List of Abbreviations
VKA – vitamin K antagonists
AH – arterial hypertension
BP – blood pressure
ASA – acetylsalicylic acid
aPTT – activated partial thromboplastin time
ICU – intensive care unit
ARB – angiotensin II receptor blockers (ATC C09CA, angiotensin II antagonists)
BoNT-A – botulinum toxin type A** (ATC M03AX01, botulinum toxin)
IV RT – intravenous thrombolytic therapy
ICA – internal carotid artery
EVT – endovascular thrombectomy (A16.23.034.013 Local endovascular transarterial thrombectomy)
VTE – venous thromboembolism
ICH – intracranial hypertension
ICP – intracranial pressure
Brain – brain
DWI – diffusion-weighted imaging
DC – decompressive craniotomy
ДС – dislocation syndrome
ЗМА – posterior cerebral artery
ЗЧЯ – posterior cranial fossa
ИАПФ – angiotensin-converting enzyme inhibitors (ATC C09AA, agents acting on the renin-angiotensin system)
IMV – invasive mechanical ventilation
IS – ischemic stroke
ИМ – myocardial infarction
BMI – body mass index
CT – computed tomography
КТА – computed tomography angiography
Лп(а) - lipoprotein (a) – macromolecular complex of low-density lipoprotein and apolipoprotein (a) protein
МК – cerebral blood flow
INR – international normalized ratio
MV – minute volume of respiration
МРА – magnetic resonance angiography
MRI – magnetic resonance imaging
НОАК – novel oral anticoagulants
НМГ – low molecular weight heparins
НФГ – unfractionated heparin
ACS – acute coronary syndrome
CVA – cerebrovascular accident
ООГ – acute occlusive hydrocephalus
ОЦАС – central retinal artery occlusion
ПВИ – perfusion-weighted imaging
ПКН – post-stroke cognitive impairment
ПИД – post-stroke dementia
ПМА – anterior cerebral artery
ПОАК – direct oral anticoagulants
ПСО – primary vascular center
РСЦ – regional vascular center
сВМК – symptomatic intracerebral hemorrhage
DM – diabetes mellitus
СИОЗС – selective serotonin reuptake inhibitors (ATC N06AB selective serotonin reuptake inhibitors)
СМА – middle cerebral artery
СМП – emergency medical service
СЧЯ – middle cranial fossa
ТА – thromboaspiration
DVT – deep vein thrombosis
TIA – transient ischemic attack
ТЛТ – thrombolytic therapy
Dura – dura mater
ТЦА – tricyclic antidepressants (ATC N06AA non-selective monoamine reuptake inhibitors)
ТЭ – thromboembolectomy
PE – pulmonary embolism
AF – atrial fibrillation
Chol – cholesterol
ЦВТ – cerebral venous thrombosis
ЦПД – cerebral perfusion pressure
ECG – electrocardiography
EEG – electroencephalography
ITT группа (intention to treat) – intention-to-treat patient population in a trial, receiving therapy as assigned (at least once)
PCSK9 – proprotein convertase subtilisin/kexin type 9 (ATC C10AX Other lipid-modifying agents)
PP группа (per protocol) – per-protocol patient population, having received therapy fully in accordance with the study protocol.
rtPA – recombinant tissue plasminogen activator, (ATC B01AD antithrombotic agents, enzymes)
Terms and Definitions
Basic therapy – a set of measures aimed at normalizing vital functions (respiration, circulation), managing cerebral edema, controlling epileptic seizures and autonomic disorders, correcting hyperglycemia and hyperthermia, and preventing thromboembolic and infectious complications.
Hemorrhagic transformation – formation of hemorrhage of varying severity within the cerebral infarction zone.
Differentiated therapy – a type of stroke treatment carried out in accordance with its pathogenetic subtype, localization, and volume of the brain lesion, which includes reperfusion (medical and/or via interventional revascularization), neuroprotection, and secondary prevention.
Evidence-based medicine – an approach to medical practice in which decisions about the use of preventive, diagnostic, and therapeutic measures are made based on available evidence of their efficacy and safety, and such evidence is searched for, compared, summarized, and widely disseminated for use in the best interests of patients.
Malignant ischemic stroke – cerebral infarction complicated by edema of the infarcted area, leading to dislocation of brain structures with a risk of brainstem compression. A malignant course is characteristic of extensive (massive) forms of ischemic stroke.
Acute occlusive hydrocephalus – acute impairment of cerebrospinal fluid outflow through the ventricular system of the brain. It occurs due to obstruction or compression of CSF pathways, leading to acute ventricular enlargement and brainstem damage.
Working group means two or more people of the same or different professions working together and harmoniously to create clinical guidelines and bearing joint responsibility for the results of this work.
Level of evidence certainty – reflects the degree of certainty that the found effect of a medical intervention is true.
Level of recommendation consensus – reflects not only the degree of confidence in the validity of the intervention effect, but also the degree of confidence that following the recommendations will do more good than harm in a given situation.
1. Brief information on the disease or condition
1.1 Definition of the disease or condition
Acute cerebrovascular accident (ACVA) – a clinical syndrome characterized by the sudden onset of focal neurological symptoms due to a suspected cerebrovascular etiology. This term is used as a preliminary diagnosis at the pre-hospital or early hospital stages prior to neuroimaging. Following neuroimaging, the terms "ischemic stroke" and "transient ischemic attack" are used [1].
Ischemic stroke (IS) – a clinical syndrome caused by focal cerebral infarction.
Cerebral infarction – necrosis of brain cells caused by ischemia.
Infarction criteria:
1. Pathological, neuroimaging, or other objective evidence of focal ischemic injury in a defined vascular territory of the brain,
or
2. Clinical evidence of focal ischemic injury in a defined vascular territory of the brain, with symptoms persisting for ≥ 24 hours or until death, and other potential causes excluded.
CNS infarction – death of cells of the brain, spinal cord, or retina caused by ischemia.
Criteria for CNS infarction:
1. Pathological, imaging, or other objective evidence of focal ischemic injury of the brain, spinal cord, or retina in a defined vascular territory;
or
2. Clinical signs of focal ischemic injury of the brain, spinal cord, or retina, based on symptoms persisting for ≥24 hours or until death, with alternative etiologies excluded [2].
Asymptomatic ("silent") cerebral infarction – neuroimaging or neuropathological evidence of cerebral infarction without a history of acute neurological deficit associated with this lesion [2].
Retinal infarction — death of retinal cells associated with ischemia.
Criteria for retinal infarction:
1) Pathological, imaging, or other objective evidence of focal ischemic injury of the retina in a defined vascular territory;
or
2) Clinical signs of focal ischemic injury of the retina based on persisting symptoms for ≥24 hours, or until exclusion of other causes, or death [3].
Retinal artery occlusion — a form of ischemic stroke characterized by impaired blood flow in the central retinal artery or its branches due to thromboembolism or vasospasm, with or without retinal ischemia. Central retinal artery occlusion (CRAO) is divided into non-arteritic CRAO and arteritic CRAO. Non-arteritic CRAO, taking into account anatomical features, is subdivided into CRAO with or without a cilioretinal artery [2-4].
Transient ischemic attack (TIA) – a transient episode of neurological dysfunction caused by focal brain ischemia without infarction.
TIA criteria:
1. A brief episode of neurological deficit caused by focal cerebral ischemia with clinical symptoms lasting ≤ 24 h
and
2. No evidence of acute cerebral infarction on neuroimaging (including diffusion-weighted MRI sequences) [5].
Retinal transient ischemic attack ("amaurosis fugax", transient monocular blindness) is transient painless monocular blindness without residual visual impairment [3].
Stroke caused by cerebral venous thrombosis is infarction and/or hemorrhage in the brain caused by thrombosis of cerebral venous structures [2].
These clinical guidelines do not cover the issues of perinatal stroke (ICD-10 class P).
1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)
1.2.1. Arterial stroke
The main mechanisms of ischemic arterial stroke include:
embolism (passage of embolic material from cardiac, aortic, or arterial sources into the cerebral arteries);
thrombosis (thrombotic obstruction of an extra- and/or intracranial artery in situ);
hypoperfusion (a decrease in systemic or regional cerebral blood flow with predominant involvement of watershed areas).
Ischemic stroke typically develops against the background of cerebral artery occlusion due to embolism or thrombosis. Embolism is the leading pathogenetic mechanism, originating from cardiac, aortic, and arterial sources, and may also be paradoxical in the presence of a patent foramen ovale or atrial septal defect (see Section 1.5) [6–9]. Arterio-arterial embolism is most commonly associated with unstable atherosclerotic plaques located in the proximal segments of the carotid or vertebral arteries (extracranial atherosclerosis). Damage to the fibrous cap of an atherosclerotic plaque usually initiates thrombus formation and distal embolism, although in some cases proximal thrombotic occlusion in situ develops [10]. Less commonly, atherosclerotic lesions involve intracerebral arteries (intracranial atherosclerosis), causing in situ thrombosis and/or embolism [11]. Cerebral microangiopathy (cerebral small vessel disease), developing against the background of hypertension and/or diabetes mellitus, leads to lipohyalinosis, arteriolosclerosis, and microatheromatosis, which occlude perforating (lenticulostriate) and penetrating arteries and arterioles, manifesting as a lacunar infarct [12]. In young patients without cardiovascular risk factors, stroke frequently develops due to dissection of the cervical or cerebral segments of major arteries [13]. Other causes of ischemic stroke include non-inflammatory, inflammatory, hereditary, and toxic arteriopathies, migraine-associated stroke, and hematological disorders [14] (see Section 1.5).
Occlusion of a cerebral artery or arteriole leads to hypoperfusion and focal cerebral ischemia. The hypoperfusion zone is heterogeneous in severity: in the center lies the infarct core (the zone of irreversibly damaged tissue, necrosis, with cerebral blood flow velocity below 10 mL per 100 g per minute), surrounded by the ischemic penumbra zone (potentially viable tissue with cerebral blood flow velocity reduced from 10 to 20 mL per 100 g per minute) and benign oligemia (recovers spontaneously, with cerebral blood flow velocity reduced from 50 to 20 mL per 100 g per minute) [15].
Cerebral ischemia represents a process of gradual transition from normal cerebral perfusion to hypoperfusion, initially manifesting as functional impairment of neuronal and glial structures (penumbra) and, with a critical decrease in blood flow, structural damage (infarction) of the brain. The rate of development of cerebral ischemia depends primarily on the duration and severity of the occlusion and the status of collateral blood flow [16]. Cerebral infarction forms within the glutamate-calcium cascade; changes in brain tissue are accompanied by severe energy depletion, loss of ion gradients, membrane depolarization, and irreversible cell damage [17, 18]. The rapid rate of brain tissue death during ischemia justifies the need for emergency reperfusion therapy, the goal of which is to restore cell function in the penumbra zone and prevent the development of cerebral infarction [19].
The development of cerebral infarction progresses through stages of cytotoxic (disruption of ion gradients with an intact blood-brain barrier), ionic (intermediate stage), and vasogenic (destruction of cellular structures, opening of the blood-brain barrier) edema within the cerebral ischemia zone [20]. Disruption of the integrity of the blood-brain barrier can cause hemorrhagic transformation of the ischemic focus [21]. When an extensive ischemic zone forms, severe edema with mass effect and intracranial hypertension may occur, leading to the development of displacement syndrome (brain herniation) and/or acute obstructive hydrocephalus [22].
1.2.2. Venous stroke
Thrombosis of cerebral veins and/or venous sinuses is a rare and often unrecognized cause of stroke [23]. Conditions associated with cerebral venous thrombosis are subdivided into predispositions (genetic prothrombotic disorders, antiphospholipid syndrome, cancer, etc.) and precipitating factors (oral contraceptives, infections, prothrombotic drugs) [24, 25]. Cerebral vein and/or sinus thrombosis obstructs blood outflow from brain tissue, leading to increased venous and capillary pressure followed by disruption of the blood-brain barrier, vasogenic edema, and plasma leakage into the interstitial space. Further increases in venous pressure can lead to hemorrhagic transformation of the infarct focus [26].
As a result of impaired venous outflow, adequate cerebrospinal fluid drainage through the arachnoid granulations becomes impossible, causing increased pressure in the subarachnoid spaces. Patients with superior sagittal sinus thrombosis and thrombosis of more than two sinuses are at risk [27].
1.3 Epidemiology of the Disease or Condition
According to The 2016 Global Burden of Disease report published in 2019, one in four people will suffer a stroke in their lifetime. An estimated 9.6 million strokes occur worldwide each year, with incidence increasing as the population ages, and 85% of cases being ischemic strokes [28].
Circulatory system diseases are the leading cause of mortality in the Russian Federation (47%). Mortality from cerebrovascular diseases in 2018 accounted for 31% of mortality from circulatory system diseases (263,600 people). Among individuals of working age, mortality from cerebrovascular diseases was 29.2 per 100,000 population [29]. Globally, stroke is the second leading cause of death (after ischemic heart disease). For example, in 2016, 5.5 million people died from stroke worldwide (2.7 million from ischemic stroke and 2.8 million from hemorrhagic stroke) [28].
Stroke is the predominant cause of disability in the Russian Federation (3.2 per 1000 population) [29]. In terms of disability-adjusted life years (DALYs) globally in 2016, stroke was the second leading cause (after oncological diseases) [28].
The incidence of stroke in the Russian Federation in 2010 was 3.27 cases per 1000 population, with a mortality rate of 0.96 per 1000 population. By 2014, stroke incidence decreased to 2.85 per 1000 population (a 30% reduction compared to 2009), and mortality was 0.4 per 1000 population [30, 31].
The incidence of recurrent stroke is 0.79 per 1000 population. The proportion of ischemic stroke among recurrent strokes is 87.5%. The prevalence rate of recurrent stroke among all strokes is 25.5%, indicating insufficient efficacy of secondary prevention [31].
In 25% of patients, ischemic stroke is cardioembolic, in 20% it is associated with large artery atherosclerosis, in 25% with small artery occlusion, in 25% a cryptogenic stroke is diagnosed, and in 5% rare causes are identified [32].
In recent decades, the incidence of ischemic stroke at a young age has increased by approximately 40%, which is not least due to improvements in diagnostic approaches [33, 34].
The incidence of cerebral venous thrombosis in high-income countries is 1.3–1.6 per 100,000 population per year [35, 36]. Cerebral venous thrombosis accounts for 0.5–1.0% of admissions to stroke centers [37].
Over recent decades, the detection rate of cerebrovascular diseases in children has increased, yet it remains 1,000 times lower than in the adult population. In a prospective study in Canada (January 1992 – December 2001) based on a registry, the incidence of ischemic stroke (IS) among children was 1.72 per 100,000 [38]. In Switzerland, based on the Swiss Neuropaediatric Stroke Registry for the period from January 2000 to December 2012, the incidence of IS and cerebral sinovenous thrombosis (CSVT) in children under 16 years of age was 2.1 per 100,000 per year [39]. According to data from the Sverdlovsk Region, the incidence of ischemic stroke in children aged 0 to 18 years for 2011–2015 was: 3.46 (2011), 4.99 (2012), 4.99 (2013), 4.62 (2014), and 5.01 (2015) per 100,000 child population per year [40].
According to the Center for the Treatment of Cerebrovascular Pathology in Children and Adolescents of the Morozov Children's City Clinical Hospital of the Moscow Healthcare Department, the incidence of cerebrovascular diseases was 6.59 cases per 100,000 child population of Moscow in 2015, 6.51 per 100,000 in 2016, 6.43 per 100,000 in 2017, 5.86 per 100,000 in 2018, and 6.69 per 100,000 in 2019 [41]. According to the Center's data, the incidence of childhood IS in Moscow in 2018–2021 was 1.6–2.5, and CSVT was 0.5–1.38 per 100,000 child population [42].
It should be noted that this figure remains closer to the lower threshold of the values reported in the literature (2–26.7 per 100,000 per year). We have observed a steady upward trend in the registration frequency and incidence of stroke in children in our region, which over the past decade has also been evident across all countries tracking pediatric acute cerebrovascular accidents. In the Russian Federation, there is still no unified pediatric stroke registry, which complicates the objective assessment of epidemiological data.
1.4 Features of Coding the Disease or Condition
Transient cerebral ischemic attacks and related syndromes (G45):
G45.0 – Vertebro-basilar artery syndrome
G45.1 – Carotid artery syndrome (hemispheric)
G45.2 – Multiple and bilateral precerebral artery syndromes
G45.3 – Amaurosis fugax
G45.4 – Transient global amnesia
G45.8 – Other transient cerebral ischemic attacks and related syndromes
G45.9 – Transient cerebral ischemic attack, unspecified
Cerebral infarction due to thrombosis of precerebral arteries (I63.0):
I63.0 – Cerebral infarction due to thrombosis of precerebral arteries
I63.1 – Cerebral infarction due to embolism of precerebral arteries
I63.2 – Cerebral infarction due to unspecified occlusion or stenosis of precerebral arteries
I63.3 – Cerebral infarction due to thrombosis of cerebral arteries.
I63.4 – Cerebral infarction due to embolism of cerebral arteries.
I63.5 – Cerebral infarction due to unspecified occlusion or stenosis of cerebral arteries.
I63.6 – Cerebral infarction due to nonpyogenic thrombosis of cerebral veins.
I63.8 – Other cerebral infarction.
I63.9 – Cerebral infarction, unspecified.
I64 – Stroke, not specified as haemorrhage or infarction
I65.0 – Occlusion and stenosis of vertebral artery.
I65.1 – Occlusion and stenosis of basilar artery.
I65.2 – Occlusion and stenosis of carotid artery.
I65.3 – Occlusion and stenosis of multiple and bilateral precerebral arteries.
I65.8 – Occlusion and stenosis of other precerebral arteries.
I65.9 – Occlusion and stenosis of unspecified precerebral artery.
I66.0 – Occlusion and stenosis of middle cerebral artery.
I66.1 – Occlusion and stenosis of anterior cerebral artery.
I66.2 - Occlusion and stenosis of posterior cerebral artery.
I66.3 - Occlusion and stenosis of cerebellar arteries.
I66.4 - Occlusion and stenosis of multiple and bilateral cerebral arteries.
I66.8 – Occlusion and stenosis of other cerebral artery.
I66.9 – Occlusion and stenosis of unspecified cerebral artery.
I67.6 – Nonpyogenic thrombosis of intracranial venous system.
1.5 Classification of the disease or condition
Classification of ischemic stroke time periods
The following periods of ischemic stroke are distinguished [43]:
hyperacute period – first 3 days;
acute period – up to 28 days;
early recovery period – up to 6 months;
late recovery period – up to 2 years;
period of residual effects – after 2 years.
Classification of SSS-TOAST pathogenetic subtypes. According to the SSS-TOAST classification, the automated version of which is called the Causative Classification System (available at https://ccs.mgh.harvard.edu/ccs_title.php), five pathogenetic subtypes of ischemic stroke are distinguished [44]:
Due to large artery atherosclerotic disease (atherothrombotic).
Due to cardiogenic embolism (cardioembolic).
Due to small vessel occlusion (lacunar).
Due to other determined cause (other determined etiology).
Due to undetermined cause (undetermined etiology).
Each of the first three subtypes is subdivided into definite, probable, and possible.
Differentiation of stroke pathogenetic subtypes based solely on clinical presentation is impossible and requires a comprehensive analysis of anamnestic, clinical, and neuro-/angiimaging data.
Atherothrombotic stroke (due to large artery atherosclerotic disease) – Ischemic stroke in the territory of a large extra- or intracranial artery with > 50% stenosis or occlusion according to neuroimaging [45].
Two methods are used to measure the degree of ICA stenosis – according to NASCET (North American Symptomatic Carotid Endarterectomy Trial) [46] and ECST (European Carotid Surgery Trial) [47]. The ECST scale uses the ratio of the preserved arterial lumen diameter to the estimated true size (measured at the level of the ICA bulb). The NASCET scale uses the ratio of the preserved arterial lumen in the bulb area to the ICA diameter above the stenosis area where the artery walls become parallel to each other. A 50% stenosis degree on the NASCET scale corresponds to 75% on the ECST scale, and 60% on the NASCET scale corresponds to 80% on the ECST scale. The NASCET technique is considered a priority [48, 49.].
In the presence of stenosis of less than 50%, the atherothrombotic genesis of stroke may be confirmed by the high emetogenic potential of the atherosclerotic plaque. The main mechanisms of stroke development include artery-to-artery embolism (passage of a thrombus or atheroma fragment), hypoperfusion, or a combination thereof. The clinical picture of atherothrombotic stroke is nonspecific and depends on the specific pathogenetic mechanism, but several clinical clues can be distinguished: TIA in the relevant arterial territory, transient ipsilateral monocular blindness, atherosclerotic lesions of other arterial territories (coronary, peripheral arteries), localization of cerebral infarction in border-zone circulation areas (especially internal ones), and the presence of old infarctions in the same vascular territory [50, 51] (Table 1).
Cardioembolic stroke – Ischemic stroke due to arterial occlusion by an embolus presumably formed in the heart [45]. In most cases, cardioembolic stroke develops against the background of atrial fibrillation, and is often characterized by acute development of neurological deficit and its maximal severity at disease onset. Involvement of proximal cerebral arteries manifests as severe neurological deficit, but distal migration of the embolus can lead to rapid symptom regression. Imaging may reveal cerebral infarctions (both acute and chronic) in multiple vascular territories [52, 53].
Table 1
Ischemic stroke due to large artery atherosclerotic disease (atherothrombotic)
Level certainty | Diagnostic criteria |
|---|---|
Definite | 1. Atherosclerotic occlusion or stenosis (≥ 50% of the arterial lumen or < 50% in the presence of signs of ulceration or plaque thrombosis) of extra- or intracranial arteries clinically involved in the pathological process, and 2. Absence of acute infarctions in the supply territories of arteries that do not show signs of atherosclerotic occlusion or stenosis |
Probable | 1. Occurrence within the past month of one or more episodes of transient monocular blindness, TIA, or stroke in the territory of the clinically involved artery showing signs of atherosclerosis, or 2. Signs of subocclusion or acute occlusion, presumably of atherosclerotic origin, in clinically involved extra- or intracranial arteries (excluding vertebral arteries), or 3. Presence of unilateral infarcts in the watershed zone or multiple infarcts of varying ages exclusively within the affected arterial territory |
Possible | 1. Atherosclerotic stenosis < 50% of the lumen of the clinically involved artery with no signs of plaque ulceration or thrombosis, and a history of two or more (and at least one within the past month) episodes of transient monocular blindness, TIA, or stroke in the territory of the clinically involved artery showing signs of atherosclerosis, or 2. Presence of large-artery atherosclerosis in the absence of a complete patient workup, making it impossible to exclude other potential mechanisms of ischemic stroke |
Table 2
Ischemic stroke due to cardiogenic embolism (cardioembolic)
Level certainty | Diagnostic criteria |
|---|---|
Definite | Presence of high-risk cardiac sources of embolism |
Probable | 1. Presence of systemic embolism, or 2. Presence of multiple acute infarcts of comparable age located in both cerebral hemispheres within carotid artery territories, or located in both carotid and vertebrobasilar territories in the absence of signs of arterial subocclusion or occlusion. Absence of other conditions that could account for multiple cerebral infarcts (vasculitis, vasculopathies, hemostatic or hemodynamic disorders) |
Possible | 1. Presence of low- or undetermined-risk cardiac sources of embolism, or 2. Presence of an established source of cardiogenic embolism in the absence of a complete patient workup, making it impossible to exclude other potential mechanisms of ischemic stroke |
Sources of high cardioembolic risk include:
Atrial fibrillation and flutter.
Left atrial or left ventricular thrombus.
Sick sinus syndrome.
Mitral stenosis or rheumatic valve disease.
Bioprosthetic and mechanical heart valves.
Recent myocardial infarction (< 1 month before stroke).
Sequelae of myocardial infarction with reduced ejection fraction (< 28%).
Dilated cardiomyopathy (previously established diagnosis or left ventricular dilation with ejection fraction < 40% or fractional shortening < 25%).
Infective endocarditis, nonbacterial thrombotic endocarditis.
Papillary fibroelastoma.
Left atrial myxoma.
Sources of low and undetermined cardioembolic risk include:
Mitral annular calcification.
Patent foramen ovale and/or atrial septal aneurysm.
Left ventricular aneurysm without thrombus.
Spontaneous echo contrast in the left atrium.
Congestive heart failure with ejection fraction < 30%.
Wall motion abnormalities (hypokinesia, akinesia, dyskinesia), apical akinesia.
Hypertrophic cardiomyopathy, left ventricular hypertrophy.
Left ventricular hypertrabeculation/noncompaction.
Atheroma in the ascending aorta or proximal arch (> 4 mm or mobile or ulcerated plaque) is identified separately as a low and undetermined risk source [53].
Lacunar stroke. The clinical presentation of lacunar stroke is nonspecific; lacunar syndromes (hemihypesthesia and hemiparesis, isolated hemihypesthesia, isolated hemiparesis, dysarthria–clumsy hand syndrome, and ataxic hemiparesis) frequently occur in patients with other pathogenetic stroke subtypes. Isolated hemihypesthesia and ataxic hemiparesis syndromes have higher specificity. An uncommon but important clinical sign of lacunar stroke is the capsular warning syndrome, which manifests as recurrent transient motor or sensory-motor lacunar symptoms involving two of the three body parts (face, arm, leg) with complete recovery between episodes. In more than one-third of patients with a lacunar syndrome, neurological deficits progress during the first days of the disease. The basis for verifying a lacunar stroke is visualization of an infarct measuring less than 20 mm in the territory of a perforating artery (deep structures of the cerebral hemispheres, pons). If an infarct smaller than 20 mm is located in the corticosubcortical zone, the lacunar stroke subtype is invalid [54–56].
In most patients, the cause of lacunar stroke is sporadic cerebral microangiopathy associated with hypertension and/or diabetes mellitus, neuroimaging markers of which include white matter hyperintensities, lacunes, enlarged perivascular spaces, and cerebral microbleeds in the deep brain structures [57, 58]. If lacunar stroke develops against the background of severe cerebral microangiopathy, the clinical picture may include vascular cognitive impairment, postural and urinary disturbances in addition to focal neurological deficits [59].
Table 3
Ischemic stroke due to small artery occlusion (lacunar)
Level certainty | Diagnostic criteria |
|---|---|
Definite | 1. Presence of an isolated and clinically significant acute infarct < 20 mm in maximum diameter, located in the projection of the basal ganglia or brainstem, in the absence of other pathological changes in the large artery from which the perforating arteries originate (atheroma, dissection, vasculitis, vasospasm, etc.) |
Probable | 1. Occurrence within the past week of recurrent stereotyped TIAs with the development of a lacunar syndrome, or 2. Presence of a typical lacunar syndrome in the clinical picture |
Possible | 1. Presence of a typical lacunar syndrome in the clinical picture in the absence of neuroimaging evidence of infarction (using sufficiently sensitive neuroimaging methods), or 2. Presence of an infarct caused by perforating artery occlusion in the absence of a complete patient workup, making it impossible to exclude other potential mechanisms of ischemic stroke |
Stroke of other determined etiology. Other causes of ischemic stroke include non-inflammatory arteriopathies (dissection; fibromuscular dysplasia, notably carotid web; reversible cerebral vasoconstriction syndrome; moyamoya disease; Fabry disease; CADASIL, etc.), inflammatory arteriopathies (primary angiitis of the central nervous system; giant cell arteritis; vasculitis associated with connective tissue diseases; infectious vasculitis due to syphilis, tuberculosis, other bacterial infections, varicella-zoster, HIV, etc.); toxic arteriopathy; migraine-associated stroke; MELAS; and hematological disorders (hereditary thrombophilias, antiphospholipid syndrome, sickle cell anemia, polycythemia vera, essential thrombocytosis, etc.) [14].
Table 4
Ischemic stroke due to other determined etiology
Level certainty | Diagnostic criteria |
|---|---|
Definite | Presence of another established cause that led to the lesion of the arteries clinically involved in the pathological process |
Probable | Development of stroke in close temporal relationship with arterial dissection or surgical interventions on the arteries and/or heart |
Possible | Presence of another established cause of stroke in the absence of a complete patient workup, making it impossible to exclude other potential mechanisms of ischemic stroke listed above |
Spontaneous dissection of the cervical and cerebral arteries is the most frequent cause of ischemic stroke in young patients [60]. Dissection is usually preceded by a mechanical trigger, and the clinical presentation includes cephalgia and/or cervicalgia on the side of the affected artery. An important clinical clue regarding internal carotid artery dissection is Horner's syndrome or peripheral hypoglossal nerve palsy [61–63].
Diagnostic criteria for dissection as a potential cause of stroke according to the ASCOD classification (A (Atherosclerosis), S (Small vessel disease), C (Cardiac pathology), O (Other cause), and D (Dissection)):
Direct signs of dissection: evidence of hematoma formation based on one of the studies — T1 FS MRI, TOF-MRA, CT (axial slices), autopsy — thickening of the arterial wall due to hematoma with luminal narrowing; or ultrasound (hypoechoic arterial wall with luminal narrowing and a sharp increase in the diameter of the carotid or vertebral (V2) artery)
Indirect signs of dissection or use of a less sensitive or less specific diagnostic test (only extended arterial stenosis distal to the carotid bifurcation or in the V2, V3, or V4 segment of the vertebral artery without signs of arterial wall hematoma on selective angiography and/or ultrasound, and/or CTA, and/or MRA) or ultrasound findings consistent with recanalization during the follow-up period [64].
Stroke of undetermined etiology
Stroke of undetermined etiology includes the following clinical situations.
Stroke of undetermined etiology. To designate cases of stroke where a full diagnostic workup could not be performed, it is advisable to use the term "stroke of undetermined etiology".
Stroke of unknown etiology (cryptogenic stroke) is a neuroimaging-confirmed stroke with an unknown source despite a thorough diagnostic workup [45].
Embolic stroke of undetermined source (ESUS) is a stroke with a non-lacunar pattern on neuroimaging, with no obvious sources of embolism after diagnostic workup and exclusion of known causes of stroke, particularly cardioembolic sources and atherosclerosis proximal to the stroke zone [45].
The diagnosis of embolic stroke of undetermined source is established based on the following criteria:
Presence of a non-lacunar ischemic lesion on CT or MRI.
Absence of extra- or intracranial stroke-related cerebral artery stenosis (with lumen narrowing ≥ 50%).
Absence of high-risk cardiac sources.
Absence of other causes of stroke: arteritis, dissection, migraine/vasospasm, drug abuse.
Potential causes of ESUS include paroxysmal atrial fibrillation, atrial cardiomyopathy (unrelated to atrial fibrillation), embolic atherosclerotic plaques with arterial lumen narrowing of less than 50%, aortic arch atheroma, and patent foramen ovale.
Two or more causes. It is common to encounter a situation where a patient has two or more potential causes of stroke, such as atrial fibrillation and ipsilateral internal carotid artery stenosis greater than 50%. It may also happen that there are causes, the severity of each of which is insufficient to explain the stroke, such as ipsilateral internal carotid artery stenosis of 30% to 50% and left ventricular apical akinesia. In such situations, it is advisable to use the ASCOD phenotypic classification [64].
The pediatric patient group is heterogeneous, and the concept of pediatric stroke applies to children from 28 days to 17 years and 11 months of age [65.]. The timeframes for AIS in children correspond to those in the adult population.
Strokes in childhood differ significantly in their etiological factors compared to older patients. According to early studies, it is impossible to classify the etiology of pediatric stroke using adult population criteria due to the mismatch with the criteria for atherosclerotic, cardioembolic, and small vessel occlusion-induced AIS [66]. The International Pediatric Stroke Study (IPSS) classification, 2007 (the Pediatric Stroke Classification) and Dr. G. Sebire's classification of arteriopathies (the Sebire Criteria), 2004 [67] have not become widespread.
In 2012, the International Pediatric Stroke Organization (IPSO) expert consensus developed the criteria for the Childhood AIS Standardized Classification and Diagnostic Evaluation (CASCADE, Table 4a) [68].
Table 4a. Childhood AIS Standardized Classification and Diagnostic Evaluation.
Type | Subtype | Diagnostic criteria |
|---|---|---|
Stroke due to small cerebral vessel arteriopathy | A | Confirmed - multifocal small artery stenosis on angiogram - confirmation of small vessel arteriopathy on biopsy |
B | Radiologically confirmed - multifocal small vessel arterial narrowing on contrast-enhanced angiogram. | |
C | Biopsy-confirmed | |
D | Probable: - location of ischemia lesion(s) corresponds to the territory of small arteries, - data from non-contrast (non-invasive) neuroimaging and/or - presence of a concomitant pathological process associated with small vessel arteriopathy (e.g., meningitis or systemic lupus erythematosus) | |
Stroke due to unilateral focal childhood cerebral arteriopathy | A | Carotid territory with collaterals (includes moyamoya angiopathy and primary CNS angiitis) - unilateral stenosis or irregularity of a large artery (MCA, ICA, ACA*) supplying the infarction zone - excessive collateral network of small vessels distal to the stenosis site. |
B | Carotid territory without collaterals (includes transient cerebral arteriopathy, post-varicella arteriopathy, and large-vessel primary CNS angiitis): - unilateral stenosis or irregularity of a large artery (MCA, ICA, ACA) supplying the infarction zone - absence of a collateral network of small vessels distal to the stenosis site | |
C | Vertebrobasilar territory: - unilateral stenosis or irregularity of a major intracranial artery (PCA, basilar) supplying the infarction zone and not meeting dissection criteria. | |
D | Other | |
Stroke due to bilateral childhood cerebral arteriopathy | A | With collaterals (moyamoya disease or syndrome): - bilateral stenosis or irregularity of a large artery (MCA, ICA, ACA) supplying the infarction zone - excessive collateral network of small vessels distal to the stenosis site |
B | Without collaterals (includes moyamoya angiopathy, CNS angiitis): - bilateral stenosis or irregularity of a large artery (MCA, ICA, ACA) supplying the infarction zone - absence of a collateral network of small vessels distal to the stenosis site | |
C | other | |
Cervical vessel arteriopathy | A | Dissection: - angiographic findings of a double lumen, floating intimal flap, or pseudoaneurysm, presence of high-intensity signal from the arterial wall on fat-suppressed MRI; - history of neck or head trauma, neck pain or headache less than 6 weeks prior to detection of cervical artery stenosis (occlusion); - stenosis (or occlusion) of the vertebral artery at the level of the C2 vertebra, even without a known history of trauma. |
C | Takayasu arteritis - Stenosis (occlusion) of the aorta and/or its branches PLUS at least one of the following criteria: Decreased peripheral pulses and/or intermittent claudication Blood pressure difference between limbs of more than 10 mmHg Auscultatory bruits over the aorta or its main branches Arterial hypertension | |
C | Other | |
Cardioembolic stroke | A | Confirmed - presence of a concurrent condition with a high risk of embolism (e.g., congenital heart disease with hemodynamic abnormalities, arrhythmia, or endocarditis) or cardiac surgery within a month prior to stroke onset - ischemia zone corresponds to a large/medium cerebral artery or 2 or more vascular territories |
C | probable: - ischemia zone corresponds to 2 or more vascular territories in a child without another identifiable etiology And one of the following criteria: Patent foramen ovale with right-to-left shunt or other minor cardiac anomaly Abrupt occlusion without signs of preceding stenosis and not meeting the criteria for arteriopathy | |
Other | - Etiology remains undetermined despite comprehensive evaluation - Other disease not meeting other criteria | |
Stroke from multiple sources | - The disease meets the criteria of multiple types in this classification; it is impossible to determine the dominating significance of any single type. |
Notes: *ACA – anterior cerebral artery, ICA – internal carotid artery, MCA – middle cerebral artery.
The CASCADE classification is based on an anatomical principle aimed at identifying the primary source of arterial thrombosis/embolism in the brain (small cerebral arteries, large cerebral arteries, aorta and neck arteries, heart), which dictates specific diagnostic interventions [69-72].
The CASCADE classification distinguishes the following sections:
I. Classification of acute AIS in children (period up to 1 month from symptom onset).
Stroke due to small vessel cerebral arteriopathy (SCA)
Stroke due to childhood unilateral focal cerebral arteriopathy (UFCA)
Stroke due to childhood bilateral cerebral arteriopathy (BCA)
Stroke due to aortocervical arteriopathy (ACA)
Cardioembolic stroke
Stroke due to other determined or undetermined etiology
Multifactorial stroke
II. Evolution of cerebral arteriopathy – classification of chronic AIS in children (period > 1 month from disease debut).
Progressive arteriopathy
Stable arteriopathy
Reversible arteriopathy
Indeterminate arteriopathy
Classification of venous ischemic stroke (cerebral venous thrombosis) in children according to localization [73]:
Superficial cerebral venous thrombosis
Deep cerebral venous thrombosis
Cerebral sinus thrombosis
Jugular vein thrombosis
1.6 Clinical presentation of the disease or condition
Ischemic stroke or TIA develops as a result of a sudden decrease in perfusion of a specific brain region, leading to a loss of the corresponding neurological function. Thus, the main feature of the clinical picture of stroke and TIA is the sudden onset of focal (and in some cases generalized) neurological symptoms. Symptoms can be transient (lasting from a few seconds to several hours) or persist for a prolonged period. The clinical picture does not allow for a reliable determination of the stroke type (ischemic or hemorrhagic); therefore, performing brain CT or MRI is mandatory for all patients with suspected stroke. Nevertheless, clinical symptoms can serve as the basis for a topical diagnosis when the infarct lesion is not visualized (e.g., in the early stages; when brain MRI is not feasible).
Table 5
Characteristic focal symptoms in lesions of the carotid and vertebrobasilar territories [74]
Artery | Possible symptoms |
|---|---|
Anterior cerebral artery | Contralateral hemiparesis and/or hemihypesthesia with predominance in the leg (compared to the arm and face). Acute cognitive impairment, abulia, gait apraxia |
Middle cerebral artery | Contralateral hemiparesis and/or hemihypesthesia and/or hemianopsia; Gaze palsy. Acute cognitive impairment. Dominant hemisphere: motor and/or sensory aphasia, agraphia, alexia, apraxia. Nondominant hemisphere: neglect (including anosognosia) |
Anterior choroidal artery | Hemiparesis (often plegia in the arm), hemihypesthesia (often superficial sensory loss with spared deep sensation), hemianopsia (often sectorial), facial asymmetry, and dysarthria |
Ophthalmic artery | Acute painless monocular vision loss |
Posterior cerebral artery | Homonymous hemianopsia, alexia without agraphia (occipital lobe lesion), hemihypesthesia, dystonia/choreoathetosis, hyperpathy, acute cognitive impairment (thalamic involvement), hemiparesis, oculomotor nerve palsy, vertical gaze palsy (midbrain involvement) |
Basilar artery | Depression of consciousness. Tetraparesis (bilateral motor symptoms). Internuclear ophthalmoplegia, one-and-a-half syndrome, unilateral or bilateral horizontal gaze palsy, pinpont pupils. Trigeminal and facial nerve involvement. Acute vestibular syndrome. Cortical blindness (distal basilar artery occlusion) |
Vertebral artery artery | Medial medullary syndrome (ipsilateral tongue paresis, contralateral hemiparesis, and loss of deep sensation); Lateral medullary syndrome (Wallenberg-Zakharchenko): dizziness, ataxia, Horner's syndrome, dysarthria, dysphagia, dysphonia, hiccups, ipsilateral facial hypesthesia and/or contralateral hemihypesthesia |
Cerebellar arteries | Cerebellar ataxia (truncal and/or appendicular). Acute vestibular syndrome. Unilateral hearing loss (anterior inferior cerebellar artery occlusion) |
Perforating arteries | Lacunar syndromes: pure motor stroke, pure sensory stroke, sensori-motor stroke, dysarthria-clumsy hand syndrome, ataxic hemiparesis |
Generalized symptoms include: headache, nausea/vomiting, altered level of consciousness (drowsiness, stupor, coma), and altered mental status.
Other important clinical and anamnestic data that should be actively elicited in stroke patients are presented in Table 6. These data may play an important role in decision-making regarding the scope of initial imaging and/or reperfusion therapy.
Table 6
Important clinical and anamnestic data in patients with suspected stroke
Sign | Interpretation | |
|---|---|---|
Dizziness, nystagmus | Suspicion of vertebrobasilar stroke | |
Headache | More common in vertebrobasilar stroke. May indicate dissection, cerebral venous thrombosis, less commonly vasculitis, reversible cerebral vasoconstriction syndrome, migrainous stroke, stroke mimics (migraine with aura, HaNDL – syndrome of transient headache with neurological deficits and cerebrospinal fluid lymphocytosis) | |
Neck pain | May indicate dissection | |
Unilateral hearing loss | May indicate stroke in the anterior inferior cerebellar artery territory | |
Horner's syndrome | May indicate internal carotid artery dissection (or lateral medullary syndrome) | |
Peripheral tongue paresis | May indicate internal carotid artery dissection (or medial medullary syndrome) | |
Epileptic seizure at onset | Embolic mechanism, cerebral venous thrombosis, stroke mimic (post-ictal neurological deficit) | |
Maximum severity of neurological deficit at onset followed by regression | Embolic mechanism | |
Stepwise or fluctuating course | Small or large artery pathology (lacunar or atherothrombotic stroke) | |
Stereotyped TIAs | Perforator occlusion (including "internal capsule warning syndrome"), severe extra- and intracranial atherosclerosis (hypoperfusion TIAs) | |
Presence of mechanical (potentially traumatic) factors: sports, gymnastics, fitness, heavy lifting, abrupt cervical spine movement or forced head position, massage, or manual therapy | May indicate dissection in young patients | |
Prior immobilization (recent prolonged travel, flight, illness, surgery); DVT and PE; dehydration; symptom onset upon awakening or during situations associated with the Valsalva maneuver (heavy lifting, straining, sexual intercourse, coughing, sneezing, and others) | May indicate paradoxical embolism in young patients | |
Thromboses (arterial, venous, or microvascular), pregnancy-related pathology (miscarriages, late intrauterine fetal death, and severe preeclampsia) | May indicate antiphospholipid syndrome | |
Hyperthermia | May indicate infective endocarditis | |
Vision loss in one eye | History of vision loss in one eye, including transient monocular blindness (amaurosis fugax) | Internal carotid artery stenosis |
Vision loss in one eye and contralateral hemiparesis | Acute internal carotid artery occlusion or combined embolism in the central retinal artery and middle cerebral artery | |
Vision loss in one eye, ipsilateral temporal pain, tenderness of the temporal artery upon palpation | May indicate giant cell arteritis | |
The acute period of stroke in children differs significantly from stroke in adults. Up to 35-40% of children present with low-grade fever of "unknown" etiology prior to acute cerebrovascular events. General cerebral symptoms may predominate over focal symptoms in the clinical picture, partly due to the child's inability to describe subjective symptoms (visual impairment, weakness or clumsiness in a limb, sensory disturbances, severe headache). Very young patients may not demonstrate focal symptoms during the hyperacute phase of AIS. The most frequent symptom is focal epileptic seizures involving a single limb [65].
Table 7. Frequency of clinical symptoms in the hyperacute period of arterial ischemic stroke in 162 children aged 0-18 years [40].
One of the main challenges in the pre-hospital diagnosis of stroke in children is the difficulty of differential diagnosis with stroke "mimics", which may account for 50 to 93% of all cases in children and adolescents with initial suspected AIS, whereas in the adult population "stroke mimics" occur in only a third of patients with sudden onset of focal neurological deficit.
Several researchers have attempted to analyze the most frequent "stroke mimics" encountered in pediatric stroke (Table 8).
Table 8. Frequency of stroke and "stroke mimics" in the pediatric age group [75]
Diagnosis | Mackay&Yock-Corrales, 2016 (n=102; 280) |
|---|---|
Stroke | |
Ischemic stroke | 53,9% |
Hemorrhagic stroke | 36,3% |
Transient ischemic attack | 9,8% |
Stroke mimics | |
Migraine | 30% |
Epilepsy | 16,4% |
Bell's palsy | 10,4% |
Conversion disorder | 6,4% |
Syncope | 5% |
Cerebral venous thrombosis. Cerebral venous thrombosis should be considered as a potential cause of AIS when presented with atypical clinical and neuroimaging findings, especially in young patients [76]. Acute symptom onset occurs in half of the patients, and subacute onset in a third of patients. Headache is the most frequent symptom of CVT and may be the sole manifestation of the disease. Headache characteristics are nonspecific, but it is most often progressive (over hours or days), and much less frequently thunderclap, as in subarachnoid hemorrhage. Suspicion for CVT should be raised by the following headache features: new-onset cephalgia, unilaterality, exacerbation in the supine position, with physical exertion, coughing, straining, progression, and refractoriness to non-opioid analgesics and non-steroidal anti-inflammatory drugs [77]. The second most frequent sign of CVT is the development of focal neurological symptoms, most commonly as a motor deficit. Symptoms suspicious for cerebral venous thrombosis also include isolated vomiting, seizures, behavioral changes, confusion/amnesia, visual disturbances, fever, nuchal rigidity, and papilledema [78].
The localization of thrombosis, along with individual features of pathological and compensatory mechanisms, accounts for the significant variability of clinical manifestations, which can be attributed to one of three syndromes: isolated intracranial hypertension syndrome, focal brain lesion syndrome, and encephalopathy syndrome [79, 80].
In children, symptoms of venous stroke and CVT can be subtle and nonspecific, complicating timely diagnosis and treatment [81]. Unlike AIS, symptoms may develop subacutely. Pediatric patients typically exhibit signs of intracranial hypertension (headache, nausea and vomiting, lethargy, sixth nerve palsy, diplopia) or focal symptoms associated with infarction and hemorrhage [82]. Cavernous sinus thrombosis has a more specific presentation with unilateral ptosis and cranial nerve palsies (III-VI) located directly within the cavernous sinus. Isolated cortical vein thrombosis is rare (6% of all CVT cases). Clinically, it may manifest as partial seizures followed by the development of hemiparesis, aphasia, hemianopia, or other focal neurological dysfunction (depending on the thrombosis localization) even in the absence of signs of increased intracranial pressure [72]. CVT in children may also be clinically asymptomatic and diagnosed via neuroimaging following head trauma or surgery [83].
2. Diagnostics, medical indications and contraindications for diagnostic methods
Criteria for establishing the diagnosis of ischemic stroke and transient ischemic attack. The clinical picture forms the basis for the diagnosis of ischemic stroke and transient ischemic attack. The syndromes specified in section 1.6 serve as the clinical criteria for establishing these diagnoses.
Diagnostic criteria for ischemic stroke:
1. Pathological, neuroimaging, or other objective evidence of focal ischemic injury in a defined vascular territory of the brain,
or
2. Clinical evidence of focal ischemic injury in a defined vascular territory of the brain, with symptoms persisting for ≥ 24 hours or until death, and other potential causes excluded.
Diagnostic criteria for TIA:
1. A brief episode of neurological deficit caused by focal cerebral ischemia with clinical symptoms lasting ≤ 24 h
and
2. Absence of acute cerebral infarction signs on neuroimaging data (including MRI diffusion-weighted imaging sequences).
2.1 Complaints and Anamnesis
It is recommended that all patients with suspected stroke or TIA undergo evaluation to detect findings indicating the presence or absence of focal (motor, sensory, coordination, cognitive, speech, and cranial nerves) and general cerebral (altered consciousness, headache, nausea, etc.) symptoms of brain damage for the purpose of timely diagnosis [84, 99].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: in pediatric patients, complaints and medical history are gathered and/or clarified from legal representatives and witnesses of the disease onset, including potential data collection via phone conversation. In pediatric patients, the presence of first-degree relatives with an onset of thrombosis of any localization at an atypical (young and pediatric) age is ascertained. To assess neurological deficit, the National Institutes of Health Stroke Scale (NIHSS, Appendix G1, PedNIHSS for the pediatric population, Appendix G2) is used; to assess the level of consciousness, the Glasgow Coma Scale (Appendix G9) and the FOUR score (Appendix G8) are used, while for the pediatric group, the use of the adapted Glasgow Coma Scale (Appendix G10) and the FOUR score is recommended.
It is recommended that all patients with suspected CVT undergo assessment of vital functions (airway patency, respiratory and circulatory functions) and neurological status (general cerebral symptoms with determination of the level of consciousness, meningeal signs, focal neurological deficit) in order to determine management and diagnostic tactics [23, 85-88].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: To assess neurological deficit, the National Institutes of Health Stroke Scale (NIHSS, Appendix G1, PedNIHSS for pediatric patients, Appendix G2) is used; to assess the level of consciousness, the Glasgow Coma Scale (Appendix G9) and the FOUR score (Appendix G8) are used; for the pediatric group, the use of the adapted Glasgow Coma Scale (Appendix G10) and the FOUR score is recommended.
It is recommended that the exact time of symptom onset be established in all patients with suspected stroke or TIA in order to determine management tactics; if it is unknown, it is necessary to clarify the time when the patient was last seen without these symptoms (time of last known well) [89].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in every third stroke patient, the exact time of symptom onset is unknown. This is most often due to stroke occurring during night sleep ("wake-up stroke"), as well as the patient's inability to provide medical history data due to speech disorders, altered consciousness, neglect, or lack of insight into their condition [90–92]. In such cases, for patients of all age groups, it is necessary to ascertain the time of disease onset and medical history from the patient's relatives or other informants (including via telephone conversation) to increase the likelihood of using reperfusion therapy methods.
It is recommended to obtain data on the presence or absence of acute or chronic diseases/conditions in the history and current medications in all patients with suspected stroke or TIA in order to determine management tactics [84, 89].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in stroke patients, it is necessary to identify the presence of risk factors in their history. According to large-scale studies (Framingham Heart Study, 3C-study, REGARDS, INTERSTROKE, South London Stroke Register, Asian Stroke Registry), these include: arterial hypertension, diabetes mellitus, heart diseases (atrial fibrillation, coronary artery disease), peripheral artery disease, dyslipidemia, obesity, a history of stroke, lifestyle factors (low physical activity, non-compliance with diet, active tobacco smoking and alcohol abuse), psychosocial stress, and depression [91–95]. The process of identifying risk factors should not delay the initiation of reperfusion therapy. When determining indications for thrombolytic therapy (TLT), it is necessary to identify a history of diseases/conditions that are contraindications to systemic thrombolysis, as well as the use of anticoagulant therapy with clarification of the time of the last dose. Identifying a history of migraine, epilepsy, alcohol abuse, head trauma, and somatic pathology (including oncological) can be important information in the differential diagnosis of stroke and its mimics.
It is recommended during the physical examination of a patient with suspected cerebral venous thrombosis (CVT) to focus on looking for signs of head and neck infection (otitis, mastoiditis, sinusitis, rhinitis, facial and cranial lesions) to determine the cause of the disease [23, 85-88].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: otitis, mastoiditis, sinusitis, rhinitis, facial and cranial lesions can cause secondary septic CVT, particularly cavernous sinus thrombosis. Attention should be paid to the presence of sore throat, neck swelling, anterior cervical lymphadenopathy, toothache or earache, as well as dyspnea, hemoptysis, chest pain, and trismus (Lemierre's syndrome) (spread of thrombosis to the internal jugular vein).
2.2 Physical Examination
It is recommended that all patients with a suspected acute cerebrovascular accident undergo an evaluation (examination, consultation) by a neurologist (B01.023.001) no later than 10 minutes from admission to the inpatient facility in order to reduce the time to initiation of reperfusion and basic therapy [41, 96, 97, 1121].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: stroke patients need a reduction in the time from stroke onset to the application of reperfusion methods to increase the likelihood of a favorable outcome. Thus, when TLT is performed within 90 minutes after symptom onset, the NNT (number needed to treat to achieve one favorable outcome) is 4.5, increasing to 9 when TLT is performed 91–180 minutes later, which dictates the need for rapid medical care [98].
It is recommended that all patients with ischemic stroke or TIA undergo an assessment of vital functions (patency of the upper airway, respiratory and circulatory functions) and neurological status (general cerebral symptoms with determination of the level of consciousness, meningeal signs, focal neurological deficit) in order to determine therapeutic and diagnostic tactics [41, 84, 1121].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: to assess neurological deficit, the National Institutes of Health Stroke Scale (NIHSS, see Appendix G1) is used; for the pediatric age group, an adapted scale (pedNIHSS, Appendix G2) is used [99]. The scales help objectify the patients' condition, have prognostic value, and are important tools for making clinical decisions regarding the scope of basic therapy, determining indications for reperfusion treatment methods, and monitoring the patient's condition (including detecting deterioration in malignant infarction, hemorrhagic transformation) [100–102].
It is recommended that all patients with ischemic stroke or TIA use the Glasgow Coma Scale and/or FOUR score (Full Outline of UnResponsiveness, see Appendices G8–G10) to assess the level of arousal (before the administration of sedatives) and signs of progressive brain herniation [103, 104].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended that all patients with ischemic stroke or TIA undergo an evaluation of swallowing function to identify early signs of dysphagia. The initial swallowing screening should be performed before meals or oral medications within the first 3 hours of the patient's admission to the ICU or intensive care unit to reduce the risk of aspiration [84, 1122].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: dysphagia is a frequent manifestation of acute stroke, which is a risk factor for aspiration pneumonia and is associated with higher mortality [105, 106]. Dysphagia screening helps reduce the risk of pneumonia (1.9% vs. 13.1%), while non-instrumental methods (swallowing screening tests) have high sensitivity (64–79%) and specificity (61–81%) for detecting swallowing disorders [107, 108]. Detailed information on dysphagia is presented in the Russian clinical guidelines "Diagnosis and Treatment of Dysphagia in Central Nervous System Diseases" [109]. The initial assessment of swallowing function is preferably performed using a swallowing screening test. The dysphagia test ("three-swallow test" using a pulse oximeter) should be performed within the first 24 hours of the patient's stay in the department. If swallowing function testing is impossible or dysphagia is detected, placement of a nasogastric tube for nutritional support is indicated.
It is recommended that all patients with ischemic stroke undergo regular standard assessments of activities of daily living, self-care, functional mobility, and communication abilities in order to plan and evaluate the effectiveness of rehabilitation measures [110, 1123].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended that adult patients with ischemic stroke undergo cognitive function testing using the Montreal Cognitive Assessment (Appendix G20) with assessment of unilateral neglect syndrome in order to timely recognize them and formulate an individual rehabilitation treatment plan [111].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
2.3 Laboratory Diagnostics
It is recommended that all patients with suspected acute cerebrovascular accident undergo blood glucose testing, which is performed at the prehospital stage (optimally) and/or upon admission to the hospital to detect hypo- or hyperglycemia, in order to determine diagnostic and therapeutic tactics [84, 523].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: assessing glycemia levels in patients with suspected acute cerebrovascular accident allows for the exclusion of hypo- or hyperglycemia as a stroke mimic ("masquerade"). If there are indications for TLT, blood glucose determination is the only laboratory parameter required before thrombolysis [84]. Hyperglycemia is associated with the risk of hemorrhagic transformation and worse clinical outcomes [115, 116].
It is recommended that adult patients with ischemic stroke and indications for intravenous thrombolysis undergo an INR test when taking warfarin** (B01AA03) or a thrombin time test when taking dabigatran etexilate** (B01AE07) to determine the feasibility of using this treatment method [84, 117].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: if coagulopathy is not suspected, routine hemostasis tests (INR, aPTT, platelets) prior to thrombolytic therapy (TLT) are impractical [84] "Unexpected" coagulopathy, which is a potential contraindication to TLT, occurs in only 0.4% of cases; therefore, thrombolysis should not be delayed while awaiting laboratory test results [118]. If the patient is taking warfarin** (B01AA03), assessing the INR level helps determine the feasibility of TLT; if taking dabigatran etexilate** (B01AE07), blood thrombin time must be evaluated. For patients taking apixaban** (B01AF02) or rivaroxaban** (B01AF01), determining anti-Xa activity is advisable [117]. If reliable information is available that the patient has not taken NOACs within the past 48 hours, combined with normal renal filtration function, TLT may be performed.
It is recommended that all patients with ischemic stroke, TIA, or cerebral venous thrombosis undergo mandatory laboratory testing (Table 9) to determine diagnostic and therapeutic management [84–88, 523].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Table 9
Mandatory laboratory tests in all patients with ischemic stroke or TIA
Tests whose results must be provided from the time of admission | Characteristic |
|---|---|
Within 3 hours | Complete blood count (CBC) with differential and ESR |
General clinical blood chemistry panel (ALT, AST, bilirubin, creatinine, urea, total protein, potassium, sodium). Coagulogram (preliminary assessment of the hemostatic system) (aPTT, INR, fibrinogen) | |
Urinalysis | |
Within 48 h | Biochemical blood test for lipid metabolism disorders (B03.016.005) (triglycerides, total cholesterol, low-density lipoproteins, high-density lipoproteins) |
Comment: determination of laboratory parameters presented in Table 9 is necessary to monitor the patient's condition, timely detect complications, and determine stroke risk factors. Depending on the clinical situation (rare causes of stroke, comorbidities, stroke mimics), various laboratory tests may be indicated. Tests for genetic thrombophilia and rare causes of stroke not performed in the inpatient setting should be included in the discharge summary recommendations for outpatient follow-up.
It is recommended that children with a confirmed diagnosis of stroke or TIA of undetermined origin, a history of thrombosis of any localization, or a first-degree relative with proven thrombophilia undergo additional examination to screen for thrombophilia, systemic infections, vasculitis, autoimmune diseases, and genetic causes of stroke [119-121].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: thrombophilia screening should include the evaluation of the following parameters: antithrombin III (A09.05.047 Determination of antithrombin III activity in blood), protein C (A09.05.125 Assay of protein C level in blood) and S (A09.05.126 Determination of protein S activity in blood ), factor V Leiden mutation (A27.05.018 Molecular genetic testing for G1691A mutation in factor V gene (Leiden mutation in coagulation factor V)), prothrombin G20210A gene mutation (A27.05.002 Determination of prothrombin G20210A polymorphism in blood coagulation factor II gene) and MTHFR (A27.05.003 Determination of C677T polymorphism of methylenetetrahydrofolate reductase), homocysteine (A09.05.214 Assay of homocysteine level in blood), APS screening (anticardiolipin antibodies (A12.06.029 Determination of anticardiolipin antibodies in blood), anti-beta-2-glycoprotein antibodies (A12.06.051 Determination of anti-beta-2-glycoprotein antibodies in blood), lupus anticoagulant). Thrombophilias resulting from hereditary or acquired conditions are directly associated with the onset of stroke in childhood [122-123]. They are believed to act as a trigger in the presence of other etiological factors (e.g., heart disease). The association with recurrent stroke in children was demonstrated in a single-center longitudinal study in protein C and lipoprotein (a) deficiency [124].
Genetic testing may include screening for the following conditions: CADASIL, CARASIL, retinal vasculopathy with cerebral leukodystrophy, FOXC1, COL4A1, COL4A2, Fabry disease, pseudoxanthoma elasticum, type 1 neurofibromatosis, genetic forms of hyperhomocysteinemia, Ehlers-Danlos syndrome type IV, fibromuscular dysplasia, arterial tortuosity syndrome, Marfan syndrome, moyamoya disease, sickle cell anemia, hereditary hemorrhagic telangiectasia, and MELAS. Screening for autoimmune diseases includes the determination of antinuclear antibodies (ANA) and antineutrophil cytoplasmic antibodies (ANCA) in blood serum. These tests can be performed in an outpatient setting.
It is recommended to perform thrombophilia screening in selected adult patients with unprovoked cerebral venous thrombosis (CVT) in order to select appropriate secondary prevention and reduce the risk of recurrent thrombotic events [85-88].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: Thrombophilia screening may be recommended in the following clinical situations: unprovoked cerebral venous thrombosis (without risk factors), recurrent cerebral venous thrombosis, a history of deep vein thrombosis and pulmonary embolism, and a family history burdened by venous thrombosis. Thrombophilia screening should include the evaluation of the following parameters: antithrombin III (A09.05.047 Determination of antithrombin III activity in blood), protein C (A09.05.125 Assay of protein C level in blood) and S (A09.05.126 Determination of protein S activity in blood), factor V Leiden mutation (A27.05.018 Molecular genetic testing for G1691A mutation in factor V gene (Leiden mutation in coagulation factor V), prothrombin G20210A gene mutation (A27.05.002 Determination of prothrombin G20210A polymorphism in blood coagulation factor II gene) and MTHFR (A27.05.003 Determination of C677T polymorphism of methylenetetrahydrofolate reductase), homocysteine (A09.05.214 Assay of homocysteine level in blood), APS screening (anticardiolipin antibodies (A12.06.029 Determination of anticardiolipin antibodies in blood), anti-beta-2-glycoprotein antibodies (A12.06.051 Determination of anti-beta-2-glycoprotein antibodies in blood), lupus anticoagulant). It is preferable to perform tests for protein C, protein S, and antithrombin at least two weeks after discontinuation of oral anticoagulants, since their levels may decrease temporarily during acute cerebral venous thrombosis, and the use of warfarin** can lead to a decrease in protein C and S levels as well as an increase in antithrombin levels.
2.4 Instrumental Diagnostics
2.4.1. Neuroimaging of the brain and head and neck vessels
It is recommended that adult patients with signs of acute cerebrovascular accident (ACVA) undergo emergency non-contrast brain CT (A06.23.004) or brain MRI (A05.23.009) with results (report) provided within 40 minutes of patient admission to the hospital for differential diagnosis of ACVA in order to determine treatment tactics [125–131, 1121-1123].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: Reducing the time interval from hospital admission to the initiation of brain neuroimaging helps shorten the time to treatment initiation and, consequently, results in a better clinical outcome. Non-contrast CT or MRI is a reliable and rapid method to rule out acute intracranial hemorrhage as an absolute contraindication to subsequent thrombolytic therapy and/or thrombectomy in the first hours of stroke. Early CT signs of cerebral ischemia include: loss of gray-white matter differentiation, effacement of sulci along the convexity, loss of the ribbon-like structure of the insular gyri, and decreased attenuation of the basal ganglia. Hypodense changes (decreased X-ray attenuation of the brain tissue) are detected by the end of the first day from the onset of ischemic stroke [126]. In most cases, non-contrast CT provides the necessary information to decide on the management strategy in the hyperacute period. The use of diffusion-weighted imaging (DWI) during MRI makes it possible to diagnose pathological changes within the first minutes and hours of ischemic stroke onset. Compared to conventional T2- and T1-weighted images (T2-WI and T1-WI), DWI is more sensitive to early brain tissue changes in stroke. DWI has a sensitivity of 94% and a specificity of 100% in the first six hours of ischemic stroke. The use of susceptibility-weighted imaging (SWI, SWAN, FSBB, SWIp, BSI) in the MRI protocol allows differentiation of the intracerebral hemorrhage lesion from the brain tissue at any stage of hemorrhage [126].
It is recommended to perform computed tomography angiography (A06.12.056 Computed tomography angiography of cerebral vessels) or magnetic resonance angiography of intracranial vessels (A05.23.009.008) starting from the aortic arch level in adult patients with ischemic stroke admitted within 6 hours of disease onset with a neurological deficit severity of ≥ 6 points on the NIHSS, an evaluation of early brain tissue changes by ASPECTS ≥ 6 points (Appendix G12), and a pre-stroke disability level of 0–2 points on the modified Rankin scale regardless of the cause of disability, in order to determine occlusive lesions of extracranial and/or intracranial arteries [132–151, 1124-1126].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: the use of computed tomography angiography and contrast-enhanced magnetic resonance angiography allows for the detection of occlusions and stenoses of pre- and cerebral vessels, as well as the evaluation of structural variants of the Circle of Willis and other vascular structures. Angiography makes it possible to determine the location and cause of occlusion and to identify patients at high risk of recurrent stroke. Knowledge of vascular anatomy and information regarding the presence of extracranial dissections, stenoses, and vascular occlusions can assist in planning endovascular interventions or in identifying patients for whom this type of therapy is unsuitable due to vessel tortuosity or the inability to access intracranial vessels [125, 126].
It is recommended to perform a duplex ultrasound scan of the carotid arteries (A04.12.005.003 Duplex scanning of brachiocephalic arteries with color Doppler blood flow mapping, A04.12.005.005 Duplex scanning of extracranial segments of brachiocephalic arteries, A04.12.005.006 Duplex scanning of intracranial segments of brachiocephalic arteries) within 24 hours of hospitalization in adult patients with ischemic stroke in the carotid territory with a modified Rankin scale score of 0–2 who are candidates for carotid endarterectomy or stenting, in order to determine treatment tactics [153–162, 1127].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended to perform blood flow assessment in the neck and head vessels using imaging and/or ultrasound diagnostic methods (A06.12.056 Computed tomography angiography of cerebral vessels, A05.23.009.008 Magnetic resonance angiography of intracranial vessels, A06.12.058.001 Computed tomography angiography of the intracranial segment of brachiocephalic arteries of the Circle of Willis, A04.12.005.003 Duplex scanning of brachiocephalic arteries with color Doppler blood flow mapping, A04.12.005.005 Duplex scanning of extracranial segments of brachiocephalic arteries, A04.12.005.006 Duplex scanning of intracranial segments of brachiocephalic arteries) in adult patients with transient ischemic attack (TIA) to identify stenotic or occlusive lesions [168, 169].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
It is recommended to use the ASPECTS scale (Appendix G12) during brain CT scans in adult patients with ischemic stroke to determine the extent of the lesion [170, 171, 1128-1130].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is not recommended to wait for the results of serum creatinine concentration assessment in adult patients with ischemic stroke prior to performing CT angiography (A06.12.058 Computed tomography angiography of brachiocephalic arteries, A06.12.058.001 Computed tomography angiography of the intracranial segment of brachiocephalic arteries of the Circle of Willis) or MR angiography (A05.23.009.008 Magnetic resonance angiography of intracranial vessels) when determining indications for endovascular treatment, provided the patient has no history of renal failure [172–177].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: analysis of a number of observational studies shows that the risk of contrast-induced nephropathy after CTA is relatively low, especially in patients with no history of renal failure. Moreover, waiting for creatinine concentration results may lead to a delay in performing mechanical thrombectomy [178–183].
It is recommended to perform an emergency repeat brain CT in adult patients with ischemic stroke if there is an increase in NIHSS severity by ≥ 4 points from baseline, or upon the appearance of symptoms corresponding to a lesion in another vascular territory, in order to determine treatment tactics [184].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended to perform a repeat brain CT (A06.23.004 Computed tomography of the brain) or brain MRI (A05.23.009 Magnetic resonance imaging of the brain) between 22 and 36 hours from disease onset in adult patients with ischemic stroke who have undergone intravenous thrombolysis and/or mechanical thrombectomy, in the presence of signs of clinical deterioration, in order to determine treatment tactics [185].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended to perform a repeat brain CT (A06.23.004 Computed tomography of the brain) in adult patients with ischemic stroke presenting with malignant cerebral infarction secondary to acute occlusion of the proximal segment of the middle cerebral artery to clarify the volume of the infarction and the presence of lateral and/or axial brain displacement [191, 192].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: in the acute period of stroke with CT-negative findings obtained within the first 8 hours of the disease in a patient with severe hemiparesis and gaze palsy, it is necessary to perform a repeat brain CT for targeted detection of early indirect signs of massive hemispheric ischemia: compression of subarachnoid spaces and increased signal density of the MCA stem.
It is recommended to interpret the course of stroke as malignant in adult patients with ischemic stroke if brain CT (A06.23.004) reveals axial displacement of more than 2 mm within the first 24 hours of disease onset or more than 7 mm within the first 48 hours of disease onset, in order to determine treatment tactics [192].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended to visualize the ischemic core and/or penumbra using one of the following methods in adult patients with ischemic stroke who are potential candidates for mechanical thromboembolectomy and have symptom duration ranging from 6 to 24 hours from disease onset in the presence of a large vessel occlusion in the carotid territory: computed tomography perfusion of the brain (A06.23.004.001) or magnetic resonance perfusion of the brain (A05.23.009.003) with automated calculation of ischemic core and penumbra volumes, or brain MRI (A05.23.009) with diffusion-weighted imaging to assess the ischemic core zone [194].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: The DAWN trial (Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention With Trevo) used clinical-imaging mismatch (a combination of the NIHSS score and imaging results via brain computed tomography perfusion or brain magnetic resonance diffusion) as a selection criterion for suitability in patients with large vessel occlusion in the carotid territory for mechanical thrombectomy within the 6- to 24-hour window from symptom onset. This trial demonstrated overall benefit regarding functional outcome at 90 days in the experimental group [193]. The DEFUSE 3 trial (Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution) used perfusion-to-infarct core mismatch as well as maximum core size determined by imaging as selection criteria for patients with large vessel occlusion in the carotid territory within 6 to 16 hours of symptom onset undergoing mechanical thrombectomy. A better functional outcome at 90 days was demonstrated in the experimental group [194]. Benefit was independently demonstrated for the subgroup of patients meeting the DAWN trial eligibility criteria as well as for the subgroup not meeting these criteria. The DAWN and DEFUSE 3 trials are the only RCTs that have demonstrated the benefit of mechanical thrombectomy beyond 6 hours after stroke onset. Therefore, patient selection should strictly follow the criteria used in these trials (NIHSS > 6 points, presence of proximal arterial occlusion, small infarct core volume, preserved collateral blood flow). In clinical practice, the criteria used in the DAWN and DEFUSE 3 trials must be strictly followed.
In the event that collateral blood flow is visualized in the patient according to CT angiography or MR angiography, and the patient meets the other requirements of the MR CLEAN LATE randomized clinical trial, advanced imaging modalities (computed tomography perfusion, magnetic resonance perfusion, magnetic resonance imaging with diffusion-weighted imaging) are not performed [152].
It is recommended to perform brain MRI (A05.23.009) with intracranial vessel MRA (A05.23.009.008) in all children with signs of acute cerebrovascular accident on an emergency basis for the purpose of differential diagnosis, verification of the diagnosis, and selection of treatment tactics [195-196].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that all children with signs of acute cerebrovascular accident undergo emergency brain CT (A06.23.004) and CT angiography of brachiocephalic arteries (A06.12.058) if emergency MRI cannot be performed [196-197].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that all children with established ischemic stroke and TIA (based on brain CT data) undergo brain MRI (A05.23.009) and intracranial vessel MRA (A05.23.009.008) in order to clarify the pathogenetic variant, perform differential diagnosis, and choose treatment tactics [195-196].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comments: When performing a brain MRI, the following sequences should be included: DWI, FLAIR, T1 and T2); the pediatric brain MRI protocol may also include: GRE or SWI, T1WI (Mirsky DM, Beslow LA, Amlie-Lefond C, Krishnan P, Laughlin S, Lee S, et al. Pathways for neuroimaging of childhood stroke. Pediatr Neurol. 2017;69:11–23). If necessary, MRI, MRA, CT, and CTA are performed using combined inhalation anesthesia (including the use of xenon) (B01.003.004.012)
It is recommended in adult patients with suspected cerebral venous thrombosis to evaluate direct and indirect signs of the disease on non-contrast brain CT (A06.23.004) to verify the diagnosis and perform differential diagnosis [85, 198].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: CT is often the primary neuroimaging method in patients with acute cerebral pathology; therefore, native tomograms must be evaluated for signs of cerebral venous thrombosis. Direct signs (present in 25–30% of patients) include: the "dense thrombus" sign (direct visualization of the thrombus), the "dense triangle" sign (in thrombosis of the superior sagittal sinus), the "cord" sign (thrombosis of cortical or deep veins). The increased CT density is due to the elevated hemoglobin and erythrocyte content in the thrombus. This sign may be false-positive in dehydration and hemoconcentration. Indirect signs include: cerebral infarction outside typical arterial territories, hemorrhagic infarction, bilateral parasagittal infarctions and hemorrhages, lobar intracerebral hemorrhage, intracerebral hemorrhage adjacent to a sinus, convexity (juxtacortical) subarachnoid hemorrhage (the "cashew" sign), and vasogenic edema [85, 198, 200-201].
It is recommended to perform contrast-enhanced MR venography (A05.12.005 Magnetic resonance venography (one region)) or CT venography (A06.12.056 Computed tomographic angiography of cerebral vessels) as the primary angioimaging in all patients with clinically suspected cerebral venous thrombosis for timely diagnosis [23, 85, 198-201].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: the key sign of cerebral venous thrombosis on contrast-enhanced MR venography (post-contrast T1 images) or CT venography is the "empty delta" sign, which represents a contrast-impermeable thrombus surrounded by collateral veins of the sinus wall. CT venography is a sensitive method for verifying cerebral venous thrombosis and is appropriate when MRI is unavailable or contraindicated. CTA has a sensitivity of 79% and a specificity of 90% [202]. The CTA "empty delta" sign occurs in one-third of patients with cerebral venous thrombosis. It may be absent in the acute phase (first 5 days) due to sinus hyperattenuation and appear only in the subacute phase. The diagnostic value of CT venography as a standalone diagnostic method is limited, as anatomical variants (atresia, hypoplasia, asymmetry, arachnoid granulations, septa) can mimic thrombosis [199].
When interpreting MRI results, it must be taken into account that the MR signal from a thrombus changes over time due to the sequential transformation of oxyhemoglobin into deoxyhemoglobin and methemoglobin. T1- and T2-weighted images may yield a false-negative result in the acute phase (first 5 days); therefore, it is advisable to use T2* or SWI (SWAN) MR sequences, which allow visualization of the thrombus as a hypointense "blooming" area. These sequences are most informative for verifying cortical vein thrombosis. In the subacute phase (5–15 days), the thrombus becomes hyperintense on T1- and T2-weighted images. In the chronic phase (more than 15 days), the thrombus is homogeneous, and signal intensity decreases across all sequences. Contrast-enhanced MR venography has higher sensitivity compared to time-of-flight (TOF) mode. The use of unenhanced MR venography as a standalone technique is not recommended. MRI has a sensitivity of 88–87% and a specificity of 77–100% compared to DSA. The positive predictive value is 94%, and the negative predictive value is 58% [202-204]. Difficulties in interpreting MRI results include phenomena resembling cerebral venous thrombosis (MRI pitfalls): arachnoid granulations, flow voids disruption in the transverse sinus, absence of flow voids, slowed blood flow, etc. [205]. An important MRI phenomenon in cerebral venous thrombosis is vasogenic and cytotoxic edema (often in combination). In the case of intracerebral hemorrhage, MRI frequently demonstrates bilateral hemorrhages, multifocal hemorrhages, or hemorrhagic infarctions atypical for arterial territory involvement. At the same time, the localization of parenchymal damage can indicate the location of venous thrombosis. For example, involvement of the frontal, parietal, and occipital lobes is typical for superior sagittal sinus thrombosis, whereas temporal lobe involvement is typical for transverse and sigmoid sinus thrombosis. If edema or cortical/subcortical localized hemorrhage is detected, the signal intensity of adjacent cortical veins should be evaluated, especially when the lesion does not correspond to an arterial territory [200, 206].
It is recommended to perform total selective cerebral angiography (catheter subtraction cerebral angiography) (A06.12.031.001) in adult patients with suspected cerebral venous thrombosis when non-invasive angioimaging data are inconclusive, when an arteriovenous fistula is suspected, or when endovascular treatment is planned, in order to determine the treatment strategy [85-87].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: although catheter cerebral angiography remains the "gold standard" of angioimaging in cerebral venous thrombosis, in most cases the use of this invasive technique is not required. Inconclusive CT and MRI results may be related to the difficulty of differentiating cerebral venous thrombosis from conditions and phenomena such as atresia, hypoplasia, sinus asymmetry, arachnoid granulations, septa, flow voids disruption in the transverse sinus, absence of flow voids, slowed blood flow, etc. [205]. Angiography is a highly informative diagnostic method for rare isolated cortical vein thrombosis, the detection of which on CT and MR venography can be difficult.
2.4.2. Other instrumental diagnostic methods
It is not recommended to routinely perform targeted chest X-ray (A06.09.007.001) upon hospital admission in adult patients with ischemic stroke or TIA who are candidates for reperfusion therapy, in order to reduce the time to initiation of reperfusion therapy [207, 208].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: routine chest X-ray upon hospital admission reveals potentially significant abnormalities in only 3.8% of patients and may delay the initiation of intravenous thrombolysis [207, 208].
It is recommended to record an electrocardiogram (A05.10.006) in all patients with ischemic stroke and TIA upon hospital admission to detect atrial fibrillation, ischemic and other myocardial changes, congenital and acquired heart defects, and cardiac arrhythmias; however, this should not delay reperfusion therapy if indicated [209–211, 523, 536].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: performing a 12-lead electrocardiography upon hospital admission is necessary both to optimize emergency treatment and to determine the cause of ischemic stroke (IS) or transient ischemic attack (TIA). Electrocardiography can detect atrial fibrillation, though its absence during screening does not rule out the possibility of detecting the arrhythmia upon longer monitoring. IS/TIA may be combined with acute myocardial infarction. Furthermore, IS can cause neurogenic stress cardiomyopathy with electrocardiographic changes via hyperactivation of the sympathetic system [209–211].
It is recommended to perform bedside ECG monitoring (A05.10.007 Electrocardiographic data monitoring) or 24-hour Holter heart rhythm monitoring (A05.10.008) for at least 24 hours in adult patients with ischemic stroke or TIA to detect atrial fibrillation, ischemic, and other myocardial changes [212–214].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comments: bedside ECG monitoring (telemetry) for two to three days makes it possible to detect significant arrhythmias in 25–30% of patients, which entails a change in treatment. Most arrhythmia episodes are detected within the first 24 hours after hospital admission. 24-hour Holter monitoring has lower sensitivity in detecting paroxysmal fibrillation compared to telemetry [212–214].
It is recommended to perform Holter heart rhythm monitoring (A05.10.008) lasting at least 72 hours or implant a loop recorder for long-term recording of the electrical activity of the cardiac conduction system (A05.10.012) in adult patients with ESUS and signs of atrial cardiopathy to detect latent atrial fibrillation [215–221].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: latent atrial fibrillation is a frequent cause of ESUS, especially in elderly and senile patients. The detection rate of arrhythmia ranges from 4.3% with 72-hour Holter monitoring to 22% with 3-week monitoring. Prolonged cardiac monitoring using loop recorders makes it possible to detect atrial fibrillation within 3 years in 41% of patients with ESUS. In patients with cryptogenic IS/TIA, prolonged cardiac monitoring is associated with more frequent prescription of anticoagulants and a lower rate of recurrent strokes. Indicators of a high probability of detecting atrial fibrillation after IS/TIA include: age over 75 years, left atrial diameter greater than 46 mm, number of supraventricular extrasystoles ≥ 480/day or the presence of an episode of supraventricular tachycardia lasting > 20 cardiac cycles during initial monitoring, NT-proBNP concentration > 400 pg/mL, P-wave terminal force > 5000 μVxms. Prolonged monitoring in patients with markers of atrial cardiopathy is more effective [222]. The longer the ECG monitoring, the higher the probability of detecting atrial fibrillation. Other ways to determine indications for long-term ECG monitoring include evaluation using scoring scales: C2HEST and ESUS-AF. According to the C2HEST scale, at 0–1 points, the AF detection rate is 0.34% per year; at 2–3 points, 2.60% per year; and at 3 or more points, 15.98% per year. According to the ESUS-AF scale, the rate of newly diagnosed AF is 26.9% among patients with a score > 0 and 1.97% among patients with 0 points [222-227].
It is recommended to perform echocardiography (EchoCG) (A04.10.002) in all patients with ischemic stroke or TIA to identify cardiac sources of embolism [228–234, 523, 536, 1131-1133].
Level of Evidence CReliability of Evidence 4Level of Clinical Recommendation C (Reliability of Evidence 4 for adults, 5 for children)
Comment: using standard transthoracic echocardiography (TTE) (A04.10.002) in elderly patients, it is possible to diagnose the following causes of ischemic stroke / transient ischemic attack (IS/TIA): thrombi, cardiac chamber tumors, left ventricular akinesia and aneurysm (with or without thrombus), reduced ejection fraction, mitral stenosis, infective endocarditis, and prosthetic valve dysfunction (thrombosis). Although clinically significant changes are infrequently detected on routine TTE, their identification leads to a substantial change in therapeutic management. It should be noted that the absence of the aforementioned sources of cardiac embolism on TTE can be a false negative. TTE is also necessary to assess left atrial size in order to determine dilation, which increases the likelihood of occult atrial fibrillation. Indications for transesophageal echocardiography (TEE) (A04.10.002.001) include: suspected infective endocarditis (even if TTE yielded negative results), left ventricular aneurysm to search for flat mural thrombi, the need to assess the left atrial appendage, the need to evaluate prosthetic valves, a positive bubble test to verify the source of a shunt and assess its anatomical characteristics, and suspected aortic arch atheroma [228–234].
It is recommended for all patients with unprovoked epileptic seizures to undergo electroencephalography with activation procedures (A05.23.001.001) according to a standard protocol (lasting at least 30 minutes of artifact-free EEG recording), as well as electroencephalography with video monitoring (A05.23.001.002) to identify and localize epileptiform changes on the EEG [597, 598, 1111, 1112].
Level of Evidence CReliability of Evidence 4Level of Clinical Recommendation C (Reliability of Evidence - 4)
It is recommended for all patients in the acute period of IS presenting with paroxysmal conditions with an atypical clinical picture / decreased level of alertness to undergo electroencephalography with activation procedures (A05.23.001.001) (lasting at least 30 minutes) or electroencephalography with video monitoring (A05.23.001.002) for the differential diagnosis of non-motor epileptic seizures and non-convulsive status epilepticus [1113, 1114, 1134].
Level of Evidence CReliability of Evidence 5Level of Clinical Recommendation C (Reliability of Evidence - 5)
Comments: During prolonged EEG recording with activation procedures (A05.23.001.001), seizures in the acute period of acute cerebrovascular accident (ACVA) are recorded in 6 - 27% of patients. EEG with activation procedures (A05.23.001.001) for 30 - 60 minutes makes it possible to record non-motor epileptic seizures or non-convulsive status epilepticus (if present) in 48 - 58% of cases, and within 24 - 48 hours in 80 - 95% of cases [1114].
It is recommended for adult patients with post-stroke epileptic seizures to undergo brain CT or MRI: in the event of an epileptic seizure or convulsive status epilepticus, brain CT is recommended to rule out hemorrhagic stroke or the hemorrhagic component of IS, or recurrent ACVA (if possible in CT perfusion mode) [1115, 1116, 1117].
Level of Evidence CReliability of Evidence 5Level of Clinical Recommendation C (Reliability of Evidence — 5)
Comments: brain MRI is a more sensitive method for ruling out causes of epileptic seizures other than ACVA. For unprovoked epileptic seizures or status epilepticus, a brain MRI of at least 1.5 Tesla is recommended to clarify the diagnosis and optimize treatment tactics [1107, 1118].
2.5 Other Procedures
It is recommended to perform ultrasonic Doppler location of microbubbles (transcranial Doppler with a bubble study) (A04.12.001.008) in ESUS patients aged 18 to 55 years to diagnose paradoxical embolism [235–237].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: transcranial Doppler with a bubble study has 96% sensitivity and 92% specificity in diagnosing a right-to-left shunt compared to TEE, which is considered the "gold standard". The examination must obligatorily be supplemented by the Valsalva maneuver. The result of transcranial Doppler must include a quantitative assessment of microbubble signals (High Intensity Transient Signals – HITS). The grading of shunt volume according to TCD is classified into five degrees: degree 0 – absence of HITS; degree 1 – 1–10 HITS; degree 2 – 11–25 HITS; degree 3 – more than 25 HITS ("shower" effect); degree 4 – "curtain" [235–237]. An alternative to transcranial Doppler is performing a transthoracic echocardiogram with a bubble study, which has 46% sensitivity and 99% specificity [238].
It is recommended to perform contrast-enhanced MR venography (contrast-enhanced magnetic resonance angiography, A05.12.006) or CT venography (computed tomographic angiography of cerebral vessels, A06.12.056) in adult patients with ischemic stroke presenting with appropriate clinical signs to diagnose cerebral venous thrombosis [239–246].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: in a quarter of patients, direct signs of cerebral venous thrombosis (CVT) are present on CT: the "dense triangle" sign (in thrombosis of the superior sagittal sinus), the "empty delta" sign (in thrombosis of the superior sagittal or transverse sinus), and the "cord sign" (thrombosis of cortical or deep veins). On MRI, T1- and T2-weighted images may show false-negative results in the acute phase (the first 5 days); therefore, it is advisable to use T2* or SWI (SWAN) MR sequences, which allow visualization of the thrombus as a hypointense zone. In the subacute phase (5–15 days), the thrombus becomes hyperintense on T1- and T2-weighted images. In the chronic phase (more than 15 days), the thrombus is homogeneous, and the signal intensity decreases on all sequences. Contrast-enhanced MR venography has a higher sensitivity compared to time-of-flight (TOF) imaging. The use of non-contrast MR venography as the sole technique is not recommended. Digital subtraction angiography should remain a backup method and be used when CT and MRI results are contradictory, to rule out arteriovenous fistulas, or when planning endovascular intervention [239–246].
It is recommended that all patients with cryptogenic stroke undergo additional workup, if clinically indicated, to screen for thrombophilia, systemic infections, vasculitis, autoimmune diseases, and genetic causes of stroke [119-121, 247–250].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: thrombophilia screening should include the evaluation of the following parameters: antithrombin III, protein C and S, factor V Leiden mutation, prothrombin G20210A and MTHFR mutations, homocysteine, antiphospholipid syndrome (APS) screening (anticardiolipin antibodies, anti-beta-2-glycoprotein antibodies, lupus anticoagulant). Genetic testing may include screening for the following conditions: CADASIL, CARASIL, retinal vasculopathy with cerebral leukodystrophy, FOXC1, COL4A1, COL4A2, Fabry disease, pseudoxanthoma elasticum, neurofibromatosis type 1, genetic forms of hyperhomocysteinemia, Ehlers-Danlos syndrome type IV, fibromuscular dysplasia, arterial tortuosity syndrome, Marfan syndrome, moyamoya disease, sickle cell anemia, hereditary hemorrhagic telangiectasia, and MELAS. Screening for autoimmune diseases includes the determination of antinuclear antibodies (ANA) and antineutrophil cytoplasmic antibodies (ANCA) in blood serum. These tests can be performed on an outpatient basis. Infection screening includes tests for HIV, syphilis, and viral hepatitis, as well as cerebrospinal fluid analysis, and should be performed in an inpatient setting [247–250].
It is recommended to perform a lumbar puncture (A11.23.001) in all patients with CVT and suspected meningitis for the timely diagnosis of septic venous thrombosis [23, 251].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: CVT can be a complication of meningitis, which should be clinically suspected in the presence of hyperthermia and meningeal syndrome. In aseptic CVT, cerebrospinal fluid changes are nonspecific and may include lymphocytic pleocytosis, an increased red blood cell count, and elevated protein levels (in 30–50% of patients) [251].
It is recommended to perform cancer screening in adult patients with CVT older than 40 years in the absence of other identified risk factors for the timely diagnosis of an underlying malignancy [252].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: 7.4% of all CVT cases are associated with malignancies [252]; therefore, it is advisable to screen for tumors when other risk factors for venous thrombosis are absent.
3. Treatment, including drug and non-drug therapies, diet therapy, and pain management
3.1. Conservative therapy
3.1.1. Basic therapy
It is recommended that patients with ischemic stroke or TIA undergo monitoring of neurological status, heart rate, blood pressure, body temperature, and oxygen saturation for at least 24 hours to improve disease outcomes [253–255, 523, 536].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: active monitoring of neurological status and vital signs such as blood pressure, heart rate, blood glucose, and body temperature is standard practice Based on randomized clinical trials, there are no direct guidelines specifying how frequently monitoring should be performed. However, studies concerning the organization of stroke units [255] practiced observation and assessment at least every 4 hours during the first 72 hours from symptom onset.
3.1.1.1. Airway, breathing and oxygenation
It is recommended for patients with ischemic stroke presenting with a decreased level of consciousness or bulbar dysfunction to maintain a patent airway to prevent aspiration complications [256, 257].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended for patients with ischemic stroke presenting with depressed consciousness, signs of increased intracranial pressure, generalized seizure attacks, cerebral infarction, or signs of brain tissue displacement on neuroimaging to consider the feasibility of mechanical ventilation to prevent secondary hypoxic brain injury [257, 258, 259].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with ischemic stroke receive oxygen therapy (oxygen insufflation) (A20.30.026) to maintain blood oxygen saturation measured by pulse oximetry if saturation drops below 94% [260].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: routine use of oxygen therapy in the absence of indications is not recommended.
It is recommended in adult patients with ischemic stroke who are predicted to require prolonged mechanical ventilation or have been diagnosed with severe dysphagia to consider early tracheostomy (A16.08.003 Placement of a temporary tracheostomy) (within the first 7 days of mechanical ventilation) to improve the disease prognosis [261].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: early tracheostomy helps reduce the risk of accidental endotracheal extubation, increases patient comfort compared to orotracheal intubation, and facilitates tracheobronchial hygiene.
It is not recommended for adult patients with ischemic stroke to undergo hyperbaric oxygen therapy to improve disease outcomes, except in cases where the stroke is caused by an air embolism [262, 263].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
3.1.1.2. Blood pressure
It is not recommended for adult patients in the hyperacute period of ischemic stroke or TIA to lower blood pressure to improve disease outcomes if it does not exceed 220/120 mm Hg, except for patients selected for reperfusion therapy [264–266].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: early treatment of hypertension in patients with acute ischemic stroke may be necessary in the presence of comorbid conditions:
acute coronary syndrome (immediate reduction of systolic blood pressure below 140 mm Hg is recommended)
cardiogenic pulmonary edema (immediate reduction of systolic blood pressure below 140 mm Hg is recommended)
aortic dissection (immediate reduction of systolic blood pressure below 120 mm Hg and heart rate below 60 bpm is recommended; in preeclampsia/eclampsia, immediate reduction of systolic blood pressure below 160 mm Hg and diastolic blood pressure below 105 mm Hg is recommended).
Nevertheless, it is important to bear in mind that excessive blood pressure reduction may aggravate cerebral ischemia [267]. In patients with a significant increase in blood pressure (> 220/120 mm Hg) who have no indications for reperfusion therapy, it is recommended to lower blood pressure by 15% during the first 24 hours from stroke onset. In patients with preexisting arterial hypertension, a gradual and smooth reduction of blood pressure levels is recommended, along with stabilization and maintenance of blood pressure at 15–20 mm Hg above the mean blood pressure level (if anamnestic data are available). Usually, blood pressure is lowered to 180/100–105 mm Hg in patients with a history of hypertension, and in other cases, to 160–180/90–100 mm Hg. For patients receiving antihypertensive therapy prior to the stroke, it is advisable to resume it 24 hours after the onset of acute cerebrovascular accident in the absence of specific contraindications and once neurological and somatic status has stabilized. Initiating or resuming antihypertensive therapy within the first 48–72 hours after ischemic stroke onset in patients with severe hypertension (> 220/120 mm Hg) who did not receive reperfusion therapy, in the absence of comorbid conditions requiring intensive blood pressure lowering, is safe, but it does not reduce mortality rates or affect functional outcomes [268–271].
In patients receiving reperfusion therapy, blood pressure must be maintained at no higher than 185/110 mmHg prior to intravenous thrombolysis and no higher than 180/105 mmHg during intravenous thrombolysis and/or mechanical thrombectomy [272].
It is recommended that adult patients with ischemic stroke or TIA undergo correction of hypotension and hypovolemia to maintain systemic perfusion levels [273].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: no studies have been conducted aimed at evaluating the correction of low blood pressure in stroke patients, although it is known that a drop in blood pressure in the acute phase of the disease is associated with an unfavourable outcome [274]. There are no data to guide the volume and duration of parenteral fluid administration. There are also no studies comparing different isotonic fluids. Most stroke patients are dehydrated upon hospital admission, which may be a poor prognostic sign associated with an unfavourable disease outcome [275].
It is recommended that adult patients with ischemic stroke immediately prior to systemic thrombolytic therapy have their blood pressure stabilized at < 185 mmHg for systolic and < 110 mmHg for diastolic pressure to improve disease outcomes [276–281].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
Comment: in RCTs involving intravenous administration of alteplase** (B01AD02), the following requirements were established: systolic BP < 185 mmHg, diastolic BP < 110 mmHg before initiating therapy; for at least the first 24 hours after therapy, BP must be maintained at < 180/105 mmHg. If hypertension correction is necessary, short-acting agents administered intravenously should be preferred. The exact BP values that increase the risk of bleeding after thrombolytic therapy are unknown, although it has been shown that in cases of successful recanalization, an increase in BP is associated with a higher risk of intracranial hemorrhage of any type [280]. Therefore, it is advisable to maintain BP at the target level used in RCTs investigating IV thrombolysis.
It is not recommended for adult patients with ischemic stroke to reduce systolic blood pressure below 120 mmHg in the first 72 hours after mechanical thrombectomy [282].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: the randomized clinical trial ENCHANTED2/MT (n=821) demonstrated a negative effect of correcting systolic blood pressure to levels below 120 mmHg on functional outcomes of the disease (increased probability of an unfavorable outcome – OR 1.37, 95% CI 1.07-1.76). Optimal blood pressure figures after mechanical thrombectomy are unknown.
It is recommended for adult patients with ischemic stroke who are scheduled for mechanical thrombectomy and have not received intravenous thrombolytic therapy to maintain blood pressure at < 185/110 mmHg to improve disease outcomes [283–288].
COVID CLEL 5Level of Evidence Recommendations C (Level of Confidence of Evidence – 5)
Comment: out of 6 RCTs that independently demonstrated the clinical benefit of mechanical thrombectomy using a stent retriever when performed within < 6 hours after stroke onset, 5 RCTs (REVASCAT, SWIFT PRIME, EXTEND-IA, THRACE, and MR CLEAN [250–252, 254]) established a procedural exclusion criterion of BP > 185/110 mmHg. The sixth RCT, ESCAPE [288], did not establish a procedure exclusion criterion based on blood pressure. The DAWN study [132] also used a BP > 185/110 mmHg exclusion criterion. RCT data regarding optimal approaches to maintaining an appropriate blood pressure level in these settings are missing. Since the vast majority of patients included in these RCTs had their blood pressure maintained below 185/110 mmHg prior to the procedure, it is appropriate to use this level as the target.
It is not recommended to prescribe vasodilators to adult patients with ischemic stroke or TIA to improve disease outcomes [289–292].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
3.1.1.3. Water-electrolyte balance
It is recommended that adult patients with ischemic stroke undergo daily monitoring of fluid and, where indicated, electrolyte balance to maintain homeostasis [293–296].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
It is not recommended to use a 5% dextrose solution** (B05CX01) as part of infusion therapy in adult patients with ischemic stroke [293, 297, 298].
GCR ALEL 3Grade of Recommendation A (Level of Evidence – 3)
It is not recommended to routinely use hemodilution to improve hemorheological parameters in adult patients with ischemic stroke or TIA [299].
GCR ALEL 3Grade of Recommendation A (Level of Evidence – 3)
It is not recommended to administer albumin** (ATC B05AA) for the prevention of cerebral edema in adult patients with ischemic stroke or TIA [293, 300].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
3.1.1.4. Temperature
It is recommended to prescribe antipyretics to reduce body temperature when it rises above 37.5 °C in adult patients with ischemic stroke or TIA [301–307].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
Comment: hyperthermia is a frequent complication occurring in 50% of patients with acute ischemic stroke [308] and has been shown to be accompanied by a poor treatment outcome. Hyperthermia also increases oxygen demand and can exacerbate heart or lung failure, as well as trigger delirium in patients with brain disorders. The QASC study showed that the implementation of fever, dysphagia, and hyperglycemia management protocols improved treatment outcomes and resulted in a 16% reduction in mortality and disability at 90 days and in-hospital [309]. Although it was impossible to precisely determine which of the three components of this intervention had a beneficial effect, multiple logistic regression analysis showed that hyperglycemia and fever management were the primary determinants [305].
It is recommended in adult patients with ischemic stroke or TIA, upon body temperature elevation above 37.5 °C, to screen for a concomitant infection, including novel coronavirus infection, to adjust therapy and improve outcomes [310–312].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is not recommended to use systemic antibacterial drugs (J01) prophylactically in adult patients with ischemic stroke to improve disease outcomes [313–315].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
It is not recommended to use induced hypothermia in adult patients with ischemic stroke or TIA to improve disease outcomes [316–318].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: hypothermia is a promising neuroprotective strategy, but its benefit in treating ischemic stroke patients has not been confirmed. Most studies indicate that inducing hypothermia is associated with an increased risk of infection, including pneumonia. Therapeutic hypothermia should only be used in the context of clinical trials.
3.1.1.5. Glycemia
It is recommended for all patients with ischemic stroke to undergo careful monitoring of glycemia levels (A09.05.023 Blood glucose test) and, in the presence of hyperglycemia, its correction in the range from 7.8 to 9.9 mmol/l to improve functional outcomes and prevent additional cerebral damage [319–326, 523].
For children, Level of Evidence C (Level of Confidence of Evidence – 5); for adults, Level of Evidence A (Level of Confidence of Evidence – 2)
Comment: Available evidence indicates that persistent hyperglycemia lasting during the first 24 hours of hospital stay following ischemic stroke onset is associated with more unfavorable outcomes compared to normoglycemia and is an independent predictor of increased infarct size, poor functional outcome, and a higher risk of death [319]. Although based on a smaller body of data, it has been conclusively shown that hyperglycemia is also independently associated with poor functional outcome in patients with cerebral venous thrombosis [320]. Optimal glycemic management and target blood glucose levels following ischemic stroke remain controversial, particularly in critically ill stroke patients. Preliminary data from the Stroke Hyperglycemia Insulin Network Effort (SHINE) trial, which enrolled 1151 patients from 63 stroke centers in the USA, demonstrate that intensive glucose control targeting 4.4–7.2 mmol/L (80–130 mg/dL) using insulin infusions and analogues (A10A) does not improve 90-day functional outcomes compared to standard control <10 mmol/L (< 180 mg/dL) with intermittent subcutaneous administration of insulin aspart** [321]. Furthermore, intensive glucose control increased the risk of hypoglycemia and required increased nursing surveillance in this trial. It appears reasonable to use intravenous insulin for blood glucose control in patients with ischemic stroke exclusively in an intensive care unit setting where such practice is routine and the risk of hypoglycemia is lower than in acute stroke units [322].
Current guidelines recommend careful monitoring of blood glucose levels following ischemic stroke and treatment of hyperglycemia to maintain glucose levels in the range of 7.7–9.9 mmol/L (140–180 mg/dL), while avoiding or immediately treating hypoglycemia <3.7 mmol/L (< 60 mg/dL) [323]. An important argument in favor of rigorous glycemic control is the fact that effective glycemic control facilitates the maintenance of collateral blood flow [327].
3.1.1.6. Nutrition
It is recommended to initiate enteral nutrition within the first 48 hours of intensive care in adult patients with ischemic stroke receiving tube feeding, giving preference to clinical nutrition products for the prevention of malnutrition [326, 328–330].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: critically ill patients have the highest risk of developing malnutrition. Such patients require artificial nutrition with monitoring of energy requirements and protein loss. Delayed initiation of feeding is accompanied by worsening clinical and neurological outcomes and an increased number of complications.
It is recommended that adult patients with ischemic stroke receiving tube feeding be prescribed targeted artificial nutrition of 25 kcal per kg of body weight per day (or 70% of calculated energy requirements) and 1.3 g of protein per kg of body weight per day to meet baseline metabolic needs [331, 332].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: a hypocaloric diet is preferred over an isocaloric diet during the first week after initiating intensive care in patients. Early protein intake of 1.2–1.3 g/kg/day is associated with improved clinical and neurological outcomes [331, 332].
It is recommended to prescribe parenteral nutrition for adult patients with ischemic stroke to correct nutritional status only when enteral nutrition is impossible or ineffective [328, 333].
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: the enteral route of nutrition is preferred. If adequate enteral feeding is impossible, parenteral nutrition is used (when it is impossible to provide up to 50% of the required nutritional volume via the enteral feeding route within 3–7 days) [328, 333].
It is recommended to place a nasogastric tube in adult patients with ischemic stroke and diagnosed dysphagia to prevent aspiration and facilitate feeding [330, 334, 336].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is recommended to consider the placement of a percutaneous gastrostomy within 2–4 weeks from disease onset to prevent aspiration in adult patients with ischemic stroke who continue to require tube feeding [330].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke follow an oral hygiene protocol to reduce the risk of pneumonia [337–339].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke (IS) presenting with malnutrition or at high risk of malnutrition, and without dysphagia, receive specialized high-energy and high-protein nutritional supplements to reduce the risk of mortality and improve functional recovery [340, 341].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: polymorbid patients with IS who require nutritional support should receive 1.2–1.5 g of protein/kg of body weight per day as a cost-effective and highly efficient measure to prevent weight loss, reduce the risk of mortality, complications, and readmission, as well as to improve functional outcomes and quality of life.
It is recommended that adult patients with IS use a texture-modified diet and/or thickened liquids to maintain fluid balance and nutrient intake [342].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: a meta-analysis of the safety and therapeutic efficacy of xanthan gum-based powdered and liquid thickeners demonstrated that xanthan gum-based thickeners are superior to starch-based thickeners due to better texture perception, greater stability (e.g., over time and temperature), and higher resistance to salivary amylase. Both thickener formulations (liquid or powder) are clinically safe and effective for improving swallowing safety in individuals with oropharyngeal dysphagia, although published clinical data supporting the safety and efficacy of liquid xanthan gum are more limited [343, 344].
It is recommended that adult patients with IS and malnutrition or at high risk of malnutrition continue nutritional support after hospital discharge to maintain or improve body weight and enhance functional recovery [345].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with IS aged over 65 years with malnutrition or at high risk of malnutrition continue nutritional support after hospital discharge via additional intake of specialized medical nutrition products to reduce mortality [345].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
3.1.1.7. Deep vein thrombosis prophylaxis
It is recommended that immobilized adult patients with ischemic stroke undergo an individualized selection of the method and duration for deep vein thrombosis (DVT) and pulmonary embolism (PE) prophylaxis [346–348].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: the frequency of symptomatic DVT and PE in ischemic stroke is 5% and 2%, respectively (increasing to 43% and 10% when instrumental screening is performed), with the peak incidence occurring on days 2–7 [349–351].
There are no universally accepted criteria for immobilization in stroke patients. According to the design of the CLOTS 1 and 3 randomized clinical trials, an immobilized patient was defined as one who was unable to get out of a bed or chair and walk to the toilet unassisted, regardless of the cause of reduced mobility [347, 352]. The choice of prevention method (antithrombotic agents (anticoagulants) (B01A), intermittent pneumatic compression, or a combination thereof) can be made taking into account the following factors. Factors favoring the use of intermittent pneumatic compression: patient compliance, high risk of extra- and/or intracranial hemorrhagic complications associated with anticoagulant therapy. To assess the risk of extracranial bleeding, the IMPROVE Bleeding Risk score (Appendix G18) can be used, with a score of 7 or higher indicating a high risk of bleeding [353, 354]. A high risk of intracranial hemorrhage is determined by the following main factors: poorly controlled arterial hypertension, large cerebral infarction size (greater than 5 cm), dual antiplatelet therapy, thrombocytopenia below 50,000, severe anemia, presence of multiple cerebral microbleeds (> 10), and a history of non-traumatic intracranial hemorrhages [355–357].
Factors favoring the prescription of antithrombotic agents (anticoagulants) (B01A): inability to perform prolonged intermittent pneumatic compression / presence of contraindications, low patient compliance (cognitive impairment, pain syndrome), low risk of extracranial (IMPROVE score less than 7) and/or intracranial hemorrhagic complications during anticoagulant therapy.
Measures for DVT and PE prophylaxis may be discontinued once the patient's mobility is restored (able to walk to the toilet unassisted) [347].
It is recommended that immobilized adult patients with ischemic stroke receive intermittent pneumatic compression (A21.12.002 Intermittent pneumatic compression) to prevent deep vein thrombosis and pulmonary embolism [347, 358, 359].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: The CLOTS (Clots in Legs or stockings After Stroke) 3 randomized clinical trial demonstrated that, compared with standard care (ASA** and hydration), the use of intermittent pneumatic compression in immobilized patients with ischemic stroke is associated with a reduced risk of deep vein thrombosis (odds ratio [OR] 0.65; p = 0.001) and improved 6-month survival (p = 0.042) [347]. A meta-analysis incorporating the results of CLOTS 3 and two smaller studies [358, 359] confirmed these findings.
It is advisable to perform lower extremity venous duplex ultrasonography prior to initiating intermittent pneumatic compression. However, intermittent pneumatic compression may be initiated in patients without prior mobility limitations within the first 72 hours of stroke onset without prior lower extremity venous duplex ultrasonography [347]. Patients with pre-stroke mobility limitations (mRS score of 4 or 5) or those in whom pneumatic compression is initiated later than 3 days after stroke onset require prior lower extremity venous duplex ultrasonography. Thigh-length cuffs should be used, and pneumatic compression must be applied for extended periods (interruptions are permitted for hygiene and physical rehabilitation). The method is contraindicated in patients with open lower extremity wounds, deep vein thrombosis, decompensated heart failure, severe peripheral arterial disease, or confusion/severe cognitive impairment (where attempts to stand may lead to falls and injury).
It is recommended to prescribe prophylactic doses of heparin sodium** (unfractionated heparin [UFH]**) (5,000 units subcutaneously 2 or 3 times daily) or low-molecular-weight heparins (ATC group: B01AB Heparin group, LMWH) to immobilized adult patients with ischemic stroke for the prevention of deep vein thrombosis and pulmonary embolism, provided that the benefit of reducing the risk of venous thromboembolism outweighs the potential risk of intracranial and extracranial bleeding [346, 361, 362].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: A meta-analysis demonstrated that anticoagulant prophylaxis is associated with a reduced risk of deep vein thrombosis (OR = 0.21) and pulmonary embolism (OR = 0.69), but is accompanied by an increased risk of symptomatic intracranial hemorrhage (OR = 1.68) and symptomatic extracranial bleeding (OR = 1.65). Meanwhile, the absolute risk of intracranial hemorrhage during treatment increases by only 0.4%, whereas the absolute risk of deep vein thrombosis decreases by 32.8% [314]. When indicated, UFH/LMWH administration should be initiated on the first day of ischemic stroke; in cases of systemic thrombolysis, no earlier than 24 hours later.
It is recommended that immobilized adult patients with ischemic stroke be preferentially prescribed LMWHs (ATC B01AB) rather than UFH** to prevent deep vein thrombosis and pulmonary embolism [314, 327, 328].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: A meta-analysis [352] showed that the use of LMWHs (ATC B01AB) compared with UFH is associated with a greater reduction in the incidence of deep vein thrombosis (OR = 0.55), with a trend toward a greater, albeit statistically non-significant, reduction in the risk of pulmonary embolism and symptomatic intracranial hemorrhage, alongside a statistically significant increase in the risk of major extracranial bleeding (OR = 3.79). Once-daily administration of LMWHs (ATC B01AB) is more convenient for the patient and easier for medical staff compared to UFH, but it is associated with a substantially higher treatment cost and may increase the bleeding risk in elderly patients with reduced renal function; therefore, the choice of a specific anticoagulant must be individualized [346, 352, 362].
It is not recommended to use compression stockings in adult patients with ischemic stroke and transient ischemic attack for the prevention of deep vein thrombosis and pulmonary embolism [363, 364].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: The use of compression stockings in patients with ischemic stroke does not lead to a significant reduction in the risk of deep vein thrombosis or death [363]. A meta-analysis incorporating the results of the large CLOTS 1 trial [352] and an earlier smaller study [365] demonstrated that compression stockings have no significant effect on mortality, deep vein thrombosis, or pulmonary embolism, but are associated with a significantly increased risk of skin damage [348].
3.1.1.8. Other therapy and nursing care
It is not recommended to routinely place an indwelling urinary catheter to manage urinary function in patients with ischemic stroke who have lower urinary tract dysfunction, due to the increased risk of urinary tract infection [366–369].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: In the acute period of ischemic stroke, one manifestation of voiding dysfunction is urgent urinary incontinence. A clear association has been established between urgent urinary incontinence and severe motor and mental impairments. The cause of urgent urinary incontinence in stroke is detrusor overactivity resulting from the loss of cortical inhibitory control over the micturition reflex. In the absence of post-void residual urine, anticholinergics (trospium chloride) are recommended as the drugs of choice with proven efficacy for treating neurogenic detrusor overactivity. It is advisable to use external condom catheters in men and absorbent pads in women. Another form of lower urinary tract dysfunction can be urinary retention. Short-term (no more than 7 days) urethral catheterization under aseptic conditions is indicated. Routine placement of an indwelling urinary catheter (A11.28.007 Urinary bladder catheterization) is not recommended due to the increased risk of urinary tract infection. Intermittent catheterization is preferred, coupled with diuresis monitoring, ultrasound assessment of post-void residual volume (A04.28.002.005 Ultrasound examination of the urinary bladder with determination of residual urine), and documented tracking of spontaneous voiding volumes or volumes obtained via intermittent catheterization.
It is recommended that adult patients with ischemic stroke undergo daily skin inspections with pressure ulcer risk assessment to prevent disease-related complications [370].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
3.1.1.9. Management of progressive cerebral edema and other complications
Edema accompanied by a mass effect is the primary cause of clinical deterioration and death in patients with large supratentorial infarctions. Life-threatening cerebral edema typically develops between the 2nd and 5th days after the onset of ischemic stroke, although neurological symptoms may progress within 24 hours of symptom onset in one-third of patients.
It is recommended that patients with ischemic stroke and extensive cerebral infarction undergo close monitoring for signs of neurological deterioration during the first days of the disease to ensure the timely initiation of anti-edema therapy [371–374, 523, 536].
For children: Level of recommendation C (evidence level – 5); for adults: Level of recommendation C (evidence level – 3)
It is recommended that patients with ischemic stroke undergo positioning with the head of the bed elevated and the head aligned in the midline, along with pain management, maintenance of normoxia and normothermia, to prevent cerebral edema [371, 375–377, 523, 536].
For children: Level of recommendation C (evidence level – 5); for adults: Level of recommendation A (evidence level – 3)
It is recommended to obtain an early evaluation (examination, consultation) by a neurosurgeon (B01.024.001) in patients with ischemic stroke who are at high risk for malignant cerebral edema, in order to address the indications for surgical decompression [378–380, 523, 536, 1124].
For children: Level of recommendation C (evidence level – 5); for adults: Level of recommendation A (evidence level – 1)
It is recommended to use mannitol** (B05BC01) for the treatment of suspected elevated intracranial pressure in adult patients with ischemic stroke presenting with clinical deterioration, in order to reduce intracranial hypertension [381, 382].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is not recommended to use hypothermia for the treatment of cerebral edema without intracranial pressure monitoring in adult patients with ischemic stroke [388].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is not recommended to administer glucocorticoids (H02AB) for the treatment of cerebral edema and elevated intracranial pressure in adult patients with ischemic stroke, due to the lack of evidence of efficacy and an increased potential risk of infectious complications [389].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
3.1.2. Specific therapy
3.1.2.1. Reperfusion techniques
Currently, the following reperfusion technologies are approved for use in patients with acute ischemic stroke (AIS):
intravenous (systemic, medical) thrombolytic therapy (IV TLT);
mechanical thrombectomy (thromboextraction/thromboaspiration);
staged reperfusion therapy — a combination of IV TLT and mechanical thrombectomy.
3.1.2.1.1. Intravenous thrombolytic therapy
It is recommended to perform intravenous thrombolytic therapy with alteplase** (B01AD02) within the first 4.5 hours from the onset of the disease in AIS patients aged 16 years and older to improve functional outcomes [390–392].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: A meta-analysis of 10 RCTs by Wardlaw J.M. et al. (6,887 patients) [391] showed that the use of alteplase** (B01AD02) within 6 hours after AIS onset reduces the risk of death or disability, defined as a mRS score of 3–6 [OR 0.84; 95% CI: 0.77–0.93, p = 0.0006], and that the effect is greatest within the first 3 hours (OR 0.68; 95% CI: 0.53–0.87, p = 0.002). A meta-analysis of individual participant data from 9 RCTs by Emberson J. et al. (6,756 patients) [393] demonstrated that the administration of alteplase** (B01AD02) significantly increases the probability of a favorable outcome (absence of symptoms or disabling symptoms, mRS score 0–1) at 3 months after disease onset (6 months in the Third International Stroke Study [IST-3]) [390], with earlier treatment leading to proportionally greater benefit. Alteplase** (B01AD02) significantly increased the likelihood of a favorable outcome when administered within 3 hours (OR 1.75; 95% CI: 1.35–2.27, p < 0.0001) and from 3 to 4.5 hours (OR 1.26; 95% CI: 1.05–1.51, p = 0.0132), but not after 4.5 hours (OR 1.15; 95% CI: 0.95–1.40, p = 0.15).
It is recommended that adult patients with AIS undergo intravenous thrombolysis using a recombinant protein containing the staphylokinase amino acid sequence** (B01AD) within the first 4.5 hours of disease onset to improve functional outcomes [394].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
Comment: The FRIDA RCT (n = 385) demonstrated the non-inferiority of the recombinant protein containing the staphylokinase amino acid sequence** (B01AD) compared to alteplase** (B01AD02), with a notable advantage of the non-immunogenic recombinant protein containing the staphylokinase amino acid sequence** being its bolus administration. The use of the recombinant protein containing the staphylokinase amino acid sequence** at a dose of 10 mg within the first 4.5 hours from AIS onset is associated with a favorable functional outcome (mRS 0–1) at 90 days in 50% of patients compared to 40% of patients who received alteplase** at a dose of 0.9 mg/kg (p non-inferiority < 0.0001). Symptomatic ICH developed in 3% of patients in the recombinant protein containing the staphylokinase amino acid sequence** group and in 8% of patients in the alteplase** group (p = 0.087). 3-month mortality and the number of serious adverse events did not differ between the groups. Of note, patients undergoing mechanical thrombectomy were not included in the study [394]. It is also important to note that the FRIDA study did not investigate the feasibility of using alteplase** with advanced neuroimaging methods beyond the 4.5-hour therapeutic window (MRI criteria, CT or MR perfusion criteria).
It is recommended to perform CT or MRI perfusion with automated calculation of the ischemic core and penumbra volume in patients over 16 years of age (if appropriate software is available) with AIS within 4.5 to 9 hours from disease onset (or from the time last known well), in whom mechanical thrombectomy is not indicated or planned, to undergo intravenous thrombolysis with alteplase** (B01AD02) to improve functional outcomes if a mismatch between the hypoperfused area and the ischemic core volume is detected on CT or MRI [395].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: in an individual participant data meta-analysis by Campbell B. et al. [395] the mismatch between the hypoperfusion volume and the infarct volume was assessed using automated software processing and defined as follows:
– infarct volume *≤ 70 mL
and
– critical hypoperfusion volume** / infarct volume* > 1.2
and
– mismatch between the hypoperfusion volume and the infarct volume > 10 mL.
In the meta-analysis by Campbell B. et al. [395], of individual participant data from the EPITHET, ECASS-4, and EXTEND trials, data were included for all patients who met the inclusion criteria of the original trials (n = 414; 52% assessed by perfusion-diffusion MRI, 48% by perfusion CT); IV thrombolysis was associated with a higher rate of excellent outcome (36% with alteplase** (B01AD02) vs. 29% with placebo, OR 1.86; 95% CI: 1.15–2.99; p = 0.01) and a higher rate of symptomatic intracranial hemorrhage (5% vs. < 1%; OR 9.7; 95% CI: 1.23–76.55; p = 0.03), with no significant difference in mortality (14% vs. 9%; OR 1.55; 95% CI: 0.81–2.96; p = 0.19). However, 51% of the included patients had a wake-up stroke. Analysis of three predefined time strata (4.5–6 h, 6–9 h, wake-up stroke) showed no evidence of treatment effect modification for alteplase** (B01AD02). In subgroups of patients with a known stroke onset treated within the 4.5–6 h and 6–9 h time windows, the ORs for an excellent outcome (0–1 points on the mRS) were 2.19 (95% CI: 0.82–5.85) and 2.27 (95% CI: 0.83–6.24), respectively. Similar results were observed for good outcome and improved functional outcome. The authors performed a sensitivity analysis restricted to a subgroup of 303 patients meeting the mismatch criteria in the EXTEND trial [396]. For this purpose, individual patient imaging data were re-analyzed using automated software. The use of alteplase** (B01AD02) remained associated with an excellent outcome (OR 2.06; 95% CI: 1.17–3.62). However, after excluding patients with wake-up stroke, the association between IV thrombolysis and excellent/good outcome or improved functional outcome did not reach statistical significance. Of note, 62% of patients whose data were analyzed in the meta-analysis had a large vessel occlusion, but thrombectomy was not performed, except for one protocol-deviation procedure; therefore, this recommendation applies only to patients in whom mechanical thrombectomy is not planned.
Due to the fact that this clinical indication is not listed in the official prescribing information for alteplase** (B01AD02), administering IV thrombolysis in accordance with this recommendation is only possible upon the decision of a medical commission.
It is not recommended to perform intravenous thrombolysis in adult patients with acute ischemic stroke between 4.5 and 9 hours from symptom onset (with known onset time) to improve clinical outcomes based solely on non-contrast brain CT findings [397–399].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comments: the majority (98.5%) of patients included in the individual participant data meta-analysis of 9 RCTs were randomized after brain neuroimaging using conventional CT [397]. In 6 RCTs, patients could be randomized within the time window from 4.5 to 6 hours after symptom onset (1229 patients receiving alteplase** (B01AD02) compared with 1166 patients receiving placebo) [400–405] This meta-analysis revealed no evidence of a significant benefit of alteplase** (B01AD02) compared with placebo after 4.5 hours from stroke onset or the time last known well (OR for excellent outcome at 3–6 months: 1.15; 95% CI: 0.95–1.40). Qualitatively similar results were obtained for a good outcome (mRS 0–2) and using an ordinal logistic regression model (OR for better functional outcome after 4.5 hours: 1.03; 95% CI: 0.90–1.18) [406]. The estimated time when the lower 95% CI for the expected treatment benefit (mRS 0–1) crossed 1.0 was 5.1 hours [407].
In the study-level meta-analysis, the 4.5-hour threshold was not specifically evaluated [408], but no significant effect of alteplase** was observed in patients randomized later than 3 hours after stroke onset (OR 0.97; 95% CI: 0.85–1.09; 5 studies, 1449 participants), although this estimate did not statistically differ from that in patients randomized less than 3 hours after stroke onset.
It is recommended to administer intravenous thrombolysis with alteplase** (B01AD02) to adult patients with acute ischemic stroke whose symptoms were detected upon awakening from sleep, or with an unknown time of symptom onset, provided it is within 12 hours of the last known well time, brain MRI is available, and there are no indications for mechanical thromboembusectomy, in case DWI/FLAIR mismatch is identified on MRI, with the aim of improving functional outcomes [409, 410].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: the WAKE-UP trial included 503 patients with wake-up stroke and last known well >4.5 h ago who had acute ischemic lesions on DWI but no prominent parenchymal hyperintensity on FLAIR (DWI-FLAIR mismatch) [409, 411]. Patients scheduled for thrombectomy were excluded. Patients were randomized to alteplase** (B01AD02) 0.9 mg/kg or placebo, and the primary endpoint was excellent functional outcome (mRS 0–1 at 90 days). The adjusted OR for excellent outcome with alteplase** (B01AD02) was 1.61 (95% CI: 1.09–2.36; p = 0.02), and the OR for a shift toward a better functional outcome was 1.62 (95% CI: 1.17–2.23; p = 0.003). Alteplase** (B01AD02) was also associated with a non-significant increase in the risk of symptomatic ICH (2.0% vs. 0.4%, p = 0.15) and a non-significant increase in 90-day mortality (4.1% vs. 1.2%, p = 0.07). The Thrombolysis for Acute Wake-Up and Unclear-Onset Strokes With Alteplase (THAWS) trial used the same patient selection criteria as the WAKE-UP trial, and patients with DWI-FLAIR mismatch on MRI were randomized to low-dose alteplase** (B01AD02) (0.6 mg/kg) or placebo [412]. The trial was terminated early following the positive results of WAKE-UP after enrolling 131 of the planned 300 patients, resulting in low statistical power. The THAWS trial found no difference in excellent outcome (mRS score 0–1) at 3 months between the alteplase** (B01AD02) and control groups (relative risk 0.97; 95% CI: 0.68–1.41; p = 0.89). There were also no differences in mortality (relative risk 0.85; 95% CI: 0.06–12.58; p > 0.99). Only one patient in the alteplase** (B01AD02) group experienced symptomatic ICH compared with 0 in the placebo group.
The systematic review and meta-analysis of individual participant data from randomized controlled trials of IV thrombolysis with alteplase** (B01AD02) (Evaluation of unknown Onset Stroke thrombolysis trials [EOS]) in patients with unknown-onset stroke [410] included 843 patients based on DWI-FLAIR mismatch (WAKE-UP and THAWS trials) or perfusion-core mismatch (EXTEND and ECASS-4 trials [413]). Perfusion data were automatically processed using RAPID software, and the authors used the definition of the ischemic penumbra size from the EXTEND trial (ischemic core volume < 70 mL, absolute perfusion lesion volume > 10 mL, and perfusion-to-core mismatch ratio > 1.2). The median time from last known well to the start of treatment was 10.5 hours, and imaging was performed using MRI in 85% of cases. Compared with placebo or standard care, IV thrombolysis was significantly associated with an excellent outcome (primary endpoint: adjusted OR, 1.49; 95% CI: 1.10–2.03; p = 0.01) and a better functional outcome (OR, 1.39; 95% CI: 1.05–1.80; p = 0.02), at the cost of a higher risk of symptomatic ICH (3% vs. 0.5%, p = 0.02) and 3-month mortality (adjusted OR, 2.06; 95% CI: 1.03–4.09; p = 0.04). The effect of alteplase** (B01AD02) was consistent across all predefined subgroups, including imaging modality (CT vs. MRI) and large vessel occlusion status.
Since this clinical indication is not listed in the official prescribing information for alteplase** (B01AD02), performing IV thrombolysis in accordance with this recommendation is only possible based on a decision by a medical board (v врачебная комиссия). The upper limit of the time window for the last known well time was set at 12 hours based on the upper quartile of this time in the group of patients who received thrombolytic therapy according to MRI criteria in the WAKE-UP trial.
It is recommended to administer intravenous thrombolysis with #alteplase** (B01AD02) at a dose of 0.9 mg/kg of body weight (maximum dose 90 mg, 10% of the dose administered as an IV bolus over 1 minute, 90% as an IV infusion) to adult patients with acute ischemic stroke whose symptoms were detected upon awakening from sleep and who have a mismatch between the volumes of hypoperfusion and infarction zones on CT or MRI within 9 hours from the midpoint of sleep, in the absence of indications for mechanical thrombectomy or if it is not planned, in order to improve functional outcomes [411, 414].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: perfusion-to-core mismatch is evaluated using automated processing software and is defined as follows:
– infarct core volume *≤ 70 mL
and
– volume of critical hypoperfusion region** / infarct core volume * > 1.2
and
– mismatch between hypoperfusion volume and infarct core volume > 10 mL.
Data from the WAKE-UP trial [409], which evaluated the efficacy and safety of IV thrombolysis in wake-up stroke (WUS), indicate that when the exact time of symptom onset is unknown, performing thrombolysis with alteplase following preliminary MRI is associated with more favorable functional outcomes. In the presence of ischemic brain injury on DWI MRI and the absence of hyperintensity in the parenchyma on FLAIR MRI, it can be assumed that the stroke onset is within 4.5 hours, which in turn allows for the administration of intravenous alteplase** (B01AD02) to patients. This approach to deciding on IV thrombolysis in patients with WUS helps increase the number of patients with more favorable 90-day functional outcomes (OR, 1.62; 95% CI: 1.17–2.23; p = 0.003), despite a statistically non-significant increase in hemorrhagic complications (2.0% vs. 0.4%; p = 0.15).
In the EXTEND trial [396] alteplase** (B01AD02) was compared with placebo in patients with treatment initiation between 4.5 and 9 hours from stroke onset or in patients with symptom onset upon awakening if the midpoint of sleep was within 9 hours of treatment initiation. Inclusion criteria were: ischemic core volume < 70 mL, critical hypoperfusion volume / ischemic core volume > 1.2, volume mismatch > 10 mL, rCBF < 30% (perfusion CT). Patient enrollment was completed early following the publication of the WAKE-UP trial data. The trial demonstrated more favorable functional outcomes at day 90 in the alteplase group (mRS 0–1: OR, 1.44; 95% CI: 1.01–2.06; p = 0.04), despite a higher frequency of hemorrhagic complications (adjusted OR, 7.22; 95% CI: 0.97–53.5; p = 0.05).
Because this clinical indication is not included in the official prescribing information for alteplase** (B01AD02), performing IV thrombolysis in accordance with this recommendation is only possible based on a decision by a medical board.
It is recommended to use alteplase** (B01AD02) at the standard (0.9 mg/kg) rather than a reduced dose in adult patients with acute ischemic stroke within 4.5 hours of symptom onset who meet the criteria for intravenous thrombolysis, with the aim of improving disease outcomes [415].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: the ENCHANTED trial (3310 patients, 2/3 from Asian countries) did not prove the non-inferiority of the 0.6 mg/kg dose of alteplase** (B01AD02) compared to the standard 0.9 mg/kg dose regarding unfavorable functional outcomes (mRS score 2–6): 53.2% vs. 51.1% (OR, 1.09; 95% CI: 0.95–1.25, P for non-inferiority = 0.51). Meanwhile, the rate of symptomatic ICH was lower in the reduced-dose group (1.0% vs. 2.1%, p = 0.01) [415]. A pre-planned subgroup analysis did not identify any patients who benefited from low-dose IV thrombolysis [416–418].
It is recommended that adult patients with ischemic stroke receive antithrombotic therapy (antiplatelet agents other than heparin (B01AC)) within 24 hours after intravenous administration of alteplase** (B01AD02), if it is known that withholding antithrombotic therapy carries a substantial risk of thrombotic/thromboembolic events, to improve clinical outcomes [419].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: in most clinical scenarios, the initiation of antithrombotic therapy is postponed for 24 hours from the moment of intravenous thrombolysis (IV TLT); however, in certain cases, there is a need for early administration of anticoagulant or antiplatelet drugs (emergency stenting, thrombosis of prosthetic heart valves, etc.). A retrospective analysis of ischemic stroke patients admitted to a vascular center in Seoul revealed no increased risk of hemorrhagic complications when antiplatelet agents or anticoagulants were administered within the first 24 hours after IV alteplase** (B01AD02) thrombolysis or endovascular treatment compared to administration after 24 hours [412]. The study may have been subject to bias; therefore, the administration of antithrombotic drugs should be guided by an individual risk-benefit assessment.
The administration of antithrombotic agents within the first 24 hours following the administration of alteplase** (B01AD02) contradicts the official drug label and therefore must be justified by a medical board decision.
It is recommended that adult patients with ischemic stroke undergo intravenous thrombolysis with alteplase** (B01AD02) within 4.5 hours of symptom onset, regardless of prior antiplatelet therapy, to improve clinical outcomes [420–425].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment:the use of antiplatelet agents prior to ischemic stroke may increase the risk of symptomatic intracerebral hemorrhage (sICH) in patients receiving alteplase** (B01AD02)[426]. However, antiplatelet therapy(antiplatelet agents except heparin (B01AC))was not an exclusion criterion in randomized controlled trials (RCTs) on IV thrombolysis. A secondary analysis of the IST-3 study showed that the proportion of sICH in patients who received antiplatelet(antiplatelet agents except heparin (B01AC)) therapy within 48 hours prior to stroke onset exceeds that in patients who did not receive antiplatelet therapy(antiplatelet agents except heparin (B01AC))(9% vs 5%, p = 0.019), which does not affect the 6-month functional outcome[420].A secondary analysis of the ENCHANTED trial indicated an association between the standard dose of alteplase** (B01AD02) and the risk of sICH in patients receiving antiplatelet agents(antiplatelet agents except heparin (B01AC))prior to stroke[427],however, after adjustment for potential confounding factors, the use of antiplatelet agents(antiplatelet agents except heparin (B01AC))prior to stroke treatment was not associated with a poorer functional outcome[428].Other data also indicate that the use of one or two antiplatelet agents(antiplatelet agents except heparin (B01AC)) prior to IV thrombolysis is not associated with poorer functional outcomes or a higher risk of hemorrhagic complications[422–424].A recent meta-analysis of 9 observational studies involving over 66,000 ischemic stroke patients who received IV thrombolysis failed to confirm any association between dual antiplatelet(antiplatelet agents except heparin (B01AC)) therapy and the development of ICH, functional outcome, and mortality in adjusted analyses accounting for potential confounders[425].Thus, the use of antiplatelet agents(antiplatelet agents except heparin (B01AC)), including dual therapy, should not be regarded as a reason to withhold treatment.
It is recommended that adult patients with ischemic stroke presenting within 4.5 hours of symptom onset who are taking DOACs (dabigatran etexilate** (B01AE07), rivaroxaban** (B01AF01), apixaban** (B01AF02)), provided their last dose was taken more than 48 hours ago and they have normal renal function (Cockcroft-Gault creatinine clearance > 80 ml/min), undergo intravenous thrombolysis with alteplase** to reduce the risk of hemorrhagic complications [429, 430].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: performing IV thrombolysis is contraindicated in patients in a state of hypocoagulation. Considering that the half-life of DOACs in patients with normal renal function does not exceed 17 hours [431], 48 hours after the last dose is the period after which the anticoagulant effect of the drug has already worn off in a patient with normal renal function (creatinine clearance > 80 ml/min) [432].
It is recommended that adult patients with ischemic stroke presenting within 4.5 hours of symptom onset who are taking dabigatran etexilate** (B01AE07), provided their last dose was taken within the preceding 12–48 hours, or in the presence of a Cockcroft-Gault creatinine clearance below 80 ml/min, or if the time of the last dose is unknown, undergo intravenous thrombolysis with alteplase** (B01AD02) if thrombin time values are within the local laboratory reference range, with the goal of reducing the risk of hemorrhagic complications [433].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: the half-life of dabigatran etexilate** (B01AE07) in patients with normal renal function (creatinine clearance > 80 ml/min) does not exceed 12–17 hours [431]. If less than 48 hours have passed since the last dose, an anticoagulant effect of the drug may still be present. In patients with renal impairment, the half-life of dabigatran etexilate** (B01AE07) is prolonged; therefore, even when more than 48 hours have elapsed since the last dose, the presence of an anticoagulant effect cannot be ruled out. Consequently, evaluation of thrombin time is recommended in these clinical patient groups to rule out the presence of the anticoagulant effect of dabigatran etexilate** (B01AE07). Thrombin time is the test most sensitive to the action of dabigatran etexilate** (B01AE07). Normal thrombin time values completely rule out the presence of dabigatran etexilate** (B01AE07) in blood plasma [434].
It is recommended that adult patients with ischemic stroke presenting within 4.5 hours of symptom onset who are taking dabigatran etexilate** (B01AE07), provided their last dose was taken within the preceding 12–48 hours, or in the presence of a Cockcroft-Gault creatinine clearance below 80 ml/min, or if the time of the last dose is unknown, receive a specific reversal agent (idarucizumab (V03AB37)) prior to intravenous thrombolysis if thrombin time values are outside the local laboratory reference range, with the goal of reducing the risk of hemorrhagic complications [435-437].
GCR BLOE 3Grade of Recommendation B (Level of Evidence – 3)
Comment: an elevated thrombin time in a patient receiving dabigatran etexilate** (B01AE07) indicates the presence of the anticoagulant effect of dabigatran etexilate** (B01AE07). Idarucizumab (V03AB37) is a specific reversal agent for dabigatran etexilate** (B01AE07). Administration of idarucizumab (V03AB37) rapidly and sustainably neutralizes the effect of dabigatran etexilate** (B01AE07), as convincingly demonstrated in the RE-VERSE AD trial [438]. The feasibility of using idarucizumab (V03AB37) to neutralize the anticoagulant effect of dabigatran etexilate** (B01AE07) prior to IV thrombolysis in ischemic stroke patients has been demonstrated in a large series of clinical cases [435, 436].
According to the results of phase I–III studies of the specific dabigatran etexilate** (B01AE07) reversal agent idarucizumab (V03AB37), neutralization of the effect of dabigatran etexilate** (B01AE07) is achieved immediately after intravenous administration of idarucizumab (V03AB37) [438, 439]. Therefore, initiation of IV thrombolysis can be performed immediately after the end of the 5 g idarucizumab (V03AB37) infusion and subsequent blood draw for thrombin time determination, without waiting for the results of the latter. If the obtained thrombin time values exceed the upper limit of the local laboratory reference range, it is recommended to stop the IV thrombolysis procedure.
It is recommended that adult patients with ischemic stroke presenting within 4.5 hours of symptom onset who are taking dabigatran etexilate** (B01AE07), provided their last dose was taken within the preceding 12 hours, receive a specific reversal agent (idarucizumab (V03AB37)) prior to intravenous thrombolysis, with the goal of reducing the risk of hemorrhagic complications [435-437].
GCR BLOE 3Grade of Recommendation B (Level of Evidence – 3)
Comment: the half-life of dabigatran etexilate** (B01AE07) ranges from 12 to 17 hours [431]. Therefore, in situations where less than 12 hours have passed since the last dose of dabigatran etexilate** (B01AE07), it is highly likely that the drug is present in the blood plasma and, accordingly, that its anticoagulant effect is present. Administration of idarucizumab (V03AB37) rapidly and sustainably neutralizes the effect of dabigatran etexilate** (B01AE07), as convincingly demonstrated in the RE-VERSE AD trial [438]. The feasibility of using idarucizumab (V03AB37) to neutralize the anticoagulant effect of dabigatran etexilate** (B01AE07) prior to IV thrombolysis in ischemic stroke patients has been demonstrated in a large series of clinical cases [435, 436].
It is recommended that adult patients with ischemic stroke within 4.5 hours of symptom onset who are taking direct factor Xa inhibitors (B01AF) (rivaroxaban** (B01AF01), apixaban** (B01AF02)), provided their last dose was taken within the preceding 12–48 hours, or with a Cockcroft-Gault creatinine clearance of less than 80 mL/min, or if the time of the last dose is unknown, and in the absence of detectable plasma anti-Xa activity, receive intravenous thrombolysis with alteplase** (B01AD02) to reduce the risk of hemorrhagic complications [440, 441].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: The half-lives of factor Xa inhibitors in patients with normal renal function (creatinine clearance > 80 mL/min) do not exceed 14 hours. If less than 48 hours have elapsed since the last dose, an anticoagulant effect of the drug may still be present. In patients with renal impairment, the half-life of factor Xa inhibitors can be prolonged, meaning that even if more than 48 hours have passed since the last dose, the possibility of an ongoing anticoagulant effect cannot be excluded. Therefore, in these clinical patient groups, tests are recommended to rule out the presence of an anticoagulant effect. The only laboratory test that allows for a reasonably accurate assessment of the presence or absence of the anticoagulant effect of factor Xa inhibitors is the measurement of plasma anti-Xa activity. If a detectable level of plasma anti-Xa activity is identified, the patient should be considered to be in a state of hypocoagulation. Given the lack of a specific reversal agent to neutralize the anticoagulant effect of these drugs, intravenous thrombolysis in such patients is not recommended [441].
It is not recommended to administer intravenous thrombolysis with alteplase** (B01AD02) to adult patients with ischemic stroke within 4.5 hours of symptom onset who are taking direct factor Xa inhibitors (B01AF) (rivaroxaban** (B01AF01), apixaban** (B01AF02)) with a last-dose administration time of less than 12 hours, for the purpose of improving disease outcome [440, 441].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: The half-lives of direct factor Xa inhibitors (B01AF) in patients with normal renal function range from 5 to 14 hours depending on the patient's age and the specific drug [441]. Consequently, in situations where less than 12 hours have elapsed since the last dose of apixaban** (B01AF02) or rivaroxaban** (B01AF01), it is highly probable that the drug is present in the plasma and, accordingly, exerts an anticoagulant effect. Given the lack of a specific reversal agent to neutralize the anticoagulant effect of these drugs, performing intravenous thrombolysis in such patients is not recommended.
It is recommended that adult patients over 80 years of age with ischemic stroke within 4.5 hours of symptom onset and without other contraindications undergo intravenous thrombolysis with alteplase** (B01AD02) to improve functional outcome [442, 443].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: In an individual participant data meta-analysis [442] the odds ratio for an excellent outcome (mRS score 0–1) in patients older than 80 years who received alteplase** (B01AD02) was 1.56 (95% CI: 1.17–2.08), compared to 1.25 (95% CI: 1.10–1.42) in patients aged 80 years or younger, with no evidence of a difference in efficacy between the groups; there was also no evidence that the risk of intracranial hemorrhage was higher in patients over 80 years of age compared to younger patients.
It is recommended that adult patients with disabling ischemic stroke and a neurological deficit severity of NIHSS < 5 points within 4.5 hours of symptom onset, with no other contraindications, undergo intravenous thrombolysis with alteplase** (B01AD02) to improve functional outcome [445].
GOR ALE 2Grade of Recommendation A (Level of Evidence – 2)
Comment: Approximately half of all ischemic strokes are initially mild (usually defined as an NIHSS score < 5), but up to a third of patients with minor stroke become disabled or die within 3 months of disease onset [445, 446]. Meta-analysis has shown that in patients with mild, moderate, and severe strokes, the proportional beneficial effect of alteplase** (B01AD02) did not statistically differ. In patients with a baseline NIHSS score of 0–4, the odds ratio for an excellent outcome (mRS score 0–1 at 3 months) was 1.48 (95% CI: 1.07–2.06) [444] These findings support the use of alteplase** (B01AD02) in patients with minor disabling stroke.
A disabling deficit should be considered any deficit that, if left unchanged, would prevent the patient from performing activities of daily living (i.e., bathing, mobility, using the toilet, personal hygiene, and eating) or returning to work [447]. Potential scenarios may include (but are not limited to) the following clinical situations: complete hemianopia, severe aphasia, hemispatial neglect, motor deficit limiting effort against gravity (the patient cannot keep the paretic arm and/or leg elevated against gravity), or any other focal symptoms that can be considered disabling for a specific patient depending on the nature of their work and lifestyle characteristics.
It is recommended that adult patients with non-disabling ischemic stroke and a neurological deficit severity of NIHSS < 5 points within 4.5 hours of symptom onset, with large vessel occlusion and no other contraindications, undergo intravenous thrombolysis with alteplase** (B01AD02) to prevent the progression of neurological deficit [446, 447].
GCR BLOE 3Grade of Recommendation B (Level of Evidence – 3)
Comment: Patients with large vessel occlusion have a higher risk of stroke progression and unfavorable prognosis compared to other patients [447]. Multicenter observational studies indicate a potential beneficial effect of intravenous thrombolysis [445] and staged reperfusion therapy [446] in patients with minor ischemic stroke and large vessel occlusion.
In accordance with the official prescribing information for alteplase** (B01AD02), the use of the drug in patients with mild stroke is not recommended; therefore, a medical board (consilium) decision is required to implement this recommendation.
It is recommended that adult patients with ischemic stroke within 4.5 hours of disease onset and a systolic blood pressure > 185 mmHg or diastolic blood pressure > 110 mmHg, provided their blood pressure is lowered to < 185 and < 110 mmHg respectively, undergo intravenous thrombolysis with alteplase** (B01AD02) or a recombinant protein containing the amino acid sequence of staphylokinase** (B01AD) to improve functional outcome [394, 448, 449].
GGR BLoE 2Recommendation Grade B (Level of Evidence – 2)
Comment: Pre-treatment blood pressure lowering to less than 185/110 mmHg was permitted in all completed randomized controlled trials of the efficacy and safety of alteplase in patients with ischemic stroke, and thus their results can be extrapolated to this category of patients.
In the ENCHANTED trial, 2,196 patients with systolic blood pressure values ranging from 150 to 185/110 mmHg, meeting the inclusion criteria for potential intravenous thrombolysis with alteplase** (B01AD02), were randomized into two groups: intensive systolic blood pressure lowering (target values of 130–140 mmHg within one hour) and target systolic blood pressure lowering below 180 mmHg, with the goal of maintaining target values for at least 72 hours [448]. The mean systolic blood pressure at 24 hours was 144 ± 10 mmHg in the intensive blood pressure-lowering group and 150 ± 12 mmHg in the control group. However, the degree of functional recovery at 90 days did not differ between patients in both groups (OR 1.01; 95% CI: 0.87–1.17; p = 0.87). The intensive blood pressure-lowering group showed a statistically significantly lower incidence of any intracerebral hemorrhage (14.8%) compared to the control group (18.7%) [OR 0.75; 0.60–0.94; p = 0.01]. Blood pressure reduction was also associated with a statistically non-significant decrease in the number of type 2 parenchymal hemorrhages (OR 0.71; 95% CI: 0.50–1.01). Analysis of data from the IST-3 trial showed that the use of antihypertensive therapy in the first 24 hours of monitoring is associated with a lower risk of an unfavorable outcome (3–6 points on the Oxford Handicap Scale) at 6 months of follow-up (OR 0.78; 95% CI: 0.65–0.93; p = 0.007), regardless of whether intravenous thrombolysis with alteplase** (B01AD02) was performed or not [449].
It is recommended that adult patients with ischemic stroke presenting within 4.5 hours of symptom onset who have a history of diabetes mellitus undergo intravenous thrombolysis to improve functional outcomes [394, 450].
GCR CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: only two of the nine RCTs (ECASS-3 and IST-3) included in the individual patient data meta-analysis evaluated the efficacy of intravenous thrombolysis with alteplase depending on the presence or absence of a history of diabetes mellitus. It was demonstrated that a history of diabetes mellitus does not negatively affect the degree of functional recovery in patients, according to either ECASS-3 or IST-3 results. Furthermore, a history of diabetes mellitus in patients in the intravenous thrombolysis group with alteplase** (B01AD02) did not affect the increase in mortality and the frequency of symptomatic intracranial hemorrhage. It should be noted that an analysis of data from 54,206 SITS registry patients who received intravenous thrombolysis with alteplase** (B01AD02) revealed no effect of a history of diabetes mellitus on the incidence of symptomatic intracranial hemorrhage, the degree of functional recovery, or 90-day mortality [450].
It is not recommended to perform intravenous thrombolysis in adult patients with ischemic stroke within 4.5 hours of symptom onset and subacute ST-elevation myocardial infarction (from 6 hours to 7 days) in order to reduce the risk of complications (myocardial rupture, cardiac tamponade, embolism from the ventricular cavity) [451–453].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: the literature contains case reports of alteplase** (B01AD02) treatment in ischemic stroke patients with acute myocardial infarction complicated by rupture and cardiac tamponade [451–453]. A retrospective review of 102 cases of treatment in patients with ischemic stroke and a history of acute myocardial infarction showed that 4 patients who received r-tPA died from confirmed or suspected cardiac rupture/tamponade; all of them had an ST-elevation myocardial infarction within the week prior to the ischemic stroke. In the group that did not receive r-tPA, this complication occurred in one patient. None of the patients with non-ST-elevation myocardial infarction who received r-tPA experienced cardiac complications [454]. Therefore, when deciding on intravenous thrombolysis in patients with ischemic stroke and recent or concurrent myocardial infarction, the type of infarction and the time elapsed between the two events must be taken into account.
It is not recommended to perform intravenous thrombolysis in adult patients with ischemic stroke within 4.5 hours of symptom onset and confirmed or suspected infective endocarditis, in order to reduce the risk of hemorrhagic complications [455–457].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: cerebral infarctions caused by septic emboli are particularly prone to hemorrhagic transformation resulting from septic arteritis with erosion of the arterial wall and the formation of mycotic aneurysms [458].
It is recommended to consider the use of #tenecteplase** (ATX B01AD11) at a dose of 0.25 mg/kg, administered as a single bolus injection within 4.5 hours of ischemic stroke symptom onset, including in patients with large vessel occlusion scheduled for mechanical thrombectomy (thromboextraction), as an alternative to alteplase** (B01AD02) at 0.9 mg/kg in adult patients with ischemic stroke, to improve functional outcomes [459-467].
GCR ALoE 2Grade of Recommendation A (Level of Evidence – 2).
Comments: this approach is based on the results of the randomized clinical trials TNK-S2B, TAAIS, ATTEST, EXTEND-IA TNK, TRACE, TASTE-A, AcT, NOR-TEST, and NOR-TEST 2 [459-467] and the recommendations of the European Stroke Organisation (ESO) based on a meta-analysis of 2,842 ischemic stroke patients, which showed that the rates of achieving an optimal functional outcome (mRS 0–1 score) in patients who received thrombolysis with #tenecteplase** (ATX B01AD11) 0.25 mg/kg did not significantly differ from those with alteplase** (B01AD02) 0.9 mg/kg (OR 1.17 [95% CI: 0.98–1.39; p=0.08; I2=0%]). Meanwhile, for #tenecteplase** (ATX B01AD11) at 0.40 mg/kg, the estimate for achieving an mRS score of 0–1 was 0.73 (95% CI: 0.36–1.48; p=0.38; I2=76%), failing to demonstrate non-inferiority to alteplase** (B01AD02). The incidence of symptomatic intracranial hemorrhage and extracranial bleeding did not differ between treatment groups, nor did 3-month mortality rates, which were comparable (OR=0.88; 95% CI: 0.65–1.19; p=0.39; I2=7%). There was also no significant difference in door-to-needle time (median difference = −3.7 min; 95% CI: −9.5 to 2.2 min; p=0.22; I2=83%) [468]. Based on available data, #tenecteplase** (ATX B01AD11) was approved for use in ischemic stroke in Europe in 2024 [469, 470]. For ischemic stroke, #tenecteplase** (ATX B01AD11) is used at a dose of 0.25 mg/kg (maximum dose not to exceed 25 mg) within 4.5 hours of symptom onset and after ruling out intracranial hemorrhage. The required dose of #tenecteplase** (ATX B01AD11) is administered as a rapid single bolus injection over 5–10 seconds [471].
It is not recommended to perform intravenous thrombolysis in adult patients with verified ischemic stroke due to cerebral venous thrombosis in order to reduce the risk of hemorrhagic complications [472, 473.].
Level of Evidence AGrade of Evidence 3Level of Recommendations A (Grade of Evidence – 3)
Comment: Data regarding the efficacy of intravenous thrombolysis in cerebral venous thrombosis are extremely limited. Published studies have demonstrated a high incidence of major hemorrhagic complications (9.8–11.5%) and intracranial hemorrhage (7.6–11.5%), including symptomatic events [472, 473]. An additional argument against systemic thrombolysis in cerebral venous thrombosis is the need to initiate therapeutic doses of anticoagulants as early as possible.
3.1.2.1.2. Mechanical recanalization using endovascular devices
General Provisions
It is recommended that adult patients with ischemic stroke undergo thrombolysis, if indicated, when planning mechanical thrombectomy (A16.23.034.013) to restore cerebral blood flow [474-480].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: the results of the randomized trials MR CLEAN-NO IV, SKIP, DEVT, and data from several registries do not support omitting thrombolysis when planning mechanical thrombectomy A16.23.034.013. Nor do they allow for the identification of a patient subgroup in which omitting thrombolysis would be justified [474–480].
It is recommended that adult patients with ischemic stroke not have mechanical thrombectomy (A16.23.034.013) delayed while awaiting thrombolysis results, with the aim of restoring cerebral blood flow [481].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: a meta-analysis of individual patient data from 7 randomized trials (728 patients) showed a significant decrease in the probability of reperfusion with increasing time from hospital arrival to arterial puncture (a relative reduction of 22% per hour), as well as with increasing time from imaging to puncture (26% per hour); therefore, time to mechanical thrombectomy (A16.23.034.013) must be minimized [481]. As a meta-analysis of 5 randomized trials demonstrated, mechanical thrombectomy (A16.23.034.013) was equally effective both in the group undergoing endovascular intervention combined with thrombolysis (OR = 2.45; 95% CI 1.68–3.57) and without thrombolysis (OR = 2.43; 95% CI 1.3–4.55) compared to standard care [482].
3.1.2.1.3. Endovascular interventions in the carotid system
It is recommended that adult patients with ischemic stroke and a large intracranial artery occlusion in the anterior circulation, with a neurological deficit severity of 6 or more on the NIHSS and an ASPECTS of 6 or more, undergo mechanical thrombectomy (A16.23.034.013) within 6 hours of symptom onset or last known well time, with the aim of restoring cerebral blood flow [482].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: modern meta-analyses of randomized trials of mechanical thrombectomy (A16.23.034.013) for anterior circulation ischemic stroke indicate higher efficacy of endovascular interventions compared to standard care in the presence of verified large intracranial artery occlusion [489–492]. A meta-analysis of data from the HERMES Collaboration also showed improved functional outcomes when mechanical thrombectomy (A16.23.034.013) was performed in the M2 middle cerebral artery segment occlusion group compared to standard care (OR = 2.39; 95% CI 1.08–5.28) [482].
It is recommended that adult patients with ischemic stroke and an NIHSS score of 6 or more, with a major intracranial artery occlusion in the anterior circulation, an ischemic core volume of less than 70 mL, a ratio of perfusion deficit volume to ischemic core volume of at least 1.8, and a mismatch volume (penumbra) of at least 15 mL, undergo mechanical thrombectomy (A16.23.034.013) between 6 and 16 hours to improve functional outcomes [133].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: the multicenter randomized DEFUSE-3 trial demonstrated improved functional outcomes in patients undergoing mechanical thrombectomy (A16.23.034.013) of the ICA and proximal MCA M1 segment at 6–16 hours from stroke onset when selected based on perfusion imaging assessment of ischemic core structure. Mechanical thrombectomy (A16.23.034.013) compared with standard medical therapy was associated with a favorable shift in the distribution of functional outcomes on the modified Rankin scale at 90 days (OR = 2.77, p < 0.001) and a higher proportion of functionally independent patients (0–2 points on the modified Rankin scale) — 45% vs. 17% (p < 0.001). The 90-day mortality was 14% in the mechanical thrombectomy group and 26% in the medical therapy group (p = 0.05); the incidence of symptomatic intracranial hemorrhage did not significantly differ between the groups (7% and 4%, respectively, p = 0.75) [133].
It is recommended to perform mechanical thrombectomy (A16.23.034.013) within 6 to 24 hours in adult patients with acute ischemic stroke due to large intracranial arterial occlusion in the anterior circulation, aged 80 years and older with an NIHSS score of 10 or more and an ischemic core volume of less than 21 ml, aged under 80 years with an NIHSS score of 10–19 and an ischemic core volume of less than 31 ml, as well as with an NIHSS score of 20 or more and an ischemic core volume of 31–50 ml according to neuroimaging data, to improve functional outcome [132].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: the multicenter randomized DAWN trial demonstrated improved functional outcomes after mechanical thrombectomy (A16.23.034.013) of the ICA and proximal MCA M1 segment within the first 6–24 hours compared with standard medical therapy when selecting patients based on stroke severity and ischemic core volume. The rate of functional independence at 90 days was 49% in the mechanical thrombectomy group (A16.23.034.013) compared with 13% in the control group. The incidence of symptomatic intracranial hemorrhage did not significantly differ between the two groups (6% in the mechanical thrombectomy group and 3% in the control group, p = 0.50) [132].
It is recommended to perform mechanical thrombectomy (A16.23.034.013) in adult patients with acute ischemic stroke and large intracranial arterial occlusion in the anterior circulation with NIHSS < 6 points to prevent disabling neurological deficit and improve outcome [490].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: a systematic review of randomized trials with meta-analysis showed a comparable effect across the entire spectrum of neurological deficit severity (by NIHSS); however, in the subgroup with 10 points or less, mechanical thrombectomy (A16.23.034.013) showed lesser efficacy compared with standard therapy (OR = 1.67; 95% CI 0.8–3.5), possibly due to the small sample size of this subgroup [490]. A meta-analysis on endovascular treatment of "minor stroke" (NIHSS < 6) showed similar 90-day functional outcomes when treating these patients with mechanical thrombectomy versus medical therapy [493]. According to another meta-analysis, performing mechanical thrombectomy (A16.23.034.013) for "minor stroke" (defined as NIHSS < 9) resulting from large intracranial artery occlusion led to improved 90-day outcomes (OR = 1.68; 95% CI 1.08–2.61) [494].
It is recommended for patients with acute ischemic stroke meeting specific criteria (confirmed large intracranial artery occlusion in the anterior circulation with grade 1–3 collateral blood flow on multiphase CT angiography, age 18 years and older, NIHSS score of 2 or more points) to undergo mechanical thrombectomy (A16.23.034.013) as an alternative approach within 6 to 24 hours from symptom onset (or time last known well) to improve functional outcome [495].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: the multicenter randomized MR CLEAN LATE trial (n=535) evaluated the feasibility of performing mechanical thrombectomy (A16.23.034.013) in the late time window of 6–24 hours from symptom onset (or time last known well) bypassing CT perfusion, based solely on collateral cerebral blood flow assessment on CT angiography or MR angiography. Patients treated according to the MR CLEAN LATE criteria in the 6–24 hour window bypassing CT perfusion had more favorable 90-day functional outcomes assessed by the modified Rankin scale compared with the control group receiving no endovascular treatment (adjusted OR 1.67, 95% CI 1.20–2.32). This approach avoids the time delay of CT perfusion and accelerates the initiation of surgical treatment in a subset of patients. Patient selection criteria included: confirmed large intracranial artery occlusion in the anterior circulation, age 18 years and older, time from symptom onset (or time last known well) of 6–24 hours, NIHSS score of 2 or more points, and confirmed collateral blood flow in the territory of the infarct-related artery based on multiphase (visualizing arterial, capillary, and venous phases) CT angiography.
The presence of grade 1 collateral blood flow (filling of 50% or less of collaterals, but greater than 0%), grade 2 (filling of more than 50% of collaterals), and grade 3 (100% collateral filling) was chosen as the criterion for collateral blood flow [496, 497].
It is recommended that adult patients with ischemic stroke presenting with combined extracranial and intracranial occlusion of the carotid artery system undergo extracranial stenting (A16.12.026.020 Endovascular angioplasty and stenting of brachiocephalic vessels) combined with EVTE (A16.23.034.013 Local endovascular transarterial thromboextraction) to ensure access to the intracranial lesion, eliminate hemodynamically significant symptomatic stenosis, and/or prevent re-occlusion [498].
GCR CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: a large meta-analysis demonstrated that the use of EVTE (A16.23.034.013) was equally effective both in the presence of tandem extracranial and intracranial carotid artery lesions (OR = 2.95; 95% CI 1.38–6.32) and in isolated intracranial occlusion (OR = 2.35; 95% CI 1.68–3.28) compared to standard therapy [499]. A systematic review with meta-analysis including 1,000 patients from 23 studies showed no effect of emergency carotid angioplasty in tandem lesions (no differences in successful recanalization rate, good functional outcomes, and 90-day mortality) while increasing operative time and complication risk [500]. A non-randomized comparative study showed that performing carotid angioplasty with stenting prior to EVTE (A16.23.034.013) in tandem lesions provided better functional outcomes than in the EVTE group (A16.23.034.013) without tandem lesions. It was noted that dual antiplatelet therapy did not increase the likelihood of symptomatic intracranial hemorrhage, while #clopidogrel** (B01AC04) was safer than #ticagrelor** (B01AC24) [501]. Data from the TITAN registry also demonstrate that patients undergoing EVTE (A16.23.034.013) and carotid angioplasty with stenting prescribed with antiplatelet therapy more frequently achieved successful reperfusion and good 90-day functional outcomes [498]. Thus, in cases of emergency stenting, the administration of DAPT is indicated
3.1.2.1.4. Endovascular interventions in the vertebrobasilar system
It is recommended that adult patients with ischemic stroke presenting with acute occlusion of the basilar artery or the intracranial segment of the vertebral artery undergo EVTE (A16.23.034.013) within 24 hours of stroke onset to improve functional outcomes [504].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: in patients with basilar artery occlusion, successful reperfusion is an important predictor of 90-day functional outcome, with the proportion of mRS 0–2 reaching 36.8–44.8% [505, 506]. A large systematic review and meta-analysis including 102 articles showed better functional outcomes and recanalization rates in patients with acute basilar artery occlusion treated with EVTE (A16.23.034.013) compared to thrombolytic therapy (systemic, intra-arterial) groups [507]. According to the BASILAR registry, which included 829 patients, performing EVTE (A16.23.034.013) within 24 hours of occlusion of the basilar artery and the V4 segment of the vertebral artery reduced mortality and increased the proportion of good functional outcomes [508].
It is recommended that adult patients with ischemic stroke presenting with acute isolated occlusion of the posterior cerebral artery undergo EVTE (A16.23.034.013) within the first 24 hours from disease onset to improve functional outcomes [509, 510].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
3.1.2.1.5. Special cases
It is recommended that adult patients with ischemic stroke in the carotid and vertebrobasilar territories undergo balloon angioplasty and/or intracranial artery stenting (Endovascular angioplasty and stenting of major intracranial vessels, A16.12.026.019) in cases of failed mechanical thrombectomy (A16.23.034.013) due to intracranial atherosclerotic disease or dissection, in order to restore cerebral blood flow [511].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: intracranial atherosclerotic disease or arterial dissection are potential causes of mechanical thrombectomy (A16.23.034.013) failure in large intracranial arteries. In a series of 34 patients undergoing intracranial angioplasty and stenting (A16.12.028.016) for acute reocclusion or significant stenosis, technical success was achieved in 97%, and successful reperfusion (mTICI 2b–3) in 76% of cases. At 90 days, a good functional outcome (mRs 0–2) was observed in 22% of patients with carotid ischemic stroke and 38% of patients with vertebrobasilar ischemic stroke [512].
In a systematic review and meta-analysis involving 1,315 ischemic stroke patients caused by intracranial atherosclerotic disease, intracranial stenting with or without prior angioplasty (A16.12.028.016) was performed in 261 cases (32.7%), and angioplasty without stenting in 98 patients (12.3%). Compared to the group of patients with embolic ischemic stroke, a comparable rate of recanalization and good functional outcomes was noted. The incidence of symptomatic intracranial hemorrhage in the intracranial atherosclerotic disease group, who more frequently required intracranial stenting (A16.12.028.016), was significantly lower (OR = 0.60; 95% CI 0.46–0.77) [513].
A retrospective analysis of experience from seven centers, including 210 ischemic stroke patients who underwent emergency intracranial stenting (64.8% in the carotid circulation), showed a higher incidence of symptomatic intracranial hemorrhages with carotid stenting (86.4%) compared to vertebrobasilar stenting (13.6%), with an overall good functional outcome rate of 44.8% [514]. These findings can be explained by the fact that intracranial atherosclerotic disease as a stroke etiology is more frequent in the vertebrobasilar territory, and the rate of hemorrhagic complications is lower in atherosclerotic lesions compared to embolic ones [514].
According to the ANGEL-ACT registry, stenting (A16.12.028.016) in acute basilar artery occlusion achieved successful reperfusion (mTICI 2b–3) in 92.6% of cases, leading to a higher rate of mRs 0–3 functional outcome (59.1%) and reduced mortality (18.5%) at 90 days without increasing the incidence of symptomatic intracranial hemorrhage [515].
It is recommended that adult patients with acute occlusion of a major intracranial artery occurring during any endovascular procedure undergo immediate mechanical thrombectomy (A16.23.034.013) in the absence of intracranial hemorrhage signs to prevent ischemic stroke [516].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: occlusion of a major intracranial artery during an endovascular procedure (coronary angioplasty/stenting, carotid angioplasty/stenting, cerebral aneurysm/arteriovenous malformation embolization, diagnostic angiography, and other therapeutic and diagnostic interventions) may be the cause of procedural embolic ischemic stroke. In the absence of clinical and neuroimaging evidence of intracranial hemorrhage, such occlusion should be considered a procedural complication and managed by immediate endovascular thrombectomy to prevent ischemic stroke, without delaying reperfusion time or performing additional diagnostic workup [516].
It is not recommended to withhold mechanical thrombectomy (A16.23.034.013) in adult ischemic stroke patients aiming to improve functional outcomes based solely on criteria such as antithrombotic (anticoagulant) therapy use or laboratory coagulation abnormalities (elevated INR, aPTT, etc.) [517].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
Comment: coagulation abnormalities are frequently observed both in patients receiving anticoagulant therapy (e.g., following artificial valve replacement, in atrial fibrillation, etc.) and as a result of the natural course of various diseases and pathological conditions. Anticoagulant therapy may be used by approximately 16% of patients undergoing mechanical thrombectomy (A16.23.034.013) [517]. Considering contraindications to thrombolytic therapy, mechanical thrombectomy (A16.23.034.013) often remains the only reperfusion modality with the potential to improve functional outcomes.
A large multicenter cohort study (1,932 patients) demonstrated that mechanical thrombectomy (A16.23.034.013) in patients taking vitamin K antagonists is associated with an increased risk of symptomatic intracranial hemorrhage (OR = 1.92; 95% CI 1.16–3.17) and mortality (OR = 1.68; 95% CI 1.21–2.33), whereas direct oral anticoagulants did not affect the rate of these events [517]. Furthermore, patients taking direct oral anticoagulants had a higher rate of technical success compared to those taking vitamin K antagonists (mTICI 2b–2c–3: 93.2% vs. 81.5%, respectively; p = 0.016). The rate of good functional outcome at 90 days post-thrombectomy was lower in patients taking vitamin K antagonists compared to those on direct oral anticoagulants or no anticoagulation (33%, 43.9%, and 44.7%, respectively), although multivariable analysis revealed no statistically significant differences [517]. A meta-analysis of observational studies (7,462 patients) confirms these findings regarding a higher rate of symptomatic intracranial hemorrhage in vitamin K antagonist users undergoing mechanical thrombectomy [517]. Conversely, data from the RESCUE-Japan Registry 2 showed no differences in successful reperfusion rates (mTICI 2b–3), good functional outcomes (mRs 0–2) at 90 days, and symptomatic intracranial hemorrhage rates between warfarin** users with an INR ≤ 1.7 vs. > 1.7, compared to direct oral anticoagulant users [518]. The decision to perform mechanical thrombectomy (A16.23.034.013) in patients receiving vitamin K antagonists should be made on an individual basis after balancing the risks and benefits of the procedure.
It is recommended to consider endovascular treatment for adult patients with severe cerebral venous thrombosis who show clinical and/or radiological signs of disease progression despite adequate anticoagulation therapy, with the aim of reducing mortality [519].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: Endovascular treatment can rapidly achieve sinus recanalization and arrest the pathophysiology of life-threatening cerebral venous thrombosis complications, such as symptomatic hemorrhagic transformation and cerebral edema. The main endovascular techniques for cerebral venous thrombosis include mechanical thrombectomy, local thrombolysis (including prolonged infusions), and combinations thereof. In the TO-ACT trial (Thrombolysis or Anticoagulation for CVT), clinical benefit from endovascular treatment over anticoagulation alone was not proven [520]. However, a subsequent systematic analysis of 10 studies (n=339) demonstrated that endovascular treatment can be an effective and safe option for cerebral venous thrombosis patients in whom anticoagulants fail or are contraindicated. Complete or partial recanalization rates reached 90%. Seventy-two percent of patients were discharged with minimal or no neurological deficit. The rate of hemorrhagic transformation was 3%, and mortality was 7% [519]. Endovascular treatment should be considered only as second-line therapy in the presence of clinical and/or radiological signs of cerebral venous thrombosis progression despite adequate anticoagulation [521].
3.1.2.2. Antithrombotic therapy
It is recommended to prescribe antithrombotic therapy to pediatric patients with ischemic stroke, provided there is no intracranial hemorrhage, with the aim of improving functional outcomes [41, 72, 326, 523].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: clinical studies have established the safety of anticoagulant and antiplatelet therapy in children. The risk of intracerebral hemorrhage with anticoagulant therapy is 11% [522].
It is recommended to administer heparin sodium** (unfractionated heparin) to pediatric patients diagnosed with arterial ischemic stroke before etiology is established, for 5–7 days, with the aim of improving functional outcomes [50, 72, 523].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: Initial dose – 75–100 IU/kg IV bolus over 10 minutes. Maintenance dose: children aged 1–3 months – 25–30 IU/kg/hour (800 IU/kg/day), children aged 4–12 months – 25–30 IU/kg/hour (700 IU/kg/day), children older than 1 year – 18–20 IU/kg/hour (500 IU/kg/day) IV drip. The dose of heparin sodium** should be adjusted based on blood coagulation parameters (target aPTT level 60–85 seconds). Continuous intravenous infusion of heparin sodium** without a loading dose is possible. Monitoring of aPTT is required before administration and 4 hours after administration; dosage titration is performed until target aPTT values are achieved. If anti-Xa activity determination is available, the target level is 0.35–0.7 IU/ml [524.].
It is recommended to prescribe low-molecular-weight heparin (LMWH, ATC group: heparin group B01AB) prior to etiology determination for 5–7 days in pediatric patients diagnosed with arterial ischemic stroke in order to improve functional outcome [72, 326, 523, 525].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in pediatric practice, LMWHs (B01AB) are not approved according to the prescribing information and must be prescribed in accordance with an off-label protocol. When prescribing LMWHs (B01AB), anti-Xa activity monitoring is required 4–6 hours after subcutaneous injection, with target values of 0.5–1.0 [524.].
Therapeutic dosages of LMWHs (B01AB): in patients older than 2 months, #enoxaparin** 1 mg/kg every 12 hours; younger than 2 months, 1.5 mg/kg every 12 hours; #dalteparin** 129 ± 43 IU/kg every 24 hours. Prophylactic dosages of #LMWHs: in patients older than 2 months, #enoxaparin** 0.5 mg/kg every 12 hours; younger than 2 months, 0.75 mg/kg every 12 hours; #dalteparin** 92 ± 52 IU/kg every 24 hours [72, 525].
It is recommended to prescribe #acetylsalicylic acid** (#ASA**) prior to etiology determination for 5–7 days in pediatric patients diagnosed with arterial ischemic stroke in order to improve functional outcome [50, 72, 523].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in pediatric practice, #ASA** drugs are not approved according to the prescribing information and must be prescribed in accordance with an off-label protocol. The recommended dosage is 3–5 mg/kg/day [524]. If dose-dependent side effects occur (epistaxis, gastrointestinal lesions), the dosage may be reduced to 1–3 mg/kg/day [72, 524]
It is recommended to prescribe #ASA** (B01AC06) to pediatric patients with a confirmed diagnosis of ischemic stroke for the prevention of recurrent ischemic strokes over a period of 2 years, provided that dissection of major arteries (CASCADE type 4a) and cardioembolic ischemic stroke (CASCADE type 5a) are excluded [50, 72, 524].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: There is no safety or efficacy advantage of anticoagulants over antiplatelet agents [526].
It is recommended to prescribe gastroprotective therapy (A02BC Proton pump inhibitors) in children with ischemic stroke receiving long-term #ASA** (B01AC06) therapy [326].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to administer varicella vaccination and annual influenza vaccination to pediatric patients with ischemic stroke receiving #ASA** (B01AC06) to reduce the risk of Reye's syndrome [50, 72].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to perform platelet aggregation testing (A12.05.017) (with arachidonic acid) in pediatric patients with ischemic stroke receiving #ASA** to reduce the risk of bleeding and detect #ASA** resistance [527–529].
GGR BLEL 3Grade of Recommendation B (Level of Evidence – 3)
Comment: It is known that the administration of modern antithrombotic agents (except for warfarin**) in adult patients does not require laboratory monitoring due to their receptor-oriented nature, proven dosing regimen, and numerous studies demonstrating the safety of these drugs at doses recommended by the manufacturer. However, these statements cannot be unconditionally extrapolated to the pediatric population of patients with ischemic stroke (IS) and/or transient ischemic attack (TIA). Given the combined etiological factors of acute cerebrovascular accident (CVA), the instability of the hemostatic system in children, potential resistance to therapy, age-related features of drug pharmacokinetics, and the potentially high risk of complications, including those of a non-hemorrhagic spectrum, there is a need to monitor the safety profile in pediatric patients. Target aggregation values in children with stroke/TIA receiving #ASA** are considered achieved when aggregation indices with arachidonic acid decrease below 30 U (using the Multiplate Analyzer) or when aggregation with ADP decreases by at least 30% from the lower limit of normal. According to studies by Lvova O.A. and Gusev V.V. (2014, 2017) in 82 patients who underwent IS with onset under the age of 18 and received aspirin and clopidogrel, monitoring of platelet aggregation capacity necessitated therapy adjustment in 35.4% (n=29) of children [40, 530 – 532].
It is recommended to switch pediatric patients with ischemic stroke from #ASA** to #LMWH (B01AB) or #warfarin** (B01AA03) if side effects occur and/or in the event of a TIA and/or recurrent ischemic stroke [524, 533].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: the most commonly prescribed vitamin K antagonist is warfarin** (B01AA03). Its use in children older than 6 years is permitted in the Russian Federation. The starting dose is 0.2 mg/kg with normal liver function and 0.1 mg/kg with impaired liver function; titration is performed to target INR values (2 to 3). INR monitoring is recommended on the 5th day of administration and, after achieving target values, once every 4–8 weeks. The prescription of #warfarin** in children under 6 years of age must comply with an off-label protocol. For infants, a starting dosage of 0.33 mg/kg is possible, with target INR values from 2 to 3 [525]. In pediatric practice, LMWHs (B01AB) are not approved according to the prescribing information and must be prescribed in accordance with an off-label protocol. Therapeutic dosages of LMWHs (B01AB): in patients older than 2 months, #enoxaparin sodium** 1 mg/kg every 12 hours; younger than 2 months, 1.5 mg/kg every 12 hours; #dalteparin sodium** 129 ± 43 IU/kg every 24 hours. Prophylactic dosages of #LMWHs: in patients older than 2 months, #enoxaparin sodium** 0.5 mg/kg every 12 hours; younger than 2 months, 0.75 mg/kg every 12 hours; #dalteparin sodium** 92 ± 52 IU/kg every 24 hours [72, 525].
It is recommended to continue therapy with #LMWH (B01AB) or #warfarin** (B01AA03) for 3–6 months or longer if indicated, in pediatric patients with confirmed ischemic stroke due to major artery dissection (CASCADE 4a) [50, 524].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: The use of #warfarin** (B01AA03) in children older than 6 years is permitted in the Russian Federation. The starting dose is 0.2 mg/kg with normal liver function and 0.1 mg/kg with impaired liver function; titration is performed to target INR values (2 to 3). INR monitoring is recommended on the 5th day of administration and, after achieving target values, once every 4–8 weeks. The prescription of #warfarin** in children under 6 years of age must comply with an off-label protocol. For infants, a starting dosage of 0.33 mg/kg is possible, with target INR values from 2 to 3 [525]. Continuing anticoagulant therapy for more than 6 months is advisable in patients with recurrent TIAs and/or ischemic strokes. If radiological signs of dissection persist, continuation of antiplatelet therapy may be considered [72, 536].
It is recommended to administer anticoagulant therapy for at least 1 year or until the correction of the cardiac defect responsible for the embolism in pediatric patients with confirmed ischemic stroke of cardioembolic etiology (CASCADE 5a) to reduce the risk of recurrent stroke. If the risk of cardiac embolism remains high one year later or after defect correction, anticoagulant therapy should be continued indefinitely [50, 72, 536].
GRC BLoE 5Grade of Recommendation B (Level of Evidence – 5)
It is recommended to prescribe anticoagulant therapy for 3–6 months in pediatric patients with cerebral venous thrombosis (CVT) and/or venous stroke without intracranial hemorrhage to prevent recurrence [50, 524, 536].
GGR ALEL 5Grade of Recommendation A (Level of Evidence – 5)
Comment: radiological follow-up is recommended in CVT and venous thrombosis at 3 months; if clinical and/or radiological features persist, therapy should be continued up to 6 months. A potential anticoagulant therapy regimen is UFH transitioning to LMWH [524]. Continuation of therapy beyond 6 months may be warranted if thrombophilia is detected or risk factors for thrombosis persist. Currently, there are no trial results in the pediatric population regarding direct thrombin inhibitors and factor Xa inhibitors [50].
3.1.2.3. Drug therapy aimed at neuroprotection and improving the recovery of neurological functions
From the standpoint of evidence-based medicine, prescribing this category of drugs is not absolutely justified (with a recommendation strength grade of A and a level of evidence of 1); therefore, there is no "gold standard" for metabolic therapy in the treatment of ischemic stroke or TIA. At the same time, according to domestic and foreign RCTs, positive clinical experience has been accumulated with a number of drugs from various pharmacological groups with different metabolic effects, including those without the use of reperfusion therapy methods, which makes it possible to consider this group of drugs as promising for improving the functional outcomes of the disease.
It is recommended that adult patients with ischemic stroke, with the exception of patients with atrial fibrillation and a cardioembolic stroke subtype, as well as patients requiring carotid artery surgery, be administered protein-free hemoderivative of calf blood (B06AB) to restore cognitive functions and during the recovery period of ischemic stroke [537].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: it is advisable to use it in elderly patients (over 60 years of age) with acute supratentorial cerebral infarction, with varying severity of neurological deficit (NIHSS 3–18 points) and post-stroke cognitive impairment, with the exception of severe and total aphasia syndrome. The drug is administered at a dose of 2000 mg/250 ml in the form of a solution for injection (0.9% sodium chloride solution** 250 ml/200 mg) for up to 20 infusions, followed by a switch to oral administration of the drug at a dose of 1200 mg/day for six months. The ARTEMIDA study was dedicated to studying the efficacy of protein-free hemoderivative of calf blood (B06AB) in the acute period of ischemic stroke. This multicenter, randomized, double-blind, placebo-controlled parallel-group study evaluated the efficacy and safety of protein-free hemoderivative of calf blood (B06AB) for the treatment of post-stroke cognitive impairment. The ARTEMIDA study involved 503 patients from 33 medical institutions in Russia, Belarus, and Kazakhstan. The study consisted of a screening and randomization period (≤ 7 days post-stroke), a 6-month double-blind treatment period, and a 6-month follow-up period. The primary endpoint of the study was the assessment of cognitive functions using the ADAS-Cog+ scale at 6 months after the start of therapy compared to baseline ADAS-Cog+ values. No changes in neurological status according to the NIHSS scale and daily activities according to the Barthel index were detected. Functional outcomes according to the Modified Rankin Scale were not assessed. It is important to note that changes in the MoCA scale score at 3, 6, and 12 months were assessed as secondary endpoints, and a statistically significant more positive dynamic of cognitive status was noted in patients receiving protein-free hemoderivative of calf blood (B06AB) compared to placebo [537].
It is recommended that adult patients with ischemic stroke and TIA who do not have hemodynamically significant steno-occlusive lesions of precerebral and cerebral arteries, with a low risk of hemorrhagic complications, and who do not require heparin group drugs** (B01AB) and anticoagulant therapy, be administered vinpocetine** (N06BX18) in the early and late recovery periods of the disease to restore self-care function, cognitive functions, social activity, and the functional outcome of the disease [538–543].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: it is advisable to prescribe #vinpocetine** (N06BX18) as part of complex pharmacotherapy to patients who have suffered an ischemic stroke in the internal carotid artery system, in the early and late recovery periods of the disease. The drug is prescribed as a drip infusion (infusion rate should not exceed 80 drops/min), single dose of 1 mg/kg body weight per 500 ml of isotonic sodium chloride solution**, course duration 14 days. Vinpocetine** (N06BX18) inhibits type 1 phosphodiesterase, which determines its vasodilating effect [539]. There are individual clinical studies demonstrating the effect of vinpocetine** (N06BX18) on cerebral perfusion and oxygenation in the acute, early, and late recovery periods of ischemic stroke, as well as on inflammatory processes in the acute period of the disease [540–543]. Also, a number of studies have shown the antioxidant and anti-inflammatory potential of vinpocetine** (N06BX18).
According to a Cochrane review that included the results of two randomized clinical trials (63 patients), there is no convincing evidence of the efficacy of vinpocetine** (N06BX18) regarding survival or disability in acute ischemic stroke [538]; however, more recent data were not included in the review, and the endpoints on which the review is based do not fully characterize the quality of life of patients in the long-term period of the disease. At the same time, according to a meta-analysis that included a total of 4 RCTs in which 601 patients with ischemic stroke received vinpocetine** (N06BX18) and 236 received placebo, it was shown that there is a faster and more complete regression of neurological deficit, a more complete restoration of self-care function, cognitive functions, social activity, and the functional outcome of the disease.
The prescription of vinpocetine** (N06BX18) requires special caution in patients with steno-occlusive lesions of extra- and intracranial cerebral vessels due to the possible formation of a steal syndrome in the carotid or vertebrobasilar system. In elderly and senile age, the sensitivity of cerebral vessels to the vasodilator effect of vinpocetine** (N06BX18) increases, which is due to the sensitization of the adenylate cyclase-cAMP system during aging. In most cases, vinpocetine** (N06BX18) has no drug interactions; however, one must keep in mind the impossibility of its simultaneous use (parenterally) with heparin sodium. When vinpocetine** (N06BX18) is used against the background of heparin therapy, the risk of hemorrhagic complications increases.
It is recommended that adult patients with mild ischemic stroke in the carotid territory be prescribed bovine cerebral cortex polypeptides** (N06BX) for the early restoration of impaired functions [544–546].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: it is advisable to use it in middle-aged and elderly patients with ischemic stroke in the carotid system (severity of neurological deficit less than 20 NIHSS points). Treatment should be carried out according to the scheme: 2 courses of intramuscular injections of the drug 20 mg (10 + 10) for 10 days of ischemic stroke with a 10-day break. A complex of polypeptides and neurotransmitters capable of exerting a tissue-specific effect on the cerebral cortex, normalizing the ratio of excitatory and inhibitory amino acids in the brain, and regulating the content of dopamine and serotonin. According to a randomized clinical trial that included 408 patients receiving bovine cerebral cortex polypeptides** (N06BX) and 72 patients receiving placebo in the first 24 hours of ischemic stroke, it was shown that bovine cerebral cortex polypeptides** (N06BX) promote a significantly faster and more significant restoration of the patient's daily activity and cognitive functions, confirming the high rehabilitation potential of the drug [546].
It is recommended that adult patients with ischemic stroke or TIA who have a preserved and stable swallowing function be prescribed glycine** (N06BX) sublingually at a daily dose of 1.0 g for five days to improve the functional outcome [547].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: The drug can be dissolved, while the exclusion of dysphagia is possible by screening using the three-sip test, which takes a minimal amount of time. The molecular basis of the drug's action is the effect of amplification of metabolic and neurotransmitter processes, regulation of glycine and glutamate reception, and alpha1-adrenolytic action. Glycine** (N06BX) is a central inhibitory neurotransmitter and a universal conjugate of low-molecular-weight toxic compounds. Glycine** (N06BX) limits the toxic effect of excitatory aminoacidergic neurotransmitters (aspartate, glutamate) and promotes the binding of aldehydes and phenols released during cerebral ischemia. Activation of glutathione synthesis leads to an increase in the cell's compensatory capabilities during oxidative stress.
The efficacy of glycine** (N06BX) was demonstrated in a randomized, double-blind, placebo-controlled trial (1992/1997) involving 200 patients in the acute phase of ischemic stroke from onset up to 6 hours at a dose of 1–2 g/day for the first 5 days. A statistically significant trend toward a reduction in 30-day mortality was demonstrated (5.9% in the "glycine** (N06BX) 1 g daily" group and 10% in the "glycine** (N06BX) 2.0 g daily" group compared to 14% in the "placebo" group and 14.3% in the "glycine** (N06BX) 0.5 g daily" group). Statistically significantly more favorable outcomes were also noted according to the Orgogozo stroke scale, the Scandinavian Stroke Scale, and a better functional outcome according to the Barthel Index ($p < 0.01$ in the "glycine** (N06BX) 1 g daily" group compared to "placebo") [547].
It is recommended to prescribe inosine + nicotinamide + riboflavin + succinic acid** (N07XX) to adult patients of middle, elderly, and senile age (up to 85 years) with ischemic stroke, regardless of the localization of the vascular brain lesion, with the aim of a more complete recovery of impaired neurological functions [549–552].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
Comment: inosine + nicotinamide + riboflavin + succinic acid** (N07XX) is a drug whose pharmacological effects are due to the combined action of its constituent components (antihypoxant, antioxidant, and energy corrector). The pharmacological effects are associated with the improvement of cellular respiration processes, increased activity of antioxidant defense factors, activation of glucose and oxygen metabolism processes, intracellular protein synthesis, and gamma-aminobutyric acid synthesis in neurons. Treatment for severe forms of ischemic stroke should be initiated within the first 10 days using the parenteral form of the drug 20 ml (in 400 ml of 0.9% NaCl) twice daily, and then from the 11th to the 35th day – the oral form (850 mg twice daily) [550–552].
It is recommended for adult patients with ischemic stroke to use inosine + nicotinamide + riboflavin + succinic acid** (N07XX) with the aim of regressing the volume of ischemic brain tissue and improving functional outcome [552-555].
GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)
Comment: in a multicenter randomized clinical trial involving eight vascular centers and 373 patients with acute ischemic stroke, the addition of inosine + nicotinamide + riboflavin + succinic acid** (N07XX) at a dose of 20 ml for 10–20 days to baseline therapy was associated with a better functional outcome according to the Rivermead and Rankin scales and a significantly more pronounced regression of ischemic brain tissue volume according to CT data by day 21 compared to the control group receiving baseline therapy and ascorbic acid**. The advantage of long-term therapy (20 days compared to 10 days) was revealed only for patients with severe stroke (NIHSS ≥ 16 scores upon admission) [552]. Another multicenter randomized trial involving 600 patients with ischemic stroke demonstrated a reduction in mortality and better recovery of cognitive functions when inosine + nicotinamide + riboflavin + succinic acid** (N07XX) at a dose of 20 ml/day was added to baseline therapy compared to placebo. The greatest effect was achieved when therapy was initiated within 6–12 hours from symptom onset [553]. A meta-analysis of studies investigating the efficacy of inosine + nicotinamide + riboflavin + succinic acid** (N07XX) in various CNS diseases (including 21 publications, 11 of which were for strokes) showed that inosine + nicotinamide + riboflavin + succinic acid** (N07XX) consistently increases the probability of a positive outcome across a set of assessment indicators in various types of neurological pathology [554].
It is recommended to prescribe citicoline** (N06BX06) to adult patients with ischemic stroke to improve functional outcome [556–558].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: 10 double-blind placebo-controlled RCTs have been conducted to evaluate the efficacy of citicoline** (N06BX06) on patient recovery after ischemic stroke. Administration of citicoline** (N06BX06) was associated with a significantly higher rate of independence (mRS score 0–2), regardless of the assessment method used (OR = 1.56; 95% CI = 1.12–2.16 under random effects). The use of citicoline** (N06BX06) was associated with a reduction in long-term mortality and disability rates. Furthermore, citicoline** (N06BX06) increased the rates of complete recovery in patients with moderate or severe ischemic stroke. Two completed meta-analyses of RCTs on the use of citicoline** (N06BX06) in ischemic stroke indicate a decrease in the effect of citicoline** (N06BX06) in patients who received reperfusion therapy, which was explained by the primary contribution of the latter to the reduction of neurological symptom severity. The ICTUS study showed a nonsignificant effect due to the inclusion of patients with intravenous thrombolysis (IVT) and the possible attainment of a "ceiling" effect after IVT [556–558].
It is recommended to prescribe choline alfoscerate** (N07AX02) to adult patients with ischemic stroke to improve functional outcome [559].
GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)
Comment: the use of choline alfoscerate** (N07AX02) in ischemic stroke was studied in a non-randomized GlIA study, which evaluated the proportion of patients without disability after a stroke and the preservation of the ischemic penumbra zone. In the group receiving therapy with 2000 mg IV of choline alfoscerate** (N07AX02), there was a significantly lower number of disabled patients by day 90 after stroke onset ($p < 0.01$), and tomogram comparisons (MRI diffusion-weighted imaging on day 1 and T2-weighted imaging at 28–30 days) showed greater preservation of the ischemic penumbra zone. Data from studies were used as comparison groups: for the main group – Clark W.M. et al. (1999), for the expanded neuroimaging study – Warach S. et al. (2000) [559].
It is recommended to use cerebrolysin** (N06BX) in adult patients in the acute period with non-severe ischemic stroke to improve upper extremity motor function [560–562].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: the drug should be prescribed within the first 72 hours of an ischemic stroke episode according to the regimen: 30 ml once daily for 14–21 days (IV infusion) in addition to rehabilitation methods [560–562].
It is recommended to use cerebrolysin** (N06BX) in adult patients in the acute period of ischemic stroke to improve functional outcome [560-563].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: the drug should be prescribed within the first 72 hours of an ischemic stroke episode according to the regimen: 30 ml once daily for 14–21 days (IV infusion) in addition to rehabilitation methods [560–563]. In the meta-analysis by Bornstein et al. (2018) [563], the results of nine ischemic stroke studies evaluating the efficacy of cerebrolysin** (N06BX) regarding overall neurological improvement in the early post-stroke period were combined. All included studies were prospective, randomized, double-blind, and placebo-controlled in design. Patients received 30–50 ml of cerebrolysin** (N06BX) once daily for 10–21 days, with treatment initiated within 72 hours after the development of ischemic stroke. While early effects of the drug were observed in all patients regardless of stroke severity, outcome assessment on day 90 indicates that patients with more severe stroke generally derived greater benefit from therapy. It was shown that the clinical benefit of cerebrolysin** (N06BX) begins to manifest very early (with the most pronounced differences from placebo from day 5 to day 30), and the drug was also more effective compared to placebo on day 90 regarding neurological function recovery (NIHSS), functional outcome/overall disability (mRS), and activities of daily living. The meta-analysis results also indicate an increased benefit on day 90 in patients with milder stroke (NIHSS < 10 scores) when cerebrolysin** (N06BX) treatment is extended from 10 to 21 days, preferably in combination with an early rehabilitation program initiation.
Additionally, it is important to note that a 2023 systematic review presents moderate-certainty evidence indicating that in ischemic stroke, there is no positive effect of cerebrolysin** on all-cause mortality, no positive effect of cerebrolysin** on the number of patients with serious adverse events, and a potential increase in the number of non-fatal serious adverse events in patients receiving cerebrolysin** [1120].
It is recommended for adult patients with ischemic stroke to use cerebrolysin** (N06BX) at a dose of 30 ml IV concurrently with or immediately after reperfusion therapy to reduce the risks of hemorrhagic transformation of the ischemic focus [564].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comments: the use of Cerebrolysin** (N06BX) for 14 days. According to the prospective, randomized, multicenter pilot clinical study CEREHETIS by Khasanova D.R. et al. (2023), which included 341 patients with acute ischemic stroke, treatment with Cerebrolysin** (N06BX) at a dose of 30 mL/day for 14 days combined with rtPA resulted in a significant reduction in the incidence of symptomatic hemorrhagic transformation of ischemic stroke in the ITT group (3.2% vs. 9.3%, p=0.03), as well as any hemorrhagic transformation of ischemic stroke in the PP (per protocol) group [564]. No serious adverse events associated with Cerebrolysin** (N06BX) administration were identified. On day 14, the Cerebrolysin** (N06BX) group showed:
a significant decrease in NIHSS scores (p=0.045);
statistically significant differences in diffusivity and fractional anisotropy indices in the core of the infarction between the main and control groups, indicating effective neuroprotection against the background of achieved recanalization, which is consistent with the reduction in final infarct volume and blood-brain barrier permeability.
It is recommended to prescribe methionyl-glutamyl-histidyl-phenylalanyl-prolyl-glycyl-proline** (N06BX) to adult patients with IS during stages 2 and 3 of medical rehabilitation (with preserved ability for intranasal administration) to reduce upper and lower limb muscle paresis [565, 566].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: it is advisable to prescribe it to patients with moderate IS within the first 6–12 h from the onset of the disease. Hard endpoints related to stroke outcomes were not studied in the conducted trials, and the sample size was limited; therefore, the level of recommendation confidence and evidence level are low [565]. At the same time, a study involving 110 patients in the recovery period of IS receiving methionyl-glutamyl-histidyl-phenylalanyl-prolyl-glycyl-proline** (N06BX) therapy showed an increase in systemic levels of brain-derived neurotrophic factor, which contributed to an accelerated and more complete reduction of upper and lower limb muscle paresis [566].
It is recommended to use ethylmethylhydroxypyridine succinate** (N07XX) in adult patients with IS who did not undergo thrombolytic therapy, to improve disease outcomes [567, 568].
Strong recommendation grade CLOE 2Level of Evidence C (Level of Evidence — 2)
Comment: to study the efficacy and safety of early administration of ethylmethylhydroxypyridine succinate** (N07XX) in the acute period of IS, a multicenter, randomized, double-blind, placebo-controlled parallel-group study was conducted to evaluate the efficacy and safety of ethylmethylhydroxypyridine succinate** (N07XX) (solution for IV and IM administration / film-coated tablets) for long-term sequential therapy in patients with hemispheric ischemic stroke in the acute and early recovery periods [567]. The clinical trial evaluated the efficacy and safety of long-term sequential therapy with ethylmethylhydroxypyridine succinate** (N07XX) compared to placebo in patients with hemispheric ischemic stroke in the acute and early recovery periods. Ethylmethylhydroxypyridine succinate** (N07XX) was administered against the background of standard baseline therapy. The study included 151 patients. The primary endpoints were the results of the mRS score evaluation at the end of the therapy course (in the study and control groups). Evaluation of the change in mRS score at the end of therapy relative to baseline (Visit 1 – Visit 5) revealed statistically significant differences (p = 0.04) between the treatment groups: in the ethylmethylhydroxypyridine succinate** (N07XX) group, the value was 1.098; in the placebo group, it was 1.460. Secondary endpoints included test results on the following scales at the end of the therapy course: NIHSS, Barthel Index, Mini-Cog, FAB, Beck Depression Inventory, and EQ-5D. Evaluation of the change in NIHSS score at the end of therapy relative to baseline (Visit 1 – Visit 5) revealed statistically significant differences (p = 0.038) between the treatment groups in the subpopulation of patients with diabetes mellitus: in the ethylmethylhydroxypyridine succinate** (N07XX) group, the value was 5.364; in the placebo group, it was 4.
3.2. Surgical treatment
Decompressive craniectomy is the only surgical treatment method for malignant ischemic infarction. The decision to perform decompressive craniectomy is made by a multidisciplinary team including a neurosurgeon, neurologist, and anesthesiologist-intensivist.
It is recommended to perform decompressive craniectomy (A16.23.002) in adult patients aged 60 years or younger with malignant ischemic infarction in the middle cerebral artery territory in case of worsening neurological symptoms despite medical therapy, within 48 hours of stroke onset, and with a midline shift of 7 mm or more, to improve the functional outcome of the disease and reduce mortality [326, 523, 573–576, 1125].
For children – Level of recommendation confidence C (level of evidence – 5), for adults – Level of recommendation confidence A (level of evidence – 1)
Comment: a pooled analysis of the DECIMAL, DESTINY, and HAMLET trials showed that, compared to the control group, patients who underwent decompressive surgery had better functional recovery with a modified Rankin scale score < 4 or < 3, as well as a higher percentage of survivors (NNT = 2, 4, and 2, respectively) [573, 575, 576].
It is not recommended to perform decompressive craniectomy (A16.23.002) in adult patients with malignant ischemic infarction presenting with coma-level impaired consciousness, severe concomitant somatic pathology, and absence of hemorrhagic transformation of the ischemic focus with intracerebral hematoma formation, aimed at reducing mortality. A craniectomy size greater than 14 cm does not improve functional treatment outcomes [576, 577].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: It is permissible to perform decompressive craniectomy (A16.23.002) if impaired consciousness deepens to a coma during preoperative preparation. If impairment of wakefulness progresses to deep coma during the preoperative preparation stage, surgery is no longer viable [576]. It must be taken into account that despite a significant reduction in mortality, only 14% of patients are able to care for themselves in the postoperative period. In addition, decompressive craniectomy (A16.23.002) can lead to complications such as syndrome of the trephined and dysresorptive hydrocephalus. Patients who have undergone decompressive craniectomy require cranioplasty [575].
It is recommended to perform ventriculostomy (A16.23.007) in adult patients with malignant cerebellar infarction and obstructive hydrocephalus in the absence of clinical and CT signs of brainstem compression to reduce mortality [578–581].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended to perform posterior fossa decompressive craniectomy (A16.23.002) in adult patients with malignant cerebellar infarction in the presence of clinical and CT signs of brainstem compression when conservative therapy is ineffective, to improve disease outcomes and reduce mortality [578–581].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: Decompressive craniectomy can be performed either simultaneously with ventriculostomy or as a second stage in case of increasing edema and brainstem compression. Standard decompressive suboccipital craniectomy may be supplemented by C1 laminectomy and/or resection of infarcted cerebellar tissue.
It is not recommended to perform posterior fossa decompressive craniectomy (A16.23.002) in adult patients with malignant cerebellar infarction presenting with deep coma and signs of brainstem ischemia, aimed at reducing mortality [578–581].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to perform decompressive craniectomy (A16.23.002) in adult patients with severe cerebral venous thrombosis in the presence of clinical and/or radiological signs of progressive cerebral edema with the development of herniation syndrome, despite adequate anticoagulant therapy, to reduce mortality [582].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: The international prospective cohort study DECOMPRESS2 (Decompressive Surgery for Patients With Cerebral Venous Thrombosis, Part 2) demonstrated that performing decompressive craniectomy (A16.23.002) in severe cerebral venous thrombosis ensures the survival of 2/3 of patients and functional independence of more than 1/3 of patients with severe cerebral venous thrombosis [582]. Surgical treatment should only be considered when signs of herniation syndrome appear, which is most commonly observed in superior sagittal sinus thrombosis.
3.3. Seizures in the acute period of ischemic stroke
Ischemic stroke is one of the most common causes of epilepsy in the elderly. The prevalence of epileptic seizures (ES) after ischemic stroke has two peaks: within the first 24 hours and from 6 months to 1 year [583]. Early or acute symptomatic (provoked) seizures, including serial seizures (2 or more per day), develop within the first 7 days after ischemic stroke. Late (unprovoked) seizures develop 7 days or more after ischemic stroke [584, 585]. Acute cerebrovascular accidents, including ischemic stroke, are the most frequent cause of symptomatic status epilepticus (SE) in adults (14–22% of all symptomatic SE cases), particularly in the elderly (36–61%), and are characterized by high mortality (about 35%), especially in prolonged status and among elderly patients [1106, 1107].
The most frequent type of SE registered in ischemic stroke is convulsive SE with focal motor seizures involving paretic limbs, as well as SE with bilateral tonic-clonic seizures with focal onset, although non-convulsive SE may also develop [1108]. Status epilepticus following ischemic stroke is a life-threatening condition associated with high mortality and requires immediate intensive care in a neuro-ICU setting.
In the pediatric population, the incidence of ischemic stroke-associated ES is reliably unknown due to the relative rarity of ischemic stroke, small cohort sizes, and the lack of uniform terminology. Acute symptomatic ES develop in up to 50% of children with acute cerebrovascular accidents and represent one of the significant risk factors for post-stroke epilepsy, along with younger age and cerebral cortex involvement. Given the specific features of children's nervous system, ongoing synapse growth, and neurotransmitter system characteristics, acute symptomatic ES can increase the volume of cytotoxic edema and expand the ischemic injury zone, which dictates the need for careful monitoring and timely identification of high-risk patients. The cumulative risk of developing post-stroke epilepsy in children is up to 30% within 10 years after ischemic stroke. Post-stroke epilepsy in childhood significantly limits rehabilitation potential and negatively impacts quality of life [1126].
Risk factors for symptomatic seizures and SE include: severity of ischemic stroke (higher NIHSS score, a score of more than 3 on the modified Rankin Scale), supratentorial location of the cerebral infarction, lesion focus in the ACA and/or MCA territory, presence of a hemorrhagic component in the cerebral infarction, cardioembolic etiology of ischemic stroke, and patient age under 65 years [1109, 1110].
It is recommended to prescribe diazepam** (N05BA01) intravenously at a dose of 0.1–0.2 mg/kg body weight (maximum dose 10 mg) as a first-line drug to adult patients with ischemic stroke presenting with acute symptomatic seizures, in order to terminate the seizure [1127, 1128].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: when administering diazepam** (N05BA01) intravenously, it is necessary to consider the possibility of respiratory depression up to arrest, as well as blood pressure decrease and increased sedation levels, particularly in elderly patients.
It is recommended to initiate treatment with intravenous administration of diazepam** (N05BA01) at a dose of 0.1–0.2 mg/kg body weight (maximum dose 10 mg) in adult patients with ischemic stroke presenting with acute symptomatic status epilepticus [1127].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: diazepam** (N05BA01) is administered intravenously at a dose of 0.1–0.2 mg/kg (meanwhile, re-administration is possible within 20 min, and the total dose must not exceed 10 mg). Therapy should be initiated: within 5 min for bilateral tonic-clonic seizures, and no later than 10 min for focal seizures. When administering diazepam** intravenously, it is necessary to consider the possibility of respiratory depression up to arrest, as well as blood pressure decrease and increased sedation levels, particularly in elderly patients.
It is not recommended to prescribe antieptic drugs to adult patients with ischemic stroke for the purpose of preventing post-stroke epilepsy [588, 1129].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
Comment: short-term (weeks) administration of antiepileptic drugs is possible for individual indications, for example, in patients with severe comorbid conditions where the risk of exacerbation upon seizure recurrence is high.
It is recommended to prescribe levetiracetam** (N03AX14) as a first-line drug to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [1130, 1131].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: it is advisable to prescribe the drug as monotherapy. It is necessary to take into account the potential sedative effect of the drug or, conversely, the onset of irritability and agitation during its use, particularly in elderly patients and patients with impaired renal function.
It is recommended to prescribe lamotrigine** (N03AX09) as a first-line drug to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [1128, 1131, 1132].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: it is advisable to prescribe the drug as monotherapy. A gradual dose escalation is required taking into account the potential development of allergic reactions. Lamotrigine** (N03AX09) is prescribed with caution if the patient has cardiac arrhythmias.
It is recommended to prescribe eslicarbazepine (N03AF04) to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [589].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: it is advisable to prescribe the drug as monotherapy. The possibility of hyponatremia development must be taken into account.
It is recommended to prescribe oxcarbazepine** (N03AF02) to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [1133].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: it is advisable to prescribe the drug as monotherapy. The possibility of hyponatremia development must be taken into account.
It is recommended to prescribe gabapentin (N03AX12) to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [1134].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
It is recommended to prescribe zonisamide (N03AX15) as a first-line drug to adult patients with ischemic stroke and a confirmed diagnosis of post-stroke epilepsy in order to prevent seizures [590, 1135].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: all the above-mentioned drugs are advisable to be prescribed as monotherapy. Preference should be given to drugs with good tolerability and minimal drug interactions. Carbamazepine** (N03AF01) and valproic acid** (N03AG01) are effective, but inferior to the aforementioned drugs due to drug interactions. The choice of drug for the treatment of post-stroke epilepsy depends on a number of factors, including patient age, presence of comorbid conditions, and concurrent medications. Better tolerability has been demonstrated for levetiracetam** (N03AX14) and lamotrigine** (N03AX09) compared to carbamazepine** (N03AF01) [591, 592]. In elderly patients, given the decline in renal function and accumulation of comorbid diseases, it is recommended to initiate therapy with lower drug doses, choose a slower titration rate, and use prolonged-release formulations and monotherapy whenever possible.
It is recommended to prescribe antiepileptic drugs (N03A) to pediatric patients presenting with acute symptomatic epileptic seizures resulting from acute cerebrovascular accidents, in order to prevent seizures [593-598].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: therapy for post-stroke epilepsy is carried out in accordance with the clinical guidelines "Epilepsy and Status Epilepticus in Adults and Children".
It is recommended to consider surgical treatment of epilepsy in patients with pharmacoresistant course of post-stroke epilepsy [1136, 1137].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
3.4. Post-stroke depression
Post-stroke depression is diagnosed when a patient exhibits the classic "depressive triad": depressed mood, motor activity reduction, and ideational slowing. The primary disturbance consists in a mood shift toward depression, frequently accompanied by suicidal ideation. It is caused by the impact of the underlying disease on various aspects of a person's life, including physical health, mobility, and communication skills, which can lead to feelings of helplessness, lowered self-esteem, and dependence on others for care. The resulting psychosocial damage is characterized by sudden onset, prolonged persistence of distressing circumstances, prognostic uncertainty regarding the degree of possible recovery of lost functions, and the likelihood of recurrent stroke. Depression arising against this background is a psychopathological state with a possible blending of various affective components (melancholy, apathy, anhedonia). Most commonly, it is accompanied by anxiety, a decrease in overall activity levels, sleep-wake cycle disturbances, and other psycho-vegetative manifestations. The symptomatology is secondary to the cerebrovascular accident, although the likelihood of clinically defined depressive episodes in the history should also be assessed. According to ICD-10, post-stroke depression should be diagnosed as "Other nonpsychotic mental disorders due to brain damage and dysfunction and to physical disease" F06.361. Its treatment involves prescribing antidepressants combined with psychosocial rehabilitation and psychotherapy. SSRIs (N06AB) are generally prescribed as first-line agents. It is advisable to initiate antidepressant therapy with minimal doses, especially in elderly and senile patients, gradually increasing the dose to a therapeutic level while monitoring the severity of adverse effects. The duration of treatment is typically at least 6 months.
It is recommended that adult patients with a history of ischemic stroke and signs of affective disorders undergo an evaluation (examination, consultation) by a psychiatrist to diagnose post-stroke depression, select therapy, and provide subsequent clinical monitoring [599, 600].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended to prescribe fluoxetine** (N06AB03) as a drug of choice to adult patients with post-stroke depression for etiotropic therapy [601-604].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: the recommended dosage of fluoxetine** (N06AB03) for the treatment of post-stroke depression is 20 mg, with a possible gradual increase up to 60 mg per day. Adverse effects of fluoxetine** (N06AB03) include: sexual dysfunction, insomnia, sedation, headache, tremor, dizziness, hyperhidrosis, syndrome of inappropriate antidiuretic hormone secretion [604].
It is recommended to prescribe sertraline** (N06AB06) as a drug of choice to adult patients with post-stroke depression for etiotropic therapy [601, 605–607].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: according to RCTs, the highest efficacy and tolerability, along with the lowest discontinuation rates, were observed with sertraline. The therapeutic range of sertraline** (N06AB06) is quite broad, ranging from a minimum single daily dose of 50 mg to a maximum single daily dose of 200 mg. Drug dosage selection is determined by the severity of post-stroke depression. The advantage of sertraline** (N06AB06) over other SSRIs is its simultaneous effect on both the components of the depressive state and the anxiety disorder. Adverse effects include phenomena such as: sexual dysfunction, insomnia, sedation, headache, tremor, dizziness, hyperhidrosis, rarely hyponatremia (primarily in elderly patients and usually reversible upon discontinuation of sertraline), and syndrome of inappropriate antidiuretic hormone secretion [604].
It is recommended to prescribe paroxetine** (N06AB05) as a drug of choice to adult patients with post-stroke depression for etiotropic therapy [607, 608].
GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: treatment of post-stroke depression with paroxetine** (N06AB05) at therapeutic dosages (20–50 mg) is effective for post-stroke depression, including over a 6–12 week period. Adverse effects of paroxetine** (N06AB05) include: sexual dysfunction, insomnia, sedation, headache, tremor, dizziness, hyperhidrosis, weight gain, and syndrome of inappropriate antidiuretic hormone secretion [604]. Due to the risk of weight gain, paroxetine** (N06AB05) should be prescribed with caution to overweight patients.
It is recommended to use escitalopram (N06AB10) as a drug of choice for etiotropic therapy in adult patients with post-stroke depression [608, 609].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: according to RCTs, escitalopram (N06AB10) demonstrated good therapeutic efficacy and tolerability, as well as the lowest discontinuation rates; pharmacological effects of the drug were observed in the dose range of 5–20 mg/day. Long-term therapy with escitalopram (N06AB10) (10–20 mg/day for 12 months) has been shown to improve cognitive functions, particularly verbal and visual memory, in patients with a history of ischemic stroke [610]. Adverse effects include phenomena such as: sexual dysfunction, insomnia, sedation, headache, tremor, dizziness, hyperhidrosis, rarely hyponatremia (primarily in elderly patients and usually reversible upon discontinuation of escitalopram), and syndrome of inappropriate antidiuretic hormone secretion [604].
It is recommended to use duloxetine (N06AX21) as a drug of choice for etiotropic therapy in adult patients with post-stroke depression [607, 611].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: duloxetine (N06AX21) belongs to the group of serotonin and norepinephrine reuptake inhibitors (SNRIs, included in the "Other antidepressants" group according to the ATC classification), meaning it selectively blocks the reuptake of both norepinephrine and serotonin. The therapeutic range of duloxetine (N06AX21) is 60 to 120 mg/day depending on the severity of the depressive state. Duloxetine (N06AX21) is effective for post-stroke depression, but its tolerability profile was inferior to that of SSRIs. Adverse effects of duloxetine (N06AX21) include: nausea, diarrhea, decreased appetite, dry mouth, constipation (a dose-dependent effect), sleep disturbances, sedation, dizziness, sexual dysfunction, sweating, elevated blood pressure, and urinary retention [604].
It is recommended to prescribe citalopram (N06AB04) as a drug of choice for etiotropic therapy in adult patients with post-stroke depression [612].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: citalopram (N06AB04) is initiated at dosages of 20 mg/day with a possible gradual increase up to 40 mg/day depending on the severity of depression. Adverse effects of citalopram (N06AB04) include: sexual dysfunction, insomnia, sedation, headache, tremor, dizziness, hyperhidrosis, and syndrome of inappropriate antidiuretic hormone secretion [604].
It is not recommended to use non-selective monoamine reuptake inhibitors (N06AA, tricyclic antidepressants) as first-line drugs in patients with post-stroke depression due to the high risk of adverse effects and the availability of alternative therapeutic strategies [603, 613, 614].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: adverse reactions associated with anticholinergic and antiadrenergic effects of tricyclic antidepressants (TCAs), such as glaucoma, confusion, urinary retention, hypotension, and dizziness, preclude the use of TCAs as first-line drugs, despite their good therapeutic efficacy in post-stroke depression compared to SSRIs or SSRIs + psychotherapy. The prescription of TCAs when SSRIs are ineffective should be decided after assessing the individual risk/benefit ratio for the patient.
3.5. Post-stroke anxiety
The diagnosis of anxiety disorder in stroke survivors, according to ICD-10, should be defined as "Organic anxiety disorder due to brain damage and dysfunction and to physical disease" F06.41. The incidence of anxiety disorder in ischemic stroke survivors can reach 22%, significantly worsening the functional outcome of the disease [615]. In most cases, post-stroke anxiety is associated with depression; therefore, the treatment of anxiety disorders is carried out with antidepressants and, if necessary, anxiolytics.
It is recommended that adult patients with a history of ischemic stroke undergo an evaluation (examination, consultation) by a psychiatrist for the early clinical diagnosis of anxiety disorder [616–618].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended to prescribe antidepressants from the SSRI group (N06AB selective serotonin reuptake inhibitors) as the drugs of choice for adult patients with established post-stroke anxiety disorder with the aim of reducing symptoms of anxiety disorder [619–621].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: therapy with SSRI antidepressants (N06AB) is advisable in this group of patients due to the high comorbidity of anxiety and depression.
It is recommended to temporarily add benzodiazepine derivatives (N05BA) at the start of therapy in adult patients with post-stroke anxiety disorder in order to alleviate symptoms of the disease and allow the use of lower initial doses of SSRIs (N06AB) [1138, 1139].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: benzodiazepine derivatives (N05BA) are prescribed in minimal dosages for a duration of no more than 14 days. Long-term use of benzodiazepine derivatives (N05BA) is not recommended as it may lead to excessive sedation, ataxia, and carries a risk of developing dependence [604].
It is recommended to prescribe buspirone (N05BE01) to adult patients with post-stroke anxiety to relieve symptoms of anxiety disorder [624].
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: the recommended initial daily dose is 15 mg; the dosage can be increased by 5 mg per day every 2–3 days in the absence of an anxiolytic effect. The maximum single dose is 30 mg; the maximum daily dose should not exceed 60 mg. Adverse effects of buspirone (N05BE01) include: headache, irritability, sedation, agitation, nausea, anxiety [604].
It is recommended to prescribe pregabalin** (N02BF02) to adult patients with post-stroke anxiety disorder in the presence of concomitant pain syndrome to simultaneously affect anxiety symptoms and pain [625, 1140].
Strong recommendation grade CLOE 2Level of Evidence C (Level of Evidence — 2)
Comment: the mechanism of action of the drug consists in binding to the alpha-2-delta subunit of voltage-gated calcium channels, which blocks the transmission of pain impulses, binds presynaptic N and P/Q calcium channels, reducing their excessive activity, thereby lowering neurotransmitter transmission, which leads to a decrease in the manifestation of anxiety symptoms. Dosing regimen: initial dose is 150 mg/day. Depending on the achieved effect and tolerability, the dose can be increased to 300 mg/day after 3 to 7 days. Long-term use of the drug is safe for the patient. Adverse effects of pregabalin** (N02BF02) include such phenomena as: sedation, dizziness, tremor, dysarthria, paresthesia, memory impairment, coordination disturbance, attention disturbance, confusion, euphoria, irritability, dry mouth, constipation, weight gain, increased appetite, flatulence, blurred vision, diplopia, peripheral edema, decreased libido, erectile dysfunction [604].
3.6. Pain management
It is recommended that adult patients with ischemic stroke undergo endovascular thrombectomy (A16.23.034.013) in the carotid circulation under general anesthesia (B01.003.004.010) or sedation (B01.003.004.009) to improve outcomes [627].
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: A large meta-analysis by the HERMES Collaboration group included individual data from seven randomized trials (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT-PRIME, REVASCAT, PISTE, and THRACE) on 797 patients who underwent endovascular thrombectomy (A16.23.034.013), of whom 236 were under general anesthesia. According to the meta-analysis, even after adjustment for major prognostic indicators, worse outcomes after endovascular thrombectomy were associated with general anesthesia (B01.003.004.010). At the same time, interventions under general anesthesia did not demonstrate greater safety or a lower complication rate than interventions without general anesthesia. Among the advantages of endovascular thrombectomy (A16.23.034.013) without general anesthesia are the ability to assess neurological status during the intervention, simplified intensive care requirements, and reduced procedure cost. Serious limitations of this meta-analysis include the lack of randomization by anesthesia type and formalized anesthesia protocol in the included studies, as well as an unknown proportion of interventions performed under general anesthesia due to indications versus operator choice [626]. In another systematic review and meta-analysis (SIESTA, ANSTROKE, and GOLIATH) including 368 patients (183 under general anesthesia), performing endovascular thrombectomy (A16.23.034.013) under general anesthesia compared with sedation (B01.003.004.009) was associated with significantly lower disability at three months post-intervention. The authors suggest considering their findings preliminary, as the meta-analysis used single-center randomized trials, and disability was the primary outcome in only one of them. An important fact is that, according to the meta-analysis results, a higher rate of successful reperfusion (mTICI 2b-3) was observed when endovascular thrombectomy was performed under general anesthesia compared to sedation—72.7% and 63.3%, respectively, likely due to the absence of patient movement during the procedure [627].
3.7. Diet therapy
It is recommended that adult patients with ischemic stroke adhere to the Mediterranean diet and DASH diet to correct stroke risk factors and prevent stroke [1141, 1142].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Mediterranean diet and DASH diet
Mediterranean diet | DASH diet |
|---|---|
High mono-unsaturated/saturated fat ratio (use of olive oil as the primary cooking ingredient and/or consumption of other traditional foods high in mono-unsaturated fats, such as tree nuts) | Limited consumption of saturated fats and cholesterol and increased consumption of nuts |
High consumption of plant foods, including fruits, vegetables, and legumes | Emphasis on consumption of fruits, vegetables, and legumes |
High consumption of whole grains and cereals | Emphasis on whole grains |
Increased fish consumption | – |
Low consumption of meat and meat products Discourages red and processed meat | Limits red and processed meat |
Low to moderate red wine consumption | – |
Moderate consumption of milk and dairy products | Emphasis on low-fat/fat-free dairy products |
Consumption of carbonated drinks, pastries, sweets, commercial bakery products, and vegetable fats is not recommended | Limits sweets, added sugars, sodium, and sugar-sweetened beverages |
*rCBF < 30% (perfusion CT) or ADC < 620 µm2/s (diffusion MRI);
**Tmax > 6 s (perfusion CT or perfusion MRI).
* *rCBF < 30% (perfusion CT) or ADC < 620 µm2/s (diffusion MRI);
**Tmax > 6 s (perfusion CT or perfusion MRI).
4. Medical Rehabilitation and Sanatorium-Resort Treatment
The rehabilitation goal must be specialized, quantifiable, achievable, and take into account the individual requirements of the patient. Rehabilitation measures should include, as indicated, kinesiotherapy, occupational therapy, speech therapy, management of dysphagia, nutritional support, cognitive training, management of emotional status, including counseling of patients, families and caregivers, physical modalities, and pharmacological treatment. Medical rehabilitation for patients with ischemic stroke is carried out with an intensity commensurate with the expected benefit and load tolerance [628, 629].
It is recommended that adult patients with ischemic stroke begin medical rehabilitation measures no later than 48 hours from admission to the hospital in order to prevent complications, improve functional outcomes, and reduce mortality [628–633].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: early mobilization is the process of improving a patient's functional activity, specifically the ability to turn in bed, sit up, stand up, and take steps as early as possible. Minimal yet independent muscle activity prevents the development of muscle atrophy as an early sign of immobilization syndrome. Rehabilitation mobilization activities are divided, depending on the degree of patient participation, into active (for those capable of cooperation with multidisciplinary rehabilitation team members) and passive (for patients with a low quantitative and/or altered qualitative level of consciousness). Passive procedures include movements in all joints matching their physiological range of motion, which are performed by an exercise therapy specialist (appendix: A3-1).
It is recommended that medical rehabilitation measures for adult patients with ischemic stroke be carried out by a multidisciplinary rehabilitation team (MDRT) of specialists, with coordinated work and participation of the patient, family members, and caregivers, with the aim of increasing independence in daily life and reducing mortality [628, 634, 635].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: At the present stage, the leading coordinator of the team's work is a physician in physical and rehabilitation medicine, whose task is to formulate an individual rehabilitation program, goals and objectives of medical rehabilitation, and working models for MDRT members. Numerous studies and systematic reviews (78 publications by European authors over a 10-year period; a review of databases from 2001–2015 (MBASE, CINAHL, PubMED, ProQuest, PsycINFO, AMED, and Scopus)) have proven that the use of a multidisciplinary model, compared to a linear rehabilitation model, provides a significant improvement in the condition of patients with ischemic stroke in the hyperacute period, as assessed by the modified Rankin scale (mRS) at the end of the rehabilitation course (Appendix A3-2).
It is recommended that patients with ischemic stroke undergo joint monitoring of the development of complications by a multidisciplinary rehabilitation team in order to improve functional outcomes and reduce mortality [636–639].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: complications refer to aspiration, nutritional deficiency, trophic disorders, urination disorders, immobilization syndrome, central and peripheral pain syndromes, muscle tone disorders, contractures, and other clinical conditions developing in the patient during treatment (Appendix A3-3).
It is recommended that adult patients with ischemic stroke and speech disorders undergo intensive sessions with a speech therapist to improve functional outcomes and prevent cognitive impairment [628, 640, 641] (Appendix A3-4).
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke undergo regular training to improve personal activities of daily living skills in order to increase independence and quality of life [642] (Appendix A3-5).
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke undergo early mobilization and physical training after assessing individual exercise tolerance in order to reduce mortality and improve functional outcomes [643–645].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: Low physical activity after stroke is widespread. Recommendations for physical activity and exercise should be included in the management of stroke survivors. The use of physical exercise (aerobic, resistance training) improves functional capacity, the ability to perform activities of daily living, and quality of life, and also reduces the risk of subsequent cardiovascular events. The goals of physical activity and the exercise program are individual for each patient; it is important to ensure long-term adherence to the treatment regimen.
Special attention is recommended to be paid to low-to-moderate intensity aerobic activity, muscle-strengthening activity, reduction of sedentary behavior, and risk management for secondary stroke prevention [646] (Appendix A3-6).
It is not recommended to initiate mobilization in an adult patient with ischemic stroke earlier than 24 hours from the onset of the stroke in order to reduce the likelihood of an unfavorable outcome at three months [628, 643, 644].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: A Cochrane review analyzing 19 databases of stroke patients (up to August 2017) presented the results of 9 RCTs with 2,958 participants. Early mobilization (within 24 hours of stroke onset) did not increase the number of people who survived or recovered well after a stroke. At the same time, there was a reduction in hospital stay by one day (low-certainty evidence). Early mobilization was associated with a slightly higher number of deaths and participants with a poor outcome compared to delayed mobilization. The review authors express concern that rehabilitation initiated within 24 hours may carry an increased risk of an unfavorable outcome in certain stroke patients. Given the uncertainty of these effect estimates for early versus delayed rehabilitation, more detailed studies are needed to resolve this issue.
It is recommended that an adult patient with ischemic stroke start active and/or passive (using a tilt table, 116940) verticalization from the second day onwards, after assessing individual load tolerance, in order to reduce mortality and improve functional outcomes [643, 644, 647].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: this mobilization stage holds a special place in early rehabilitation, as it significantly mitigates the negative effects of bed rest and prepares the patient for a prompt transfer from the ICU to another ward. Verticalization involves raising the head of the bed, followed by lowering the foot section. The gravitational gradient is typically increased every 15 min in the absence of symptoms that limit or halt further mobilization. Upon reaching a 90° elevation angle, the patient can potentially transition to passive transfer into a armchair. The sitting position helps maintain central and peripheral perfusion, an acceptable blood oxygen saturation level, prevents pneumonia, improves muscle metabolism, and counteracts venous stasis and deep vein thrombosis of the calf (Appendix A3-7).
It is recommended that adult patients with ischemic stroke and shoulder subluxation undergo limb positioning using special devices and splints to restore limb motor function and improve functional outcomes [653, 654] (Appendix A3-10).
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended that adult patients with ischemic stroke use functional electrical stimulation of muscles to restore limb motor function and improve functional outcomes [655–657].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: data from meta-analyses (2010–2016) indicate the benefits of functional electrical stimulation of muscles for improving walking speed over distances greater than 10 m, functional load capacity, and increasing patient mobility time (Appendix A3-11).
It is recommended that adult patients with ischemic stroke and upper extremity paresis undergo instrumental (electromechanical and robotic) rehabilitation (A19.23.002.016 Mechanotherapy for central nervous system and brain disorders, A19.23.002.017 Robotic mechanotherapy for central nervous system and brain disorders) to improve arm function [658, 659].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
Comment: the efficacy of instrumental (electromechanical and robotic) rehabilitation for gross arm movement training is demonstrated in a systematic review that included 45 RCTs involving a total of 1,619 patients [658]. Furthermore, significant improvements in proximal arm movements, increased muscle strength, and pain reduction are observed. Another systematic review showed that robotic devices increase rehabilitation efficacy only when used as an adjuvant method (in addition to basic rehabilitation methods) [659] (Appendix A3-12).
It is recommended that patients with ischemic stroke and limb paresis use specialized positioning to prevent spasticity and the development of joint contractures [628, 661].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that an adult patient with ischemic stroke and early spasticity receive botulinum therapy using botulinum toxin type A-hemagglutinin complex** (M03AX01) and botulinum toxin type A** (M03AX01) preparations to prevent contractures, reduce pain, restore limb motor function, and improve functional outcomes [661-665].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: according to meta-analyses [661, 662, 665], the inclusion of botulinum therapy in comprehensive rehabilitation reduces spasticity in central upper and lower limb paresis, pain syndrome, muscle spasms, and increases walking speed. The duration of action of botulinum toxin type A (M03AX01), which is 12–24 weeks, should be utilized as a "therapeutic window" to implement intensive physical rehabilitation methods against the background of reduced muscle hypertonus. At the same time, the efficacy and safety of high doses of botulinum toxin type A** (M03AX01) in pronounced spasticity, optimal doses and injection sites for various target muscles, as well as the optimal timing for botulinum therapy, have not currently been established. Botulinum therapy is prescribed to patients with focal/multifocal spasticity according to specific indications: spasticity grade according to the modified Ashworth scale (Appendix G4) (Ashworth, 1964) ≥ 2 points; however, botulinum therapy is ineffective for fixed joint contractures, as the range of motion in the joint will not increase.
During botulinum toxin therapy, clinical monitoring must be performed to rule out local and systemic adverse effects of botulinum toxin therapy. The efficacy of botulinum toxin type A** (M03AX01) for upper limb post-stroke spasticity (≥ 2 points on the Modified Ashworth Scale) has been demonstrated in clinical trials involving more than 1,500 patients with ischemic stroke [661-665] (Appendix A3-13).
It is recommended that patients with ischemic stroke who received botulinum toxin therapy for early spasticity undergo active physical rehabilitation (A19.23.002 Exercise therapy for diseases of the central nervous system and brain) to improve motor function [628, 664].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: physical rehabilitation should include: A19.23.002.014 Individual exercise therapy session for diseases of the central nervous system and brain, A21.30.006 Occupational therapy, A19.23.002.016 Mechanotherapy for diseases of the central nervous system and brain, A19.23.002.017 Robotic mechanotherapy for diseases of the central nervous system and brain, A17.23.004.001 Transcranial magnetic stimulation, A22.30.015 Shock wave therapy (Appendix A3-14).
It is recommended to use multi-functional neuromuscular electrical stimulation (A17.24.010) or vibrational massage of spastic limb muscles as an adjunct to comprehensive therapy for post-stroke spasticity in adult patients with ischemic stroke to temporarily reduce muscle hypertonus and improve motor function [666] (Appendix A3-15).
GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)
It is recommended that adult patients with ischemic stroke and neuropathic pain syndrome use an interdisciplinary approach to improve functional outcomes [667].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: the onset of central neuropathic pain (CPSP – Central Neuropathic Pain Syndromes) varies from the time of disease onset to several months or years. Stroke localization is more important for the risk of CPSP than etiology. There is a high risk of developing CPSP when the lesion is located in the thalamus (excluding infarctions in the medial and centromedian nuclei), with involvement of the posteroventral nuclei – 25%, and in Wallenberg-Zakharchenko syndrome – 25%. Some studies have shown that CPSP is more likely in younger patients, as well as with right-hemispheric lesion localization (Appendix A3-16).
It is recommended that adult patients with ischemic stroke undergo neurodevelopmental Bobath therapy to improve functional outcomes (active verticalization, balance, gait function) [668–670] (Appendix A3-17).
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke undergo occupational therapy and training to increase activities of daily living in order to restore personal skills, increase independence levels, and improve quality of life [671] (Appendix A3-18).
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke and lower limb paresis with impaired balance and weight-bearing function undergo gait training with body weight support, using robotic and mechanical devices to restore mobility and gait function [672].
Strong recommendation grade CLOE 2Level of Evidence C (Level of Evidence — 2)
Comment: the main measures for restoring lost gait ability in this group of patients involve the maximum possible number of gait movement repetitions. This is achieved by incorporating robotic equipment into rehabilitation programs. When using robotic gait support, two therapeutic principles are distinguished: the end-effector-based approach (with the patient's feet fixed immovably at the bottom on a treadmill and free simulation of movements in the knee and hip joints) and the exoskeleton principle (with additional fixation and robotic control of movements in the knee and hip joints). Both therapeutic approaches use partial body weight support systems and feedback systems. To date, no conclusive evidence of the superiority of one approach over the other has been obtained, and the debate continues. Convincing evidence has been obtained demonstrating the superiority of the robotic rehabilitation approach over conventional training (overground walking, preparatory sitting exercises, complete absence of assistive-mechanical gait training) (Appendix A3-19).
It is recommended that adult patients with ischemic stroke and cognitive impairment undergo cognitive rehabilitation to improve functional outcomes and independence [673, 674].
GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)
Comment: a systematic review of data from 181 studies (2000–2011) demonstrates the efficacy of remedial (e.g., computerized working memory training) and compensatory interventions for improving executive functions and functional abilities [675] (Appendix A3-20).
It is recommended that adult patients with ischemic stroke be considered for compensatory cognitive training strategies to improve attention, memory, and executive functions, as well as internal (e.g., encoding and retrieval strategies, self-efficacy training) and external (assistive technologies, computers, prompting devices, notebooks) compensatory strategies to improve post-stroke memory functions [676, 677] (Appendix A3-21).
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with ischemic stroke and neglect syndrome undergo comprehensive rehabilitation to improve functional outcomes and increase independence [678] (Appendix A3-22).
GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)
It is recommended that adult patients with ischemic stroke who have limitations in independent mobility, communication, and self-care, provided there is a prospect for recovery, receive multidisciplinary rehabilitation to reduce functional deficits [679] (Appendix A3-23).
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with ischemic stroke and hemiparesis undergo mirror therapy to restore limb motor function and improve functional outcomes [680, 681, 640].
GCR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: mirror therapy (MT) has demonstrated efficacy in post-stroke arm motor recovery in studies involving a total of over 500 patients. Several studies have shown the effect of MT on improving basic self-care skills. MT is one of the basic methods of motor rehabilitation for patients with hand plegia, primarily due to the impossibility of using most other types of rehabilitation interventions in this category of patients (Appendix A3-24).
It is recommended that adult patients with ischemic stroke and limb paresis use virtual reality technologies to improve activities of daily living [682].
GCR BLEL 1Grade of Recommendation B (Level of Evidence – 1)
Comment: the efficacy of virtual reality technology as an adjunct method has been shown in RCTs involving more than 500 patients. To achieve a therapeutic effect, at least 15 hours of training is required. Studies did not reveal an increase in grip strength during virtual reality training, but an overall increase in daily activity was demonstrated (Appendix A3-25).
It is recommended that adult patients with ischemic stroke and upper limb paresis undergo constraint-induced movement therapy to restore arm motor function [685].
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: patient selection based on the presence of active wrist and finger extension should be considered a key factor determining the potential to overcome the "learned non-use" phenomenon of the paretic arm. With a constraint-induced movement therapy dosage regimen of 60 to 72 hours over two weeks, better results in restoring paretic arm function (manipulation of objects) were achieved. In the late recovery period of the disease, the duration of intact arm constraint should be 90% of the patient's waking time, with intensive training lasting 6 hours a day for 10 working days over two weeks (Appendix A3-27).
It is recommended that adult patients with ischemic stroke and impaired fine motor skills (excluding plegia) use robotic systems for hand and finger function recovery in any rehabilitation period as an adjunct to basic physical rehabilitation methods [686].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: robotic systems for hand and finger function recovery have become widespread and implemented into practice relatively recently; therefore, there is a lack of clinical studies to confirm their efficacy.
A meta-analysis (2008–2015) of 34 RCTs (1160 patients) compared the results of electromechanical and robotic arm training with other rehabilitation interventions or no treatment. The authors concluded that the use of electromechanical and robotic systems for the rehabilitation of patients with upper limb and hand dysfunction can improve activities of daily living, arm and hand function, and upper limb and muscle strength. However, the quality of evidence in the analyzed studies was low; there were differences between trials in intensity, duration, number of training sessions, and type of treatment [648] (Appendix A3-28).
It is recommended to use medical treadmills and stationary bicycles (including those utilizing movement resistance technologies, voice prompting commands, biofeedback, functional electrical stimulation, respiratory and cardiovascular monitoring systems) as well as robotic devices in adult patients with ischemic stroke during comprehensive medical rehabilitation to increase exercise tolerance and improve functional outcomes [687].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: a meta-analysis (2003–2017) of 56 studies (3105 patients) showed that the use of treadmills significantly increased walking speed and walking endurance. The use of body-weight-supported treadmill training in stroke survivors did not lead to an increase in walking speed or walking endurance. To improve patient mobility, it is necessary to establish and separate basic goals: restoring the ability to walk when impossible, improving walking function when impaired, increasing walking speed and distance, and restoring balance. Walking speed and duration (distance) are the main clinical criteria for evaluating the effectiveness of gait rehabilitation after stroke. Walking speed has become a method for stratifying individuals with neurological impairments and a criterion for evaluating outcomes in clinical trials (Appendix A3-29).
It is recommended that patients with ischemic stroke timely select and use assistive devices to improve independence [628] (Appendix A3-30).
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that patients with ischemic stroke and motor impairments undergo therapeutic exercise (A19.23.002 Therapeutic exercise for diseases of the central nervous system and brain), including goal-directed training and high-repetition movement training in any rehabilitation period to improve functional outcomes [652].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: despite the heterogeneity of the study designs, therapeutic exercise is a universally recognized standard for motor rehabilitation in post-stroke patients (Appendix A3-31).
It is recommended that adult patients with ischemic stroke and preserved ability to perform voluntary movements undergo strength training to hypertrophy the trained muscle group, restore limb function, and improve functional outcomes [688].
GGR CLeE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: strength training is an adjuvant method and should be a component of comprehensive rehabilitation, as it affects muscle strength rather than motor learning or relearning. During strength training, the correct selection of trained muscle groups and vigilance regarding the development or increase of spasticity are important. The primary impact should be directed at the muscles antagonistic to the spastic muscles (Appendix A3-32).
It is recommended that adult patients with ischemic stroke include low-intensity aerobic cyclic exercises in their individual rehabilitation plan to increase exercise tolerance, improve cardiovascular status, and reduce the risk of recurrent stroke [688, 689].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: in a study of stroke survivors who received medical care regarding risk factors, physical inactivity was the strongest independent predictor of recurrent stroke. These data indicate that physical inactivity is a critical risk factor that must be addressed. American Stroke Association guidelines suggest 20 to 60 minutes of aerobic exercise 3 to 5 days a week (Appendix A3-33).
It is recommended that adult patients with ischemic stroke with developing moderate to mild contractures of the elbow and wrist joints undergo staged use of orthoses or static adjustable splints (fixation devices) [690] (Appendix A3-34).
GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)
It is recommended that adult patients with ischemic stroke use adaptive (splints) and assistive equipment to enhance safety and increase activity in patients' daily lives if other methods are unavailable or cannot be mastered by the patient [628] (Appendix A3-35).
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with ischemic stroke and generalized or multifocal spasticity use central-acting oral muscle relaxants (tizanidine** (M03BX02), baclofen** (M03BX01), tolperisone (M03BX04)) as part of a comprehensive antispastic therapy to improve motor function, prevent contracture formation, and increase rehabilitation efficiency [691–694].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: for a better therapeutic effect, patients with central paralysis/paresis of the upper and/or lower extremity, when indicated, must be provided with a comprehensive post-stroke spasticity management program that includes multiple technologies (kinesiotherapy, massage, orthotics, physiotherapy methods, drug therapy). The choice of medications depends on the severity, anatomical distribution of spasticity (multifocal, generalized, regional), and comorbid conditions. In mild to moderate spasticity, the use of oral muscle relaxants generally leads to a positive therapeutic effect. Central-acting muscle relaxants are usually not combined. Treatment with muscle relaxants starts with the minimum dose and is then slowly increased to achieve the effect. However, with long-term use, their effectiveness decreases, while increasing the dosages of muscle relaxants leads to an enhancement of the systemic effect of the drugs and an increase in the frequency of side effects. In severe focal/regional spasticity, the use of oral muscle relaxants is ineffective, so priority is given to other therapeutic strategies (Appendix A3-35).
It is recommended that adult patients with ischemic stroke and generalized or regional spasticity, in case of ineffectiveness of conservative treatment for severe spastic syndrome, undergo the installation of a pump (FSZ 2010/07863, Programmable Implantable Pump) with baclofen** (intrathecal solution) to reduce spasticity [695].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: intrathecal baclofen** (M03BX01) therapy using implantable pumps is a highly effective method for managing severe spastic syndrome, with the ability to regulate the therapeutic effect. A reduction in muscle tone by ≥ 1 point on the modified Ashworth scale indicates a positive therapeutic effect. However, the high cost of treatment, as well as the likelihood of developing severe complications due to drug infusion failure, impose certain limitations on the clinical use of this method.
It is recommended that adult patients with ischemic stroke undergo training to improve instrumental activities of daily living based on individual needs and taking into account functional deficits in order to improve functional deficits [628].
GGR BLoE 2Recommendation Grade B (Level of Evidence – 2)
Comment: recommendations regarding approaches to the diagnosis and correction of activities of daily living are based on a conceptual approach endorsed by the World Health Organization. The recommended total duration of therapeutic exercise is 900–1200 minutes within 4–6 weeks after the acute period. Subsequently, the intensity of therapeutic exercise should be determined by the patient's general condition, the nature of the motor deficit, and rehabilitation goals (Appendix A3-36).
It is recommended that adult patients with ischemic stroke and post-stroke shoulder pain syndrome develop an individualized comprehensive rehabilitation program taking into account pathogenetic factors and pain severity, including pharmacotherapy (botulinum toxin type A-hemagglutinin complex** (M03AX01) and botulinum toxin type A** (M03AX01) for spasticity) and correction of the osteoarticular and muscular system of the shoulder girdle to reduce pain [696–700].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: post-stroke pain syndrome can be associated with several pathogenetic factors, including local damage to periarticular tissues, myogenic pain from the scalene muscles, neuropathic pain including complex regional pain syndrome, central post-stroke pain, and spasticity-related pain. To measure pain intensity, the visual analog scale (VAS) is used. Depending on the nature of the shoulder pain syndrome, various treatment algorithms can be used: glucocorticoid injections into the shoulder and/or subacromial joints, suprascapular nerve block, electrical stimulation of the shoulder muscles, injections of botulinum toxin type A: botulinum toxin type A-hemagglutinin complex** (M03AX01) and botulinum toxin type A** (M03AX01) into the subscapularis and/or pectoralis major muscle, etc., use of shoulder orthoses, nonsteroidal anti-inflammatory and antirheumatic drugs, massage and gentle mobilization techniques for the shoulder muscles, acupuncture [696–700] (Appendix A3-37).
It is recommended to use transcutaneous electrical nerve stimulation (TENS) (A17.30.006) as an adjuvant method in the motor rehabilitation of adult patients with post-stroke arm paresis with a stroke duration of more than one month in the late recovery period of stroke and the period of residual effects [653].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: sensory TENS refers to electrical stimulation of a peripheral nerve with series of pulses of 0.125–1 ms duration at a frequency of 80–100 Hz (high-frequency TENS), which produces a sensory rather than motor response, or at a frequency of 1–5–10 Hz (low-frequency TENS), which, in addition to a sensory response, causes muscle contraction. It is used mainly for pain relief. In addition, the methodology of TENS varies significantly regarding electrode placement, pulse frequency and duration, current intensity, session duration (from 20 min to 2 h), session frequency (from 1 to 6 times per week), and duration of the course of therapy (from a single session to sessions for 8 weeks) (Appendix A3-39).
It is recommended for adult patients with ischemic stroke to undergo low-frequency passive neuromuscular electrical stimulation (NMES) or EMG-triggered NMES of the wrist and finger flexors and extensors as an adjuvant method when the rehabilitation goal is to restore hand and finger movements in patients with a stroke duration of less than 6 months [653].
GCR CLoE 5Grade of Recommendation C (Level of Evidence – 5)
Comment: low-frequency NMES, unlike sensory electrical nerve stimulation, is capable of producing a motor response, i.e., muscle contraction. In this case, stimulation is performed in the low-frequency range (10–50 Hz), and electrodes are placed over motor endplates (areas of high concentration of neuromuscular synapses). Low-frequency NMES can be passive or triggered by available preserved muscle activity (recorded using electromyography, EMG-NMES) or limb position in space (recorded using an accelerometer). The latter two techniques are also used to provide biofeedback to the patient and increase their engagement in goal-directed training when muscle contraction can be generated, but its strength is insufficient (functional NMES). According to a systematic review, NMES combined with standard motor rehabilitation is effective in increasing active range of motion and, in some cases, muscle strength. Low-frequency passive NMES of the wrist and finger extensors can also be used for temporary reduction of spasticity as an adjuvant method (Appendix A3-40).
It is recommended for adult patients with ischemic stroke to perform mental practice with movement imagery as an adjuvant rehabilitation method for patients with post-stroke central arm paresis of any severity to improve functional outcomes [702].
GCR BLoE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: the inclusion of movement imagery training in comprehensive motor rehabilitation increases the efficacy of arm movement recovery, as shown in studies involving more than 500 patients. No effect of this therapy on the improvement of basic self-care skills has been identified.
It is recommended for adult patients with post-stroke arm muscle paresis of varying severity to include a course of training using kinesthetic movement imagery technology with a brain–computer interface coupled with a hand exoskeleton in the comprehensive motor rehabilitation program (stages 2 and 3 of medical rehabilitation) to improve arm motor function in both proximal and distal segments [703–705].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: The use of an interface with functional electrical stimulation and non-invasive electroencephalography, controlling a robotic orthosis on the paretic limb, to solve visual abstraction tasks on a monitor [705]. In addition, the advantages of interface-linked functional electrical stimulation contributed to training precise hand movements with robotic orthosis control (Appendix A3-41).
It is not recommended for adult patients with ischemic stroke and lower urinary tract dysfunction to routinely insert an indwelling urinary catheter to correct urination disorders due to an increased risk of urinary tract infection [706–710].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: in the acute period of ischemic stroke, one of the forms of urination disorders is urinary urge incontinence. A clear correlation has been revealed between the presence of urge urinary incontinence and severe motor and mental impairments. The cause of urge incontinence in stroke is detrusor overactivity due to the loss of the inhibitory influence of cortical centers on the micturition reflex. It is advisable to use external condom catheters for men and absorbent pads for women. Another form of lower urinary tract dysfunction can be urinary retention. Short-term (no more than 7 days) urethral catheterization (A11.28.007 Urinary bladder catheterization) under aseptic conditions is indicated. Intermittent catheterization is preferred with diuresis monitoring, ultrasound assessment of post-void residual urine volume (A04.28.002.005 Ultrasound examination of the urinary bladder with determination of residual urine), and documented records of spontaneous urination volumes or volumes obtained during intermittent catheterization (Appendix A3-42).
It is recommended for adult patients with ischemic stroke and urination dysfunction to regularly assess and record post-void residual urine volume using ultrasound to determine the indications and schedule for intermittent catheterization (A04.28.002.005 Ultrasound examination of the urinary bladder with determination of residual urine) [706–710].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: incomplete bladder emptying is a major risk factor for urinary tract infections (UTIs), increased intravesical pressure during the filling phase, and urinary incontinence. Normally, the residual urine volume should not exceed 50 ml. Ultrasound assessment of residual urine volume is carried out in two stages: with a full bladder (the patient must first drink 1 liter of fluid 1.5–2 hours before the study) and after urination. Intermittent catheterization should be considered as a method of symptomatic treatment for impaired bladder emptying function. The recommended catheterization frequency is 4–6 times a day, performed upon the urge to urinate or its equivalent. If the urge to urinate becomes more frequent, therapy aimed at reducing detrusor hypersensitivity and overactivity is performed, and fluid intake is regulated. In the absence of the urge to urinate, catheterization is performed every 4 hours. Such a catheterization regimen prevents bladder overdistension (normally, the bladder volume during catheterization should not exceed 400–500 ml) and reduces the risk of UTI (Appendix A3-43).
It is recommended for adult patients with ischemic stroke in whom incontinence treatment is impossible or associated with high risks of anticholinergic drugs (group G04BD, drugs for urinary frequency and incontinence) to use absorbent products (280360) [708]. If contractile function of the perineal muscles is preserved, pelvic floor muscle training, including with biofeedback, can be used to improve functional outcomes [709, 710]
}$.) CLevel of reliability of evidence – 5Level of recommendation C (level of reliability of evidence – 5)
Comment: if conservative treatment for urinary incontinence is ineffective or impossible, patients may prefer absorbent products and urine collection devices over active treatment with its associated risks. These devices include absorbent pads, urethral catheters, external urine collection devices, male compression devices, and intravaginal devices for women. Pelvic floor muscle training, including biofeedback, is used in patients with a preserved ability for partial or complete voluntary contraction of the perineal muscles (Appendix A3-44).
It is recommended to prescribe botulinum toxin type A** (M03AX01) to adult patients with ischemic stroke (IS) complicated by chronic sialorrhea to reduce the risk of aspiration complications [711-714].
GPR 2Level of Evidence Recommendation B (Level of Confidence of Evidence – 2)
Comment: The efficacy of botulinum toxin type A** (M03AX01) (incobotulinumtoxinA) has been demonstrated in several small studies, as well as in a large prospective, multicenter, randomized, double-blind, placebo-controlled SIAXI trial involving 184 patients with chronic sialorrhea due to various neurological conditions, including stroke. A statistically significant reduction in drooling was shown by week 4 after the injection of 75 and 100 U of botulinum toxin type A** (M03AX01) compared with placebo. The drug showed a favorable safety profile with a low incidence of treatment-related adverse events, the most frequent of which was dry mouth [711].
It is recommended for adult patients with IS and hemiparesis in the early recovery period of stroke to undergo correction of motor function using computer technologies (A 19.23.004, gait training with biofeedback) targeting the stance phase parameter, in order to reduce functional asymmetry and harmonize gait [715-717].
LEC BLOCE 3Level of Evidence Recommendation B (Level of Confidence of Evidence – 3)
It is recommended for adult patients with IS in the acute period of stroke to use eye-tracking to provide alternative communication and stimulate oculomotor reactions [718-724].
LEC CLOCE 2Level of Evidence Recommendation C (Level of Confidence of Evidence – 2)
It is recommended for adult patients with IS and communication impairment due to speech disorders in the early and late recovery periods to use the eye-tracking method to provide alternative communication [725-729].
LEC BLOCE 3Level of Evidence Recommendation B (Level of Confidence of Evidence – 3)
It is recommended that adult patients with cerebral stroke in the early and late recovery periods undergo therapeutic exercises for the extraocular muscles (A19.23.002.00) using semi-immersive virtual environments with biofeedback based on objective eye movement parameters (saccades and fixations) to restore visual fields and visuo-oculomotor functions associated with visual attention [730-736].
LEC ALOCE 2Level of Evidence Recommendation A (Level of Confidence of Evidence – 2)
Comment: for rehabilitation exercises in patients with saccadic dysfunction, visual attention disorders, and visual field defects, it is recommended to use eye-tracking with biofeedback, preferably in the early recovery period. For diagnostics to identify saccadic disorders or visual attention deficits (including neglect syndrome), as well as to conduct objective diagnostics of the rehabilitation effect, it is recommended to use the eye-tracking method in both early and late recovery periods.
It is recommended that adult patients with IS undergo neuropsychological diagnostics of higher mental functions within the first 48 hours after disease onset to determine treatment tactics [737, 738].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with IS use the A.R. Luria neuropsychological syndrome analysis method for diagnosing higher mental function disorders [739-742].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comments. Most studies use short screening neuropsychological tests, such as MoCa (Appendix G20). These tests are mainly used for a rapid assessment of cognitive functions during initial diagnosis by the attending physician. However, the sensitivity of such tests to the specific features of higher mental function disorders in patients with organic brain lesions is relatively low. Accordingly, this factor necessitates the use of more detailed diagnostic tools. A.R. Luria's neuropsychological syndrome analysis method makes it possible to determine the structural and functional organization of mental functions, such as perception, movement and action, attention, memory, speech, thinking, regulation of mental activity, and the characteristics of disorders of these functions in patients with cerebral pathology.
5. Prevention and Dispensary Observation
5.1. General provisions
It is recommended to initiate secondary prevention early (no later than 48 hours after the onset of acute cerebrovascular accident) in adult patients with IS/TIA to improve functional outcomes and reduce the risk of recurrent vascular events [743–746].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in patients who have suffered an ischemic stroke or TIA, the risk of recurrent stroke is increased almost 10-fold and is about 25–30 %. The risk of recurrent stroke is highest in the first few weeks, and for recurrent TIA – within the first days following onset. Therefore, secondary prevention should be started as early as possible: immediately after the diagnosis of TIA and no later than 48 hours after the onset of ischemic stroke. Individualized secondary prevention of stroke reduces the risk of recurrent cerebrovascular events by 20–30 %. The main areas of secondary prevention of ischemic stroke include both non-pharmacological methods (risk factor correction, lifestyle modification) and drug therapy (antihypertensive drugs, antithrombotic agents, statins) and surgical treatments.
5.2. Lifestyle modification
Diet. It is recommended that adult patients with IS/TIA adhere to a Mediterranean-style diet emphasizing monounsaturated fats, plant-based foods, and fish consumption, or supplemented with high-quality extra virgin olive oil or nuts, which is preferable to simply following a low-fat diet to reduce the risk of recurrent stroke [747, 748, 1142].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: currently, there is limited data supporting the benefit of prescribing special diets for secondary stroke prevention compared to well-established recommendations regarding the benefits of diets for individuals at high risk for cardiovascular disease and coronary artery disease, as well as the impact of nutrition on stroke risk factors such as blood pressure and cholesterol. The REGARDS (Reasons for Geographic and Racial Differences in Stroke Study) cohort study found that higher adherence to a Southern diet (high in fats, fried foods, eggs, processed meats, and sugar-sweetened beverages) was associated with a 39 % increased risk of stroke (hazard ratio [HR] 1.39 [95 % CI 1.05–1.84]) [749].
It is recommended that adult patients with IS/TIA who do not restrict dietary sodium intake in daily life reduce salt (sodium chloride) consumption by at least 2.5 g/day (1 g/day of sodium) to reduce the risk of cardiovascular disease, including stroke [750, 751].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: the results of meta-analyses of long-term studies on salt reduction in individuals with established cardiovascular disease [750] showed that a reduction in sodium intake of 1 g/day (salt 2.5 g/day) is associated with a 20% reduction in subsequent cardiovascular events (RR = 0.80 [95 % CI = 0.66–0.97]). The DASH-sodium study [751] demonstrated that against the background of the DASH diet typical of the US in the 1990s, reducing sodium intake from 3.3 to 2.4 g/day decreased systolic blood pressure by 2.1 mm Hg (p < 0.001), and a further reduction in sodium intake from 2.4 to 1.5 g/day led to an additional decrease of 4.6 mm Hg (p < 0.001). The DASH diet was associated with significantly lower systolic blood pressure levels at every sodium level compared to the control diet.
Physical activity. It is recommended that physically active adult patients with ischemic stroke / transient ischemic attack (IS/TIA) perform moderate-intensity aerobic physical activity for at least 10 minutes 4 times a week, or high-intensity aerobic physical activity for at least 20 minutes twice a week to reduce the risk of recurrent stroke, death from recurrent stroke, myocardial infarction, or other vascular causes [752].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: participants in the SAMMPRIS study [752] who did not achieve the target level of physical activity defined by the Physician-Based Assessment and Counselling for Exercise score ≥ 4 points had a significantly higher chance of developing stroke, myocardial infarction, and death from vascular causes compared to those who achieved this indicator (OR = 5.4 [95% CI = 2.4–12.1]). A physical activity score of 4 points on the Physician-Based Assessment and Counselling for Exercise scale is equivalent to 10-minute sessions of moderate physical activity (sufficient to cause sweating or a noticeable increase in heart rate, e.g., brisk walking, stationary cycling) 4 times a week or 20-minute sessions of vigorous physical activity (e.g., jogging) twice a week. For the endpoint of ischemic stroke, physical activity was the only risk factor associated with a lower number of stroke events; among those who did not reach the target levels for specific physical activity, the OR was 6.7 (95% CI = 2.5–18.1) for recurrent stroke compared to those who reached the target levels of physical activity.
It is recommended that adult patients with IS/TIA who are forced to lead a sedentary lifestyle break up sitting time with standing or light activity lasting 3 minutes every 30 minutes in order to maintain normal cardiovascular system function [753].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: prolonged sitting and physical inactivity increase the risk of recurrent stroke, as these levels are generally associated with cardiovascular mortality (HR = 1.15 [95% CI = 1.11–1.19]) and the development of cardiovascular disease (HR = 1.143 [95% CI = 1.00–1.73]), with risks becoming more pronounced at lower levels of physical activity [754]. Preliminary results from the BUST-Stroke (Breaking Up Sitting Time After Stroke) study established that sitting time interrupted by 3-minute bouts of light standing physical activity every 30 minutes reduced systolic blood pressure by 3.5 mm Hg.
It is recommended that adult patients with IS/TIA avoid exposure to ambient tobacco smoke (passive smoking), and that those who continue to smoke stop smoking (or reduce daily smoking) to reduce the risk of recurrent stroke [759–762].
Level of Evidence AGrade of Evidence 3Level of Recommendations A (Grade of Evidence – 3)
It is recommended that adult patients with IS/TIA who consume alcohol in amounts exceeding two standard drinks per day for men or one standard drink per day for women quit or reduce alcohol consumption to lower the risk of recurrent stroke (one standard drink = 14 g or 17.7 ml of pure ethanol) [763–766].
Level of Evidence AGrade of Evidence 3Level of Recommendations A (Grade of Evidence – 3)
It is recommended that adult patients with IS/TIA who are overweight or obese undergo weight loss and lifestyle modification to improve their cardiovascular risk factor profile and reduce the risk of recurrent stroke [767, 768, 769, 770, 771].
GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)
Comment: approximately 24 to 30% of patients with ischemic stroke suffer from obesity [769]. In population-based studies, obesity increases the risk of ischemic stroke by 50–100% compared to normal-weight patients [770]. A weight loss of just 5–10% leads to a significant reduction in the risk of vascular events [771]. Observational studies provide some evidence that weight loss following bariatric surgery may reduce the risk of stroke [772, 773].
5.2.1. Arterial hypertension
It is recommended that adult patients with IS and TIA suffering from hypertension be prescribed drugs from the groups of thiazide diuretics (thiazides) (C03AA), ACE inhibitors (C09AA), and angiotensin II receptor blockers (C09CA) to control blood pressure levels and reduce the risk of recurrent IS [775–778].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: Diuretics, ACE inhibitors (C09AA) and angiotensin II receptor blockers (C09CA) have demonstrated benefit in RCTs or systematic reviews of RCTs.
It is recommended for the majority of adult patients with IS and TIA suffering from hypertension to achieve a target blood pressure value of less than 130/80 mm Hg to reduce brain and other target-organ damage and lower the risk of recurrent IS, intracranial hemorrhage, and other cardiovascular events [775–780].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: achievement of the target blood pressure level should be accomplished within three months with titration steps (increasing drug dosage or switching to a 2-/3-component therapy regimen) of approximately 4 weeks [781]. Achieving a target blood pressure level of less than 130/80 mm Hg may not be advisable in patients over 80 years of age, when stroke develops against the background of precerebral artery dissection, or in hemodynamically significant stenosis of brachiocephalic arteries.
It is recommended that adult patients with IS and TIA without a confirmed diagnosis of hypertension, but having a blood pressure level greater than 130/80 mm Hg, be prescribed antihypertensive therapy (ACE inhibitors (C09AA) and angiotensin II receptor blockers (C09CA)) to reduce the risk of recurrent IS, intracranial hemorrhage, and other cardiovascular events [778, 782–784].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: patients who suffered an IS and had a blood pressure level in the range of 130/80–140/90 mm Hg were included in a number of studies. For example, in the PRoFESS study, more than 33% of patients who suffered an IS had a systolic blood pressure level of less than 135 mm Hg [783], and in the PAST-BP study, more than half of the patients had an SBP level of less than 140 mm Hg [784]. All of the aforementioned studies demonstrated the efficacy and safety of prescribing antihypertensive therapy as part of secondary prevention of IS in patients with BP < 140/90 mm Hg.
5.2.2. Dyslipidemia
It is recommended for the majority of adult patients with IS and TIA to be prescribed lipid-lowering therapy (HMG-CoA reductase inhibitors C10AA) to achieve a target LDL-C level < 1.4 mmol/L or at least a ≥ 50% reduction in LDL-C levels compared to baseline in order to reduce the progression of atherosclerotic vascular damage and lower the risk of recurrent stroke [785].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: additional benefits of lowering LDL-C levels below 1.8 mmol/L were demonstrated in the TST (Treat Stroke to Target) study: in patients with a prior IS, choosing this treatment strategy reduced the risk of recurrent cardiovascular events by 22% [785]. The results of the IMPROVE-IT study and two meta-analyses showed an additional reduction in the risk of CV events when lowering LDL-C levels to < 1.4 mmol/L, allowing the formula to be defined: "the lower the LDL-C, the lower the risk of CV events" [788].
It is recommended that adult patients with IS who are at extremely high risk for recurrent CV events achieve a target LDL-C value of < 1.0 mmol/L to reduce the risk of recurrent stroke [789].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: extremely high risk for recurrent CV events is defined by the following clinical situations:
– an adult patient with atherosclerotic IS who, within the next two years while receiving maximally tolerated lipid-lowering therapy (statins + ezetimibe) and PCSK-9 targeted therapy ((alirocumab** (C10AX14), evolocumab** (C10AX13), inclisiran (C10AX16))) / while achieving the target LDL-C value (less than 1.4 mmol/L), experienced a recurrent atherosclerotic CV event (myocardial infarction, unstable angina, percutaneous coronary intervention, coronary artery bypass grafting, intermittent claudication, recurrent TIA/IS).
It is recommended that adult patients with IS/TIA under 55 years of age undergo blood lipoprotein testing (A09.05.027) with the aim of adjusting lipid-lowering therapy to reduce the risk of recurrent stroke [791].
CUALEL 2 Level of Evidence A (Level of Certainty of Evidence – 2)
It is recommended that adult patients with IS/TIA who had an early onset (under 45 years of age) of atherosclerotic heart disease (CHD, myocardial infarction, IS/TIA, lower extremity ischemia) undergo blood lipoprotein testing (A09.05.027) with the aim of adjusting lipid-lowering therapy to reduce the risk of recurrent stroke [792].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that the majority of adult patients with IS/TIA be prescribed high-intensity statin therapy (C10AA, HMG-CoA reductase inhibitors) at maximum tolerated doses to achieve target LDL-C levels in order to reduce the risk of cardiovascular events [793].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
Comment: high-intensity statin therapy refers to the administration of atorvastatin** (C10AA05) at doses of 40–80 mg/day or rosuvastatin (C10AA07) at doses of 20–40 mg/day [794]. When triglyceride (TG) levels exceed the target value (2.3 mmol/L), statin therapy is also the first-line treatment [795].
It is recommended that adult patients over 75 years of age with a history of IS/TIA, when indicated, initiate moderate-intensity statin therapy to reduce the risk of recurrent stroke [796, 797].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
Comment: moderate-intensity statin therapy refers to the administration of atorvastatin** (C10AA05) 10–20 mg/day, or rosuvastatin 5–10 mg/day [798].
It is recommended that patients over 75 years of age with IS/TIA who were previously receiving high-intensity statin therapy continue statin therapy to reduce the risk of recurrent stroke without changing the intensity regimen [799–801].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended that adult patients with IS/TIA who have not reached target LDL-C levels on therapy with maximally tolerated statin doses for 4–12 weeks receive the addition of ezetimibe (C10AX09) to therapy to reduce the risk of recurrent stroke [803].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended that adult patients with IS/TIA and statin intolerance be prescribed ezetimibe (C10AX09) to achieve the target LDL-C level in order to reduce the risk of recurrent stroke [803].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: statin intolerance is defined as the development of side effects following discontinuation and subsequent rechallenge with a statin, including when using a different statin and/or a reduced dose.
It is recommended that adult patients with IS/TIA receive PCSK9-targeted therapy (alirocumab** (C10AX14), evolocumab** (C10AX13), inclisiran** (C10AX16)) added to ongoing statin and ezetimibe therapy to achieve the target LDL-C level [806–808, 1119].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is recommended that adult patients with IS/TIA undergo evaluation of the efficacy of ongoing lipid-lowering therapy, its safety, and patient adherence to treatment (including lifestyle modifications) [809].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: it is advisable to evaluate laboratory parameters (fasting lipid profile, ALT, AST) 4–12 weeks after initiating statin therapy or increasing its dose. After achieving target LDL-C and TG levels (the target for TG is less than 2.3 mmol/L), annual laboratory monitoring is recommended (in the absence of adherence issues or other specific reasons for more frequent monitoring). Routine monitoring of liver enzymes during statin treatment is not recommended unless symptoms indicative of liver pathology are present.
5.3. Non-cardioembolic stroke or TIA
It is recommended that adult patients with non-cardioembolic IS and TIA receive antiplatelet therapy to reduce the risk of recurrent IS [815, 816].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: adult patients with non-cardioembolic IS and TIA are prescribed antiplatelet therapy (ASA** (B01AC06) at a dose of 75–150 mg/day, or clopidogrel** (B01AC04) 75 mg/day to reduce the risk of recurrent cardiovascular events [815, 816].
It is recommended that adult patients with minor (NIHSS score of 3 or less) non-cardioembolic acute ischemic stroke or high-risk TIA (more than 3 points on the ABCD2 scale) receive early dual antiplatelet therapy (ASA** (B01AC06) and clopidogrel** (B01AC04)), initiated 12–24 hours after symptom onset (possibly later, but no later than 7 days from symptom onset) for a duration of at least 21 days (but not more than 90 days), followed by transition to single antiplatelet therapy (ASA** (B01AC Antiplatelet agents excluding heparin) and clopidogrel** (B01AC Antiplatelet agents excluding heparin)), to reduce the risk of recurrent ischemic stroke [821–823].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended that adult patients with non-cardioembolic IS with a neurological deficit of less than 6 NIHSS points, or high-risk TIA (ABCD2 score greater than 5), or any TIA in the presence of symptomatic stenosis of at least 50% of an extracranial or intracranial artery, receive early (within 24 hours) dual antiplatelet therapy (ASA** (B01AC06) and ticagrelor** (B01AC24)) for a duration of 30 days to reduce the risk of recurrent IS [824].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: the THALES study demonstrated that the combined use of ticagrelor** (B01AC24) and ASA** (B01AC06) in adults reduces the risk of recurrent stroke compared to ASA** (B01AC06) monotherapy.
It is not recommended (due to a high risk of bleeding) in adult patients with non-cardioembolic ischemic stroke or TIA to use dual antiplatelet therapy (ASA** (B01AC06) and clopidogrel** (B01AC04)) for more than 90 days or triple antiplatelet therapy to reduce the risk of recurrent ischemic stroke [825–827].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended to prescribe ASA** (B01AC06) 325 mg/day to adult patients with ischemic stroke or TIA due to 50–99% major intracranial artery stenosis to reduce the risk of recurrent ischemic stroke and vascular death [828, 829].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended to add clopidogrel** (B01AC04) 75 mg/day to ASA** (B01AC06) for up to 90 days in adult patients who have suffered an ischemic stroke or TIA due to severe 70–99% major intracranial artery stenosis to reduce the risk of recurrent stroke [830–833].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended to maintain systolic blood pressure at no higher than 140 mm Hg, high-intensity statin therapy (C10AA HMG-CoA reductase inhibitors), and moderate to vigorous physical activity in adult patients with ischemic stroke or TIA due to 50–99% major intracranial artery stenosis to prevent recurrent stroke [834–837].
Level of Evidence AGrade of Evidence 3Level of Recommendations A (Grade of Evidence – 3)
Comment: the goal of antihypertensive therapy is to reduce the risk of intracranial hemorrhagic complications. After three months (90 days), the tolerability of antihypertensive therapy should be evaluated.
It is not recommended to perform angioplasty and stenting of the corresponding artery as initial treatment in adult patients with ischemic stroke or TIA due to 50–99% major intracranial artery stenosis to reduce the risk of recurrent stroke [838–840].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: this recommendation applies to patients with newly diagnosed stenosis, as well as to patients who previously received antithrombotic therapy. The optimality of the prescribed therapy and patient adherence to the previously prescribed preventive treatment should be evaluated.
It is not recommended to perform extracranial-intracranial bypass surgery for the prevention of recurrent stroke in adult patients who have suffered an ischemic stroke or TIA within the last 120 days due to symptomatic middle cerebral/internal carotid artery stenosis [841, 842].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: currently, there is insufficient data to recommend this surgical intervention for the prevention of recurrent stroke.
It is recommended to provide optimal medical therapy—including antiplatelet (B01 Antithrombotic agents), high-intensity lipid-lowering (C10 Lipid-modifying agents), and antihypertensive therapy (C02 Antihypertensive drugs)—to adult patients with ischemic stroke or TIA due to carotid artery stenosis to reduce the risk of recurrent stroke [843, 1143, 1144].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: the target value for low-density lipoprotein cholesterol is less than 1.4 mmol/L, and the target systolic blood pressure level is less than 140 mm Hg.
It is recommended to perform revascularization within two weeks after disease onset in adult patients with TIA or non-disabling stroke due to > 50% carotid artery stenosis to increase the probability of a favorable stroke outcome [844].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: a non-disabling stroke is defined as a condition corresponding to 3 points or less on the modified Rankin scale.
It is not recommended to perform revascularization via carotid endarterectomy or carotid stenting in adult patients with ischemic stroke/TIA and < 50% carotid artery stenosis to reduce the risk of recurrent stroke [845].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is not recommended to perform extracranial-intracranial bypass surgery for the prevention of recurrent stroke in adult patients who have suffered an ischemic stroke or TIA within the last 120 days due to symptomatic stenosis or occlusion of the middle cerebral/internal carotid artery [846].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended to prescribe optimal medical therapy, including antiplatelet (B01 Antithrombotic agents), high-intensity lipid-lowering (C10 Lipid-modifying agents), and antihypertensive therapy (C02 Antihypertensive agents), to adult patients with ischemic stroke or TIA in the setting of symptomatic extracranial vertebral artery stenosis to reduce the risk of recurrent stroke [843, 1145].
COVID CLEL 5Level of Evidence Recommendations C (Level of Confidence of Evidence – 5)
It is not recommended to perform endarterectomy and vertebral artery transposition in adult patients with ischemic stroke or TIA and extracranial vertebral artery stenosis with recurrent symptoms despite optimal medical therapy for the prevention of recurrent stroke due to insufficient evidence [847].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: The utility of open surgical interventions, such as endarterectomy and vertebral artery transposition, for the prevention of recurrent stroke has not been proven to date.
It is recommended to prescribe a combination of rivaroxaban** (B01AF01) 2.5 mg twice daily and ASA** (B01AC06) 100 mg daily one month after the event in adult patients with non-lacunar non-cardioembolic ischemic stroke or TIA combined with coronary artery disease (CAD) or other forms of atherosclerosis at low bleeding risk to reduce the risk of recurrent stroke/TIA and cardiovascular death [848, 849].
GCR BLeE 2Grade of Recommendations B (Level of Evidence – 2)
Comment: The COMPASS RCT demonstrated a significant reduction in the number of all ischemic events in the combination therapy group of rivaroxaban** (B01AF01) 2.5 mg twice daily combined with ASA** (B01AC06) 100 mg compared with ASA** (B01AC06) monotherapy: a 24% reduction in the incidence of the primary endpoint (cardiovascular death, stroke, or myocardial infarction) (HR = 0.76 at 95% CI = 0.66–0.86; p < 0.001); a 49% reduction in the incidence of ischemic or undetermined stroke (HR = 0.58 at 95% CI = 0.44–0.76, p < 0.001); a 22% reduction in cardiovascular death (HR = 0.78 at 95% CI = 0.64–0.96; p = 0.02). Major bleeding occurred more frequently in the rivaroxaban** (B01AF01) and ASA** (B01AC06) combination group (3.1%) compared to the ASA** monotherapy group (1.9%) (HR = 1.70; p < 0.001), whereas the incidence of intracranial and fatal hemorrhages did not differ.
Target patient groups for combination therapy include:
- patients with CAD older than 65 years;
- patients with CAD younger than 65 years with involvement of at least two vascular beds or having 2 or more additional risk factors (ongoing smoking, diabetes mellitus, estimated glomerular filtration rate [eGFR] < 60 mL/min, heart failure, or ischemic stroke other than lacunar, occurring ≥ one month ago);
- patients with peripheral artery disease (lower extremity revascularization or amputation, intermittent claudication combined with an ankle-brachial index [ABI] below 0.90 or peripheral artery stenosis (≥ 50%), or CAD combined with ABI below 0.90 or carotid revascularization) [848–849]. Low bleeding risk implies the absence of: a history of intracranial hemorrhage, ischemic stroke within the past month or other intracranial pathology, recent gastrointestinal bleeding (GIB) or anemia due to suspected GIB, other gastrointestinal pathology with increased bleeding risk, hepatic impairment, or renal impairment requiring dialysis or with eGFR < 15 mL/min/1.73 m2, coagulopathy or hemorrhagic diathesis, advanced age, or frailty [850]. To reduce the risk of hemorrhagic complications, it is necessary to achieve blood pressure < 140/90 mm Hg and administer proton pump inhibitors in patients at high risk for GIB. The combination of rivaroxaban** (B01AF01) and ASA** (B01AC06) is not recommended in patients with a prior hemorrhagic or lacunar stroke, severe heart failure, advanced chronic kidney disease (estimated eGFR < 15 mL/min), or when dual antiplatelet, anticoagulant, or other antithrombotic therapy other than ASA** (B01AC06) is required [851].
It is recommended to consider short-term anticoagulant therapy (30–60 days) using heparin (heparin group
B01AB) with transition to direct oral anticoagulants (B01AE Direct thrombin inhibitors and B01AF Direct factor Xa inhibitors), followed by antiplatelet monotherapy (B01A Antithrombotic agents) for secondary stroke prevention in adult patients with cryptogenic ischemic stroke associated with COVID-19 infection, occurring in the setting of hypercoagulation with elevated D-dimer, who are not in critical condition [852].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
5.4. Cardioembolic stroke or TIA
Atrial fibrillation is a major cause of cardioembolic stroke. In patients with ischemic stroke or TIA, the diagnosis of AF leads to lifelong oral anticoagulant therapy, thereby reducing the rate of recurrent strokes/TIs. Anticoagulation systemically reduces thrombus formation, including in the left atrium, and lowers the risk of stroke or systemic embolism in AF, while also increasing the risk of bleeding. Patients with ischemic stroke or TIA represent a higher risk group for recurrent strokes than the general population. Furthermore, when considering the use of the CHA2DS2-VASc risk calculator (Appendix G14), the presence of stroke or TIA immediately places the patient in the high-risk category, for which anticoagulant therapy is always recommended [853, 854].
It is recommended to prescribe oral anticoagulants (dabigatran etexilate** (B01AE07), apixaban** (B01AF02), rivaroxaban** (B01AF01), or warfarin** (B01AA03)) to adult patients with nonvalvular AF and ischemic stroke or TIA to reduce the risk of recurrent ischemic stroke [855–862].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
Comment: Nonvalvular AF refers to all variants except AF in the presence of a mechanical bi-leaflet aortic valve prosthesis***, a mechanical bi-leaflet mitral valve prosthesis***, or moderate-to-severe mitral stenosis.
It is recommended to use oral anticoagulants in adult patients with nonvalvular AF and ischemic stroke/TIA to reduce the risk of recurrent ischemic stroke regardless of the type of AF (paroxysmal, persistent, or permanent) [863].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended to prescribe direct oral anticoagulants (DOACs): apixaban** (B01AF02), dabigatran etexilate** (B01AE07), or rivaroxaban** (B01AF01) – preferably over warfarin** (B01AA03) to reduce the risk of recurrent stroke in adult patients with nonvalvular AF and ischemic stroke/TIA [863–867].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended to administer anticoagulant therapy similar to that used for AF in adult patients with atrial flutter and ischemic stroke/TIA to reduce the risk of recurrent ischemic stroke [863–867].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to use apixaban** (B01AF02), dabigatran etexilate** (B01AE07), or rivaroxaban** (B01AF01) in adult patients with nonvalvular AF and ischemic stroke/TIA in whom the time in the therapeutic range (TTR) for INR (2.0–3.0) during warfarin** (B01AA03) therapy is ≤ 70%, to reduce the risk of recurrent ischemic stroke [869, 1146].
GCR CLOC 5Grade of Recommendations C (Level of Evidence – 5)
It is recommended to delay the initiation of oral anticoagulants for 14 days in adult patients with AF and ischemic stroke at high risk of hemorrhagic transformation to reduce the risk of intracranial hemorrhagic complications [870–873].
GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)
Comment: patients with large cerebral infarctions have a high risk of hemorrhagic transformation of intracranial hemorrhage with early initiation of anticoagulation [874]; therefore, in these circumstances, it is reasonable to delay the initiation of oral anticoagulation for 14 days after stroke onset. Although there is no universally accepted definition of a large cerebral infarction, accepted definitions include an NIHSS score >15 [875] and brain infarctions involving either the entire vascular territory of one or more than one vascular territory of cerebral arteries [876]. In addition, patients with early signs of hemorrhage (but not type 1 hemorrhagic transformation) on neuroimaging are at the highest risk for further intracerebral hemorrhage and therefore it is recommended to delay the initiation of oral anticoagulation for a longer period (4–8 weeks) to allow recovery of the blood-brain barrier [877]. The timing of initiation/re-initiation of anticoagulants (B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) is determined by the rule: for small brain lesions (lacunar strokes) initiation/re-initiation is performed earlier, for large lesions – later. For patients with stroke/TIA in the carotid territory, the following scheme for determining the timing of anticoagulant therapy re-initiation can be used: for TIA – start/re-initiation of therapy within 24 hours, for mild stroke (NIHSS score <8) – after 3 days, for moderate stroke (NIHSS 8–16) – after 6–8 days, for severe stroke (NIHSS score >16) – after 12–14 days [878, 879]. In case of moderate and severe stroke, neuroimaging must be performed before re-initiation to rule out hemorrhagic complications of ischemic stroke.
It is recommended to consider prescribing ASA** (B01AC06) (in the absence of contraindications) to adult patients with AIS, TIA, and AF before starting or resuming oral anticoagulant therapy (B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) to reduce the risk of recurrent AIS and TIA [880–882].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: a pooled analysis of the CAST and IST trial data [883], which included patients with AF among others, demonstrated a reduction in the risk of recurrent stroke and death with the initiation of ASA** (B01AC06) within the first 48 hours.
It is not recommended for the majority of adult patients with AF and AIS/TIA to prescribe combination therapy with antithrombotic agents (oral anticoagulants) (B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) and antiplatelet agents (B01AC Antiplatelet agents excluding heparin) [884–888].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: this recommendation does not apply to patients requiring the prescription of antiplatelet agents excluding heparin (B01AC) and antithrombotic agents (anticoagulants) (B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) for other indications (e.g., after arterial stenting).
It is recommended to initiate anticoagulant therapy (B01AB Heparin group, B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) in adult patients with non-valvular AF and TIA after a symptomatic event and diagnosis of TIA to reduce the risk of recurrent ischemic stroke [889].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended to perform percutaneous left atrial appendage closure (A16.12.041.007 Endovascular occlusion of the left atrial appendage) in adult patients with non-valvular AF and AIS/TIA and AF who have contraindications to lifelong anticoagulant therapy (B01AB Heparin group, B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) in order to reduce the risk of recurrent stroke and hemorrhagic complications [890–893].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
Comment: in patients with stroke and non-valvular AF, the left atrial appendage is the site of embolic mass detection in 90% of cases. This observation gave rise to the concept of left atrial appendage closure to reduce the risk of stroke in AF. The Watchman device was studied in the PROTECT AF randomized trial and the PREVENT trial, which demonstrated a slight increase in thrombotic risk after implantation, alongside a reduced risk of bleeding later in patients' lives. Current clinical practice, based on clinical trial design, involves the short-term (1.5 months = 45 days) use of oral anticoagulants after Watchman device placement to reduce the risk of thrombus formation associated with the implanted device, followed by 4.5 months of dual antiplatelet therapy. In patients at high risk of bleeding due to oral anticoagulation, left atrial appendage closure can reduce the long-term bleeding risk with an ischemic stroke risk comparable to vitamin K antagonist therapy. Absolute contraindications to oral anticoagulants are:
1. Recurrent intracranial hemorrhage
2. Intracranial mass
3. End-stage liver disease – hepatic impairment according to Child-Pugh class C is a contraindication for DOACs; warfarin** is not indicated if baseline INR is above the therapeutic level.
It is recommended to initiate oral anticoagulant therapy (B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) between days 3 and 14 after the onset of acute neurological symptoms in adult patients with non-valvular AF and AIS with a low risk of hemorrhagic transformation to reduce the risk of recurrent ischemic stroke [894–896].
GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)
Comment: the decision on the timing of starting/resuming oral anticoagulant therapy is based on assessing the size of the brain lesion and the severity of the stroke, determined by the National Institutes of Health Stroke Scale (NIHSS) score. Neurologist experts consider it acceptable not to interrupt anticoagulants in patients with TIA and to start/resume anticoagulants in patients with confirmed AIS between 3 and 14 days, depending on the stability of neurological status and neuroimaging data. Patients are recommended to undergo neuroimaging on day 6 for moderate stroke, and on day 14 for severe stroke, to rule out hemorrhagic transformation.
It is recommended to use warfarin** (B01AA03) in adult patients with AF, moderate to severe mitral stenosis, and AIS and TIA to reduce the risk of recurrent ischemic stroke or TIA [898–903].
LE LoE Recommendation Strength Grade C (Level of Evidence – 2)
It is recommended to prescribe combination therapy with #ASA** (B01AC06) (75–100 mg/day) and warfarin** (B01AA03), or increase the dose of warfarin** (B01AA03) maintaining the INR within the range of 3.0–3.5 (TTR 65–70%) to adult patients with a mechanical bileaflet mitral valve prosthesis*** and a history of AIS/TIA occurring within the target INR range (at least 2.5), in order to reduce the risk of thrombosis and recurrent ischemic stroke or TIA [904, 905].
Level of Evidence AGrade of Evidence 3Level of Recommendations A (Grade of Evidence – 3)
Comment: although regular use of the combination of #ASA** (B01AC06) and warfarin** (B01AA03) in patients with mechanical heart valve prostheses is not recommended, patients with a history of ischemic stroke or TIA prior to valve replacement surgery represent a group with a inherently higher risk of thromboembolism. In this case, the benefit of the combination of warfarin** (B01AA03) and #ASA** (B01AA06 [sic]) in terms of protection against recurrent thromboembolic events may outweigh the competing bleeding risk [905].
It is recommended to prescribe antiplatelet agents (B01AC Antiplatelet agents excluding heparin) to adult patients with ischemic stroke and TIA and aortic valve pathology or non-rheumatic mitral valve pathology (mitral annular calcification, prolapse, etc.), without AF or other indications for antithrombotic agents (anticoagulants) (B01AB Heparin group, B01AE Direct thrombin inhibitors, B01AF Direct factor Xa inhibitors) to reduce the risk of recurrent ischemic stroke or TIA [906–910].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to treat adult patients with ischemic stroke/TIA and mitral stenosis without AF with anticoagulant therapy using warfarin** (B01AA03), achieving a target INR of 2.0–3.0 [907, 1147].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to prescribe long-term therapy with ASA** (B01AC06) 3 to 6 months after valve replacement to adult patients with AIS and TIA and a bioprosthetic aortic heart valve*** or bioprosthetic mitral valve*** who have no other indications for anticoagulant therapy, in order to reduce the risk of recurrent ischemic stroke or TIA [911–917].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: in patients who have undergone mitral or aortic valve replacement using bioprostheses, oral anticoagulation with warfarin** (B01AA03) targeting an INR of 2.5 (range 2.0–3.0) is reasonable for at least 3 months (or up to 6 months postoperatively in patients with a low bleeding risk) [918]. This recommendation is based on observational studies reporting an increased risk of ischemic stroke in the early period after aortic or mitral valve bioprosthesis implantation [919–921]. Long-term therapy with ASA** (B01AC06) alone at 75 to 100 mg daily is recommended 3–6 months after surgery [922–924].
It is recommended that patients with ischemic stroke, TIA, and infective endocarditis be managed in accordance with the clinical guidelines of the Russian Society of Cardiology on infective endocarditis and cardiac implantable electronic device infections [925].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with a mechanical aortic valve prosthesis and a history of ischemic stroke and TIA occurring within the target INR range (at least 2.0) receive anticoagulant monotherapy with warfarin** (B01AA03) with an increased target INR of 3.0 (range 2.5–3.5), or combination therapy with #ASA** (B01AC06) (75–100 mg/day) and warfarin** (B01AA03) maintaining the previous target INR range of 2.0–3.0, to reduce the risk of recurrent ischemic stroke and TIA [905, 939, 1148-1150].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: in real-world clinical practice, anticoagulation with warfarin** (B01AA03) in patients with a prosthetic aortic valve aims to achieve a mean INR of 2.5 (range 2.0–3.0). However, patients who have suffered an ischemic stroke/TIA require more aggressive therapy—either achieving a mean INR of 3.0 (range 2.5–3.5) or adding ASA** (B01AC06) to baseline warfarin** (B01AA03) therapy.
It is recommended that adult patients with a large cerebral infarction or intracranial hemorrhage and infective endocarditis, if hemodynamically stable, have valve surgery delayed for at least 4 weeks to reduce the risk of hemorrhagic complications [926, 927].
GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)
It is recommended that adult patients with ischemic stroke/TIA in the setting of acute myocardial infarction (MI) complicated by left ventricular (LV) mural thrombus formation receive therapy with warfarin** (B01AA) (target INR 2.5 [range 2.0–3.0]) for at least 3 months to reduce the risk of recurrent cardioembolic ischemic stroke [930–932].
Leveled of Evidence CLevel of Data Reliability 2Level of evidence C (level of data reliability – 2)
It is not recommended (due to insufficient safety data) for adult patients with ischemic stroke, TIA, and an LV thrombus (detected within the preceding 3 months) to receive NOAC therapy (dabigatran etexilate**, rivaroxaban**, apixaban**) to reduce the risk of recurrent cardioembolic ischemic stroke [931-933].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
Comment: to date, only a few small-scale studies on the efficacy and safety of NOACs for preventing LV thrombus formation or stroke in patients with acute MI have been published. Therefore, if long-term anticoagulant therapy is planned, vitamin K antagonists (VKAs) remain the drugs of choice for preventing LV thrombus formation or stroke in patients with acute MI. If administration of vitamin K antagonists with adequate INR control (TTR 65–70%) is not feasible, prescribing a NOAC should be considered.
It is recommended that adult patients with ischemic stroke and TIA, as well as a left atrial thrombus in the setting of ischemic, non-ischemic, or restrictive cardiomyopathy and LV dysfunction, receive anticoagulant therapy with warfarin** (B01AA) for at least 3 months to reduce the risk of recurrent cardioembolic ischemic stroke [934, 935].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is recommended that pediatric patients with ischemic stroke and detected atrial myxoma undergo atrial myxoma resection to reduce the risk of oncogenic cardioembolism [72, 937].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
5.5. Aortic arch atherosclerosis
It is recommended that adult patients with ischemic stroke/TIA and aortic arch atheroma receive antiplatelet therapy (B01AC platelet aggregation inhibitors excluding heparin) to prevent recurrent ischemic stroke [938–940].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with ischemic stroke/TIA and aortic arch atheroma receive intensive dyslipidemia therapy (Section 5.2.2. Dyslipidemia) targeting an LDL-C level < 1.4 mmol/L to prevent recurrent stroke [939, 941].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
5.6. Moyamoya disease
It is recommended that adult patients with Moyamoya disease and a history of ischemic stroke/TIA undergo surgical revascularization with extracranial-intracranial bypass to prevent recurrent ischemic stroke or TIA [944, 947].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended that pediatric patients with Moyamoya disease and a history of ischemic stroke/TIA undergo surgical revascularization with extracranial-intracranial bypass to prevent recurrent ischemic stroke or TIA [939].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that patients with Moyamoya disease and ischemic stroke/TIA receive antiplatelet therapy with ASA** (B01AC06) to prevent recurrent ischemic stroke or TIA [939, 947, 948].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
5.7. Patent foramen ovale
It is recommended that patients aged 18 to 60 years with ESUS in the presence of a patent foramen ovale (PFO) and a high risk of embolism undergo transcatheter closure of the PFO using a cardiac occluder device**** followed by long-term antiplatelet therapy (B01AC platelet aggregation inhibitors excluding heparin) to prevent recurrent stroke [939, 950–955].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: anatomical features associated with a high risk of embolism in PFO in studies included the size of the right-to-left shunt (significant difference for large shunts) and the presence of atrial septal aneurysm. Right-to-left shunting through a PFO was assessed using transesophageal echocardiography with a "bubble study" while the patient was at rest or during the Valsalva maneuver. Shunt size classification was based on the maximum number of microbubbles observed in the left atrium within the first three cardiac cycles following their detection in the right atrium; the absence of microbubbles was classified as no shunt, 1 to 5 microbubbles as small size, 6 to 25 microbubbles as medium size, and more than 25 microbubbles as a large shunt.
Factors reducing the benefit of closure in patients with high-risk PFO anatomical features include: a low Risk of Paradoxical Embolism (RoPE) score (0–3) [954], older age, and the need for anticoagulants. Factors increasing the benefit of PFO closure include: a high Risk of Paradoxical Embolism (RoPE) score [954], young age and the absence of traditional stroke risk factors, a history of deep vein thrombosis or prothrombotic states, prior non-lacunar or cortical strokes, and failure of antiplatelet therapy.
It is not recommended for patients aged 18 to 60 years with ESUS and a PFO to be prescribed anticoagulants (warfarin** B01AA, direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF) to prevent recurrent ischemic stroke or TIA [939, 955, 956, 1151, 1152].Level of evidence C (level of certainty of evidence – 5)
5.8. Cerebral venous thrombosis
It is recommended that adult patients with ischemic stroke/TIA and cerebral venous thrombosis (including in the presence of intracranial hemorrhage) be prescribed anticoagulant therapy (warfarin** B01AA, direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF, heparin and its derivatives B01AB) to prevent recurrent cerebral venous thrombosis [957, 959, 960].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: the recommendation is based on a Cochrane meta-analysis in which only one case of major gastrointestinal bleeding was reported during anticoagulant use. Two patients in the placebo control group were diagnosed with "probable pulmonary embolism" (one case was fatal).
It is recommended that adult patients with ischemic stroke/TIA and cerebral venous thrombosis without identified thrombophilia be prescribed anticoagulant therapy for up to 6 months (warfarin**, direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF) to prevent recurrent cerebral venous thrombosis [958, 961].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: warfarin** (B01AA03) or #dabigatran etexilate** (B01AE07) are recommended as anticoagulants. In the Re-SPECT-CVT trial, the efficacy and safety of dabigatran etexilate** (B01AE07) at a dosage of 150 mg twice daily for 24 weeks and warfarin** (B01AA03) did not differ [961].
5.9. Carotid or vertebral artery dissection
It is recommended that adult patients with ischemic stroke/TIA receive antithrombotic therapy (platelet aggregation inhibitors except heparin B01AC platelet aggregation inhibitors except heparin, warfarin** B01AA) for at least 3 months or until stabilization of the affected carotid or vertebral artery wall, as determined by imaging studies, to prevent recurrent ischemic stroke or TIA [962, 963].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: Cervical artery dissections often develop after arterial wall trauma or occur spontaneously. The most frequent mechanism of stroke in extracranial artery dissection is artery-to-artery embolism. The open-label CADISS (Cervical Artery Dissection in Stroke Study) trial compared the efficacy and safety of antiplatelet agents (Antiplatelet agents excluding heparin B01AC) and anticoagulants (warfarin** B01AA) in cervical artery dissection, with a treatment duration of 3 months. The researchers found no differences in the incidence of primary endpoints (stroke or death) (OR = 0.335 [95% CI = 0.006–4.233]; p = 0.63).
It is recommended to prescribe endovascular treatment (stenting) to adult patients with recurrent ischemic strokes or TIAs and extracranial carotid or vertebral artery dissection, despite the use of antithrombotic therapy, for the prevention of recurrent ischemic stroke [964–966].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
5.10. Hypercoagulation and related conditions
It is recommended to prescribe long-term anticoagulant therapy (warfarin** B01AA, direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF) to adult patients with primary spontaneous cerebral venous sinus thrombosis or recurrent ischemic stroke of unknown etiology and hereditary thrombophilia for the prevention of recurrent ischemic stroke [967].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to prescribe antiplatelet therapy (platelet aggregation inhibitors, B01AC Antiplatelet agents excluding heparin) to adult patients with acute ischemic stroke/TIA of unknown cause (despite thorough diagnostic workup and no history of other thrombosis) who have genotypically and phenotypically confirmed thrombophilia, for the prevention of recurrent ischemic stroke if anticoagulant therapy cannot be administered [967].
GCR CLOE 5Grade of Recommendation C (Level of Evidence – 5).
Comment: Diagnosed thrombophilia includes: homozygous prothrombin 20210A mutation, activated protein C resistance, elevated factor VIII levels, or protein C, protein S, or antithrombin III deficiency.
5.11. Hyperhomocysteinemia
It is not recommended to prescribe maintenance therapy with B vitamins (pyridoxine** (B6), folic acid** (B9), cyanocobalamin** (B12)) to adult patients with ischemic stroke or TIA associated with hyperhomocysteinemia of undetermined etiology for the prevention of recurrent ischemic stroke or TIA [968, 969].
Recommendation Grade BEvidence Level 2Recommendation Grade B (ineffective) (Level of Evidence – 2)
5.12. Vasculitis
It is recommended to treat the underlying infectious process in adult patients with ischemic stroke/TIA and infectious vasculitis (varicella-zoster virus (VZV), cerebral vasculitis, neurosyphilis, or bacterial meningitis) to reduce the risk of recurrent stroke [978–985].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to use ASA** (B01AC06) in adult patients with ischemic stroke/TIA and HIV-associated vasculopathy to reduce the risk of recurrent ischemic stroke [986–989].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended to treat the underlying disease in adult patients with ischemic stroke/TIA and neoplastic vasculitis to reduce the risk of recurrent stroke [994].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
It is recommended to prescribe antithrombotic therapy (antiplatelet agents excluding heparin B01AC, vitamin K antagonists B01AA, heparin and its derivatives B01AB) combined with hormone therapy (glucocorticoids H02AB) for 3–12 months in pediatric patients with ischemic stroke and a confirmed diagnosis of primary angiitis of the central nervous system (PACNS), and to consider prescribing immunosuppressive therapy in cases of progressive refractory course according to direct cerebral angiography to reduce the risk of recurrent stroke [992].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: hormone therapy is recommended: pulse therapy with #methylprednisolone** 30 mg/kg/day (maximum 1000 mg) IV for 3–5 days, followed by oral prednisolone 2 mg/kg/day for 3–12 months. Immunosuppressive therapy includes #cyclophosphamide** administered as monthly infusions of 500–750 mg/m2 for 6 months, followed by a maintenance dose of #mycophenolate mofetil** 800–1200 mg/m2 in 2 divided doses or #mycophenolic acid** 500–800 mg/m2 in 2 divided doses for up to 18 months [992].
5.13. Antiphospholipid syndrome
It is recommended to prescribe warfarin** (B01AA03) targeting an INR of 2.5 (range 2 to 3) to adult patients with ischemic stroke or TIA and a confirmed diagnosis of antiphospholipid syndrome (APS) for the prevention of recurrent ischemic stroke or TIA [993–1000].
Level of Evidence AGrade of Evidence 2Level of Recommendations A (Grade of Evidence – 2)
It is not recommended to prescribe DOACs (direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF) to adult patients with ischemic stroke or TIA in the setting of confirmed APS for the secondary prevention of ischemic stroke [993-1000].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
5.14. Secondary prevention of ischemic stroke or TIA during pregnancy
It is recommended to discuss with all women of childbearing potential who have suffered an ischemic stroke or TIA the potential risks and consequences of recurrent stroke that may arise during pregnancy, childbirth, and the postpartum period [1001–1003].
GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)
It is recommended in female patients with a history of ischemic stroke or TIA to avoid prescribing estrogen-containing contraceptives or hormone replacement therapy, considering alternative methods of contraception (barrier contraception, progestin-only oral contraceptives, or non-hormonal intrauterine devices) for the prevention of recurrent stroke [1004–1006].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended for female patients after an ischemic stroke or TIA to make a decision on the need for antiplatelet therapy, the choice of a specific drug and its dose at a medical board meeting, taking into account the etiology of the previous stroke and the reversibility of the factors that caused it, the time elapsed since the cerebrovascular event and the size of the lesion, as well as the period of pregnancy and obstetric history, for the secondary prevention of ischemic stroke or TIA [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended for female patients with a prior cardioembolic ischemic stroke to continue anticoagulant therapy, choosing a specific class of drugs taking into account its safety for the mother and fetus in order to prevent recurrent ischemic stroke [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended for female patients with ischemic stroke or TIA and carotid or vertebral artery dissection during pregnancy to prescribe/continue previously initiated antithrombotic therapy, selecting a specific class of drugs based on clinical characteristics (age of the aneurysm, presence of a mural thrombus, formation of a pseudoaneurysm) for the prevention of recurrent ischemic stroke [1155-1158].
LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)
Comment: for this category of patients, it is advisable to avoid surgical methods of treatment for arterial dissection. Delivery by Caesarean section in patients with carotid or vertebral artery dissection should not be considered routine practice.
It is recommended for female patients with ischemic stroke or TIA and APS to continue antithrombotic therapy during pregnancy, determining the choice of specific drugs (anticoagulant monotherapy, combination of anticoagulants (heparin group B01AB) and #ASA** (B01AC06)) taking into account the gestational age and the presence of complications for the prevention of recurrent ischemic stroke and TIA [1007].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended for female patients planning a pregnancy or already pregnant with a history of non-cardioembolic ischemic stroke or TIA to prescribe/continue #ASA** (B01AC06) 75–100 mg (or to replace previously prescribed clopidogrel**, ticagrelor**, or a combination of ASA** (B01AC06) and extended-release dipyridamole (B01AC07) with this therapy) throughout the entire pregnancy for the prevention of recurrent ischemic stroke and TIA [1007, 1009, 1010].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended for pregnant patients with ischemic stroke/TIA to prescribe LMWHs, switch from NOACs to this class of drugs, and avoid prescribing warfarin** throughout the entire pregnancy starting from the time of its detection, if there are indications for such therapy, for the secondary prevention of ischemic stroke or TIA [1007, 1013].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: if pregnancy is confirmed in a patient with a mechanical heart valve prosthesis, it is recommended to consider taking warfarin** after 12 weeks of pregnancy until delivery [1007].
It is recommended for pregnant patients with a history of ischemic stroke/TIA to use intravenous administration of UFH as an alternative to LMWH therapy in case of anticipated urgent/emergency delivery or the expected need for invasive procedures for the secondary prevention of ischemic stroke or TIA [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended for pregnant patients with a history of ischemic stroke/TIA to discontinue prophylactic doses of LMWHs at least 12 hours, and therapeutic doses of LMWHs at least 24 hours, before the initiation of regional anesthesia or planned labor induction to reduce the risk of hemorrhagic complications [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that pregnant patients with a history of IS/TIA resume UFH or LMWH therapy 4–6 hours after removal of the neuraxial anesthesia/analgesia catheter, provided there are no complications, signs, or symptoms of bleeding, and that such therapy be continued for 6–12 weeks postpartum for the secondary prevention of IS or TIA [1016].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that postpartum patients with a history of IS/TIA undergo selection of antithrombotic therapy (warfarin** B01AA, direct thrombin inhibitors B01AE, direct factor Xa inhibitors B01AF, antiplatelet agents other than heparin B01AC) on a general basis 6–12 weeks postpartum, taking into account breastfeeding and future pregnancy planning for the secondary prevention of IS or TIA [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to prescribe 75–100 mg of ASA** (B01AC06) during breastfeeding to postpartum patients with a history of non-cardioembolic IS/TIA for the prevention of recurrent IS and TIA [1007].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: when anticoagulant therapy is necessary during breastfeeding, LMWH and warfarin** are considered safe options. The safety of DOACs during breastfeeding has not been studied.
It is recommended for the majority of pregnant patients with IS or TIA and hypertension to achieve a target blood pressure of less than 140/90 mm Hg during pregnancy to reduce the risk of recurrent stroke or TIA [1007].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
It is recommended that pregnant patients with IS/TIA adhere to a lipid-lowering diet and lifestyle modification, rather than statin therapy, as the primary methods for managing dyslipidemia to reduce the risk of recurrent IS or TIA during pregnancy [1007, 1025–1027].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: discontinuation of statin therapy for this period and the timing of its postpartum resumption should be considered individually, taking into account comorbid conditions and the planned duration of breastfeeding.
It is recommended that patients with a prior history of IS or TIA who are at high risk for gestational diabetes undergo an oral glucose tolerance test within the first 20 weeks of pregnancy for early detection of diabetes mellitus, correction of hyperglycemia, and reduction of the risk of recurrent cerebrovascular events [1007, 1028].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
5.15. Surgical methods for primary and secondary prevention of ischemic stroke
It is recommended that adult patients with IS or TIA and severe ICA stenosis of 70–99% according to NASCET (or 85–99% according to ECST) undergo carotid endarterectomy for the prevention of recurrent stroke [1029, 1030]
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: a pooled analysis of data from the NASCET, ECST, and VA309 trials, including 6,092 patients, demonstrated the efficacy of carotid endarterectomy (CEA) in patients with severe (70–99%) ICA stenosis, showing 16.0% absolute benefit over 5 years [1029]. In the original trials (NASCET and ECST), selective angiography was used to measure the degree of stenosis, but in later trials (e.g., CREST) and routine clinical practice, non-invasive imaging (CT angiography, MR angiography) is typically used [1031]. Surgical treatment should be performed in centers with a perioperative complication (stroke, myocardial infarction) and mortality rate of < 6% [1032].
It is recommended that adult patients with IS or TIA and moderate ICA stenosis of 50–69% according to NASCET (or 75–84% according to ECST) undergo carotid endarterectomy for the prevention of recurrent stroke [1029, 1030].
LoR CGoE 1Level of Recommendation C (Level of Evidence – 1)
Comment: a pooled analysis of data from the NASCET, ECST, and VA309 trials, including 6,092 patients, demonstrated moderate efficacy of CEA in patients with moderate (50–69%) ICA stenosis, showing 4.6% absolute benefit over five years [1029].
It is recommended that adult patients with IS or TIA with indications for carotid revascularization undergo surgical treatment within 14 days of the ischemic event (if there are no contraindications to early surgery) to prevent recurrent stroke [1030, 1031].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: a pooled analysis of data from the NASCET and ECST trials, including 5,893 patients, demonstrated greater benefit from CEA when surgery was performed within 2 weeks of the last non-disabling IS [1029]. A large meta-analysis by De Rango P. et al. (2015), comprising 47 studies, also demonstrated the safety of CEA and carotid artery stenting (CAS) within 2 weeks after IS, with a combined perioperative stroke risk of 3.4% in the CEA group and 4.8% in the CAS group [1033]. Early CEA is indicated under the following conditions: mRS score of 0–2, infarct volume < 1/3 of the MCA territory, and no impaired consciousness during the IS. If these conditions are not met, delayed CEA (≥ one month) is advisable.
It is recommended that adult patients with IS or TIA and indications for carotid revascularization undergo carotid endarterectomy as the primary procedure. Carotid stenting is an alternative method [1030].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comments: The 30-day stroke/death risk after CEA in patients with symptomatic ICA stenosis of 50–99% should not exceed 6% [1035].
It is recommended that adult patients with IS or TIA and indications for carotid revascularization, in the presence of anatomical or medical conditions that increase the risk of carotid endarterectomy, choose carotid artery stenting to reduce the risk of perioperative complications [1040, 1041].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: in the SAPPHIRE trial, which included 334 participants, patients with high anatomical or medical risks for CEA were randomized to either CEA or CAS. The primary endpoint was stroke, myocardial infarction, or death within 30 days, or ipsilateral stroke within 12 months. The cumulative incidence of the primary endpoint was 12.2% in the stenting group and 20.1% in the CEA group (P = 0.004 for non-inferiority and P = 0.053 for superiority), which justifies the use of stenting in patients at high surgical risk [1043]. High-risk factors include: radiation-induced stenosis, prior neck surgery, restenosis after CEA, contralateral vocal cord palsy, high (above the angle of the mandible) or low (brachiocephalic trunk, origin of the left common carotid artery) location of stenosis, contralateral ICA occlusion, severe tandem lesions, high medical risks (CHF, EF ≤ 30%, unstable angina, myocardial infarction within 6 weeks, coronary artery disease (involvement of ≥ 2 arteries with stenosis ≥ 70%), positive stress test, need for major surgery (including cardiovascular), severe pulmonary disease, uncontrolled diabetes, age ≥ 75 years) [1044, 1045].
It is recommended that adult patients with IS and TIA undergo eversion carotid endarterectomy; when performing conventional endarterectomy, priority should be given to closing the arteriotomy using a patch angioplasty to reduce the risk of complications [1030, 1035].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: The choice of anesthesia method (general anesthesia (B01.003.004.010 Combined endotracheal anesthesia) or locoregional anesthesia (B01.003.004.001 Local anesthesia)), as well as the use of an intraluminal shunt during CEA, remains at the discretion of the surgical team [1035].
It is recommended that adult patients with IS and TIA undergo intraoperative monitoring (A06.12.007 Common carotid angiography, A04.11.002 Intraoperative ultrasound) during carotid endarterectomy to reduce the risk of perioperative stroke [1035].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with IS and TIA undergo surgical intervention (A16.12.011.005 Internal carotid artery resection with end-to-end anastomosis, A16.12.011.006 Internal carotid artery resection with replacement/grafting) for symptomatic pathological tortuosity of the ICA (coiling/kinking) only after excluding other causes of IS or TIA, in order to eliminate the risk of complications [1035, 1046]
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that adult patients with IS and TIA due to large intracranial artery occlusion undergo extracranial-intracranial bypass surgery (A16.12.038.009 Carotico-carotid bypass) in cases of subcompensated cerebral blood flow in the territory of the occluded artery with signs of chronic cerebral ischemia (fluctuating neurological deficit, retrograde blood flow in the ophthalmic artery, asymmetry of blood flow on transcranial Doppler ultrasound, exhausted or reduced cerebrovascular reserves according to brain CT/MR perfusion or SPECT, asymmetry of perfusion parameters on the side of the occlusion greater than 50%) for the prevention of recurrent stroke [1047-1049].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: the rate of surgical complications during extracranial-intracranial bypass surgery should not exceed 5% [1050].
It is recommended to perform surgical treatment in adult patients with asymptomatic ICA stenosis of 60–99% according to NASCET (or 80–99% according to ECST) for the prevention of primary stroke in the presence of at least one of the following factors associated with an increased risk of ischemic stroke even under best medical therapy: a history of TIA or ischemic stroke in the contralateral hemisphere, presence of "silent" ischemic lesions in the ipsilateral hemisphere according to neuroimaging, signs of atherosclerotic plaque instability and/or intraplaque hemorrhage, more than 1 embolism episode per hour during embolic detection, progression of stenosis degree by more than 20% during follow-up, impaired cerebral perfusion reserve, provided that the patient's expected life expectancy is at least 5 years [1161-1163].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
Comment: The ACAS study [1162] demonstrated a significant 53% reduction in the 5-year risk of any stroke (p=0.008) following carotid endarterectomy compared to the best medical therapy group. The ACST study [1163] demonstrated a significant reduction in the risk of any stroke over a 5- and 10-year period. The reduction in the 5-year stroke risk after carotid endarterectomy was 46% (p<0.0001) compared to the best medical therapy group.
It is recommended that patients with asymptomatic ICA stenosis and indications for carotid revascularization undergo carotid endarterectomy as a priority procedure to reduce the number of complications. Carotid stenting is an alternative technique in patients with unfavorable anatomy for open surgery and/or in patients classified as high perioperative risk for open surgery after their condition is assessed by a multidisciplinary team [1161].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
5.16. Follow-up medical observation
It is recommended to provide dispensary follow-up for all patients after discharge who have suffered an ischemic stroke or TIA, in order to implement a set of measures for secondary cardiovascular disease prevention, timely therapy adjustment, and improvement of treatment adherence [45, 1123, 1159].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
Comment: in accordance with Order of the Russian Ministry of Health No. 168n dated March 15, 2022, "On Approval of the Procedure for Dispensary Observation of Adults", dispensary observation of patients who have suffered an ischemic stroke within 24 months after receiving inpatient medical care in medical organizations is carried out by a general practitioner (therapist), at least once every 3 months in the first year of dispensary observation, and then at least once every 6 months. Monitored health indicators include blood pressure measurement, heart rate measurement, low-density lipoprotein cholesterol level testing (A09.05.028), ECG recording (A05.10.006), and for statin therapy – transaminases (A09.05.041 Determination of aspartate aminotransferase activity in blood, A09.05.04 Determination of alanine aminotransferase activity in blood) and CK (A09.05.043 Determination of creatine kinase activity in blood) (4 weeks after therapy initiation or in case of muscular symptoms). Additional preventive, diagnostic, therapeutic, and rehabilitation measures may be prescribed according to medical indications. It is advisable to assess the presence/risk of spasticity in patients who have suffered an ischemic stroke as part of dispensary observation and refer them for medical rehabilitation using botulinum toxin therapy to increase the effectiveness of rehabilitation measures and improve functional recovery. It is also recommended, in the presence of medical indications, to have an appointment (examination, consultation) with a neurologist, cardiovascular surgeon, or cardiologist in case of ineffectiveness of pharmacotherapy (refractory symptoms, failure to achieve target blood pressure, heart rate, or LDL-C levels).
It is recommended that adult patients with ischemic stroke and TIA, after undergoing carotid endarterectomy or stenting, undergo ultrasound examination of brachiocephalic arteries (A04.12.005.003 Duplex scanning of brachiocephalic arteries with color Doppler blood flow mapping, A04.12.005.005 Duplex scanning of extracranial segments of brachiocephalic arteries, A04.12.005.006 Duplex scanning of intracranial segments of brachiocephalic arteries) at 3 and 6 months after surgery, and then once a year for life for the purpose of recurrent stroke prevention [1051].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
6. Organization of Medical Care
It is recommended to arrange emergency hospitalization of patients with a suspected diagnosis of acute cerebrovascular accident (ACVA) to a medical organization that has a specialized neurological department for ACVA patients in order to improve the disease outcome [1052].
GCR ALEL 1Grade of Recommendation A (Level of Evidence – 1)
It is recommended to ensure the routing of ACVA patients within a two-tier care system: to primary vascular centers, which have a neurological department for ACVA patients capable of providing emergency specialized care, including systemic thrombolysis, and to regional vascular centers, which have a neurological department for ACVA patients where endovascular, neurosurgical, and cardiosurgical interventions can be performed, and which are capable of receiving ACVA patients in need of surgical care from primary vascular centers, with the aim of improving disease outcomes [1053–1055].
GCR ALEL 1Grade of Recommendations A (Level of Evidence – 1)
It is recommended when it is impossible to ensure round-the-clock duty of a neurologist to perform intravenous thrombolytic therapy using telemedicine technologies in order to increase the availability of reperfusion therapy [1056–1058].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
Comment: the neurologist of the teleconsulting regional vascular center must be trained in remote assessment using the NIHSS scale and have personal experience in performing intravenous thrombolytic therapy.
It is recommended that healthcare organization and public health specialists ensure regular educational events on the provision of specialized medical care for stroke for physicians, hospital staff, and emergency medical service (EMS) personnel to improve the quality of medical care [1059].
GCR ALOE 2Grade of Recommendation A (Level of Evidence – 2)
It is recommended with the aim of accelerating reperfusion therapy in patients with suspected ischemic stroke to implement a set of organizational measures at the regional level: notification of the neurologist of the receiving medical organization at the pre-hospital stage by the EMS employee directly transporting the patient; implementation of regional medical information systems with access to outpatient medical data from the regional vascular center/primary vascular center prior to patient admission; when technically feasible, pre-registration of the incoming patient and pre-preparation of referral forms for instrumental and laboratory diagnostic methods prior to patient admission; mandatory placement of a peripheral venous catheter by EMS teams at the pre-hospital stage (catheter diameter must be suitable for contrast enhancement during CT or MRI); upon patient arrival, transportation of the patient by EMS staff on an EMS stretcher to the CT/MRI room or a specialized examination room of the regional vascular center/primary vascular center; when technically feasible, initiation of thrombolytic therapy in the CT/MRI room or a specialized room [1060].
GCR ALEL 3Grade of Recommendation A (Level of Evidence – 3)
It is recommended that dispatchers and EMS personnel use pre-hospital assessment scales for emergency pre-hospital diagnosis of ACVA [1061, 1062].
GGR BLOE 1Grade of Recommendation B (Level of Evidence – 1)
Comment: all stroke scales used have high sensitivity ranging from 74 to 97%. The specificity of short tests such as FAST (13%) and CPSS (24–79%) is lower than that of scales including a larger number of subtests, such as LAPSS (85–97%), MASS (74–86%), and OPPS (86%), except for Med PACS (33%) and ROSIER (18%) [1000]. It is important to note that existing simplified pre-hospital stroke scales have higher sensitivity in detecting stroke in the carotid territory than in the vertebrobasilar territory. Despite the low quality of evidence, the recommendation is graded as strong because the potential benefit of identifying potential stroke victims clearly outweighs any potential harm with minimal resource expenditure.
It is recommended when transporting a patient with suspected ischemic stroke or TIA to a regional vascular center or primary vascular center to screen for proximal occlusion using special scales in order to identify candidates for mechanical thrombectomy [1063].
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: screening for proximal occlusion (for example, using the LAMS scale, Appendix G19) allows for optimizing the routing process for patients with suspected stroke or TIA and increasing the likelihood of endovascular treatment in the hyperacute period of the disease. Patients with a high probability of proximal occlusion should be routed to medical organizations with endovascular treatment capabilities to determine indications and contraindications for such treatment.
It is recommended that healthcare and public health organization specialists develop and implement public educational events aimed at informing the population about the stroke care delivery system and the need for rapid seeking of emergency medical care at the onset of the disease in order to improve disease outcomes [1064, 1065].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: it is advisable to conduct public information campaigns at least once every 6 months; programs should be aimed at informing various socio-demographic population groups. Most studies reported a statistically significant reduction in pre-hospital time following an information campaign. This recommendation is assigned a strong grade despite the low quality of evidence because the potential benefit of early recognition of stroke symptoms among the general public and immediate medical care-seeking clearly outweighs any potential harm.
It is recommended that in cases of suspected acute cerebrovascular accident (ACVA), emergency medical care be sought through the emergency medical services system in order to improve disease outcomes [1066–1068].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: patient hospitalization via the emergency medical services (EMS) is statistically significantly associated with earlier arrival at the emergency department, faster diagnostic workup, and more rapid initiation of treatment.
It is recommended that EMS services prioritize calls regarding suspected ACVA to ensure the fastest possible arrival of medical personnel to the patient [1069].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended that if round-the-clock CT or MRI interpretation is unavailable, a teleradiology system be utilized for timely reporting of CT or MRI results in cases of suspected ACVA [1070-1074].
GRC BLEL 2Grade of Recommendation B (Level of Evidence – 2)
It is recommended that all patients diagnosed with ACVA be initially admitted to an intensive care unit/ward/block dedicated to ACVA patients within a medical organization in order to improve disease outcomes [1075, 1076].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: the duration of stay in the intensive care unit/ward/block is determined by the scope of diagnostic procedures performed and the need for vital sign monitoring, and in most cases exceeds 24 hours.
It is recommended to implement mobile stroke units (ambulances equipped with a portable computed tomography scanner, a portable clinical laboratory, and telemedicine communication) in order to increase the availability of reperfusion therapy [1077–1081].
GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)
Comment: incorporating a mobile stroke unit into pre-hospital logistics pathways can help reduce the time to initiation of reperfusion technologies, increase their availability, and improve functional stroke outcomes.
It is recommended that the EMS team performing medical evacuation of a patient with ACVA notify the receiving medical organization in advance of the expected arrival of a patient with suspected ACVA, indicating the approximate travel time, in order to rapidly prepare and mobilize the necessary resources of the medical organization [1082, 1083].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
Comment: advance notification by EMS is associated with an increased likelihood of intravenous thrombolysis, a reduction in door-to-CT/MRI time, door-to-needle time for thrombolytic therapy, and symptom-to-treatment time. In a retrospective study including data from 9,230 adult ischemic stroke patients, advance notification was associated with a 1.75-fold increase in the likelihood of a patient receiving thrombolytic therapy (OR 1.75, 95% CI 1.36–2.24).
It is recommended that in cases of suspected ACVA with a duration of less than 4.5 hours, the fastest possible medical evacuation of the patient to the nearest medical organization capable of performing intravenous thrombolysis be ensured to improve disease outcomes [1084, 1085].
GCR BLoE 3Level of Evidence B (Level of Confidence of Evidence – 3)
It is recommended that in areas with low population density and/or limited transport accessibility, specialized medical care be provided to ACVA patients in medical organizations lacking a regional vascular center (RVC) or primary vascular center (PVC) in their structure, provided that diagnostics, round-the-clock medical monitoring in an intensive care unit/ward/block, and treatment using telemedicine technologies are ensured, in order to improve disease outcomes [1086–1089].
LoR BLoE 4Level of Recommendation B (Level of Evidence – 4)
Comment: medical care for patients with ACVA can be provided in medical organizations that ensure round-the-clock medical monitoring and treatment, and include the following round-the-clock functioning departments:
– resuscitation and intensive care unit (ward);
– CT or MRI room;
– clinical laboratory department;
– service providing telemedicine communication.
It is recommended to conduct telemedicine consultations involving specialists (neurosurgeon, vascular surgeon, endovascular surgeon, etc.) for patients with transient ischemic attack (TIA) and ischemic stroke (IS) when it is impossible to organize an emergency on-site consultation, in order to improve disease outcomes [1090, 1091].
GCR BLE 4Grade of Recommendation B (Level of Evidence – 4)
Comment: necessary consultations should be organized in accordance with the clinical situation: immediately in the presence of emergency indications, or up to 72 hours from hospitalization to determine secondary prevention tactics.
It is recommended that regional healthcare organizers develop triage algorithms and routing protocols for ACVA patients aimed at ensuring rapid delivery to a medical organization of the appropriate level of care, in order to improve disease outcomes.
GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)
Comment: routing schemes (including inter-hospital transfers) are developed by regional executive authorities in the field of healthcare, taking into account the geographical characteristics of the region, the equipment of medical institutions, and other factors.
It is recommended that hospitalization and treatment of patients with ischemic stroke (IS) combined with novel coronavirus infection COVID-19 be carried out in specialized ACVA departments repurposed for providing medical care to patients with novel coronavirus infection COVID-19, while preserving the core principles of medical rehabilitation in order to prevent complications, improve functional outcomes, and reduce mortality [1092-1096].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended to use telemedicine technologies for the management of patients with ischemic stroke (IS) and transient ischemic attack (TIA) combined with novel coronavirus infection COVID-19 at all stages of medical care delivery in order to increase the availability and quality of medical care [1092, 1097, 1098].
GDR CLE 5Grade of recommendation C (level of evidence – 5)
It is recommended that patients with ischemic stroke (IS) combined with novel coronavirus infection COVID-19 with a Rehabilitation Routing Scale score of 2–6 be referred for medical rehabilitation in accordance with the temporary clinical guidelines "Medical Rehabilitation for Novel Coronavirus Infection" [1099-1101]
GDR CLE 5Grade of recommendation C (level of evidence – 5)
7. Additional Information
No.
Criteria for Evaluating the Quality of Medical Care
№ No. | Quality criteria | Performance evaluation |
|---|---|---|
1 | Initial examination (evaluation, consultation) by a neurologist was performed with assessment of neurological status using the NIH Stroke Scale and the level of consciousness using the Glasgow Coma Scale and/or FOUR score no later than 10 minutes from the moment of hospital admission. | Yes/No |
2 | Swallowing competency was assessed using a swallowing test ("three-swallow test" using a pulse oximeter) within the first 3 hours of the patient's stay in the hospital. | Yes/No |
3 | Computed tomography of the brain or magnetic resonance imaging of the brain was performed no later than 40 minutes from the moment of hospital admission. | Yes/No |
4 | Physiotherapy exercises for central nervous system and brain diseases and/or physiotherapy exercises using devices and exercise machines for central nervous system and brain diseases and/or postural correction and/or occupational therapy and/or medical speech therapy assessment for dysphagia and/or medical speech therapy procedure for aphasia and/or medical speech therapy procedure for dysarthria were performed no later than 48 hours from the moment of hospital admission. | Yes/No |
References
Show references
Neurology: National Guidelines. Ed. by E.I. Gusev, A.N. Konovalov, V.I. Skvortsova. 2nd ed., revised and expanded. Moscow: GEOTAR-Media 2018; 1: 880.
Sacco RL, Kasner SE, Broderick JP, Caplan LR, Connors JJ, Culebras A, Elkind MS, George MG, Hamdan AD, Higashida RT, Hoh BL, Janis LS, Kase CS, Kleindorfer DO, Lee JM, Moseley ME, Peterson ED, Turan TN, Valderrama AL, Vinters HV; American Heart Association Stroke Council, Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular and Stroke Nursing; Council on Epidemiology and Prevention; Council on Peripheral Vascular Disease; Council on Nutrition, Physical Activity and Metabolism. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013 Jul;44(7):2064-89. doi: 10.1161/STR.0b013e318296aeca
Grory BM, Schrag M, Biousse V, Furie KL, Gerhard-Herman M, Lavin PJ, Sobrin L, Tjoumakaris SI, Weyand CM, Yaghi S and on behalf of the American Heart Association Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; and Council on Peripheral Vascular Disease. Management of Central Retinal Artery Occlusion: A Scientific Statement From the American Heart Association. Stroke. 2021;52:e282–e294. doi.org/10.1161/STR.0000000000000366
Chen, C., Singh, G., Madike, R. et al. Central retinal artery occlusion: a stroke of the eye. Eye. 2024. https://doi.org/10.1038/s41433-024-03029-w
Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, Lutsep HL, Miller E, Sacco RL; American Heart Association; American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Interdisciplinary Council on Peripheral Vascular Disease. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009 Jun;40(6):2276-93. doi: 10.1161/STROKEAHA.108.192218
Gusev E.I., Skvortsova V.I. Cerebral Ischemia. Moscow: Meditsina, 2001. – 328 p.
Stroke: A Guide for Physicians. Ed. by L.V. Stakhovskaya, S.V. Kotov. 2nd ed., expanded and revised. Moscow: Meditsinskoe Informatsionnoe Agentstvo 2018; 488 p.
Caplan, L. (Ed.). (2016). Caplan"s Stroke: A Clinical Approach (5th ed.). Cambridge: Cambridge University Press. doi:10.1017/CBO9781316095805
Campbell BCV, Khatri P. Stroke. Lancet. 2020 Jul 11;396(10244):129-142. doi: 10.1016/S0140-6736(20)31179-X
Barrett KM, Brott TG. Stroke Caused by Extracranial Disease. Circ Res. 2017 Feb 3;120(3):496-501. doi: 10.1161/CIRCRESAHA.117.310138
Banerjee C, Chimowitz MI. Stroke Caused by Atherosclerosis of the Major Intracranial Arteries. Circ Res. 2017 Feb 3;120(3):502-513. doi: 10.1161/CIRCRESAHA.116.308441
Regenhardt RW, Das AS, Lo EH, Caplan LR. Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review. JAMA Neurol. 2018 Oct 1;75(10):1273-1281. doi: 10.1001/jamaneurol.2018.1073
Ekker M.S., Boot E.M., Singhal A.B. et al. Epidemiology, aetiology, and management of ischaemic stroke in young adults. Lancet Neurol. 2018;17(9):790-801. doi: 10.1016/S1474-4422(18)30233-3
Cucchiara, Brett & Kasner, Scott. Treatment of “Other” Stroke Etiologies. 2022. doi: 10.1016/B978-0-323-69424-7.00058-2
Latchaw RE, Yonas H, Hunter GJ, Yuh WT, Ueda T, Sorensen AG, Sunshine JL, Biller J, Wechsler L, Higashida R, Hademenos G; Council on Cardiovascular Radiology of the American Heart Association. Guidelines and recommendations for perfusion imaging in cerebral ischemia: A scientific statement for healthcare professionals by the writing group on perfusion imaging, from the Council on Cardiovascular Radiology of the American Heart Association. Stroke. 2003 Apr;34(4):1084-104. doi: 10.1161/01.STR.0000064840.99271.9E
Paciaroni M, Caso V, Agnelli G. The concept of ischemic penumbra in acute stroke and therapeutic opportunities. Eur Neurol. 2009;61(6):321-30. doi: 10.1159/000210544
Chamorro Á, Dirnagl U, Urra X, Planas AM. Neuroprotection in acute stroke: targeting excitotoxicity, oxidative and nitrosative stress, and inflammation. Lancet Neurol. 2016 Jul;15(8):869-881. doi: 10.1016/S1474-4422(16)00114-9
Khoshnam SE, Winlow W, Farzaneh M, Farbood Y, Moghaddam HF. Pathogenic mechanisms following ischemic stroke. Neurol Sci. 2017 Jul;38(7):1167-1186. doi: 10.1007/s10072-017-2938-1
Zerna C, Thomalla G, Campbell BCV, Rha JH, Hill MD. Current practice and future directions in the diagnosis and acute treatment of ischaemic stroke. Lancet. 2018 Oct 6;392(10154):1247-1256
Liebeskind DS, Jüttler E, Shapovalov Y, Yegin A, Landen J, Jauch EC. Cerebral Edema Associated With Large Hemispheric Infarction. Stroke. 2019 Sep;50(9):2619-2625. doi: 10.1161/STROKEAHA.118.024766
Lu G, He Q, Shen Y, Cao F. Potential biomarkers for predicting hemorrhagic transformation of ischemic stroke. Int J Neurosci. 2018 Jan;128(1):79-89. doi: 10.1080/00207454.2017.1349766
Liebeskind DS, Jüttler E, Shapovalov Y, Yegin A, Landen J, Jauch EC. Cerebral Edema Associated With Large Hemispheric Infarction. Stroke. 2019 Sep;50(9):2619-2625. doi: 10.1161/STROKEAHA.118.024766
Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011 Apr;42(4):1158-92. doi: 10.1161/STR.0b013e31820a8364
Ferro JM, Aguiar de Sousa D. Cerebral Venous Thrombosis: an Update. Curr Neurol Neurosci Rep. 2019 Aug 23;19(10):74. doi: 10.1007/s11910-019-0988-x
Green M, Styles T, Russell T, Sada C, Jallow E, Stewart J, Lazariashvili O, Lubomirova I, Cotlarciuc I, Sharma S, Han TS, Sharma P. Non-genetic and genetic risk factors for adult cerebral venous thrombosis. Thromb Res. 2018 Sep;169:15-22. doi: 10.1016/j.thromres.2018.07.005
Afifi K, Bellanger G, Buyck PJ, Zuurbier SM, Esperon CG, Barboza MA, Costa P, Escudero I, Renard D, Lemmens R, Hinteregger N, Fazekas F, Conde JJ, Giralt-Steinhauer E, Hiltunen S, Arauz A, Pezzini A, Montaner J, Putaala J, Weimar C, Schlamann M, Gattringer T, Tatlisumak T, Coutinho JM, Demaerel P, Thijs V. Features of intracranial hemorrhage in cerebral venous thrombosis. J Neurol. 2020 Nov;267(11):3292-3298. doi: 10.1007/s00415-020-10008-0
Wei H, Jiang H, Zhou Y, Liu L, Zhou C, Ji X. Intracranial hypertension after cerebral venous thrombosis—Risk factors and outcomes. CNS Neurosci Ther. 2023; 29: 2540-2547. doi:10.1111/cns.14194
GBD 2016 Stroke Collaborators. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019 May;18(5):439-458. doi: 10.1016/S1474-4422(19)30034-1
Healthcare in Russia. 2019: Stat. Digest. Rosstat. Moscow 2019; 170 p.
Stakhovskaya L.V., Klyuchikhina O.A., Bogatyreva M.D., Kovalenko V.V. Epidemiology of stroke in Russia according to the territorial population-based register (2009–2010). Journal of Neurology and Psychiatry 2013; 5: 4-10.
Stakhovskaya L.V., Klochikhina O.A., Bogatyreva M.D., Chugunova S.A. Analysis of epidemiological indicators of recurrent strokes in the regions of the Russian Federation (based on the territorial-population register 2009–2014). Consilium Medicum. 2016; 18 (9): 8-11
Hart RG, Diener HC, Coutts SB, Easton JD, Granger CB, O"Donnell MJ, Sacco RL, Connolly SJ; Cryptogenic Stroke/ESUS International Working Group. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014 Apr;13(4):429-38. doi: 10.1016/S1474-4422(13)70310-7
Béjot Y., Bailly H., Durier J., Giroud M. Epidemiology of stroke in Europe and trends for the 21st century. Presse Med 2016; 45: 391-98.
Bejot Y., Daubail B., Jacquin A. et al. Trends in the incidence of ischaemic stroke in young adults between 1985 and 2011: the Dijon Stroke Registry. J Neurol Neurosurg Psychiatry 2014; 85: 509-13
Coutinho JM, Zuurbier SM, Aramideh M, Stam J. The incidence of cerebral venous thrombosis: a cross-sectional study. Stroke. 2012;43(12):3375-7.
Devasagayam S, Wyatt B, Leyden J, Kleinig T. Cerebral venous sinus thrombosis incidence is higher than previously thought: a retrospective population-based study. Stroke. 2016; 47 (9): 2180-2.
Ulivi L, Squitieri M, Cohen H, et al. Cerebral venous thrombosis: a practical guide. Pract Neurol. 2020;20(5):356-367
deVeber GA, Kirton A, Booth FA, Yager JY, Wirrell EC, Wood E, Shevell M, Surmava AM, McCusker P, Massicotte MP, MacGregor D, MacDonald EA, Meaney B, Levin S, Lemieux BG, Jardine L, Humphreys P, David M, Chan AK, Buckley DJ, Bjornson BH. Epidemiology and Outcomes of Arterial Ischemic Stroke in Children: The Canadian Pediatric Ischemic Stroke Registry. Pediatr Neurol. 2017 Apr;69:58-70. doi: 10.1016/j.pediatrneurol.2017.01.016. Epub 2017 Jan 26. PMID: 28254555
Steinlin M, Pfister I, Pavlovic J, Everts R, Boltshauser E, Capone Mori A, Gubser Mercati D, Hänggeli CA, Keller E, Luetschg J, Marcoz J, Ramelli GP, Roulet Perez E, Schmitt-Mechelke T, Weissert M; Swiss Societies of Paediatric Neurology and Neonatology. The first three years of the Swiss Neuropaediatric Stroke Registry (SNPSR): a population-based study of incidence, symptoms and risk factors. Neuropediatrics. 2005 Apr;36(2):90-7. doi: 10.1055/s-2005-837658. PMID: 15822021
Lvova, O. A. Ischemic strokes and transient ischemic attacks in children: clinical and molecular genetic aspects of the course, outcome prediction, and dynamic follow-up tactics : specialty 14.01.11 "Nervous Diseases" : dissertation for the degree of Doctor of Medical Sciences / Lvova Olga Aleksandrovna, 2017. – 249 p. – EDN CXBCPY
Shchederkina I.O. Stroke and cerebrovascular pathology in children and adolescents. A guide for physicians / Shchederkina I.O. et al. – GEOTAR-Media, 2021 - 448 p.
Shchederkina I.O., Livshits M.I., Kessel A.E., Plavunov N.F., Kuznetsova A.A., Khachaturov Yu.A., Vitvorskaya I.P., Khasanova K.A., Lim R.T., Sidorov A.M., Tenovskaya T.A., Asalkhanova S.B., Gorev V.V. Stroke in children: experience of the Center for the Treatment of Cerebrovascular Diseases in Children and Adolescents of Moscow. S.S. Korsakov Journal of Neurology and Psychiatry. 2023;123(8 iss. 2):22–31. https://doi.org/10.17116/jnevro202312308222
Neurology: National Guidelines. Ed. by E.I. Gusev, A.N. Konovalov, V.I. Skvortsova. 2nd ed., revised and expanded. Moscow: GEOTAR-Media 2018; 1: 880.
Ay H, Benner T, Arsava EM, Furie KL, Singhal AB, Jensen MB, Ayata C, Towfighi A, Smith EE, Chong JY, Koroshetz WJ, Sorensen AG. A computerized algorithm for etiologic classification of ischemic stroke: the Causative Classification of Stroke System. Stroke. 2007 Nov;38(11):2979-84. doi: 10.1161/STROKEAHA.107.490896
Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, Kamel H, Kernan WN, Kittner SJ, Leira EC, Lennon O, Meschia JF, Nguyen TN, Pollak PM, Santangeli P, Sharrief AZ, Smith SC Jr, Turan TN, Williams LS. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2021 May 24:STR0000000000000375. doi: 10.1161/STR.0000000000000375
North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. N Engl J Med 1991;325:445-53
European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. European Carotid Surgery Trialists" Collaborative Group. Lancet 1991;337:1235-43
Bonati LH, Kakkos S, Berkefeld J, de Borst GJ, Bulbulia R, Halliday A, van Herzeele I, Koncar I, McCabe DJ, Lal A, Ricco JB, Ringleb P, Taylor-Rowan M, Eckstein HH. European Stroke Organisation guideline on endarterectomy and stenting for carotid artery stenosis. Eur Stroke J. 2021 Jun;6(2):I-XLVII. doi: 10.1177/23969873211012121. Epub 2021 May 11. PMID: 34414302; PMCID: PMC8370069;
Rerkasem A, Orrapin S, Howard DP, Rerkasem K. Carotid endarterectomy for symptomatic carotid stenosis. Cochrane Database Syst Rev. 2020 Sep 12;9(9):CD001081. doi: 10.1002/14651858.CD001081.pub4. PMID: 32918282; PMCID: PMC8536099
Barrett KM, Brott TG. Stroke Caused by Extracranial Disease. Circ Res. 2017 Feb 3;120(3):496-501. doi: 10.1161/CIRCRESAHA.117.310138.
anerjee C, Chimowitz MI. Stroke Caused by Atherosclerosis of the Major Intracranial Arteries. Circ Res. 2017 Feb 3;120(3):502-513. doi: 10.1161/CIRCRESAHA.116.308441
Kamel H, Healey JS. Cardioembolic Stroke. Circ Res. 2017 Feb 3;120(3):514-526. doi: 10.1161/CIRCRESAHA.116.308407.
Sacchetti DC, Furie KL, Yaghi S. Cardioembolic Stroke: Mechanisms and Therapeutics. Semin Neurol. 2017 Jun;37(3):326-338. doi: 10.1055/s-0037-1603465
Kim JS, Caplan LR. Clinical Stroke Syndromes. Front Neurol Neurosci. 2016;40:72-92. doi: 10.1159/000448303.
He L, Xu R, Wang J, Zhang L, Zhang L, Zhou F, Dong W. Capsular warning syndrome: clinical analysis and treatment. BMC Neurol. 2019 Nov 13;19(1):285. doi: 10.1186/s12883-019-1522-0.
Regenhardt RW, Das AS, Lo EH, Caplan LR. Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review. JAMA Neurol. 2018 Oct 1;75(10):1273-1281. doi: 10.1001/jamaneurol.2018.1073
Wardlaw JM, Smith EE, Biessels GJ et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration: a united approach. Lancet Neurol. 2013;12:822–38. https://doi.org/10.1016/S1474-4422(13)70124-8/
ESO Guideline on covert cerebral small vessel disease. / Wardlaw, Joanna M.; Debette, Stephanie; Jokinen, Hanna; De Leeuw, Frank Erik; Pantoni, Leonardo; Chabriat, Hugues; Staals, Julie; Doubal, Fergus; Rudilosso, Salvatore; Eppinger, Sebastian; Schilling, Sabrina; Ornello, Raffaele; Enzinger, Christian; Cordonnier, Charlotte; Taylor-Rowan, Martin; Lindgren, Arne G. In: European Stroke Journal 2021; 24.
Kulesh A.A., Emelin A.Yu., Bogolepova A.N., Doronina O.B., Zakharov V.V., Kolokolov O.V., Kotov S.V., Korsunskaya L.L., Kutlubaev M.A., Laskov V.B., Levin O.S., Parfenov V.A. Clinical manifestations and diagnostic issues of chronic cerebrovascular disease (chronic cerebral ischemia) at the early (predementia) stage. Neurology, Neuropsychiatry, Psychosomatics. 2021;13(1):4-12. https://doi.org/10.14412/2074-2711-2021-1-4-12
Ekker M.S., Boot E.M., Singhal A.B. et al. Epidemiology, aetiology, and management of ischaemic stroke in young adults. Lancet Neurol. 2018;17(9):790-801
Debette S., Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurology. 2009; 8: 668-78. Doi: 10.1016/S1474-4422(09)70084-5
Debette S., Compter A., Labeyrie M.A., Uyttenboogaart M., Metso T.M., Majersik J.J., et al. Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection. Lancet Neurology. 2015;14:640-54. doi: 10.1016/S1474-4422(15)00009-5
Kalashnikova L.A., Dobrynina L.A., Chechetkin A.O., Dreval M.V., Krotenkova M.V., Zakharkina M.V. Cerebrovascular disorders in internal carotid and vertebral artery dissection. Diagnostic algorithm. Nervous Diseases. 2016;2:10-17
Amarenco P, Bogousslavsky J, Caplan LR, Donnan GA, Wolf ME, Hennerici MG. The ASCOD phenotyping of ischemic stroke (Updated ASCO Phenotyping). Cerebrovasc Dis. 2013;36(1):1-5. doi: 10.1159/000352050
Ferriero DM, Fullerton HJ, Bernard TJ, Billinghurst L, Daniels SR, DeBaun MR, deVeber G, Ichord RN, Jordan LC, Massicotte P, Meldau J, Roach ES, Smith ER; American Heart Association Stroke Council and Council on Cardiovascular and Stroke Nursing. Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. 2019 Mar;50(3):e51-e96. doi: 10.1161/STR.0000000000000183. PMID: 30686119
Williams LS, Garg BP, Cohen M, Fleck JD, Biller J. Subtypes of ischemic stroke in children and young adults. Neurology. 1997; 49:1541–1545; Wraige E, Hajat C, Jan W, Pohl KR, Wolfe CD, Ganesan V. Ischaemic stroke subtypes in children and adults. Dev Med Child Neurol. 2003; 45:229–232
Sébire G, Fullerton H, Riou E, deVeber G. Toward the definition of cerebral arteriopathies of childhood. Curr Opin Pediatr. 2004 Dec;16(6):617-22. doi: 10.1097/01.mop.0000144441.29899.20. PMID: 15548922.
Bernard TJ, Manco-Johnson MJ, Lo W, MacKay MT, Ganesan V, DeVeber G, et al. Towards a consensus-based classification of childhood arterial ischemic stroke. Stroke. 2012 Feb;43(2):371-7. https://doi.org/10.1161/STROKEAHA.111.624585
Komarova I.B., Zykov V.P. CASCADE classification of arterial ischemic stroke in childhood / S.S. Korsakov Journal of Neurology and Psychiatry. Special Issue. – 2013;113(5): 10-15,
Kessel A.E., Shchederkina I.O., Koltunov I.E., Drozdova I.M., Guzeva V.I. Transient cerebral arteriopathies in children and adolescents: features of clinical manifestations and course / Bulletin of Rehabilitation Medicine. 2018 №3 43-51,
Methodological recommendations: Organization of medical care for children who have suffered an ischemic stroke / ed. by T.T. Batysheva, 2018, pp. 7-8,
Federal Guide to Pediatric Neurology / ed. by V.I. Guzeva, 2nd edition, 2023, pp. 379-430
Zykov V.P., Komarova I.B., Dyakonova E.N., Guzeva V.I., Lvova O.A. Pediatric Neurology. Issue 2. Clinical guidelines for the diagnosis and treatment of strokes in children. – Moscow, 2014. – pp. 55-120
Kim JS, Caplan LR. Clinical Stroke Syndromes. Front Neurol Neurosci. 2016;40:72-92. doi: 10.1159/000448303
Mackay MT, Churilov L, Donnan GA, Babl FE, Monagle P. Performance of bedside stroke recognition tools in discriminating childhood stroke from mimics. Neurology. 2016 Jun 7;86(23):2154-61
Leigh R, Knutsson L, Zhou J, van Zijl PC. Imaging the physiological evolution of the ischemic penumbra in acute ischemic stroke. J Cereb Blood Flow Metab. 2018 Sep;38(9):1500-1516. doi: 10.1177/0271678X17700913
Ferro JM, Aguiar de Sousa D. Cerebral Venous Thrombosis: an Update. Curr Neurol Neurosci Rep. 2019;19(10):74.
Mehta A, Danesh J, Kuruvilla D. Cerebral Venous Thrombosis Headache. Curr Pain Headache Rep. 2019 May 30;23(7):47. doi: 10.1007/s11916-019-0786-9
Ulivi L, Squitieri M, Cohen H, et al. Cerebral venous thrombosis: a practical guide. Pract Neurol. 2020;20(5):356–367
Duman T, Uluduz D, Midi I, Bektas H, Kablan Y, Goksel BK, Milanlioglu A, Necioglu Orken D, Aluclu U; VENOST Study Group. A Multicenter Study of 1144 Patients with Cerebral Venous Thrombosis: The VENOST Study. J Stroke Cerebrovasc Dis. 2017 Aug;26(8):1848-1857. doi: 10.1016/j.jstrokecerebrovasdis.2017.04.020.
Cumurciuc R, Crassard I, Sarov M, Valade D, Bousser MG. Headache as the only neurological sign of cerebral venous thrombosis: a series of 17 cases. J Neurol Neurosurg Psychiatry. 2005;76:1084–1087. doi: 10.1136/jnnp.2004.056275
deVeber G, Andrew M, Adams C, Bjornson B, Booth F, Buckley DJ, Camfield CS, David M, Humphreys P, Langevin P, MacDonald EA, Gillett J, Meaney B, Shevell M, Sinclair DB, Yager J; Canadian Pediatric Ischemic Stroke Study Group. Cerebral sinovenous thrombosis in children. N Engl J Med. 2001;345:417–423. doi: 10.1056/NEJM200108093450604
Petrov D, Uohara MY, Ichord R, Ali Z, Jastrzab L, Lang SS, Billinghurst L. Pediatric cerebral sinovenous thrombosis following cranial surgery. Childs Nerv Syst. 2017;33:491–497. doi: 10.1007/s00381-016-3329-2
Powers WJ, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Kidwell CS, Leslie-Mazwi TM, Ovbiagele B, Scott PA, Sheth KN, Southerland AM, Summers DV, Tirschwell DL. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec;50(12):e344-e418. doi: 10.1161/STR.0000000000000211
Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011 Apr;42(4):1158-92.
Ferro JM, Bousser MG, Canhão P, Coutinho JM, Crassard I, Dentali F, di Minno M, Maino A, Martinelli I, Masuhr F, Aguiar de Sousa D, Stam J; European Stroke Organization. European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis - endorsed by the European Academy of Neurology. Eur J Neurol. 2017 Oct;24(10):1203-1213.
Ulivi L, Squitieri M, Cohen H, Cowley P, Werring DJ. Cerebral venous thrombosis: a practical guide. Pract Neurol. 2020 Oct;20(5):356-367.
Spadaro A, Scott KR, Koyfman A, Long B. Cerebral venous thrombosis: Diagnosis and management in the emergency department setting. Am J Emerg Med. 2021 Sep;47:24-29
Berge E, Whiteley W, Audebert H, De Marchis GM, Fonseca AC, Padiglioni C, de la Ossa NP, Strbian D, Tsivgoulis G, Turc G. European Stroke Organisation (ESO) guidelines on intravenous thrombolysis for acute ischaemic stroke. Eur Stroke J. 2021 Mar;6(1):I-LXII. doi: 10.1177/2396987321989865
Kim YJ, Kim BJ, Kwon SU, Kim JS, Kang DW. Unclear-onset stroke: Daytime-unwitnessed stroke vs. wake-up stroke. Int J Stroke. 2016 Feb;11(2):212-20. doi: 10.1177/1747493015616513.
Dufouil C, Beiser A, McLure LA, et al. Revised Framingham Stroke Risk Profile to Reflect Temporal Trends. Circulation. 2017;135(12):1145-1159. doi: 10.1161/CIRCULATIONAHA.115.021275.
Maas MB, Singhal AB. Unwitnessed stroke: impact of different onset times on eligibility into stroke trials. J Stroke Cerebrovasc Dis. 2013 Apr;22(3):241-3. doi: 10.1016/j.jstrokecerebrovasdis.2011.08.004
O"Donnell MJ, Chin SL, Rangarajan S, Xavier D, Liu L, et al; INTERSTROKE investigators. Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): a case-control study. Lancet. 2016 Aug 20;388(10046):761-75. doi: 10.1016/S0140-6736(16)30506-2.
Wafa HA, Wolfe CDA, Rudd A, Wang Y. Long-term trends in incidence and risk factors for ischaemic stroke subtypes: Prospective population study of the South London Stroke Register. PLoS Med. 2018 Oct 5;15(10): e1002669. doi: 10.1371/journal.pmed.1002669.
Tan BYQ, Tan JTC, Cheah D, Zheng H, Pek PP, et al. Long-Term Trends in Ischemic Stroke Incidence and Risk Factors: Perspectives from an Asian Stroke Registry. J Stroke. 2020 Sep;22(3):396-399. doi: 10.5853/jos.2020.00878
Bock BF. Proceedings of a National Symposium on Rapid Identification and Treatment of Acute Stroke: Response System for Patients Presenting With Acute Stroke. Available at: http://www.ninds.nih.gov/news_and_events/proceedings/ stroke_proceedings/bock.htm. Accessed August 23, 2011.
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA, Summers DR, Wang DZ, Wintermark M, Yonas H; American Heart Association Stroke Council; Council on Cardiovascular Nursing; Council on Peripheral Vascular Disease; Council on Clinical Cardiology. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013 Mar;44(3):870-947. doi: 10.1161/STR.0b013e318284056a. Epub 2013 Jan 31
Lees KR, Bluhmki E, von Kummer R, Brott TG, Toni D, Grotta JC, Albers GW, Kaste M, Marler JR, Hamilton SA, Tilley BC, Davis SM, Donnan GA, Hacke W; ECASS, ATLANTIS, NINDS and EPITHET rt-PA Study Group, Allen K, Mau J, Meier D, del Zoppo G, De Silva DA, Butcher KS, Parsons MW, Barber PA, Levi C, Bladin C, Byrnes G. Time to treatment with intravenous alteplase and outcome in stroke: an updated pooled analysis of ECASS, ATLANTIS, NINDS, and EPITHET trials. Lancet. 2010 May 15;375(9727):1695-703. doi: 10.1016/S0140-6736(10)60491-6
Ichord RN, Bastian R, Abraham L, Askalan R, Benedict S, Bernard TJ, Beslow L, Deveber G, Dowling M, Friedman N, Fullerton H, Jordan L, Kan L, Kirton A, Amlie-Lefond C, Licht D, Lo W, McClure C, Pavlakis S, Smith SE, Tan M, Kasner S, Jawad AF. Interrater reliability of the Pediatric National Institutes of Health Stroke Scale (PedNIHSS) in a multicenter study. Stroke. 2011 Mar;42(3):613-7. doi: 10.1161/STROKEAHA.110.607192. Epub 2011 Feb 11. PMID: 21317270; PMCID: PMC3065389
Kasner SE. Clinical interpretation and use of stroke scales. Lancet Neurol. 2006 Jul;5(7):603-12. doi: 10.1016/S1474-4422(06)70495-1.
Adams HP Jr, Davis PH, Leira EC, Chang KC, Bendixen BH, Clarke WR, Woolson RF, Hansen MD. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology. 1999 Jul 13;53(1):126-31. doi: 10.1212/wnl.53.1.126.
Fonarow GC, Saver JL, Smith EE, Broderick JP, Kleindorfer DO, Sacco RL, Pan W, Olson DM, Hernandez AF, Peterson ED, Schwamm LH. Relationship of national institutes of health stroke scale to 30-day mortality in medicare beneficiaries with acute ischemic stroke. J Am Heart Assoc. 2012 Feb;1(1):42-50. doi: 10.1161/JAHA.111.000034
Piradov M.A., Suponeva N.A., Ryabinkina Yu.V., et al. Validation and linguistic-cultural adaptation of the Russian version of the Full Outline of UnResponsiveness (FOUR) scale // Annals of Clinical and Experimental Neurology. 2019; 13 (3): 47-54. doi: 10.25692/ACEN.2019.3.7.
Belkin A.A., Bochkarev P.Yu., Levit A.L., Zabolotskikh I.B. Assessment of impaired consciousness: FOUR scale or Glasgow scale? A.I. Saltanov Intensive Care Bulletin. 2019;3:46–51
Martino R, Foley N, Bhogal S, Diamant N, Speechley M, Teasell R. Dysphagia after stroke: incidence, diagnosis, and pulmonary complications. Stroke 2005; 36:2756-63.
Feng MC, Lin YC, Chang YH, Chen CH, Chiang HC, Huang LC, Yang YH, Hung CH. The Mortality and the Risk of Aspiration Pneumonia Related with Dysphagia in Stroke Patients. J Stroke Cerebrovasc Dis. 2019 May;28(5):1381-1387. doi: 10.1016/j.jstrokecerebrovasdis.2019.02.011
Joundi RA, Martino R, Saposnik G, Giannakeas V, Fang J, Kapral MK. Predictors and Outcomes of Dysphagia Screening After Acute Ischemic Stroke. Stroke. 2017 Apr;48(4):900-906. doi: 10.1161/STROKEAHA.116.015332.
Chen PC, Chuang CH, Leong CP, Guo SE, Hsin YJ. Systematic review and meta-analysis of the diagnostic accuracy of the water swallow test for screening aspiration in stroke patients. J Adv Nurs. 2016 Nov;72(11):2575-2586. doi: 10.1111/jan.13013. Epub 2016 May 29
Diagnosis and treatment of dysphagia in central nervous system diseases. Clinical guidelines. Bulletin of Rehabilitation Medicine 2014; 4: 99–115.
Wondergem R, Pisters MF, Wouters EJ, Olthof N, de Bie RA, Visser-Meily JM, Veenhof C. The Course of Activities in Daily Living: Who Is at Risk for Decline after First Ever Stroke? Cerebrovasc Dis. 2017;43(1-2):1-8. doi: 10.1159/000451034. Epub 2016 Oct 18. PMID: 27750246
Hebert D, Lindsay MP, McIntyre A, Kirton A, Rumney PG, Bagg S, Bayley M, Dowlatshahi D, Dukelow S, Garnhum M, Glasser E, Halabi ML, Kang E, MacKay-Lyons M, Martino R, Rochette A, Rowe S, Salbach N, Semenko B, Stack B, Swinton L, Weber V, Mayer M, Verrilli S, DeVeber G, Andersen J, Barlow K, Cassidy C, Dilenge ME, Fehlings D, Hung R, Iruthayarajah J, Lenz L, Majnemer A, Purtzki J, Rafay M, Sonnenberg LK, Townley A, Janzen S, Foley N, Teasell R. Canadian stroke best practice recommendations: Stroke rehabilitation practice guidelines, update 2015. Int J Stroke. 2016 Jun;11(4):459-84. doi: 10.1177/1747493016643553. Epub 2016 Apr 14. PMID: 27079654
Kitchen L, Westmacott R, Friefeld S, MacGregor D, Curtis R, Allen A, Yau I, Askalan R, Moharir M, Domi T, deVeber G. The pediatric stroke outcome measure: a validation and reliability study. Stroke. 2012 Jun;43(6):1602-8. doi: 10.1161/STROKEAHA.111.639583. Epub 2012 Apr 3. PMID: 22474056.
Westmacott, R., McDonald, K. P., Roberts, S. D., deVeber, G., MacGregor, D., Moharir, M., … Williams, T. S. (2018). Predictors of Cognitive and Academic Outcome following Childhood Subcortical Stroke. Developmental Neuropsychology, 43(8), 708–728. https://doi.org/10.1080/87565641.2018.1522538
Claire M. Champigny, Angela Deotto, Robyn Westmacott, Nomazulu Dlamini & Mary Desrocher (2020) Academic outcome in pediatric ischemic stroke, Child Neuropsychology, 26:6, 817-833, DOI: 10.1080/09297049.2020.1712346
Mundiyanapurath S, Hees K, Ahmed N, et al.. Predictors of symptomatic intracranial haemorrhage in off-label thrombolysis: an analysis of the safe implementation of treatments in stroke registry. Eur J Neurol 2018; 25: e340–e311.
Paciaroni M, Agnelli G, Caso V, Corea F, Ageno W, Alberti A, Lanari A, Micheli S, Bertolani L, Venti M, Palmerini F, Billeci AM, Comi G, Previdi P, Silvestrelli G. Acute hyperglycemia and early hemorrhagic transformation in ischemic stroke. Cerebrovasc Dis. 2009; 28 (2): 119-23. doi: 10.1159/000223436
Berge E, Whiteley W, Audebert H, et al. European Stroke Organisation (ESO) guidelines on intravenous thrombolysis for acute ischaemic stroke. Eur Stroke J. 2021;6(1):I-LXII. doi:10.1177/2396987321989865
Rost NS, Masrur S, Pervez MA, Viswanathan A, Schwamm LH. Unsuspected coagulopathy rarely prevents IV thrombolysis in acute ischemic stroke. Neurology. 2009;73(23):1957-1962. doi:10.1212/WNL.0b013e3181c5b46d
van Beynum IM, Smeitink JA, den Heijer M, te Poele Pothoff MT, Blom HJ. Hyperhomocysteinemia: a risk factor for ischemic stroke in children. Circulation. 1999;99:2070–2072. Prengler M, Sturt N, Krywawych S, Surtees R, Liesner R, Kirkham F. Homozygous thermolabile variant of the methylenetetrahydrofolate reductase gene: a potential risk factor for hyperhomocysteinaemia, CVD, and stroke in childhood. Dev Med Child Neurol. 2001;43: 220–225.
Ferriero DM, Fullerton HJ, Bernard TJ, Billinghurst L, Daniels SR, DeBaun MR, deVeber G, Ichord RN, Jordan LC, Massicotte P, Meldau J, Roach ES, Smith ER; American Heart Association Stroke Council and Council on Cardiovascular and Stroke Nursing. Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. 2019 Mar;50(3):e51-e96. doi: 10.1161/STR.0000000000000183. PMID: 30686119
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ, Scott RM, Smith ER; American Heart Association Stroke Council; Council on Cardiovascular Disease in the Young. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008 Sep;39(9):2644-91. doi: 10.1161/STROKEAHA.108.189696. Epub 2008 Jul 17. Erratum in: Stroke. 2009 Jan 1;40(1):e8-10. PMID: 18635845.
Kenet G, Lütkhoff LK, Albisetti M, Bernard T, Bonduel M, Brandao L, Chabrier S, Chan A, deVeber G, Fiedler B, Fullerton HJ, Goldenberg NA, Grabowski E, Günther G, Heller C, Holzhauer S, Iorio A, Journeycake J, Junker R, Kirkham FJ, Kurnik K, Lynch JK, Male C, Manco-Johnson M, Mesters R, Monagle P, van Ommen CH, Raffini L, Rostásy K, Simioni P, Sträter RD, Young G, Nowak-Göttl U. Impact of thrombophilia on risk of arterial ischemic stroke or cerebral sinovenous thrombosis in neonates and children: a systematic review and metaanalysis of observational studies. Circulation. 2010;121:1838–1847. doi: 10.1161/CIRCULATIONAHA.109.913673
Nowak-Göttl U, Sträter R, Heinecke A, Junker R, Koch HG, Schuierer G, von Eckardstein A. Lipoprotein (a) and genetic polymorphisms of clotting factor V, prothrombin, and methylenetetrahydrofolate reductase are risk factors of spontaneous ischemic stroke in childhood. Blood. 1999;94:3678–3682
Sträter R, Becker S, von Eckardstein A, Heinecke A, Gutsche S, Junker R, Kurnik K, Schobess R, Nowak-Göttl U. Prospective assessment of risk factors for recurrent stroke during childhood: a 5-year follow-up study. Lancet. 2002;360:1540–1545. doi: 10.1016/S0140-6736(02)11520-0
Hennerici M.G., Bogousslavsky J., Sacco R.L.; translated from English; under the general editorship of Corr. Member of RAMS V.I. Skvortsova. Stroke: A Clinical Approach. 2nd ed. Moscow: MEDпресс-инфо 2008; 224.
Stroke. A guide for physicians. Edited by L.V. Stakhovskaya, S.V. Kotov. Moscow: MIA Publishing House 2014; 400.
Saver JL, Goyal M, van der Lugt A, Menon BK, Majoie CB, Dippel DW, Campbell BC, Nogueira RG, Demchuk AM, Tomasello A, et al; HERMES Collaborators. Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis. JAMA. 2016;316:1279–1288. doi: 10.1001/jama.2016.13647
Lees KR, Emberson J, Blackwell L, Bluhmki E, Davis SM, Donnan GA, Grotta JC, Kaste M, von Kummer R, Lansberg MG, et al; on behalf of the Stroke Thrombolysis Trialists’ Collaborators Group. Effects of alteplase for acute stroke on the distribution of functional outcomes: a pooled analysis of 9 trials. Stroke. 2016;47:2373–2379. doi: 10.1161/STROKEAHA.116.013644
Aghaebrahim A, Streib C, Rangaraju S, Kenmuir CL, Giurgiutiu DV, Horev A, Saeed Y, Callaway CW, Guyette FX, Martin-Gill C, et al. Streamlining door to recanalization processes in endovascular stroke therapy. J Neurointerv Surg. 2017;9:340–345. doi: 10.1136/neurintsurg-2016-012324
Messe SR, Khatri P, Reeves MJ, Smith EE, Saver JL, Bhatt DL, Grau-Sepulveda MV, Cox M, Peterson ED, Fonarow GC, et al. Why are acute ischemic stroke patients not receiving IV tPA? Results from a national registry. Neurology. 2016;87:1565–1574
Zaidi SF, Shawver J, Espinosa Morales A, Salahuddin H, Tietjen G, Lindstrom D, Parquette B, Adams A, Korsnack A, Jumaa MA. Stroke care: initial data from a county-based bypass protocol for patients with acute stroke. J Neurointerv Surg. 2017;9:631–635. doi: 10.1136/ neurintsurg-2016-012476
Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, et al; DAWN Trial Investigators. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018;378:11–21. doi: 10.1056/NEJMoa1706442
Albers GW, Marks MP, Kemp S, Christensen S, Tsai JP, Ortega-Gutierrez S, McTaggart RA, Torbey MT, Kim-Tenser M, Leslie-Mazwi T, et al; DEFUSE 3 Investigators. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med. 2018;378:708–718. doi: 10.1056/NEJMoa1713973
Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, Thornton J, Roy D, Jovin TG, Willinsky RA, Sapkota BL, et al; ESCAPE Trial Investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015;372:1019–1030. doi: 10.1056/NEJMoa1414905
Jovin TG, Chamorro A, Cobo E, de Miquel MA, Molina CA, Rovira A, San Román L, Serena J, Abilleira S, Ribó M, et al; REVASCAT Trial Investigators. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015;372:2296–2306. doi: 10.1056/NEJMoa1503780
Saver JL, Goyal M, Bonafe A, Diener HC, Levy EI, Pereira VM, Albers GW, Cognard C, Cohen DJ, Hacke W, et al; SWIFT PRIME Investigators. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med. 2015; 372: 2285-2295. doi: 10.1056/NEJMoa1415061
Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, Yassi N, Yan B, Dowling RJ, Parsons MW, Oxley TJ, et al; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015;372:1009-1018. doi: 10.1056/NEJMoa1414792
Bracard S, Ducrocq X, Mas JL, Soudant M, Oppenheim C, Moulin T, Guillemin F; THRACE Investigators. Mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRACE): a randomised controlled trial. Lancet Neurol. 2016; 15: 1138-1147. doi: 10.1016/S1474-4422(16)30177-6
Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, Yoo AJ, Schonewille WJ, Vos JA, Nederkoorn PJ, Wermer MJ, et al; MR CLEAN Investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015; 372: 11-20. doi: 10.1056/NEJMoa1411587
Lemmens R, Hamilton SA, Liebeskind DS, Tomsick TA, Demchuk AM, Nogueira RG, Marks MP, Jahan R, Gralla J, Yoo AJ, et al; DEFUSE 2, IMS III, STAR, and SWIFT Trialists; DEFUSE 2 IMS III STAR and SWIFT Trialists. Effect of endovascular reperfusion in relation to site of arterial occlusion. Neurology. 2016; 86: 762-770. doi: 10.1212/WNL.0000000000002399
Yoo AJ, Simonsen CZ, Prabhakaran S, Chaudhry ZA, Issa MA, Fugate JE, Linfante I, Liebeskind DS, Khatri P, Jovin TG, et al; for the Cerebral Angiographic Revascularization Grading Collaborators. Refining angiographic biomarkers of revascularization: improving outcome prediction after intra-arterial therapy. Stroke. 2013; 44: 2509-2512. doi: 10.1161/STROKEAHA.113.001990
Marks MP, Lansberg MG, Mlynash M, Kemp S, McTaggart R, Zaharchuk G, Bammer R, Albers GW; DEFUSE 2 Investigators. Correlation of AOL recanalization, TIMI reperfusion and TICI reperfusion with infarct growth and clinical outcome. J Neurointerv Surg. 2014; 6: 724-728. doi: 10.1136/neurintsurg-2013-010973
Muir KW, Ford GA, Messow CM, Ford I, Murray A, Clifton A, Brown MM, Madigan J, Lenthall R, Robertson F, et al; PISTE Investigators. Endovascular therapy for acute ischaemic stroke: the Pragmatic Ischaemic Stroke Thrombectomy Evaluation (PISTE) randomised, controlled trial. J Neurol Neurosurg Psychiatry. 2017; 88: 38-44. doi: 10.1136/jnnp-2016-314117
Mocco J, Zaidat OO, von Kummer R, Yoo AJ, Gupta R, Lopes D, Frei D, Shownkeen H, Budzik R, Ajani ZA, et al; THERAPY Trial Investigators. Aspiration thrombectomy after intravenous alteplase versus intravenous alteplase alone. Stroke. 2016; 47: 2331-2338. doi: 10.1161/STROKEAHA.116.013372
Broderick JP, Palesch YY, Demchuk AM, Yeatts SD, Khatri P, Hill MD, Jauch EC, Jovin TG, Yan B, Silver FL, et al; Interventional Management of Stroke (IMS) III Investigators. Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med. 2013; 368: 893-903. doi: 10.1056/NEJMoa1214300
Ciccone A, Valvassori L, Nichelatti M, Sgoifo A, Ponzio M, Sterzi R, Boccardi E; SYNTHESIS Expansion Investigators. Endovascular treatment for acute ischemic stroke. N Engl J Med. 2013; 368: 904-913. doi: 10.1056/NEJMoa1213701
Kidwell CS, Jahan R, Gornbein J, Alger JR, Nenov V, Ajani Z, Feng L, Meyer BC, Olson S, Schwamm LH, et al; MR RESCUE Investigators. A trial of imaging selection and endovascular treatment for ischemic stroke. N Engl J Med. 2013; 368: 914-923. doi: 10.1056/NEJMoa1212793
Nogueira RG, Lutsep HL, Gupta R, Jovin TG, Albers GW, Walker GA, Liebeskind DS, Smith WS; TREVO 2 Trialists. Trevo versus Merci retrievers for thrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke (TREVO 2): a randomised trial. Lancet. 2012; 380: 1231-1240. doi: 10.1016/S0140-6736(12)61299-9
Saver JL, Jahan R, Levy EI, Jovin TG, Baxter B, Nogueira RG, Clark W, Budzik R, Zaidat OO; SWIFT Trialists. Solitaire flow restoration device versus the Merci retriever in patients with acute ischaemic stroke (SWIFT): a randomised, parallel-group, non-inferiority trial. Lancet. 2012; 380: 1241-1249. doi: 10.1016/S0140-6736(12)61384-1
Ogawa A, Mori E, Minematsu K, Taki W, Takahashi A, Nemoto S, Miyamoto S, Sasaki M, Inoue T; for the MELT Japan Study Group. Randomized trial of intraarterial infusion of urokinase within 6 hours of middle cerebral artery stroke: the Middle Cerebral Artery Embolism Local Fibrinolytic Intervention Trial (MELT) Japan. Stroke. 2007; 38: 2633-2639. doi: 10.1161/STROKEAHA.107.488551
Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, et al. Intra-arterial prourokinase for acute ischemic stroke: the PROACT II study: a randomized controlled trial: Prolyse in Acute Cerebral Thromboembolism. JAMA. 1999; 282: 2003-2011. doi: 10.1001/jama.282.21.2003
Olthuis SGH, Pirson FAV, Pinckaers FME, Hinsenveld WH, Nieboer D, Ceulemans A, Knapen RRMM, Robbe MMQ, Berkhemer OA, van Walderveen MAA, Lycklama À Nijeholt GJ, Uyttenboogaart M, Schonewille WJ, van der Sluijs PM, Wolff L, van Voorst H, Postma AA, Roosendaal SD, van der Hoorn A, Emmer BJ, Krietemeijer MGM, van Doormaal PJ, Roozenbeek B, Goldhoorn RB, Staals J, de Ridder IR, van der Leij C, Coutinho JM, van der Worp HB, Lo RTH, Bokkers RPH, van Dijk EI, Boogaarts HD, Wermer MJH, van Es ACGM, van Tuijl JH, Kortman HGJ, Gons RAR, Yo LSF, Vos JA, de Laat KF, van Dijk LC, van den Wijngaard IR, Hofmeijer J, Martens JM, Brouwers PJAM, Bulut T, Remmers MJM, de Jong TEAM, den Hertog HM, van Hasselt BAAM, Rozeman AD, Elgersma OEH, van der Veen B, Sudiono DR, Lingsma HF, Roos YBWEM, Majoie CBLM, van der Lugt A, Dippel DWJ, van Zwam WH, van Oostenbrugge RJ; MR CLEAN-LATE investigators. Endovascular treatment versus no endovascular treatment after 6-24 h in patients with ischaemic stroke and collateral flow on CT angiography (MR CLEAN-LATE) in the Netherlands: a multicentre, open-label, blinded-endpoint, randomised, controlled, phase 3 trial. Lancet. 2023 Apr 22;401(10385):1371-1380. doi: 10.1016/S0140-6736(23)00575-5. Epub 2023 Mar 29. PMID: 37003289
Ois A, Cuadrado-Godia E, Rodríguez-Campello A, Jimenez-Conde J, Roquer J. High risk of early neurological recurrence in symptomatic carotid stenosis. Stroke. 2009; 40: 2727-2731. doi: 10.1161/STROKEAHA. 109.548032
De Rango P, Brown MM, Chaturvedi S, Howard VJ, Jovin T, Mazya MV, Paciaroni M, Manzone A, Farchioni L, Caso V. Summary of evidence on early carotid intervention for recently symptomatic stenosis based on meta-analysis of current risks. Stroke. 2015; 46: 3423-3436. doi: 10.1161/STROKEAHA.115.010764
Marnane M, Ni Chroinin D, Callaly E, Sheehan OC, Merwick A, Hannon N, Horgan G, Kyne L, Moroney J, McCormack PM, et al. Stroke recurrence within the time window recommended for carotid endarterectomy. Neurology. 2011; 77: 738-743. doi: 10.1212/WNL.0b013e31822b00cf
Ohansson EP, Arnerlöv C, Wester P. Risk of recurrent stroke before carotid endarterectomy: the ANSYSCAP study. Int J Stroke. 2013; 8: 220-227. doi: 10.1111/j.1747-4949.2012.00790.x
Strömberg S, Nordanstig A, Bentzel T, Österberg K, Bergström GM. Risk of early recurrent stroke in symptomatic carotid stenosis. Eur J Vasc Endovasc Surg. 2015; 49: 137-144. doi: 10.1016/j.ejvs.2014.11.004
Kazandjian C, Kretz B, Lemogne B, Aboa Eboulé C, Béjot Y, Steinmetz E. Influence of the type of cerebral infarct and timing of intervention in the early outcomes after carotid endarterectomy for symptomatic stenosis. J Vasc Surg. 2016; 63: 1256-1261. doi: 10.1016/j.jvs.2015.10.097
Azzini C, Gentile M, De Vito A, Traina L, Sette E, Fainardi E, Mascoli F, Casetta I. Very early carotid endarterectomy after intravenous thrombolysis. Eur J Vasc Endovasc Surg. 2016; 51: 482-486. doi: 10.1016/j.ejvs.2015.11.006
Dachi K, Sadato A, Hayakawa M, Maeda S, Hirose Y. Acute carotid artery stenting in symptomatic high-grade cervical carotid artery stenosis. Neurosurg Rev. 2017; 40: 45-51. doi: 10.1007/s10143-016-0737-4
Vasconcelos V, Cassola N, da Silva EM, Baptista-Silva JC. Immediate versus delayed treatment for recently symptomatic carotid artery stenosis. Cochrane Database Syst Rev. 2016; 9: CD011401. doi: 10.1002/14651858.CD011401.pub2
Ferguson GG, Eliasziw M, Barr HW, Clagett GP, Barnes RW, Wallace MC, Taylor DW, Haynes RB, Finan JW, Hachinski VC, et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999; 30: 1751-1758. doi: 10.1161/01.str.30.9.1751
Saver JL, Goyal M, van der Lugt A, Menon BK, Majoie CB, Dippel DW, Campbell BC, Nogueira RG, Demchuk AM, Tomasello A, et al; HERMES Collaborators. Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis. JAMA. 2016; 316: 1279-1288. doi: 10.1001/jama.2016.13647
Lees KR, Emberson J, Blackwell L, Bluhmki E, Davis SM, Donnan GA, Grotta JC, Kaste M, von Kummer R, Lansberg MG, et al; on behalf of the Stroke Thrombolysis Trialists’ Collaborators Group. Effects of alteplase for acute stroke on the distribution of functional outcomes: a pooled analysis of 9 trials. Stroke. 2016; 47: 2373-2379. doi: 10.1161/STROKEAHA.116.013644
Saver JL, Goyal M, van der Lugt A, Menon BK, Majoie CB, Dippel DW, Campbell BC, Nogueira RG, Demchuk AM, Tomasello A, et al; HERMES Collaborators. Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis. JAMA. 2016; 316: 1279-1288. doi: 10.1001/jama.2016.13647
Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, et al; DAWN Trial Investigators. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018; 378: 11-21. doi: 10.1056/NEJMoa1706442
Albers GW, Marks MP, Kemp S, Christensen S, Tsai JP, Ortega-Gutierrez S, McTaggart RA, Torbey MT, Kim-Tenser M, Leslie-Mazwi T, et al; DEFUSE 3 Investigators. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med. 2018; 378: 708-718. doi: 10.1056/NEJMoa1713973
R. Souillard-Scemama, M. Tisserand, D. Calvet, D. Jumadilova, S. Lion, G. Turc, M. Edjlali, C. Mellerio, C. Lamy, O. Naggara, J.-F. Meder, C. Oppenheim, An update on brain imaging in transient ischemic attack, Journal of Neuroradiology 2015; 42 (1): 3-11.
Wardlaw J, Brazzelli M, Miranda H, et al. An assessment of the cost-effectiveness of magnetic resonance, including diffusion-weighted imaging, in patients with transient ischaemic attack and minor stroke: a systematic review, meta-analysis and economic evaluation. Health Technology Assessment, Southampton (UK): NIHR Journals Library; 2014 Apr.; 18 (27).
Bracard S, Ducrocq X, Mas JL, Soudant M, Oppenheim C, Moulin T, Guillemin F; THRACE Investigators. Mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRACE): a randomised controlled trial. Lancet Neurol. 2016; 15: 1138-1147. doi: 10.1016/S1474-4422(16)30177-6
Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, Yoo AJ, Schonewille WJ, Vos JA, Nederkoorn PJ, Wermer MJ, et al; MR CLEAN Investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015; 372: 11-20. doi: 10.1056/NEJMoa1411587
Ehrlich ME, Turner HL, Currie LJ, Wintermark M, Worrall BB, Southerland AM. Safety of computed tomographic angiography in the evaluation of patients with acute stroke: a single-center experience. Stroke. 2016; 47: 2045-2050. doi: 10.1161/STROKEAHA.116.013973
Aulicky P, Mikulík R, Goldemund D, Reif M, Dufek M, Kubelka T. Safety of performing CT angiography in stroke patients treated with intravenous thrombolysis. J Neurol Neurosurg Psychiatry. 2010; 81: 783-787. doi: 10.1136/jnnp.2009.184002
Lima FO, Lev MH, Levy RA, Silva GS, Ebril M, de Camargo EC, Pomerantz S, Singhal AB, Greer DM, Ay H, et al. Functional contrastenhanced CT for evaluation of acute ischemic stroke does not increase the risk of contrast-induced nephropathy. AJNR Am J Neuroradiol. 2010; 31: 817-821. doi: 10.3174/ajnr.A1927
Hopyan JJ, Gladstone DJ, Mallia G, Schiff J, Fox AJ, Symons SP, Buck BH, Black SE, Aviv RI. Renal safety of CT angiography and perfusion imaging in the emergency evaluation of acute stroke. AJNR Am J Neuroradiol. 2008; 29: 1826-1830. doi: 10.3174/ajnr.A1257
Krol AL, Dzialowski I, Roy J, Puetz V, Subramaniam S, Coutts SB, Demchuk AM. Incidence of radiocontrast nephropathy in patients undergoing acute stroke computed tomography angiography. Stroke. 2007; 38: 2364-2366. doi: 10.1161/STROKEAHA.107.482778
Josephson SA, Dillon WP, Smith WS. Incidence of contrast nephropathy from cerebral CT angiography and CT perfusion imaging. Neurology. 2005; 64: 1805-1806. doi: 10.1212/01.WNL.0000161845.69114.62
Ehrlich ME, Turner HL, Currie LJ, Wintermark M, Worrall BB, Southerland AM. Safety of computed tomographic angiography in the evaluation of patients with acute stroke: a single-center experience. Stroke. 2016; 47: 2045-2050. doi: 10.1161/STROKEAHA.116.013973
Aulicky P, Mikulík R, Goldemund D, Reif M, Dufek M, Kubelka T. Safety of performing CT angiography in stroke patients treated with intravenous thrombolysis. J Neurol Neurosurg Psychiatry. 2010; 81: 783-787. doi: 10.1136/jnnp.2009.184002
Lima FO, Lev MH, Levy RA, Silva GS, Ebril M, de Camargo EC, Pomerantz S, Singhal AB, Greer DM, Ay H, et al. Functional contrastenhanced CT for evaluation of acute ischemic stroke does not increase the risk of contrast-induced nephropathy. AJNR Am J Neuroradiol. 2010; 31: 817-821. doi: 10.3174/ajnr.A1927
Hopyan JJ, Gladstone DJ, Mallia G, Schiff J, Fox AJ, Symons SP, Buck BH, Black SE, Aviv RI. Renal safety of CT angiography and perfusion imaging in the emergency evaluation of acute stroke. AJNR Am J Neuroradiol. 2008; 29: 1826-1830. doi: 10.3174/ajnr.A1257
Krol AL, Dzialowski I, Roy J, Puetz V, Subramaniam S, Coutts SB, Demchuk AM. Incidence of radiocontrast nephropathy in patients undergoing acute stroke computed tomography angiography. Stroke. 2007; 38: 2364-2366. doi: 10.1161/STROKEAHA.107.482778
Josephson SA, Dillon WP, Smith WS. Incidence of contrast nephropathy from cerebral CT angiography and CT perfusion imaging. Neurology. 2005; 64: 1805-1806. doi: 10.1212/01.WNL.0000161845.69114.62
Grotta JC, Welch KM, Fagan SC, Lu M, Frankel MR, Brott T, Levine SR, Lyden PD. Clinical deterioration following improvement in the NINDS rt-PA Stroke Trial. Stroke. 2001 Mar;32(3):661-8. doi: 10.1161/01.str.32.3.661. PMID: 11239184.
Llinas EJ, Max A, Khan S, Marsh EB. The Routine Follow-up Head CT: Is it Still a Necessary Step in the Thrombolysis Pathway? Neurocrit Care. 2022 Apr;36(2):595-601. doi: 10.1007/s12028-021-01348-4. Epub 2021 Sep 27. PMID: 34580828; PMCID: PMC8964541.
Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, Larrue V, Lees KR, Medeghri Z, Machnig T, Schneider D, von Kummer R, Wahlgren N, Toni D; ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008; 359: 1317-1329. doi: 10.1056/NEJMoa0804656
von Kummer R, Broderick JP, Campbell BC, Demchuk A, Goyal M, Hill MD, Treurniet KM, Majoie CB, Marquering HA, Mazya MV, San Román L, Saver JL, Strbian D, Whiteley W, Hacke W. The Heidelberg Bleeding Classification: classification of bleeding events after ischemic stroke and reperfusion therapy. Stroke. 2015; 46: 2981-2986. doi: 10.1161/STROKEAHA.115.010049
del Zoppo GJ, Higashida RT, Furlan AJ, Pessin MS, Rowley HA, Gent M. PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke: PROACT Investigators: Prolyse in Acute Cerebral Thromboembolism. Stroke. 1998; 29: 4-11.
Hacke W, Kaste M, Fieschi C, von Kummer R, Davalos A, Meier D, Larrue V, Bluhmki E, Davis S, Donnan G, Schneider D, Diez-Tejedor E, Trouillas P. Randomised double-blind placebo-controlled trial of Wahlgren N, Ahmed N, Eriksson N, Aichner F, Bluhmki E, Dávalos A, Erilä T, Ford GA, Grond M, Hacke W, Hennerici MG, Kaste M, Köhrmann M, Larrue V, Lees KR, Machnig T, Roine RO, Toni D, Vanhooren G; for the SITS-MOST Investigators. Multivariable analysis of outcome predictors and adjustment of main outcome results to baseline data profile in randomized controlled trials: Safe Implementation of Thrombolysis in Stroke-MOnitoring STudy (SITS-MOST). Stroke. 2008; 39: 3316-3322. doi: 10.1161/STROKEAHA.107.510768
Trouillas P, von Kummer R. Classification and pathogenesis of cerebral hemorrhages after thrombolysis in ischemic stroke. Stroke. 2006; 37: 556-561. doi: 10.1161/01.STR.0000196942.84707.71.
Ekundayo OJ, Saver JL, Fonarow GC, Schwamm LH, Xian Y, Zhao X, Hernandez AF, Peterson ED, Cheng EM. Patterns of emergency medical services use and its association with timely stroke treatment: findings from Get With The Guidelines–Stroke. Circ Cardiovasc Qual Outcomes. 2013; 6: 262-269. doi: 10.1161/CIRCOUTCOMES.113.000089
Nikitin A.S., Krylov V.V., Burov S.A., Petrikov S.S., Asratyan S.A., Kamchatnov P.R., Kemezh Yu.V., Belkov M.V., Zavalishin E.E. Dislocation syndrome in patients with a malignant course of massive ischemic stroke. S.S. Korsakov Journal of Neurology and Psychiatry 2015; 3 (Special Issue "Stroke"): 20-26.
Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, et al; DAWN Trial Investigators. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med. 2018;378:11–21. doi: 10.1056/NEJMoa1706442
He G, Wei L, Lu H, Li Y, Zhao Y, Zhu Y. Advances in imaging acute ischemic stroke: evaluation before thrombectomy. Rev Neurosci. 2021 Feb 19;32(5):495-512. doi: 10.1515/revneuro-2020-0061. PMID: 33600678.
Chalela JA, Kidwell CS, Nentwich LM, Luby M, Butman JA, Demchuk AM, Hill MD, Patronas N, Latour L, Warach S. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007 Jan 27;369(9558):293-8. doi: 10.1016/S0140-6736(07)60151-2. PMID: 17258669; PMCID: PMC1859855.
Sun LR, Lynch JK. Advances in the Diagnosis and Treatment of Pediatric Arterial Ischemic Stroke. Neurotherapeutics. 2023 Apr;20(3):633-654. doi: 10.1007/s13311-023-01373-5. Epub 2023 Apr 18. PMID: 37072548; PMCID: PMC10112833
Mastrangelo M, Giordo L, Ricciardi G, De Michele M, Toni D, Leuzzi V. Acute ischemic stroke in childhood: a comprehensive review. Eur J Pediatr. 2022 Jan;181(1):45-58. doi: 10.1007/s00431-021-04212-x. Epub 2021 Jul 29. PMID: 34327611; PMCID: PMC8760225
van Dam LF, van Walderveen MAA, Kroft LJM, Kruyt ND, Wermer MJH, van Osch MJP, Huisman MV, Klok FA. Current imaging modalities for diagnosing cerebral vein thrombosis - A critical review. Thromb Res. 2020 May;189:132-139. Sadik JC, Jianu DC, Sadik R, Purcell Y, Novaes N, Saragoussi E, Obadia M, Lecler A, Savatovsky J. Imaging of Cerebral Venous Thrombosis. Life (Basel). 2022 Aug 10;12(8):1215.
Buyck PJ, de Keyzer F, Vanneste D, Wilms G, Thijs V, Demaerel D. CT density measurement and H:H ratio are useful in diagnosing acute cerebral venous sinus thrombosis. AJNR Am J Neuroradiol. 2013;34:1568-72.
Sadik JC, Jianu DC, Sadik R, Purcell Y, Novaes N, Saragoussi E, Obadia M, Lecler A, Savatovsky J. Imaging of Cerebral Venous Thrombosis. Life (Basel). 2022 Aug 10;12(8):1215.
Spadaro A, Scott KR, Koyfman A, Long B. Cerebral venous thrombosis: Diagnosis and management in the emergency department setting. Am J Emerg Med. 2021 Sep;47:24-29.
Xu W, Gao L, Li T, Ramdoyal ND, Zhang J, Shao A. The Performance of CT versus MRI in the Differential Diagnosis of Cerebral Venous Thrombosis. Thromb Haemost. 2018 Jun;118(6):1067-1077
Lafitte F, Boukobza M, Guichard JP, Hoeffel C, Reizine D, Ille O, Woimant F, Merland JJ. MRI and MRA for diagnosis and follow-up of cerebral venous thrombosis (CVT). Clin Radiol. 1997 Sep;52(9):672-9.
Liang L, Korogi Y, Sugahara T, Onomichi M, Shigematsu Y, Yang D, Kitajima M, Hiai Y, Takahashi M. Evaluation of the intracranial dural sinuses with a 3D contrast-enhanced MP-RAGE sequence: prospective comparison with 2D-TOF MR venography and digital subtraction angiography. AJNR Am J Neuroradiol. 2001 Mar;22(3):481-92.
Canedo-Antelo M, Baleato-González S, Mosqueira AJ, Casas-Martínez J, Oleaga L, Vilanova JC, Luna-Alcalá A, García-Figueiras R. Radiologic Clues to Cerebral Venous Thrombosis. Radiographics. 2019 Oct;39(6):1611-1628.
Current imaging modalities for diagnosing cerebral vein thrombosis - A critical review. Thromb Res. 2020 May; 189: 132-139. Canedo-Antelo M, Baleato-González S, Mosqueira AJ, et al. Radiologic Clues to Cerebral Venous Thrombosis. Radiographics. 2019; 39(6): 1611-1628.
Goldstein LB. Stroke code chest radiographs are not useful. Cerebrovasc Dis. 2007; 24 (5): 460-2. doi: 10.1159/000108437.
Saber H, Silver B, Santillan A, Azarpazhooh MR, Misra V, Behrouz R. Role of emergent chest radiography in evaluation of hyperacute stroke. Neurology. 2016; 87: 782-785. doi: 10.1212/WNL.0000000000002964
Thijs V. Atrial Fibrillation Detection: Fishing for An Irregular Heartbeat Before and After Stroke. Stroke. 2017 Oct; 48 (10): 2671-2677. doi: 10.1161/STROKEAHA.117.017083.
Maciel R, Palma R, Sousa P, Ferreira F, Nzwalo H. Acute stroke with concomitant acute myocardial infarction: will you thrombolyse? J Stroke. 2015 Jan; 17 (1): 84-6. doi: 10.5853/jos.2015.17.1.84.
Battaglini D, Robba C, Lopes da Silva A, Dos Santos Samary C, Leme Silva P, Dal Pizzol F, Pelosi P, Rocco PRM. Brain-heart interaction after acute ischemic stroke. Crit Care. 2020 Apr 21; 24 (1): 163. doi: 10.1186/s13054-020-02885-8
Kallmünzer B, Breuer L, Kahl N, Bobinger T, Raaz-Schrauder D, Huttner HB, Schwab S, Köhrmann M. Serious cardiac arrhythmias after stroke: incidence, time course, and predictors--a systematic, prospective analysis. Stroke. 2012 Nov; 43 (11): 2892-7. doi: 10.1161/STROKEAHA.112.664318
Fernández-Menéndez S, García-Santiago R, Vega-Primo A, González Nafría N, Lara-Lezama LB, Redondo-Robles L, Montes-Montes M, Riveira-Rodríguez MC, Tejada-García J. Cardiac arrhythmias in stroke unit patients. Evaluation of the cardiac monitoring data. Neurologia. 2016 Jun; 31 (5): 289-95. English, Spanish. doi: 10.1016/j.nrl.2015.03.013
Rizos T, Güntner J, Jenetzky E, Marquardt L, Reichardt C, Becker R, Reinhardt R, Hepp T, Kirchhof P, Aleynichenko E, Ringleb P, Hacke W, Veltkamp R. Continuous stroke unit electrocardiographic monitoring versus 24-hour Holter electrocardiography for detection of paroxysmal atrial fibrillation after stroke. Stroke. 2012 Oct; 43 (10): 2689-94. doi: 10.1161/STROKEAHA.112.654954
Tsivgoulis G, Katsanos AH, Köhrmann M, Caso V, Perren F, Palaiodimou L, Deftereos S, Giannopoulos S, Ellul J, Krogias C, Mavridis D, Triantafyllou S, Alexandrov AW, Schellinger PD, Alexandrov AV. Duration of Implantable Cardiac Monitoring and Detection of Atrial Fibrillation in Ischemic Stroke Patients: A Systematic Review and Meta-Analysis. J Stroke. 2019 Sep; 21 (3): 302-311. doi: 10.5853/jos.2019.01067
Grond M, Jauss M, Hamann G, Stark E, Veltkamp R, Nabavi D, Horn M, Weimar C, Köhrmann M, Wachter R, Rosin L, Kirchhof P. Improved detection of silent atrial fibrillation using 72-hour Holter ECG in patients with ischemic stroke: a prospective multicenter cohort study. Stroke. 2013 Dec; 44 (12): 3357-64. doi: 10.1161/STROKEAHA.113.001884
Rubio Campal JM, García Torres MA, Sánchez Borque P, Navas Vinagre I, Zamarbide Capdepón I, Miracle Blanco Á, Bravo Calero L, Sáez Pinel R, Tuñón Fernández J, Serratosa Fernández JM. Detecting Atrial Fibrillation in Patients With an Embolic Stroke of Undetermined Source (from the DAF-ESUS registry). Am J Cardiol. 2020 Feb 1; 125 (3): 409-414. doi: 10.1016/j.amjcard.2019.10.050.
Kitsiou A, Rogalewski A, Kalyani M, Deelawar S, Tribunyan S, Greeve I, Minnerup J, Israel C, Schäbitz WR. Atrial Fibrillation in Patients with Embolic Stroke of Undetermined Source during 3 Years of Prolonged Monitoring with an Implantable Loop Recorder. Thromb Haemost. 2021 Jun; 121(6): 826-833. doi: 10.1055/a-1346-2899.
Triantafyllou S, Katsanos AH, Dilaveris P, Giannopoulos G, Kossyvakis C, Adreanides E, Liantinioti C, Tympas K, Zompola C, Theodorou A, Palaiodimou L, Flevari P, Kosmidou M, Voumvourakis K, Parissis J, Deftereos S, Tsivgoulis G. Implantable Cardiac Monitoring in the Secondary Prevention of Cryptogenic Stroke. Ann Neurol. 2020 Nov; 88(5): 946-955. doi: 10.1002/ana.25886.
Schnabel RB, Haeusler KG, Healey JS, Freedman B, Boriani G, Brachmann J, Brandes A, Bustamante A, Casadei B, Crijns HJGM, Doehner W, Engström G, Fauchier L, Friberg L, Gladstone DJ, Glotzer TV, Goto S, Hankey GJ, Harbison JA, Hobbs FDR, Johnson LSB, Kamel H, Kirchhof P, Korompoki E, Krieger DW, Lip GYH, Løchen ML, Mairesse GH, Montaner J, Neubeck L, Ntaios G, Piccini JP, Potpara TS, Quinn TJ, Reiffel JA, Ribeiro ALP, Rienstra M, Rosenqvist M, Themistoclakis S, Sinner MF, Svendsen JH, Van Gelder IC, Wachter R, Wijeratne T, Yan B. Searching for Atrial Fibrillation Poststroke: A White Paper of the AF-SCREEN International Collaboration. Circulation. 2019 Nov 26; 140 (22): 1834-1850. doi: 10.1161/CIRCULATIONAHA.119.040267
Poli S, Diedler J, Härtig F, Götz N, Bauer A, Sachse T, Müller K, Müller I, Stimpfle F, Duckheim M, Steeg M, Eick C, Schreieck J, Gawaz M, Ziemann U, Zuern CS. Insertable cardiac monitors after cryptogenic stroke--a risk factor based approach to enhance the detection rate for paroxysmal atrial fibrillation. Eur J Neurol. 2016 Feb; 23(2): 375-81. doi: 10.1111/ene.12843
Ntaios G. Embolic Stroke of Undetermined Source: JACC Review Topic of the Week. J Am Coll Cardiol. 2020 Jan 28; 75(3): 333-340. doi: 10.1016/j.jacc.2019.11.024
Schnabel RB, Haeusler KG, Healey JS, Freedman B, Boriani G, Brachmann J, Brandes A, Bustamante A, Casadei B, Crijns HJGM, Doehner W, Engström G, Fauchier L, Friberg L, Gladstone DJ, Glotzer TV, Goto S, Hankey GJ, Harbison JA, Hobbs FDR, Johnson LSB, Kamel H, Kirchhof P, Korompoki E, Krieger DW, Lip GYH, Løchen ML, Mairesse GH, Montaner J, Neubeck L, Ntaios G, Piccini JP, Potpara TS, Quinn TJ, Reiffel JA, Ribeiro ALP, Rienstra M, Rosenqvist M, Themistoclakis S, Sinner MF, Svendsen JH, Van Gelder IC, Wachter R, Wijeratne T, Yan B. Searching for Atrial Fibrillation Poststroke: A White Paper of the AF-SCREEN International Collaboration. Circulation. 2019 Nov 26; 140 (22): 1834-1850. doi: 10.1161/CIRCULATIONAHA.119.040267
Poli S, Diedler J, Härtig F, Götz N, Bauer A, Sachse T, Müller K, Müller I, Stimpfle F, Duckheim M, Steeg M, Eick C, Schreieck J, Gawaz M, Ziemann U, Zuern CS. Insertable cardiac monitors after cryptogenic stroke--a risk factor based approach to enhance the detection rate for paroxysmal atrial fibrillation. Eur J Neurol. 2016 Feb; 23(2): 375-81. doi: 10.1111/ene.12843
Li YG, Pastori D, Farcomeni A, et al. A Simple Clinical Risk Score (C2HEST) for Predicting Incident Atrial Fibrillation in Asian Subjects: Derivation in 471,446 Chinese Subjects, With Internal Validation and External Application in 451,199 Korean Subjects. Chest. 2019; 155(3): 510-518.
Hindricks G, Potpara T, Dagres N, Arbelo E, Bax JJ, et al; ESC Scientific Document Group. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur Heart J. 2021 Feb 1; 42(5): 373-498. doi: 10.1093/eurheartj/ehaa612
Ntaios G, Perlepe K, Lambrou D, Sirimarco G, Strambo D, Eskandari A, Karagkiozi E, Vemmou A, Korompoki E, Manios E, Makaritsis K, Vemmos K, Michel P. Identification of patients with embolic stroke of undetermined source and low risk of new incident atrial fibrillation: The AF-ESUS score. Int J Stroke. 2021 Jan; 16(1): 29-38. doi: 10.1177/1747493020925281
Pagola J, Pagola C, Juega J, González-Alujas T, Alvarez-Sabin J, Molina CA. The Role of Echocardiography Screening at the Stroke Unit. Front Neurol. 2020 Sep 11; 11:1003. doi: 10.3389/fneur.2020.01003
Zhang L, Harrison JK, Goldstein LB. Echocardiography for the detection of cardiac sources of embolism in patients with stroke or transient ischemic attack. J Stroke Cerebrovasc Dis. 2012 Oct; 21(7): 577-82. doi: 10.1016/j.jstrokecerebrovasdis.2011.01.005.
Fralick M, Goldberg N, Rohailla S, Guo Y, Burke MJ, Lapointe-Shaw L, Kwan JL, Weinerman AS, Rawal S, Tang T, Razak F, Verma AA. Value of routine echocardiography in the management of stroke. CMAJ. 2019 Aug 6; 191(31): E853-E859. doi: 10.1503/cmaj.190111.
ordan K, Yaghi S, Poppas A, Chang AD, Mac Grory B, Cutting S, Burton T, Jayaraman M, Tsivgoulis G, Sabeh MK, Merkler AE, Kamel H, Elkind MSV, Furie K, Song C. Left Atrial Volume Index Is Associated With Cardioembolic Stroke and Atrial Fibrillation Detection After Embolic Stroke of Undetermined Source. Stroke. 2019 Aug; 50(8): 1997-2001. doi: 10.1161/STROKEAHA.119.025384.
Stewart MH, Gilliland Y. Role of Transesophageal Echocardiography in Patients with Ischemic Stroke. Prog Cardiovasc Dis. 2018 Nov-Dec; 61 (5-6): 456-467. doi: 10.1016/j.pcad.2018.11.007
Katsanos AH, Giannopoulos S, Frogoudaki A, Vrettou AR, Ikonomidis I, Paraskevaidis I, Zompola C, Vadikolias K, Boviatsis E, Parissis J, Voumvourakis K, Kyritsis AP, Tsivgoulis G. The diagnostic yield of transesophageal echocardiography in patients with cryptogenic cerebral ischaemia: a meta-analysis. Eur J Neurol. 2016 Mar; 23(3): 569-79. doi: 10.1111/ene.12897
Schnabel RB, Camen S, Knebel F, Hagendorff A, Bavendiek U, Böhm M, Doehner W, Endres M, Gröschel K, Goette A, Huttner HB, Jensen C, Kirchhof P, Korosoglou G, Laufs U, Liman J, Morbach C, Nabavi DG, Neumann-Haefelin T, Pfeilschifter W, Poli S, Rizos T, Rolf A, Röther J, Schäbitz WR, Steiner T, Thomalla G, Wachter R, Haeusler KG. Expert opinion paper on cardiac imaging after ischemic stroke. Clin Res Cardiol. 2021 Jul; 110(7): 938-958. doi: 10.1007/s00392-021-01834-x
Katsanos AH, Giannopoulos S, Frogoudaki A, Vrettou AR, Ikonomidis I, Paraskevaidis I, Zompola C, Vadikolias K, Boviatsis E, Parissis J, Voumvourakis K, Kyritsis AP, Tsivgoulis G. The diagnostic yield of transesophageal echocardiography in patients with cryptogenic cerebral ischaemia: a meta-analysis. Eur J Neurol. 2016 Mar; 23(3): 569-79. doi: 10.1111/ene.12897
Mahmoud AN, Elgendy IY, Agarwal N et al. Identification and quantification of patent foramen ovale mediated shunts: echocardiography and transcranial Doppler. Interv Cardiol Clin. 2017; 6: 495-504.
Droste DW, Lakemeier S, Wichter T et al. Optimizing the technique of contrast transcranial Doppler ultrasound in the detection of right-to-left shunts. Stroke. 2002; 33: 2211-2216.
Serena J, Segura T, Perez-Ayuso MJ et al. The need to quantify right-to-left shunt in acute ischemic stroke: A case-control study. Stroke 1998; 29: 1322-1328
Buyck PJ, de Keyzer F, Vanneste D, Wilms G, Thijs V, Demaerel D. CT density measurement and H:H ratio are useful in diagnosing acute cerebral venous sinus thrombosis. AJNR Am J Neuroradiol. 2013; 34: 1568-72.
van Dam LF, van Walderveen MAA, Kroft LJM, Kruyt ND, Wermer MJH, van Osch MJP, Huisman MV, Klok FA. Current imaging modalities for diagnosing cerebral vein thrombosis - A critical review. Thromb Res. 2020 May; 189: 132-139.
Pongmoragot J, Saposnik G. Intracerebral hemorrhage from cerebral venous thrombosis. Curr Atheroscler Rep. 2012; 14(4): 382-389.
Buyck PJ, de Keyzer F, Vanneste D, Wilms G, Thijs V, Demaerel D. CT density measurement and H:H ratio are useful in diagnosing acute cerebral venous sinus thrombosis. AJNR Am J Neuroradiol. 2013; 34: 1568-72.
Canedo-Antelo M, Baleato-González S, Mosqueira AJ, et al. Radiologic Clues to Cerebral Venous Thrombosis. Radiographics. 2019; 39(6): 1611-1628.
Wasay M, Azeemuddin M. Neuroimaging of cerebral venous thrombosis. J Neuroimaging. 2005; 15: 118-28.
Rollins N, Ison C, Reyes T, Chia J. Cerebral MR venography in children: comparison of 2D time-of-flight and gadoliniumenhanced 3D gradient-echo techniques. Radiology. 2005; 235(3): 1011-7.
Conforto AB, Nader SN, Puglia Junior P, Yamamoto FI, Gonçalves MR, Vasconcelos FR, et al. Dural arteriovenous fistula and cerebral venous thrombosis. Arq Neuropsiquiatr. 2015; 73: 548.
George M.G. Risk Factors for Ischemic Stroke in Younger Adults: A Focused Update. Stroke. 2020; 51(3): 729-735
Omran S.S., Lerario M.P., Gialdini G. et al. Clinical Impact of Thrombophilia Screening in Young Adults with Ischemic Stroke. J Stroke Cerebrovasc Dis. 2019; 28(4): 882-88
Tan RY, Markus HS. Monogenic causes of stroke: now and the future. J Neurol. 2015 Dec; 262(12): 2601-16. doi: 10.1007/s00415-015-7794-4
Adams HP Jr. Cerebral vasculitis. Handb Clin Neurol. 2014; 119: 475-94. doi: 10.1016/B978-0-7020-4086-3.00031-X
Biousse V, Ameri A, Bousser MG. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology. 1999 Oct 22;53(7):1537-42. doi: 10.1212/wnl.53.7.1537
Silvis SM, Hiltunen S, Lindgren E, Jood K, Zuurbier SM, Middeldorp S, Putaala J, Cannegieter SC, Tatlisumak T, Coutinho JM. Cancer and risk of cerebral venous thrombosis: a case-control study. J Thromb Haemost. 2018 Jan;16(1):90-95. doi: 10.1111/jth.13903
Stroke Unit Trialists’ Collaboration. Organised inpatient (stroke unit) care for stroke (Cochrane review). In: The Cochrane Library. Oxford, UK: Update Software CD000213 2003; 1.
Cavallini A, Micieli G, Marcheselli S, Quaglini S. Role of monitoring in management of acute ischemic stroke patients.Stroke. 2003 Nov; 34(11): 2599-603.
Langhorne P, Pollock A: What are the components of effective stroke unit care? Age Ageing 2002; 31: 365-371.
Borsellino B, Schultz MJ, Gama de Abreu M, Robba C, Bilotta F. Mechanical ventilation in neurocritical care patients: a systematic literature review. Expert Rev Respir Med. 2016; 10: 1123-32
Rajajee V, Riggs B, Seder DB. Emergency neurological life support: airway, ventilation, and sedation. Neurocrit Care. 2017; 27(Suppl 1): 4-28.
Robba, C., Bonatti, G., Battaglini, D. et al. Mechanical ventilation in patients with acute ischaemic stroke: from pathophysiology to clinical practice. Crit Care 2019; 23: 388. doi:10.1186/s13054-019-2662-8
Jauch EC, Cucchiara B, Adeoye O, Meurer W, Brice J, Chan YY, Gentile N, Hazinski MF. Part 11: adult stroke: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care [published correction appears in Circulation. 2011;124:e404]. Circulation. 2010; 122(suppl 3): S818-S828
Ding J, Zhou D, Sui M, Meng R, Chandra A, Han J, Ding Y, Ji X. The effect of normobaric oxygen in patients with acute stroke: a systematic review and meta-analysis. Neurol Res. 2018; 40(6): 433-44.
Araujo de Franca S, Tavares WM, Salinet ASM, Paiva WS, Teixeira MJ. Early tracheostomy in stroke patients: A meta-analysis and comparison with late tracheostomy. Clin Neurol Neurosurg. 2021 Apr; 203: 106554. doi: 10.1016/j.clineuro.2021.106554. Epub 2021 Feb 10. PMID: 33607581
Bennett MH, Weibel S, Wasiak J, Schnabel A, French C, Kranke P. Hyperbaric oxygen therapy for acute ischaemic stroke. Cochrane Database Syst Rev. 2014:CD004954
Heyboer M 3rd, Sharma D, Santiago W, McCulloch N. Hyperbaric oxygen therapy: side effects defined and quantified. Adv Wound Care (New Rochelle). 2017; 6: 210-224.
Bath, PM, Krishnan, K. Interventions for deliberately altering blood pressure in acute stroke. Cochrane Database Syst Rev 2014; 10: CD000039.
Appiah, KO, Minhas, JS, Robinson, TG. Managing high blood pressure during acute ischemic stroke and intracerebral hemorrhage. Curr Opin Neurol 2018; 31: 8-13.
Lee M, Ovbiagele B, Hong KS, Wu YL, Lee JE, Rao NM, Feng W, Saver JL. Effect of blood pressure lowering in early ischemic stroke: meta-analysis. Stroke. 2015; 46: 1883-1889. doi: 10.1161/STROKEAHA.115.009552
Stead LG, Gilmore RM, Vedula KC, Weaver AL, Decker WW, Brown RD Jr. Impact of acute blood pressure variability on ischemic stroke outcome. Neurology. 2006; 66: 1878-1881. doi: 10.1212/01.wnl.0000219628.78513.b5
Potter JF, Robinson TG, Ford GA, Mistri A, James M, Chernova J, Jagger C. Controlling Hypertension and Hypotension Immediately Post-Stroke (CHHIPS): a randomised, placebo-controlled, double-blind pilot trial. Lancet Neurol. 2009; 8: 48-56. doi: 10.1016/S1474- 4422(08)70263-1
He J, ZhangY, XuT, ZhaoQ, WangD, ChenCS, TongW, LiuC, XuT, JuZ, PengY, PengH, LiQ, GengD, ZhangJ, LiD, ZhangF, GuoL, SunY, WangX, CuiY, LiY, MaD, YangG, GaoY, YuanX, BazzanoLA, ChenJ; CATIS Investigators. Effects of immediate blood pressure reduction on death and major disability in patients with acute ischemic stroke: the CATIS randomized clinical trial. JAMA. 2014; 311: 479-489. doi: 10.1001/jama.2013.282543
Sandset, EC, Bath, PM, Boysen, G, et al. The angiotensin-receptor blocker candesartan for treatment of acute stroke (SCAST): a randomised, placebo-controlled, double-blind trial. Lancet 2011; 377: 741-750.
Bath, PM, Woodhouse, L, Scutt, P, et al. ENOS trial investigators. Efficacy of nitric oxide, with or without continuing antihypertensive treatment, for management of high blood pressure in acute stroke (ENOS): a partial-factorial randomised controlled trial. Lancet 2015; 385: 617-628.
European Stroke Organisation (ESO) guidelines on blood pressure management in acute ischaemic stroke and intracerebral haemorrhage. European Stroke Journal 2021; 6(2): X48-L89.
Visvanathan A, Dennis M, Whiteley W. Parenteral fluid regimens for improving functional outcome in people with acute stroke. Cochrane Database Syst Rev. 2015:CD011138.
Wohlfahrt P, Krajcoviechova A, Jozifova M, Mayer O, Vanek J, Filipovsky J, Cifkova R. Low blood pressure during the acute period of ischemic stroke is associated with decreased survival.J Hypertens. 2015; 33: 339-345. doi: 10.1097/HJH.0000000000000414
Bhalla A, Sankaralingam S, Dundas R, Swaminathan R, Wolfe CD, Rudd AG: Influence of raised plasma osmolality on clinical outcome after acute stroke. Stroke 2000; 31: 2043-2048.
Butcher K, Christensen S, Parsons M, De Silva DA, Ebinger M, Levi C, Jeerakathil T, Campbell BC, Barber PA, Bladin C, Fink J, Tress B, Donnan GA, Davis SM; for the EPITHET Investigators. Postthrombolysis blood pressure elevation is associated with hemorrhagic transformation. Stroke. 2010; 41: 72-77.
Perini F, De Boni A, Marcon M, Bolgan I, Pellizzari M, Dionisio LD. Systolic blood pressure contributes to intracerebral haemorrhage after thrombolysis for ischemic stroke. J Neurol Sci. 2010; 10.
Mazya M, Egido JA, Ford GA, Lees KR, Mikulik R, Toni D, Wahlgren N, Ahmed N; for the SITS Investigators. Predicting the risk of symptomatic intracerebral hemorrhage in ischemic stroke treated with intravenous alteplase: safe Implementation of Treatments in Stroke (SITS) symptomatic intracerebral hemorrhage risk score. Stroke. 2012; 43: 1524-1531.
Waltimo T, Haapaniemi E, Surakka IL, Melkas S, Sairanen T, Sibolt G, Tatlisumak T, Strbian D. Post-thrombolytic blood pressure and symptomatic intracerebral hemorrhage. Eur J Neurol. 2016; 23: 1757-1762.
Anderson CS, Huang Y, Lindley RI, Chen X, Arima H, Chen G, Li Q, Billot L, Delcourt C, Bath PM, Broderick JP, Demchuk AM, Donnan GA, Durham AC, Lavados PM, Lee TH, Levi C, Martins SO, Olavarria VV, Pandian JD, Parsons MW, Pontes-Neto OM, Ricci S, Sato S, Sharma VK, Silva F, Song L, Thang NH, Wardlaw JM, Wang JG, Wang X, Woodward M, Chalmers J, Robinson TG; ENCHANTED Investigators and Coordinators.Intensive blood pressure reduction with intravenous thrombolysis therapy for acute ischaemic stroke (ENCHANTED): an international, randomised, open-label, blinded-endpoint, phase 3 trial. Lancet. 2019 Mar 2; 393(10174): 877-888.
Liu K, Yan S, Zhang S, Guo Y, Lou M. Systolic blood pressure variability is associated with severe hemorrhagic transformation in the early stage after thrombolysis. Transl Stroke Res. 2016; 7: 186-191.
Yang P, Song L, Zhang Y, Zhang X, Chen X, Li Y, Sun L, Wan Y, Billot L, Li Q, Ren X, Shen H, Zhang L, Li Z, Xing P, Zhang Y, Zhang P, Hua W, Shen F, Zhou Y, Tian B, Chen W, Han H, Zhang L, Xu C, Li T, Peng Y, Yue X, Chen S, Wen C, Wan S, Yin C, Wei M, Shu H, Nan G, Liu S, Liu W, Cai Y, Sui Y, Chen M, Zhou Y, Zuo Q, Dai D, Zhao R, Li Q, Huang Q, Xu Y, Deng B, Wu T, Lu J, Wang X, Parsons MW, Butcher K, Campbell B, Robinson TG, Goyal M, Dippel D, Roos Y, Majoie C, Wang L, Wang Y, Liu J, Anderson CS; ENCHANTED2/MT Investigators. Intensive blood pressure control after endovascular thrombectomy for acute ischaemic stroke (ENCHANTED2/MT): a multicentre, open-label, blinded-endpoint, randomised controlled trial. Lancet. 2022 Nov 5;400(10363):1585-1596. doi: 10.1016/S0140-6736(22)01882-7. Epub 2022 Oct 28. Erratum in: Lancet. 2022 Dec 3;400(10367):1926. PMID: 36341753.
Jovin TG, Chamorro A, Cobo E, de Miquel MA, Molina CA, Rovira A, San Roman L, Serena J, Abilleira S, Ribo M, Millan M, Urra X, Cardona P, Lopez-Cancio E, Tomasello A, Castano C, Blasco J, Aja L, Dorado L, Quesada H, Rubiera M, Hernandez-Perez M, Goyal M, Demchuk AM, von Kummer R, Gallofre M, Davalos A; REVASCAT Trial Investigators. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015; 372: 2296-2306.
Saver JL, Goyal M, Bonafe A, Diener HC, Levy EI, Pereira VM, Albers GW, Cognard C, Cohen DJ, Hacke W, Jansen O, Jovin TG, Mattle HP, Nogueira RG, Siddiqui AH, Yavagal DR, Baxter BW, Devlin TG, Lopes DK, Reddy VK, du Mesnilde Rochemont R, Singer OC, Jahan R; SWIFT PRIME Investigators. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med. 2015; 372: 2285-2295.
Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, Yassi N, Yan B, Dowling RJ, Parsons MW, Oxley TJ, Wu TY, Brooks M, Simpson MA, Miteff F, Levi CR, Krause M, Harrington TJ, Faulder KC, Steinfort BS, Priglinger M, Ang T, Scroop R, Barber PA, McGuinness B, Wijeratne T, Phan TG, Chong W, Chandra RV, Bladin CF, Badve M, Rice H, de Villiers L, Ma H, Desmond PM, Donnan GA, Davis SM; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015; 372: 1009-1018.
Bracard S, Ducrocq X, Mas JL, Soudant M, Oppenheim C, Moulin T, Guillemin F; THRACE Investigators. Mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRACE): a randomised controlled trial. Lancet Neurol. 2016; 15: 1138-1147.
Berkhemer OA, Fransen PS, Beumer D, vanden Berg LA, Lingsma HF,Yoo AJ, Schonewille WJ, Vos JA, Nederkoorn PJ, Wermer MJ, van Walderveen MA, Staals J, Hofmeijer J, van Oostayen JA, Lycklama a Nijeholt GJ, Boiten J, Brouwer PA, Emmer BJ, deBruijn SF, van Dijk LC, Kappelle LJ, Lo RH, van Dijk EJ, de Vries J, de Kort PL, van Rooij WJ, van den Berg JS, van Hasselt BA, Aerden LA, Dallinga RJ, Visser MC, Bot JC, Vroomen PC, Eshghi O, SchreuderTH, Heijboer RJ, Keizer K, Tielbeek AV, den Hertog HM, Gerrits DG, van den Berg- Vos RM, Karas GB, Steyerberg EW, Flach HZ, Marquering HA, Sprengers ME, JenniskensSF, BeenenLF, vandenBergR, KoudstaalPJ, vanZwamWH, Roos YB, van der Lugt A, van Oostenbrugge RJ, Majoie CB, Dippel DW; MRCLEAN Investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015; 372: 11-20.
Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, Thornton J, Roy D, Jovin TG, Willinsky RA, Sapkota BL, Dowlatshahi D, Frei DF, Kamal NR, Montanera WJ, Poppe AY, Ryckborst KJ, Silver FL, Shuaib A, Tampieri D, Williams D, Bang OY, Baxter BW, Burns PA, Choe H, Heo JH, Holmstedt CA, Jankowitz B, Kelly M, Linares G, Mandzia JL, Shankar J, Sohn SI, Swartz RH, Barber PA, Coutts SB, Smith EE, Morrish WF, Weill A, Subramaniam S, Mitha AP, Wong JH, Lowerison MW, Sajobi TT, Hill MD; ESCAPE Trial Investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015;372:1019-1030.
Bath PM, Krishnan K, Appleton JP. Nitric oxide donors (nitrates), L-arginine, or nitric oxide synthase inhibitors for acute stroke. Cochrane Database Syst Rev. 2017 Apr 21; 4: CD000398;
Bath PM, Krishnan K. Interventions for deliberately altering blood pressure in acute stroke. Cochrane Database Syst Rev. 2014 Oct 28; (10): CD000039
Bath PM. Theophylline, aminophylline, caffeine and analogues for acute ischaemic stroke. Cochrane Database Syst Rev. 2004; (3): CD000211.
Zhang J, Liu J, Li D, Zhang C, Liu M. Calcium antagonists for acute ischemic stroke. Cochrane Database Syst Rev. 2019 Feb 13; 2: CD001928.
Visvanathan A, Dennis M, Whiteley W. Parenteral fluid regimens for improving functional outcome in people with acute stroke. Cochrane Database Syst Rev. 2015:CD011138.
Mullen MT, Parthasarathy AB, Zandieh A, Baker WB, Mesquita RC, Loomis C, Torres J, Guo W, Favilla CG, Messé SR, Yodh AG, Detre JA, Kasner SE. Cerebral Blood Flow Response During Bolus Normal Saline Infusion After Ischemic Stroke. J Stroke Cerebrovasc Dis. 2019 Nov; 28(11): 104294.
Bhalla A, Wolfe CD, Rudd AG. Management of acute physiological parameters after stroke. QJM. 2001 Mar; 94(3): 167-72.
Dharmasaroja PA. Fluid Intake Related to Brain Edema in Acute Middle Cerebral Artery Infarction. Transl Stroke Res. 2016 Feb; 7(1): 49-53.
Shackford SR, Zhuang J, Schmoker J. Intravenous fluid tonicity: effect on intracranial pressure, cerebral blood flow, and cerebral oxygen delivery in focal brain injury. J Neurosurg. 1992; 76(1): 91-8.
van der Jagt, M. Fluid management of the neurological patient: a concise review. Crit Care 2016; 20: 126. Doi: 10.1186/s13054-016-1309-2
Chang TS, Jensen MB. Haemodilution for acute ischaemic stroke. Cochrane Database of Systematic Reviews. 2014; 8: CD000103. DOI:10.1002/14651858.CD000103.pub2.
Ginsberg MD, Palesch YY, Hill MD, Martin RH, Moy CS, Barsan WG, Waldman BD, Tamariz D, Ryckborst KJ; ALIAS and Neurological Emergencies Treatment Trials (NETT) Investigators. High-dose albumin treatment for acute ischaemic stroke (ALIAS) Part 2: a randomised, double-blind, phase 3, placebo-controlled trial. Lancet Neurol. 2013 Nov;12(11):1049-58. doi: 10.1016/S1474-4422(13)70223-0. Epub 2013 Sep 27. PMID: 24076337; PMCID: PMC3929943.
Middleton, S, McElduff, P, Ward, J. Implementation of evidence-based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): A cluster randomised controlled trial. Lancet 2011; 378: 1699-706.
Middleton, S, Drury, P, Levi, CR. What processes of clinical care are associated with 90-day survival and independence? Results from the quality in acute stroke care QASC trial. Int J Stroke 2012; 7: 25.
Hajat C, Hajat S, Sharma P. Effects of poststroke pyrexia on stroke outcome : a metaanalysis of studies in patients. Stroke. 2000 Feb; 31(2): 410-4.
Prasad K, Krishnan PR. Fever is associated with doubling of odds of short-term mortality in ischemic stroke: an updated meta-analysis.Acta Neurol Scand 2010; 122: 404-8.
Azzimondi G, Bassein L, Nonino F et al. Fever in acute stroke worsens prognosis. A prospective study. Stroke 1995; 26: 2040-3.
Saxena M, Young P, Pilcher D, Bailey M, Harrison D, Bellomo R, Finfer S, Beasley R, Hyam J, Menon D, Rowan K, Myburgh J. Early temperature and mortality in critically ill patients with acute neurological diseases: trauma and stroke differ from infection. Intensive Care Med. 2015; 41: 823-832.
Drury P, Levi C,McInnes E et al.Management of fever, hyperglycemia, and swallowing dysfunction following hospital admission for acute stroke in New South Wales, Australia. Int J Stroke 2014; 9: 23-3.
Castillo J, Davalos A, Marrugat J, Noya M. Timing for fever-related brain damage in acute ischemic stroke. Stroke 1998; 29: 2455-60.
Middleton, S, McElduff, P, Ward, J. Implementation of evidence-based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): A cluster randomised controlled trial. Lancet 2011; 378: 1699-706.
Saxena M, Young P, Pilcher D, Bailey M, Harrison D, Bellomo R, Finfer S, Beasley R, Hyam J, Menon D, Rowan K, Myburgh J. Early temperature and mortality in critically ill patients with acute neurological diseases: trauma and stroke differ from infection. Intensive Care Med. 2015; 41: 823-832.
Rincon F, Hunter K, Schorr C, Dellinger RP, Zanotti-Cavazzoni S. The epidemiology of spontaneous fever and hypothermia on admission of brain injury patients to intensive care units: a multicenter cohort study. J Neurosurg. 2014 Oct; 121(4): 950-60.
Niven DJ, Laupland KB. Pyrexia: aetiology in the ICU. Crit Care. 2016 Sep 1; 20: 247.
Westendorp WF, Vermeij JD, Zock E, Hooijenga IJ, Kruyt ND, Bosboom HJ, Kwa VI, Weisfelt M, Remmers MJ, ten Houten R, Schreuder AH, Vermeer SE, van Dijk EJ, Dippel DW, Dijkgraaf MG, Spanjaard L, Vermeulen M, van der Poll T, Prins JM, Vermeij FH, Roos YB, Kleyweg RP, Kerkhoff H, Brouwer MC, Zwinderman AH, van de Beek D, Nederkoorn PJ; PASS investigators. The Preventive Antibiotics in Stroke Study (PASS): a pragmatic randomised open-label masked endpoint clinical trial. Lancet. 2015 Apr 18;385(9977):1519-26.
Vermeij JD, Westendorp WF, Dippel DW, van de Beek D, Nederkoorn PJ. Antibiotic therapy for preventing infections in people with acute stroke. Cochrane Database Syst Rev. 2018 Jan 22;1:CD008530.
Liu L, Xiong XY, Zhang Q, Fan XT, Yang QW. The Efficacy of Prophylactic Antibiotics on Post-Stroke Infections: An Updated Systematic Review and Meta-Analysis. Sci Rep. 2016 Nov 14;6:36656 .
Lyden P, Hemmen T, Grotta J, Rapp K, Ernstrom K, Rzesiewicz T, Parker S, Concha M, Hussain S, Agarwal S, Meyer B, Jurf J, Altafullah I, Raman R. Results of the ICTuS 2 Trial (Intravascular Cooling in the Treatment of Stroke 2). Stroke. 2016;47:2888-2895.
Geurts M, Petersson J, Brizzi M, Olsson-Hau S, Luijckx GJ, Algra A, Dippel DW, Kappelle LJ, van der Worp HB. COOLIST (Cooling for Ischemic Stroke Trial): a multicenter, open, randomized, phase II, clinical trial. Stroke. 2017;48:219-221.
van der Worp, H. B., Macleod, M. R., Bath, P. M., Bathula, R., Christensen, H., Colam, B., Schwab, S. (2019). Therapeutic hypothermia for acute ischaemic stroke. Results of a European multicentre, randomised, phase III clinical trial. European Stroke Journal, 4(3), 254-262
Piironen K, Putaala J, Rosso C, et al. Glucose and acute stroke: evidence for an interlude. Stroke 2012; 43:898-902.
Zuurbier SM, Hiltunen S, Tatlisumak T, et al. Admission hyperglycemia and clinical outcome in cerebral venous thrombosis. Stroke 2016; 47: 390-396;
Johnston KC, Bruno A, Barrett K, et al. Stroke hyperglycemia insulin net- work effort (SHINE) trial primary results. International Stroke Conference 2019. Available at: https:// nett.umich.edu/sites /defau lt/files /docs/shine _isc_2019.final .pdf. Accessed 16 Apr 2019
Fuentes, B., Ntaios, G., Putaala, J., Thomas, B., Turc, G., & Dez-Tejedor, E. European Stroke Organisation (ESO) guidelines on glycaemia management in acute stroke. European Stroke Journal 2018; 3 (1): 5-21.
Gentile NT, Seftchick MW, Huynh T, Kruus LK, Gaughan J. Decreased mortality by normalizing blood glucose after acute ischemic stroke. Acad Emerg Med. 2006; 13: 174-180.
Baird TA, Parsons MW, Phanh T, Butcher KS, Desmond PM, Tress BM, Colman PG, Chambers BR, Davis SM. Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome. Stroke. 2003; 34: 2208-2214.
Ntaios G, Egli M, Faouzi M, Michel P. J-shaped association between serum glucose and functional outcome in acute ischemic stroke. Stroke. 2010 Oct; 41(10): 2366-70.
Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. 2019 Mar;50(3):e51-e96. doi: 10.1161/STR.0000000000000183. PMID: 30686119
Kim JT, Liebeskind DS, Jahan R, Menon BK, Goyal M, Nogueira RG, Pereira VM, Gralla J, Saver JL. Impact of hyperglycemia according to the collateral status on outcomes in mechanical thrombectomy. Stroke 2018; 49: 2706-271.
Singer P, Blaser AR, Berger MM, Alhazzani W, Calder PC, Casaer MP, Hiesmayr M, Mayer K, Montejo JC, Pichard C, Preiser JC, van Zanten ARH, Oczkowski S, Szczeklik W, Bischoff SC. ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr. 2019 Feb; 38(1): 48-79. doi: 10.1016/j.clnu.2018.08.037. Epub 2018 Sep 29.
Dennis M, Lewis S, Cranswick G, Forbes J; FOOD Trial Collaboration. FOOD: a multicentre randomised trial evaluating feeding policies in patients admitted to hospital with a recent stroke. Health Technol Assess. 2006;10:iii-iv, ix.
Geeganage C, Beavan J, Ellender S, Bath PM. Interventions for dysphagia and nutritional support in acute and subacute stroke. Cochrane Database Syst Rev. 2012; 10: CD000323.
Zusman O, Bendavid I, Kagan I, Theilla M, Cohen J, Singer P. Early administration of protein in critically ill patients: a large retrospective cohort study. Ann Intensive Care 2018. submitted for publication.
KoekkoekWACK, van Setten CCH, Olthof LE, Kars JCN, van Zanten ARH. Timing of PROTein INtake and clinical outcomes of adult critically ill patients on prolonged mechanical VENTilation: the PROTINVENT retrospective study. Clin Nutr 2018. doi: 10.1016/j.clnu.2018.02.012
Elke G, van Zanten ARH, Lemieux M, McCall M, Jeejeebhoy KN, Kott M, et al. Enteral versus parenteral nutrition in critically ill patients: an updated systematic review and meta-analysis of randomized controlled trials. Crit Care 2016; 20: 117.
Middleton S, Mc Elduff P, Ward J et al. Implementation of evidence based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): A cluster randomized controlled trial. Lancet 2011; 378: 1699-706.
Miles A, Zeng IS, McLauchlan H, Huckabee ML. Cough reflex testing in dysphagia following stroke: a randomized controlled trial. J Clin Med Res. 2013; 5: 222-233.
Joundi RA, Martino R, Saposnik G, Giannakeas V, Fang J, Kapral MK. Predictors and outcomes of dysphagia screening after acute ischemic stroke. Stroke. 2017; 48: 900-906
Sorensen RT, Rasmussen RS, Overgaard K, Lerche A, Johansen AM, Lindhardt T. Dysphagia screening and intensified oral hygiene reduce pneumonia after stroke. J Neurosci Nurs. 2013; 45: 139-146.
Brady M, Furlanetto D, Hunter RV, Lewis S, Milne V. Staff-led interventions for improving oral hygiene in patients following stroke. Cochrane Database Syst Rev. 2006: CD003864.
Wagner C, Marchina S, Deveau JA, Frayne C, Sulmonte K, Kumar S. Risk of stroke-associated pneumonia and oral hygiene. Cerebrovasc Dis. 2016; 41: 35-39.
Schuetz P, Sulo S, Walzer S, Vollmer L, Stanga Z, Gomes F, et al. Economic evaluation of individualized nutritional support in medical inpatients: secondary analysis of the EFFORT trial. Clin Nutr 2020;39:3361-8
Schuetz P, Fehr R, Baechli V, Geiser M, Deiss M, Gomes F, et al. Individualised nutritional support in medical inpatients at nutritional risk: a randomised clinical trial. Lancet 2019;393:2312-21
Dziewas R, Michou E, Trapl-Grundschober M, Lal A, Arsava EM, Bath PM, Clavé P, Glahn J, Hamdy S, Pownall S, Schindler A, Walshe M, Wirth R, Wright D, Verin E. European Stroke Organisation and European Society for Swallowing Disorders guideline for the diagnosis and treatment of post-stroke dysphagia. Eur Stroke J. 2021 Sep;6(3):LXXXIX-CXV. doi: 10.1177/23969873211039721. Epub 2021 Oct 13. PMID: 34746431; PMCID: PMC8564153
Hadde E. K. et al. The safety and efficacy of xanthan gum-based thickeners and their effect in modifying bolus rheology in the therapeutic medical management of dysphagia // Food Hydrocolloids for Health. – 2021. – Vol. 1. – P. 100038.
Bolivar-Prados M, Hayakawa Y, Tomsen N, Arreola V, Nascimento W, Riera S, Kawakami S, Miyaji K, Takeda Y, Kayashita J, Clavé P. Shear-Viscosity-Dependent Effect of a Gum-Based Thickening Product on the Safety of Swallowing in Older Patients with Severe Oropharyngeal Dysphagia. Nutrients. 2023 Jul 24;15(14):3279. doi: 10.3390/nu15143279. PMID: 37513697; PMCID: PMC10384341
Wunderle C, Gomes F, Schuetz P, Stumpf F, Austin P, Ballesteros-Pomar MD, Cederholm T, Fletcher J, Laviano A, Norman K, Poulia KA, Schneider SM, Stanga Z, Bischoff SC. ESPEN guideline on nutritional support for polymorbid medical inpatients. Clin Nutr. 2023 Sep;42(9):1545-1568. doi: 10.1016/j.clnu.2023.06.023. Epub 2023 Jul 8. PMID: 37478809
Sandercock PA, Leong TS. Low-molecular-weight heparins or heparinoids versus standard unfractionated heparin for acute ischaemic stroke. Cochrane Database Syst Rev. 2017 Apr 4; 4(4): CD000119.
CLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration, Dennis M, Sandercock P, Reid J, Graham C, Forbes J, Murray G. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicentre randomised controlled trial. Lancet. 2013 Aug 10; 382 (9891): 516-24.
Dennis M, Caso V, Kappelle LJ, Pavlovic A, Sandercock P; European Stroke Organisation. European Stroke Organisation (ESO) guidelines for prophylaxis for venous thromboembolism in immobile patients with acute ischaemic stroke. Eur Stroke J. 2016 Mar; 1(1): 6-19. doi: 10.1177/2396987316628384
Dennis M, Mardi N, Graham C, et al. for the CLOTS, trials collaboration. The timing, extent, progression and regression of DVT in immobile stroke patients: observational data from the CLOTS randomized trials. J Thromb Haem 2011; 9: 2193-2200.
Kelly J, Rudd A, Lewis RR, et al. Venous thromboembolism after acute ischemic stroke: a prospective study using magnetic resonance direct thrombus imaging. Stroke 2004; 35: 2320-2325.
Kelly J, Rudd A, Lewis R, Hunt BJ. Venous thromboembolism after acute stroke. Stroke 2001; 32: 262.
Dennis M, Sandercock PA, Reid J, Graham C, Murray G, Venables G, Rudd A, Bowler G. Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS trial 1): a multicentre, randomised controlled trial. Lancet. 2009 Jun 6; 373(9679): 1958-65.
Decousus H, Tapson VF, et al. Factors at admission associated with bleeding risk in medical patients: findings from the IMPROVE investigators. Chest. 2011; 139: 69-79.
Rosenberg DJ, Press A, et al. External validation of the IMPROVE Bleeding Risk Assessment Model in medical patients. Thromb Haemost. 2016; 116: 530-6
Muscari A, Faccioli L, Lega MV, Lorusso A, Masetti M, Pastore Trossello M, Puddu GM, Spinardi L, Zoli M. Predicting hemorrhagic transformation and its timing from maximum cerebral lesion diameter in nonlacunar ischemic strokes. Brain Behav. 2020 Jan; 10(1): e01497.
Best JG, Ambler G, Wilson D, Lee KJ, Lim JS et al.; Microbleeds International Collaborative Network. Development of imaging-based risk scores for prediction of intracranial haemorrhage and ischaemic stroke in patients taking antithrombotic therapy after ischaemic stroke or transient ischaemic attack: a pooled analysis of individual patient data from cohort studies. Lancet Neurol. 2021 Apr; 20(4): 294-303.
Li L, Poon MTC, Samarasekera NE, Perry LA, Moullaali TJ, Rodrigues MA, Loan JJM, Stephen J, Lerpiniere C, Tuna MA, Gutnikov SA, Kuker W, Silver LE, Al-Shahi Salman R, Rothwell PM. Risks of recurrent stroke and all serious vascular events after spontaneous intracerebral haemorrhage: pooled analyses of two population-based studies. Lancet Neurol. 2021 Jun; 20(6): 437-447.
Prasad BK, Banerjee AK, Howard H. Incidence of deep vein thrombosis and the effect of pneumatic compression of the calf in elderly hemiplegics. Age Ageing. 1982 Feb; 11(1): 42-4.
Spinelli M, Corea F, Bignamini V, et al. Early vital and functional outcome of acute ischaemic stroke patients: influence of deep vein thrombosis prevention with pneumatic compression devices. J Neurol 2006; 253: 135.
Sandercock PA, Leong TS. Low-molecular-weight heparins or heparinoids versus standard unfractionated heparin for acute ischaemic stroke. Cochrane Database Syst Rev 2017; 4:CD000119.
Shorr AF, Jackson WL, Sherner JH, Moores LK. Differences between low-molecular- weight and unfractionated heparin for venous thromboembolism prevention following ischemic stroke: a metaanalysis. Chest 2008; 133: 149.
Paciaroni M, Agnelli G, Venti M, et al. Efficacy and safety of anticoagulants in the prevention of venous thromboembolism in patients with acute cerebral hemorrhage: a metaanalysis of controlled studies. J Thromb Haemost 2011; 9: 893.
Naccarato M, Chiodo Grandi F, Dennis M, Sandercock PAG. Physical methods for preventing deep vein thrombosis in stroke. Cochrane Database of Systematic Reviews 2010, Issue 8. Art. No.: CD001922.
Powers WJ, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Kidwell CS, Leslie-Mazwi TM, Ovbiagele B, Scott PA, Sheth KN, Southerland AM, Summers DV, Tirschwell DL. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec; 50(12): e344-e418. doi: 10.1161/STR.0000000000000211
Muir KW, Watt A, Baxter G, Grosset DG, Lees KR. Randomized trial of graded compression stockings for prevention of deep-vein thrombosis after acute stroke. QJM. 2000 Jun; 93(6): 359-64. doi: 10.1093/qjmed/93.6.359
Neurogenic lower urinary tract dysfunction: clinical guidelines. Moscow, 2020.
Neurogenic lower urinary tract dysfunction: European Association of Urology (EAU) guidelines. Moscow, 2011; 67.
European-Asian guidelines for the management of patients with catheter-associated urinary tract infections and the prevention of catheter-associated infections. Moscow, 2008; 83-91.
European Association of Urology (EAU) and Asian Association of Urology (UAA) Guidelines // Clinical Microbiology and Antimicrobial Chemotherapy. Moscow, 2008; 10 (3).
Pressure Ulcer Prevention and Treatment Protocol: Health Care Protocol. Bloomington, MN; Institute for Clinical Systems Improvement (ICSI): 3rd edition. 2012 January.
van der Worp HB, Hofmeijer J, Jüttler E, Lal A, Michel P, Santalucia P, Schönenberger S, Steiner T, Thomalla G. European Stroke Organisation (ESO) guidelines on the management of space-occupying brain infarction. Eur Stroke J. 2021 Jun; 6(2): XC-CX. doi: 10.1177/23969873211014112.
Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. “Malignant” middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol. 1996; 53: 309-315.
Ropper AH, Shafran B. Brain edema after stroke: clinical syndrome and intracranial pressure. Arch Neurol. 1984; 41: 26-29.
Wijdicks EF, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clin Proc. 1998; 73: 829-836.
Malm J, Bergenheim AT, Enblad P, Hardemark HG, Koskinen LO, Naredi S, Nordstrom CH, Norrving B, Uhlin J, Lindgren A. The Swedish Malignant Middle Cerebral Artery Infarction Study: long-term results from a prospective study of hemicraniectomy combined with standardized neurointensive care. Acta Neurol Scand. 2006; 113: 25-30.
Bardutzky J, Schwab S. Antiedema therapy in ischemic stroke. Stroke. 2007; 38: 3084-3094.
Schizodimos, Theodoros et al. An overview of management of intracranial hypertension in the intensive care unit. Journal of anesthesia 2020; 34(5): 741-757.
Schwab S, Steiner T, Aschoff A, Schwarz S, Steiner HH, Jansen O, Hacke W. Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke. 1998; 29: 1888-1893.
Reinink, H, Jüttler, E, Hacke, W, et al. Surgical decompression for space-occupying hemispheric infarction: a systematic review and individual patient Meta-analysis of randomized clinical trials. JAMA Neurol 2021; 78: 208-216.
Vahedi, K, Hofmeijer, J, Juettler, E, et al. Early decompressive surgery in malignant Middle cerebral artery infarction: a pooled analysis of three randomised controlled trials. Lancet Neurol 2007; 6: 215-222.
Diringer MN, Scalfani MT, Zazulia AR, Videen TO, Dhar R. Cerebral hemodynamic and metabolic effects of equi-osmolar doses mannitol and 23.4% saline in patients with edema following large ischemic stroke.Neurocrit Care. 2011; 14: 11-17.
Schwarz S, Schwab S, Bertram M, Aschoff A, Hacke W. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. Stroke. 1998; 29: 1550-1555.
Holden DN, Yung FH, Entezami P. Hypertonic saline buffered with sodium acetate for intracranial pressure management. Clin Neurol Neurosurg. 2021 Feb; 201: 106435. doi: 10.1016/j.clineuro.2020.106435. Epub 2020 Dec 15. PMID: 33373834;
Chen H, Song Z, Dennis JA. Hypertonic saline versus other intracranial pressure-lowering agents for people with acute traumatic brain injury. Cochrane Database Syst Rev. 2020 Jan 17; 1(1): CD010904. doi: 10.1002/14651858.CD010904.pub3. PMID: 31978260; PMCID: PMC6984412.
Badenes R, Hutton B, Citerio G, Robba C, Aguilar G, Alonso-Arroyo A, Taccone FS, Tornero C, Catalá-López F. Hyperosmolar therapy for acute brain injury: study protocol for an umbrella review of meta-analyses and an evidence mapping. BMJ Open. 2020 Feb 6; 10(2): e033913. doi: 10.1136/bmjopen-2019-033913.
Curley G, Kavanagh BP, Laffey JG. Hypocapnia and the injured brain: more harm than benefit. Crit Care Med. 2010; 38: 1348-1359.
Muizelaar, JP, Marmarou, A, Ward, JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991; 75: 731.
Wan YH, Nie C, Wang HL, Huang CY. Therapeutic hypothermia (different depths, durations, and rewarming speeds) for acute ischemic stroke: a meta-analysis. J Stroke Cerebrovasc Dis. 2014; 23: 2736-2747.
Quizilbash N, Lewington SL, Lopez-arietta J. Corticosteroids for acute ischemic stroke. Cochrane library. Oxford (United Kingdom): Update software 2001; 1.
Wardlaw JM, Murray V, Berge E, del Zoppo G, Sandercock P, Lindley RL, Cohen G. Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis. Lancet. 2012 Jun 23; 379(9834): 2364-72.
Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014: CD000213.
Hacke W, Donnan G, Fieschi C, Kaste M, von Kummer R, Broderick JP, Brott T, Frankel M, Grotta JC, Haley EC Jr, Kwiatkowski T, Levine SR, Lewandowski C, Lu M, Lyden P, Marler JR, Patel S, Tilley BC, Albers G, Bluhmki E, Wilhelm M, Hamilton S; ATLANTIS Trials Investigators; ECASS Trials Investigators; NINDS rt-PA Study Group Investigators. Association of outcome with early stroke treatment: pooled analysis of ATLANTIS, ECASS, and NINDS rtPA stroke trials. Lancet. 2004; 363: 768–774. doi: 10.1016/S0140-6736(04)15692-4
Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E, Brott T, Cohen G, Davis S, Donnan G, Grotta J, Howard G, Kaste M, Koga M, von Kummer R, Lansberg M, Lindley RI, Murray G, Olivot JM, Parsons M, Tilley B, Toni D, Toyoda K, Wahlgren N, Wardlaw J, Whiteley W, del Zoppo GJ, Baigent C, Sandercock P, Hacke W; Stroke Thrombolysis Trialists" Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29; 384 (9958): 1929-35. doi: 10.1016/S0140-6736(14)60584-5
Eugene I Gusev, Mikhail Yu Martynov, Alexey A Nikonov, Nikolay A Shamalov, Michail P Semenov, Eugene A Gerasimets, Elena B Yarovaya, Andrey M Semenov, Alexander I Archakov, Sergey S Markin, and the FRIDA Study Group* Non-immunogenic recombinant staphylokinase versus alteplase for patients with acute ischaemic stroke 4·5 h after symptom onset in Russia (FRIDA): a randomised, open label, multicentre, parallel-group, non-inferiority trial. Lancet Neurol 2021; 20: 721–28
Campbell BCV, Ma H, Ringleb PA, Parsons MW, Churilov L, Bendszus M, Levi CR, Hsu C, Kleinig TJ, Fatar M, Leys D, Molina C, Wijeratne T, Curtze S, Dewey HM, Barber PA, Butcher KS, De Silva DA, Bladin CF, Yassi N, Pfaff JAR, Sharma G, Bivard A, Desmond PM, Schwab S, Schellinger PD, Yan B, Mitchell PJ, Serena J, Toni D, Thijs V, Hacke W, Davis SM, Donnan GA; EXTEND, ECASS-4, and EPITHET Investigators. Extending thrombolysis to 4·5-9 h and wake-up stroke using perfusion imaging: a systematic review and meta-analysis of individual patient data. Lancet. 2019 Jul 13; 394 (10193): 139-147.
Ma H, Campbell BCV, Parsons MW, Churilov L, Levi CR, Hsu C, Kleinig TJ, Wijeratne T, Curtze S, Dewey HM, Miteff F, Tsai CH, Lee JT, Phan TG, Mahant N, Sun MC, Krause M, Sturm J, Grimley R, Chen CH, Hu CJ, Wong AA, Field D, Sun Y, Barber PA, Sabet A, Jannes J, Jeng JS, Clissold B, Markus R, Lin CH, Lien LM, Bladin CF, Christensen S, Yassi N, Sharma G, Bivard A, Desmond PM, Yan B, Mitchell PJ, Thijs V, Carey L, Meretoja A, Davis SM, Donnan GA; EXTEND Investigators. Thrombolysis Guided by Perfusion Imaging up to 9 Hours after Onset of Stroke. N Engl J Med. 2019 May 9; 380 (19): 1795-1803.
Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E, Brott T, Cohen G, Davis S, Donnan G, Grotta J, Howard G, Kaste M, Koga M, von Kummer R, Lansberg M, Lindley RI, Murray G, Olivot JM, Parsons M, Tilley B, Toni D, Toyoda K, Wahlgren N, Wardlaw J, Whiteley W, del Zoppo GJ, Baigent C, Sandercock P, Hacke W; Stroke Thrombolysis Trialists" Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29; 384(9958): 1929-35.
Lees KR, Emberson J, Blackwell L, Bluhmki E, Davis SM, Donnan GA, Grotta JC, Kaste M, von Kummer R, Lansberg MG, Lindley RI, Lyden P, Murray GD, Sandercock PA, Toni D, Toyoda K, Wardlaw JM, Whiteley WN, Baigent C, Hacke W, Howard G; Stroke Thrombolysis Trialists’ Collaborators Group. Effects of Alteplase for Acute Stroke on the Distribution of Functional Outcomes: A Pooled Analysis of 9 Trials. Stroke. 2016 Sep;47(9):2373-9.
Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014 Jul 29; 2014(7): CD000213.
IST-3 collaborative group, Sandercock P, Wardlaw JM, Lindley RI, Dennis M, Cohen G, Murray G, Innes K, Venables G, Czlonkowska A, Kobayashi A, Ricci S, Murray V, Berge E, Slot KB, Hankey GJ, Correia M, Peeters A, Matz K, Lyrer P, Gubitz G, Phillips SJ, Arauz A. The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the third international stroke trial [IST-3]): a randomised controlled trial. Lancet. 2012 Jun 23; 379(9834): 2352-63.
Clark WM, Albers GW, Madden KP, Hamilton S. The rtPA (alteplase) 0- to 6-hour acute stroke trial, part A (A0276g) : results of a double-blind, placebo-controlled, multicenter study. Thromblytic therapy in acute ischemic stroke study investigators. Stroke. 2000 Apr; 31(4): 811-6.
Clark WM, Wissman S, Albers GW, Jhamandas JH, Madden KP, Hamilton S. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset. The ATLANTIS Study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA. 1999 Dec 1;282(21):2019-26.
Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von Kummer R, Boysen G, Bluhmki E, Höxter G, Mahagne MH, et al. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS). JAMA. 1995 Oct 4; 274(13): 1017-25.
Hacke W, Kaste M, Fieschi C, von Kummer R, Davalos A, Meier D, Larrue V, Bluhmki E, Davis S, Donnan G, Schneider D, Diez-Tejedor E, Trouillas P. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Second European-Australasian Acute Stroke Study Investigators. Lancet. 1998 Oct 17; 352(9136): 1245-51.
Davis SM, Donnan GA, Parsons MW, Levi C, Butcher KS, Peeters A, Barber PA, Bladin C, De Silva DA, Byrnes G, Chalk JB, Fink JN, Kimber TE, Schultz D, Hand PJ, Frayne J, Hankey G, Muir K, Gerraty R, Tress BM, Desmond PM; EPITHET investigators. Effects of alteplase beyond 3 h after stroke in the Echoplanar Imaging Thrombolytic Evaluation Trial (EPITHET): a placebo-controlled randomised trial. Lancet Neurol. 2008 Apr; 7(4): 299-309.
Lees KR, Emberson J, Blackwell L, Bluhmki E, Davis SM, Donnan GA, Grotta JC, Kaste M, von Kummer R, Lansberg MG, Lindley RI, Lyden P, Murray GD, Sandercock PA, Toni D, Toyoda K, Wardlaw JM, Whiteley WN, Baigent C, Hacke W, Howard G; Stroke Thrombolysis Trialists’ Collaborators Group. Effects of Alteplase for Acute Stroke on the Distribution of Functional Outcomes: A Pooled Analysis of 9 Trials. Stroke. 2016 Sep; 47(9): 2373-9.
Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E, Brott T, Cohen G, Davis S, Donnan G, Grotta J, Howard G, Kaste M, Koga M, von Kummer R, Lansberg M, Lindley RI, Murray G, Olivot JM, Parsons M, Tilley B, Toni D, Toyoda K, Wahlgren N, Wardlaw J, Whiteley W, del Zoppo GJ, Baigent C, Sandercock P, Hacke W; Stroke Thrombolysis Trialists" Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29; 384(9958): 1929-35.
Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014 Jul 29; 2014(7): CD000213.
Thomalla G, Simonsen CZ, Boutitie F, Andersen G, Berthezene Y, Cheng B, Cheripelli B, Cho TH, Fazekas F, Fiehler J, Ford I, Galinovic I, Gellissen S, Golsari A, Gregori J, Günther M, Guibernau J, Häusler KG, Hennerici M, Kemmling A, Marstrand J, Modrau B, Neeb L, Perez de la Ossa N, Puig J, Ringleb P, Roy P, Scheel E, Schonewille W, Serena J, Sunaert S, Villringer K, Wouters A, Thijs V, Ebinger M, Endres M, Fiebach JB, Lemmens R, Muir KW, Nighoghossian N, Pedraza S, Gerloff C; WAKE-UP Investigators. MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset. N Engl J Med. 2018 Aug 16; 379(7): 611-622.
Thomalla G, Boutitie F, Ma H, Koga M, Ringleb P, Schwamm LH, Wu O, Bendszus M, Bladin CF, Campbell BCV, Cheng B, Churilov L, Ebinger M, Endres M, Fiebach JB, Fukuda-Doi M, Inoue M, Kleinig TJ, Latour LL, Lemmens R, Levi CR, Leys D, Miwa K, Molina CA, Muir KW, Nighoghossian N, Parsons MW, Pedraza S, Schellinger PD, Schwab S, Simonsen CZ, Song SS, Thijs V, Toni D, Hsu CY, Wahlgren N, Yamamoto H, Yassi N, Yoshimura S, Warach S, Hacke W, Toyoda K, Donnan GA, Davis SM, Gerloff C; Evaluation of unknown Onset Stroke thrombolysis trials (EOS) investigators. Intravenous alteplase for stroke with unknown time of onset guided by advanced imaging: systematic review and meta-analysis of individual patient data. Lancet. 2020 Nov 14; 396(10262): 1574-1584.
Thomalla G, Cheng B, Ebinger M, Hao Q, Tourdias T, Wu O, Kim JS, Breuer L, Singer OC, Warach S, Christensen S, Treszl A, Forkert ND, Galinovic I, Rosenkranz M, Engelhorn T, Köhrmann M, Endres M, Kang DW, Dousset V, Sorensen AG, Liebeskind DS, Fiebach JB, Fiehler J, Gerloff C; STIR and VISTA Imaging Investigators. DWI-FLAIR mismatch for the identification of patients with acute ischaemic stroke within 4·5 h of symptom onset (PRE-FLAIR): a multicentre observational study. Lancet Neurol. 2011 Nov; 10(11): 978-86.
Koga M, Yamamoto H, Inoue M, Asakura K, Aoki J, Hamasaki T, Kanzawa T, Kondo R, Ohtaki M, Itabashi R, Kamiyama K, Iwama T, Nakase T, Yakushiji Y, Igarashi S, Nagakane Y, Takizawa S, Okada Y, Doijiri R, Tsujino A, Ito Y, Ohnishi H, Inoue T, Takagi Y, Hasegawa Y, Shiokawa Y, Sakai N, Osaki M, Uesaka Y, Yoshimura S, Urabe T, Ueda T, Ihara M, Kitazono T, Sasaki M, Oita A, Yoshimura S, Fukuda-Doi M, Miwa K, Kimura K, Minematsu K, Toyoda K; THAWS Trial Investigators. Thrombolysis With Alteplase at 0.6 mg/kg for Stroke With Unknown Time of Onset: A Randomized Controlled Trial. Stroke. 2020 May; 51(5): 1530-1538.
Ringleb P, Bendszus M, Bluhmki E, Donnan G, Eschenfelder C, Fatar M, Kessler C, Molina C, Leys D, Muddegowda G, Poli S, Schellinger P, Schwab S, Serena J, Toni D, Wahlgren N, Hacke W; ECASS-4 study group. Extending the time window for intravenous thrombolysis in acute ischemic stroke using magnetic resonance imaging-based patient selection. Int J Stroke. 2019 Jul; 14(5): 483-490.
Ma H, Campbell BCV, Parsons MW, Churilov L, Levi CR, Hsu C, Kleinig TJ, Wijeratne T, Curtze S, Dewey HM, Miteff F, Tsai CH, Lee JT, Phan TG, Mahant N, Sun MC, Krause M, Sturm J, Grimley R, Chen CH, Hu CJ, Wong AA, Field D, Sun Y, Barber PA, Sabet A, Jannes J, Jeng JS, Clissold B, Markus R, Lin CH, Lien LM, Bladin CF, Christensen S, Yassi N, Sharma G, Bivard A, Desmond PM, Yan B, Mitchell PJ, Thijs V, Carey L, Meretoja A, Davis SM, Donnan GA; EXTEND Investigators. Thrombolysis Guided by Perfusion Imaging up to 9 Hours after Onset of Stroke. N Engl J Med. 2019 May 9; 380(19): 1795-1803. doi: 10.1056/NEJMoa1813046.
Anderson CS, Robinson T, Lindley RI, Arima H, Lavados PM, Lee TH, Broderick JP, Chen X, Chen G, Sharma VK, Kim JS, Thang NH, Cao Y, Parsons MW, Levi C, Huang Y, Olavarría VV, Demchuk AM, Bath PM, Donnan GA, Martins S, Pontes-Neto OM, Silva F, Ricci S, Roffe C, Pandian J, Billot L, Woodward M, Li Q, Wang X, Wang J, Chalmers J; ENCHANTED Investigators and Coordinators. Low-Dose versus Standard-Dose Intravenous Alteplase in Acute Ischemic Stroke. N Engl J Med. 2016 Jun 16; 374(24): 2313-23.
Wang X, Robinson TG, Lee TH, Li Q, Arima H, Bath PM, Billot L, Broderick J, Demchuk AM, Donnan G, Kim JS, Lavados P, Lindley RI, Martins SO, Olavarria VV, Pandian JD, Parsons MW, Pontes-Neto OM, Ricci S, Sharma VK, Thang NH, Wang JG, Woodward M, Anderson CS, Chalmers J; Enhanced Control of Hypertension and Thrombolysis Stroke Study (ENCHANTED) Investigators. Low-Dose vs Standard-Dose Alteplase for Patients With Acute Ischemic Stroke: Secondary Analysis of the ENCHANTED Randomized Clinical Trial. JAMA Neurol. 2017 Nov 1; 74(11): 1328-1335.
Carr SJ, Wang X, Olavarria VV, Lavados PM, Rodriguez JA, Kim JS, Lee TH, Lindley RI, Pontes-Neto OM, Ricci S, Sato S, Sharma VK, Woodward M, Chalmers J, Anderson CS, Robinson TG; ENCHANTED Investigators. Influence of Renal Impairment on Outcome for Thrombolysis-Treated Acute Ischemic Stroke: ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study) Post Hoc Analysis. Stroke. 2017 Sep; 48(9): 2605-2609.
Chen G, Wang X, Robinson TG, Pikkemaat M, Lindley RI, Zhou S, Ping L, Liu W, Liu L, Chalmers J, Anderson CS; ENCHANTED Investigators. Comparative effects of low-dose versus standard-dose alteplase in ischemic patients with prior stroke and/or diabetes mellitus: The ENCHANTED trial. J Neurol Sci. 2018 Apr 15; 387: 1-5.
Jeong HG, Kim BJ, Yang MH, Han MK, Bae HJ, Lee SH. Stroke outcomes with use of antithrombotics within 24 hours after recanalization treatment. Neurology. 2016;87:996–1002
Lindley RI, Wardlaw JM, Whiteley WN, Cohen G, Blackwell L, Murray GD, Sandercock PA; IST-3 Collaborative Group. Alteplase for acute ischemic stroke: outcomes by clinically important subgroups in the Third International Stroke Trial. Stroke. 2015 Mar; 46(3): 746-56.
Chellinger PD, Tsivgoulis G. Another Enchantment From ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study): Are Savings and Safety More Salutary Than Efficacy? Stroke. 2017 Jul; 48(7): 1720-1722.
Pan X, Zhu Y, Zheng D, Liu Y, Yu F, Yang J. Prior antiplatelet agent use and outcomes after intravenous thrombolysis with recombinant tissue plasminogen activator in acute ischemic stroke: a meta-analysis of cohort studies and randomized controlled trials. Int J Stroke. 2015 Apr; 10(3): 317-23.
Luo S, Zhuang M, Zeng W, Tao J. Intravenous Thrombolysis for Acute Ischemic Stroke in Patients Receiving Antiplatelet Therapy: A Systematic Review and Meta-analysis of 19 Studies. J Am Heart Assoc. 2016 May 20; 5(5): e003242.
Tsivgoulis G, Katsanos AH, Zand R, Sharma VK, Köhrmann M, Giannopoulos S, Dardiotis E, Alexandrov AW, Mitsias PD, Schellinger PD, Alexandrov AV. Antiplatelet pretreatment and outcomes in intravenous thrombolysis for stroke: a systematic review and meta-analysis. J Neurol. 2017 Jun; 264(6): 1227-1235.
Malhotra K, Katsanos AH, Goyal N, Ahmed N, Strbian D, Palaiodimou L, Karapanayiotides T, Alexandrov AW, Grotta JC, Alexandrov AV, Tsivgoulis G. Safety and efficacy of dual antiplatelet pretreatment in patients with ischemic stroke treated with IV thrombolysis: A systematic review and meta-analysis. Neurology. 2020 Feb 18; 94(7): e657-e666.
Hacke W, Lichy C. Thrombolysis for acute stroke under antiplatelet therapy: safe enough to be beneficial? Nat Clin Pract Neurol. 2008 Sep; 4(9): 474-5.
Robinson TG, Wang X, Arima H, Bath PM, Billot L, Broderick JP, Demchuk AM, Donnan GA, Kim JS, Lavados PM, Lee TH, Lindley RI, Martins SCO, Olavarria VV, Pandian JD, Parsons MW, Pontes-Neto OM, Ricci S, Sato S, Sharma VK, Nguyen TH, Wang JG, Woodward M, Chalmers J, Anderson CS; ENCHANTED Investigators. Low- Versus Standard-Dose Alteplase in Patients on Prior Antiplatelet Therapy: The ENCHANTED Trial (Enhanced Control of Hypertension and Thrombolysis Stroke Study). Stroke. 2017 Jul; 48(7): 1877-1883.
Schellinger PD, Tsivgoulis G. Another Enchantment From ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study): Are Savings and Safety More Salutary Than Efficacy? Stroke. 2017 Jul; 48(7): 1720-1722.
Hankey GJ, Norrving B, Hacke W, Steiner T. Management of acute stroke in patients taking novel oral anticoagulants. Int J Stroke. 2014 Jul; 9(5): 627-32.
Steffel J, Collins R, Antz M, Cornu P, Desteghe L, Haeusler KG, Oldgren J, Reinecke H, Roldan-Schilling V, Rowell N, Sinnaeve P, Vanassche T, Potpara T, Camm AJ, Heidbüchel H; External reviewers. 2021 European Heart Rhythm Association Practical Guide on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Patients with Atrial Fibrillation. Europace. 2021 Oct 9; 23(10): 1612-1676.
Heidbuchel H, Verhamme P, Alings M, Antz M, Hacke W, Oldgren J, Sinnaeve P, Camm AJ, Kirchhof P; European Heart Rhythm Association. European Heart Rhythm Association Practical Guide on the use of new oral anticoagulants in patients with non-valvular atrial fibrillation. Europace. 2013 May; 15(5): 625-51.
Powers WJ, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Kidwell CS, Leslie-Mazwi TM, Ovbiagele B, Scott PA, Sheth KN, Southerland AM, Summers DV, Tirschwell DL. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec; 50(12): e344-e418.
Steffel J, Collins R, Antz M, Cornu P, Desteghe L, Haeusler KG, Oldgren J, Reinecke H, Roldan-Schilling V, Rowell N, Sinnaeve P, Vanassche T, Potpara T, Camm AJ, Heidbüchel H; External reviewers. 2021 European Heart Rhythm Association Practical Guide on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Patients with Atrial Fibrillation. Europace. 2021 Oct 9; 23(10): 1612-1676.
Steiner T, Köhrmann M, Schellinger PD, Tsivgoulis G. Non-Vitamin K Oral Anticoagulants Associated Bleeding and Its Antidotes. J Stroke. 2018 Sep; 20(3): 292-301.
Kermer P, Eschenfelder CC, Diener HC, Grond M, Abdalla Y, Abraham A, Althaus K, Becks G, Berrouschot J, Berthel J, Bode FJ, Burghaus L, Cangür H, Daffertshofer M, Edelbusch S, Eggers J, Gerlach R, Gröschel K, Große-Dresselhaus F, Günther A, Haase CG, Haensch CA, Harloff A, Heckmann JG, Held V, Hieber M, Kauert A, Kern R, Kerz T, Köhrmann M, Kraft P, Kühnlein P, Latta J, Leinisch E, Lenz A, Leithner C, Neumann-Haefelin T, Mäurer M, Müllges W, Nolte CH, Obermann M, Partowi S, Patzschke P, Poli S, Pulkowski U, Purrucker J, Rehfeldt T, Ringleb PA, Röther J, Rossi R, El-Sabassy H, Sauer O, Schackert G, Schäfer N, Schellinger PD, Schneider A, Schuppner R, Schwab S, Schwarte O, Seitz RJ, Senger S, Shah YP, Sindern E, Sparenberg P, Steiner T, Szabo K, Urbanek C, Sarnowksi BV, Weissenborn K, Wienecke P, Witt K, Wruck R, Wunderlich S. Antagonizing dabigatran by idarucizumab in cases of ischemic stroke or intracranial hemorrhage in Germany-Updated series of 120 cases. Int J Stroke. 2020 Aug; 15(6): 609-618.
Frol S, Sagris D, Pretnar Oblak J, Šabovič M, Ntaios G. Intravenous Thrombolysis After Dabigatran Reversal by Idarucizumab: A Systematic Review of the Literature. Front Neurol. 2021 Jun 3; 12: 666086.
Ramazanov G.R., Kokov L.S., Shamalov N.A., Kovaleva E.A., Klychnikova E.V., Akhmatkhanova L.Kh-B., Cheboksarov D.V., Khamidova L.T., Muslimov R.Sh., Rybalko N.V., Petrikov S.S. The first case of thrombolytic therapy using non-immunogenic staphylokinase in a female ischemic stroke patient receiving dabigatran etexilate, followed by thrombectomy. S.S. Korsakov Journal of Neurology and Psychiatry. 2022;122(6):145‑151
Pollack CV Jr, Reilly PA, van Ryn J, Eikelboom JW, Glund S, Bernstein RA, Dubiel R, Huisman MV, Hylek EM, Kam CW, Kamphuisen PW, Kreuzer J, Levy JH, Royle G, Sellke FW, Stangier J, Steiner T, Verhamme P, Wang B, Young L, Weitz JI. Idarucizumab for Dabigatran Reversal - Full Cohort Analysis. N Engl J Med. 2017 Aug 3; 377(5): 431-441.
Reilly PA, van Ryn J, Grottke O, Glund S, Stangier J. Idarucizumab, a Specific Reversal Agent for Dabigatran: Mode of Action, Pharmacokinetics and Pharmacodynamics, and Safety and Efficacy in Phase 1 Subjects. Am J Med. 2016 Nov; 129(11S): S64-S72.
Hankey GJ, Norrving B, Hacke W, Steiner T. Management of acute stroke in patients taking novel oral anticoagulants. Int J Stroke. 2014 Jul; 9(5): 627-32.
Steffel J, Collins R, Antz M, Cornu P, Desteghe L, Haeusler KG, Oldgren J, Reinecke H, Roldan-Schilling V, Rowell N, Sinnaeve P, Vanassche T, Potpara T, Camm AJ, Heidbüchel H; External reviewers. 2021 European Heart Rhythm Association Practical Guide on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Patients with Atrial Fibrillation. Europace. 2021 Oct 9; 23(10): 1612-1676.
Emberson J, Lees KR, Lyden P, Blackwell L, Albers G, Bluhmki E, Brott T, Cohen G, Davis S, Donnan G, Grotta J, Howard G, Kaste M, Koga M, von Kummer R, Lansberg M, Lindley RI, Murray G, Olivot JM, Parsons M, Tilley B, Toni D, Toyoda K, Wahlgren N, Wardlaw J, Whiteley W, del Zoppo GJ, Baigent C, Sandercock P, Hacke W; Stroke Thrombolysis Trialists" Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29; 384(9958): 1929-35.
Bluhmki E, Danays T, Biegert G, Hacke W, Lees KR. Alteplase for Acute Ischemic Stroke in Patients Aged >80 Years: Pooled Analyses of Individual Patient Data. Stroke. 2020 Aug; 51(8): 2322-2331.
Khatri P, Conaway MR, Johnston KC; Acute Stroke Accurate Prediction Study (ASAP) Investigators. Ninety-day outcome rates of a prospective cohort of consecutive patients with mild ischemic stroke. Stroke. 2012 Feb; 43(2): 560-2.
Khatri P, Kleindorfer DO, Devlin T, Sawyer RN Jr, Starr M, Mejilla J, Broderick J, Chatterjee A, Jauch EC, Levine SR, Romano JG, Saver JL, Vagal A, Purdon B, Devenport J, Pavlov A, Yeatts SD; PRISMS Investigators. Effect of Alteplase vs Aspirin on Functional Outcome for Patients With Acute Ischemic Stroke and Minor Nondisabling Neurologic Deficits: The PRISMS Randomized Clinical Trial. JAMA. 2018 Jul 10; 320(2): 156-166.
Tsivgoulis G, Goyal N, Katsanos AH, Malhotra K, Ishfaq MF, Pandhi A, Frohler MT, Spiotta AM, Anadani M, Psychogios M, Maus V, Siddiqui A, Waqas M, Schellinger PD, Groen M, Krogias C, Richter D, Saqqur M, Garcia-Bermejo P, Mokin M, Leker R, Cohen JE, Magoufis G, Psychogios K, Lioutas VA, Van Nostrand M, Sharma VK, Paciaroni M, Rentzos A, Shoirah H, Mocco J, Nickele C, Mitsias PD, Inoa V, Hoit D, Elijovich L, Arthur AS, Alexandrov AV. Intravenous thrombolysis for large vessel or distal occlusions presenting with mild stroke severity. Eur J Neurol. 2020 Jun; 27(6): 1039-1047.
Seners P, Perrin C, Lapergue B, Henon H, Debiais S, Sablot D, Girard Buttaz I, Tamazyan R, Preterre C, Laksiri N, Mione G, Arquizan C, Lucas L, Baron JC, Turc G; MINOR-STROKE Collaborators. Bridging Therapy or IV Thrombolysis in Minor Stroke with Large Vessel Occlusion. Ann Neurol. 2020 Jul; 88(1): 160-169.
Anderson CS, Huang Y, Lindley RI, Chen X, Arima H, Chen G, Li Q, Billot L, Delcourt C, Bath PM, Broderick JP, Demchuk AM, Donnan GA, Durham AC, Lavados PM, Lee TH, Levi C, Martins SO, Olavarria VV, Pandian JD, Parsons MW, Pontes-Neto OM, Ricci S, Sato S, Sharma VK, Silva F, Song L, Thang NH, Wardlaw JM, Wang JG, Wang X, Woodward M, Chalmers J, Robinson TG; ENCHANTED Investigators and Coordinators. Intensive blood pressure reduction with intravenous thrombolysis therapy for acute ischaemic stroke (ENCHANTED): an international, randomised, open-label, blinded-endpoint, phase 3 trial. Lancet. 2019 Mar 2; 393(10174): 877-888.
Berge E, Cohen G, Lindley RI, Sandercock P, Wardlaw JM, Sandset EC, Whiteley W. Effects of Blood Pressure and Blood Pressure-Lowering Treatment During the First 24 Hours Among Patients in the Third International Stroke Trial of Thrombolytic Treatment for Acute Ischemic Stroke. Stroke. 2015 Dec; 46(12): 3362-9.
Tsivgoulis G, Katsanos AH, Mavridis D, Lambadiari V, Roffe C, Macleod MJ, Sevcik P, Cappellari M, Nevšímalová M, Toni D, Ahmed N. Association of Baseline Hyperglycemia With Outcomes of Patients With and Without Diabetes With Acute Ischemic Stroke Treated With Intravenous Thrombolysis: A Propensity Score-Matched Analysis From the SITS-ISTR Registry. Diabetes. 2019 Sep; 68(9): 1861-1869.
Maciel R, Palma R, Sousa P, Ferreira F, Nzwalo H. Acute stroke with concomitant acute myocardial infarction: will you thrombolyse? J Stroke. 2015 Jan; 17(1): 84-6.
Dhand A, Nakagawa K, Nagpal S, Gelfand JM, Kim AS, Smith WS, Tihan T. Cardiac rupture after intravenous t-PA administration in acute ischemic stroke. Neurocrit Care. 2010 Oct; 13(2): 261-2.
Kasner SE, Villar-Cordova CE, Tong D, Grotta JC. Hemopericardium and cardiac tamponade after thrombolysis for acute ischemic stroke. Neurology. 1998 Jun; 50(6): 1857-9.
Marto JP, Kauppila LA, Jorge C, Calado S, Viana-Baptista M, Pinho-E-Melo T, Fonseca AC. Intravenous Thrombolysis for Acute Ischemic Stroke After Recent Myocardial Infarction: Case Series and Systematic Review. Stroke. 2019 Oct; 50(10): 2813-2818.
Asaithambi G, Adil MM, Qureshi AI. Thrombolysis for ischemic stroke associated with infective endocarditis: results from the nationwide inpatient sample. Stroke. 2013 Oct; 44(10): 2917-9.
Ong E, Mechtouff L, Bernard E, Cho TH, Diallo LL, Nighoghossian N, Derex L. Thrombolysis for stroke caused by infective endocarditis: an illustrative case and review of the literature. J Neurol. 2013 May; 260(5): 1339-42.
Bhuva P, Kuo SH, Claude Hemphill J, Lopez GA. Intracranial hemorrhage following thrombolytic use for stroke caused by infective endocarditis. Neurocrit Care. 2010 Feb; 12(1): 79-82.
Pruitt AA. Neurologic complications of infective endocarditis. Curr Treat Options Neurol 2013; 15: 465-476.
Haley, E Clarke Jr et al. “Phase IIB/III trial of tenecteplase in acute ischemic stroke: results of a prematurely terminated randomized clinical trial.” Stroke vol. 41,4 (2010): 707-11. doi:10.1161/STROKEAHA.109.572040
Parsons, Mark et al. “A randomized trial of tenecteplase versus alteplase for acute ischemic stroke.” The New England journal of medicine vol. 366,12 (2012): 1099-107. doi:10.1056/NEJMoa1109842
Huang X, Cheripelli BK, Lloyd SM, et al. Alteplase versus tenecteplase for thrombolysis after ischaemic stroke (ATTEST): a phase 2, randomised, open-label, blinded endpoint study. Lancet Neurol. 2015;14(4):368-376. doi:10.1016/S1474-4422(15)70017-7
Campbell BCV, Mitchell PJ, Churilov L, et al. Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke. N Engl J Med. 2018;378(17):1573-1582. doi:10.1056/NEJMoa1716405
Li S, Pan Y, Wang Z, et al. Safety and efficacy of tenecteplase versus alteplase in patients with acute ischaemic stroke (TRACE): a multicentre, randomised, open label, blinded-endpoint (PROBE) controlled phase II study. Stroke Vasc Neurol. 2022;7(1):47-53. doi:10.1136/svn-2021-000978
Bivard A, Zhao H, Churilov L, et al. Comparison of tenecteplase with alteplase for the early treatment of ischaemic stroke in the Melbourne Mobile Stroke Unit (TASTE-A): a phase 2, randomised, open-label trial. Lancet Neurol. 2022;21(6):520-527. doi:10.1016/S1474-4422(22)00171-5
Menon BK, Buck BH, Singh N, et al. Intravenous tenecteplase compared with alteplase for acute ischaemic stroke in Canada (AcT): a pragmatic, multicentre, open-label, registry-linked, randomised, controlled, non-inferiority trial. Lancet. 2022;400(10347):161-169. doi:10.1016/S0140-6736(22)01054-6
Logallo N, Novotny V, Assmus J, et al. Tenecteplase versus alteplase for management of acute ischaemic stroke (NOR-TEST): a phase 3, randomised, open-label, blinded endpoint trial. Lancet Neurol. 2017;16(10):781-788. doi:10.1016/S1474-4422(17)30253-3
Kvistad CE, Næss H, Helleberg BH, et al. Tenecteplase versus alteplase for the management of acute ischaemic stroke in Norway (NOR-TEST 2, part A): a phase 3, randomised, open-label, blinded endpoint, non-inferiority trial. Lancet Neurol. 2022;21(6):511-519. doi:10.1016/S1474-4422(22)00124-7
European Stroke Organisation (ESO) expedited recommendation on tenecteplase for acute ischaemic stroke. European Stroke Journal. 2023;8(1):8-54. doi:10.1177/23969873221150022 doi:10.1177/23969873221150022
https://www.ema.europa.eu/en/documents/smop/chmp-post-authorisation-summary-positive-opinion-metalyse-ii-70-g_en.pdf
https://www.ema.europa.eu/en/documents/product-information/metalyse-epar-product-information_en.pdf
Dentali F, Squizzato A, Gianni M, De Lodovici ML, Venco A, Paciaroni M, Crowther M, Ageno W. Safety of thrombolysis in cerebral venous thrombosis. A systematic review of the literature. Thromb Haemost. 2010 Nov;104(5):1055-62. doi: 10.1160/TH10-05-0311.
Viegas LD, Stolz E, Canhão P, Ferro JM. Systemic thrombolysis for cerebral venous and dural sinus thrombosis: a systematic review. Cerebrovasc Dis. 2014;37(1):43-50. doi: 10.1159/000356840
LeCouffe NE, Kappelhof M, Treurniet KM, Rinkel LA, Bruggeman AE, Berkhemer OA, Wolff L, van Voorst H, Tolhuisen ML, Dippel DWJ, van der Lugt A, van Es ACGM, Boiten J, Lycklama À Nijeholt GJ, Keizer K, Gons RAR, Yo LSF, van Oostenbrugge RJ, van Zwam WH, Roozenbeek B, van der Worp HB, Lo RTH, van den Wijngaard IR, de Ridder IR, Costalat V, Arquizan C, Lemmens R, Demeestere J, Hofmeijer J, Martens JM, Schonewille WJ, Vos JA, Uyttenboogaart M, Bokkers RPH, van Tuijl JH, Kortman H, Schreuder FHBM, Boogaarts HD, de Laat KF, van Dijk LC, den Hertog HM, van Hasselt BAAM, Brouwers PJAM, Bulut T, Remmers MJM, van Norden A, Imani F, Rozeman AD, Elgersma OEH, Desfontaines P, Brisbois D, Samson Y, Clarençon F, Krietemeijer GM, Postma AA, van Doormaal PJ, van den Berg R, van der Hoorn A, Beenen LFM, Nieboer D, Lingsma HF, Emmer BJ, Coutinho JM, Majoie CBLM, Roos YBWEM; MR CLEAN–NO IV Investigators. A Randomized Trial of Intravenous Alteplase before Endovascular Treatment for Stroke. N Engl J Med. 2021 Nov 11; 385(20): 1833-1844. doi: 10.1056/NEJMoa2107727
Suzuki K, Matsumaru Y, Takeuchi M, Morimoto M, Kanazawa R, Takayama Y, Kamiya Y, Shigeta K, Okubo S, Hayakawa M, Ishii N, Koguchi Y, Takigawa T, Inoue M, Naito H, Ota T, Hirano T, Kato N, Ueda T, Iguchi Y, Akaji K, Tsuruta W, Miki K, Fujimoto S, Higashida T, Iwasaki M, Aoki J, Nishiyama Y, Otsuka T, Kimura K; SKIP Study Investigators. Effect of Mechanical Thrombectomy Without vs With Intravenous Thrombolysis on Functional Outcome Among Patients With Acute Ischemic Stroke: The SKIP Randomized Clinical Trial. JAMA. 2021 Jan 19; 325(3): 244-253. doi: 10.1001/jama.2020.23522. Erratum in: JAMA. 2021 May 4; 325(17): 1795.
Zi W, Qiu Z, Li F, Sang H, Wu D, Luo W, Liu S, Yuan J, Song J, Shi Z, Huang W, Zhang M, Liu W, Guo Z, Qiu T, Shi Q, Zhou P, Wang L, Fu X, Liu S, Yang S, Zhang S, Zhou Z, Huang X, Wang Y, Luo J, Bai Y, Zhang M, Wu Y, Zeng G, Wan Y, Wen C, Wen H, Ling W, Chen Z, Peng M, Ai Z, Guo F, Li H, Guo J, Guan H, Wang Z, Liu Y, Pu J, Wang Z, Liu H, Chen L, Huang J, Yang G, Gong Z, Shuai J, Nogueira RG, Yang Q; DEVT Trial Investigators. Effect of Endovascular Treatment Alone vs Intravenous Alteplase Plus Endovascular Treatment on Functional Independence in Patients With Acute Ischemic Stroke: The DEVT Randomized Clinical Trial. JAMA. 2021 Jan 19; 325(3): 234-243. doi: 10.1001/jama.2020.23523.
Maier IL, Leha A, Badr M, Allam I, Bähr M, Jamous A, Hesse A, Psychogios MN, Behme D, Liman J. Inhouse Bridging Thrombolysis Is Associated With Improved Functional Outcome in Patients With Large Vessel Occlusion Stroke: Findings From the German Stroke Registry. Front Neurol. 2021 Jun 10; 12: 649108. doi: 10.3389/fneur.2021.649108.
Jian Y, Zhao L, Jia B, Tong X, Li T, Wu Y, Wang X, Gao Z, Gong Y, Zhang X, Wang H, Zhang R, Zhang L, Miao Z, Zhang G; ANGEL-ACT Study Group. Direct versus Bridging Mechanical Thrombectomy in Elderly Patients with Acute Large Vessel Occlusion: A Multicenter Cohort Study. Clin Interv Aging. 2021 Jul 5; 16: 1265-1274. doi: 10.2147/CIA.S313171
Volodyukhin M.Yu., Podshivalov I.A., Khasanova D.R., Demin T.V., Zagidullin B.I., Mukhamadieva Yu.S., Mingazetdinov M.A., Yusupov R.I., Khayrullin R.N. "Safety and efficacy of Fortelizin in staged reperfusion therapy of acute ischemic stroke in the carotid territory". Diagnostic and Interventional Radiology. 2023;17(1);17-24.
Volodyukhin M.Yu., Khasanova D.R., Timchenko L.V., Podshivalov I.A., Telyatnik Yu.A., Demin T.V., Zagidullin B.I., Mukhamadieva Yu.S., Mingazetdinov M.A., Yusupov R.I., Sinyutin V.N. Multicenter experience with Fortelizin in staged reperfusion therapy of acute ischemic stroke in the carotid system. S.S. Korsakov Journal of Neurology and Psychiatry. 2023;123(6):72‑77.
Bourcier R, Goyal M, Liebeskind DS, Muir KW, Desal H, Siddiqui AH, Dippel DWJ, Majoie CB, van Zwam WH, Jovin TG, Levy EI, Mitchell PJ, Berkhemer OA, Davis SM, Derraz I, Donnan GA, Demchuk AM, van Oostenbrugge RJ, Kelly M, Roos YB, Jahan R, van der Lugt A, Sprengers M, Velasco S, Lycklama À Nijeholt GJ, Ben Hassen W, Burns P, Brown S, Chabert E, Krings T, Choe H, Weimar C, Campbell BCV, Ford GA, Ribo M, White P, Cloud GC, San Roman L, Davalos A, Naggara O, Hill MD, Bracard S; HERMES Trialists Collaboration. Association of Time From Stroke Onset to Groin Puncture With Quality of Reperfusion After Mechanical Thrombectomy: A Meta-analysis of Individual Patient Data From 7 Randomized Clinical Trials. JAMA Neurol. 2019 Apr 1; 76(4): 405-411. doi: 10.1001/jamaneurol.2018.4510
Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CB, van der Lugt A, de Miquel MA, Donnan GA, Roos YB, Bonafe A, Jahan R, Diener HC, van den Berg LA, Levy EI, Berkhemer OA, Pereira VM, Rempel J, Millán M, Davis SM, Roy D, Thornton J, Román LS, Ribó M, Beumer D, Stouch B, Brown S, Campbell BC, van Oostenbrugge RJ, Saver JL, Hill MD, Jovin TG; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016 Apr 23; 387(10029): 1723-31. doi: 10.1016/S0140-6736(16)00163-X
Primiani CT, Vicente AC, Brannick MT, Turk AS, Mocco J, Levy EI, Siddiqui AH, Mokin M. Direct Aspiration versus Stent Retriever Thrombectomy for Acute Stroke: A Systematic Review and Meta-Analysis in 9127 Patients. J Stroke Cerebrovasc Dis. 2019 May; 28(5): 1329-1337. doi: 10.1016/j.jstrokecerebrovasdis.2019.01.034
Touma L, Filion KB, Sterling LH, Atallah R, Windle SB, Eisenberg MJ. Stent Retrievers for the Treatment of Acute Ischemic Stroke: A Systematic Review and Meta-analysis of Randomized Clinical Trials. JAMA Neurol. 2016 Mar; 73(3): 275-81. doi: 10.1001/jamaneurol.2015.4441.
Barral M, Boudour S, Viprey M, Giroudon C, Aulagner G, Schott AM, Turjman F, Armoiry X, Gory B. Stent retriever thrombectomy for acute ischemic stroke: A systematic review and meta-analysis of randomized controlled trials, including THRACE. Rev Neurol (Paris). 2018 May; 174(5): 319-326. doi: 10.1016/j.neurol.2017.09.009
Lapergue B, Blanc R, Costalat V, Desal H, Saleme S, Spelle L, Marnat G, Shotar E, Eugene F, Mazighi M, Houdart E, Consoli A, Rodesch G, Bourcier R, Bracard S, Duhamel A, Ben Maacha M, Lopez D, Renaud N, Labreuche J, Gory B, Piotin M; ASTER2 Trial Investigators. Effect of Thrombectomy With Combined Contact Aspiration and Stent Retriever vs Stent Retriever Alone on Revascularization in Patients With Acute Ischemic Stroke and Large Vessel Occlusion: The ASTER2 Randomized Clinical Trial. JAMA. 2021 Sep 28; 326(12): 1158-1169. doi: 10.1001/jama.2021.13827
Kang DH, Jung C, Yoon W, Kim SK, Baek BH, Kim JT, Park MS, Kim YW, Hwang YH, Kim YS, Kim BJ, Han MK, Bae HJ. Endovascular Thrombectomy for Acute Basilar Artery Occlusion: A Multicenter Retrospective Observational Study. J Am Heart Assoc. 2018 Jul 7; 7(14): e009419. doi: 10.1161/JAHA.118.009419.
Sheng K, Tong M. Therapy for acute basilar artery occlusion: a systematic review and meta-analysis. F1000Res. 2019 Feb 7; 8: 165. doi: 10.12688/f1000research.18042.1
Badhiwala JH, Nassiri F, Alhazzani W, Selim MH, Farrokhyar F, Spears J, Kulkarni AV, Singh S, Alqahtani A, Rochwerg B, Alshahrani M, Murty NK, Alhazzani A, Yarascavitch B, Reddy K, Zaidat OO, Almenawer SA. Endovascular Thrombectomy for Acute Ischemic Stroke: A Meta-analysis. JAMA. 2015 Nov 3; 314(17): 1832-43. doi: 10.1001/jama.2015.13767.
Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CB, van der Lugt A, de Miquel MA, Donnan GA, Roos YB, Bonafe A, Jahan R, Diener HC, van den Berg LA, Levy EI, Berkhemer OA, Pereira VM, Rempel J, Millán M, Davis SM, Roy D, Thornton J, Román LS, Ribó M, Beumer D, Stouch B, Brown S, Campbell BC, van Oostenbrugge RJ, Saver JL, Hill MD, Jovin TG; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016 Apr 23; 387(10029): 1723-31. doi: 10.1016/S0140-6736(16)00163-X.
Saver JL, Goyal M, van der Lugt A, Menon BK, Majoie CB, Dippel DW, Campbell BC, Nogueira RG, Demchuk AM, Tomasello A, Cardona P, Devlin TG, Frei DF, du Mesnil de Rochemont R, Berkhemer OA, Jovin TG, Siddiqui AH, van Zwam WH, Davis SM, Castaño C, Sapkota BL, Fransen PS, Molina C, van Oostenbrugge RJ, Chamorro Á, Lingsma H, Silver FL, Donnan GA, Shuaib A, Brown S, Stouch B, Mitchell PJ, Davalos A, Roos YB, Hill MD; HERMES Collaborators. Time to Treatment With Endovascular Thrombectomy and Outcomes From Ischemic Stroke: A Meta-analysis. JAMA. 2016 Sep 27; 316(12): 1279-88. doi: 10.1001/jama.2016.13647.
Touma L, Filion KB, Sterling LH, Atallah R, Windle SB, Eisenberg MJ. Stent Retrievers for the Treatment of Acute Ischemic Stroke: A Systematic Review and Meta-
analysis of Randomized Clinical Trials. JAMA Neurol. 2016 Mar; 73(3): 275-81. doi: 10.1001/jamaneurol.2015.4441
Goyal N, Tsivgoulis G, Malhotra K, Ishfaq MF, Pandhi A, Frohler MT, Spiotta AM, Anadani M, Psychogios M, Maus V, Siddiqui A, Waqas M, Schellinger PD, Groen M, Krogias C, Richter D, Saqqur M, Garcia-Bermejo P, Mokin M, Leker R, Cohen JE, Katsanos AH, Magoufis G, Psychogios K, Lioutas V, VanNostrand M, Sharma VK, Paciaroni M, Rentzos A, Shoirah H, Mocco J, Nickele C, Inoa V, Hoit D, Elijovich L, Alexandrov AV, Arthur AS. Medical Management vs Mechanical Thrombectomy for Mild Strokes: An International Multicenter Study and Systematic Review and Meta-analysis. JAMA Neurol. 2020 Jan 1; 77(1): 16-24. doi: 10.1001/jamaneurol.2019.3112
Xiong YJ, Gong JM, Zhang YC, Zhao XL, Xu SB, Pan DJ, Qu WS, Tian DS. Endovascular thrombectomy versus medical treatment for large vessel occlusion stroke with
mild symptoms: A meta-analysis. PLoS One. 2018 Aug 23; 13(8): e0203066. doi: 10.1371/journal.pone.0203066
Olthuis SGH, Pirson FAV, Pinckaers FME, Hinsenveld WH, Nieboer D, Ceulemans A, Knapen RRMM, Robbe MMQ, Berkhemer OA, van Walderveen MAA, Lycklama À Nijeholt GJ, Uyttenboogaart M, Schonewille WJ, van der Sluijs PM, Wolff L, van Voorst H, Postma AA, Roosendaal SD, van der Hoorn A, Emmer BJ, Krietemeijer MGM, van Doormaal PJ, Roozenbeek B, Goldhoorn RB, Staals J, de Ridder IR, van der Leij C, Coutinho JM, van der Worp HB, Lo RTH, Bokkers RPH, van Dijk EI, Boogaarts HD, Wermer MJH, van Es ACGM, van Tuijl JH, Kortman HGJ, Gons RAR, Yo LSF, Vos JA, de Laat KF, van Dijk LC, van den Wijngaard IR, Hofmeijer J, Martens JM, Brouwers PJAM, Bulut T, Remmers MJM, de Jong TEAM, den Hertog HM, van Hasselt BAAM, Rozeman AD, Elgersma OEH, van der Veen B, Sudiono DR, Lingsma HF, Roos YBWEM, Majoie CBLM, van der Lugt A, Dippel DWJ, van Zwam WH, van Oostenbrugge RJ; MR CLEAN-LATE investigators. Endovascular treatment versus no endovascular treatment after 6-24 h in patients with ischaemic stroke and collateral flow on CT angiography (MR CLEAN-LATE) in the Netherlands: a multicentre, open-label, blinded-endpoint, randomised, controlled, phase 3 trial. Lancet. 2023 Apr 22;401(10385):1371-1380. doi: 10.1016/S0140-6736(23)00575-5. Epub 2023 Mar 29. PMID: 37003289
Tan JC, Dillon WP, Liu S, Adler F, Smith WS, Wintermark M. Systematic comparison of perfusion-CT and CT-angiography in acute stroke patients. Ann Neurol. 2007 Jun;61(6):533-43. doi: 10.1002/ana.21130. PMID: 17431875.
Tan IY, Demchuk AM, Hopyan J, Zhang L, Gladstone D, Wong K, Martin M, Symons SP, Fox AJ, Aviv RI. CT angiography clot burden score and collateral score: correlation with clinical and radiologic outcomes in acute middle cerebral artery infarct. AJNR Am J Neuroradiol. 2009 Mar;30(3):525-31. doi: 10.3174/ajnr.A1408. Epub 2009 Jan 15. PMID: 19147716; PMCID: PMC7051470.
Panagiotis Papanagiotou, Diogo C. Haussen, Francis Turjman, Julien Labreuche, Michel Piotin, Andreas Kastrup, Henrik Steglich-Arnholm, Markus Holtmannspötter, Christian Taschner, Sebastian Eiden, Raul G. Nogueira, Maria Boutchakova, Adnan Siddiqui, Bertrand Lapergue, Franziska Dorn, Christophe Cognard, Monika Killer, Salvatore Mangiafico, Marc Ribo, Marios N. Psychogios, Alejandro Spiotta, Marc Antoine Labeyrie, Alessandra Biondi, Mikaël Mazighi, Sébastien Richard, René Anxionnat, Serge Bracard, Benjamin Gory, Jonathan Andrew Grossberg, Adrien Guenego, Julien Darcourt, Isabelle Vukasinovic, Elisa Pomero, Jason Davies, Leonardo Renieri, Corentin Hecker, Maria Muchada Muchada, Arturo Consoli, Georges Rodesch, Emmanuel Houdart, Raymond Turner, Aquilla Turk, Imran Chaudry, Paul-Emile Labeyrie, Roberto Riva, Johanna Lockau, Raphaël Blanc, Hocine Redjem, Daniel Behme, Hussain Shallwani, Maurer Christopher, Anne-Laure Derelle, Romain Tonnelet, Liang Liao, Camille Amaz, Carotid Stenting With Antithrombotic Agents and Intracranial Thrombectomy Leads to the Highest Recanalization Rate in Patients With Acute Stroke With Tandem Lesions, JACC: Cardiovascular Interventions, Volume 11, Issue 13, 2018, Pages 1290-1299, ISSN 1936-8798
Goyal M, Menon BK, van Zwam WH, Dippel DW, Mitchell PJ, Demchuk AM, Dávalos A, Majoie CB, van der Lugt A, de Miquel MA, Donnan GA, Roos YB, Bonafe A, Jahan R, Diener HC, van den Berg LA, Levy EI, Berkhemer OA, Pereira VM, Rempel J, Millán M, Davis SM, Roy D, Thornton J, Román LS, Ribó M, Beumer D, Stouch B, Brown S, Campbell BC, van Oostenbrugge RJ, Saver JL, Hill MD, Jovin TG; HERMES collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016 Apr 23; 387(10029): 1723-31. doi: 10.1016/S0140-6736(16)00163-X
Pires Coelho A, Lobo M, Gouveia R, Silveira D, Campos J, Augusto R, Coelho N, Canedo A. Overview of evidence on emergency carotid stenting in patients with acute ischemic stroke due to tandem occlusions: a systematic review and meta-analysis. J Cardiovasc Surg (Torino). 2019 Dec; 60(6): 693-702. doi: 10.23736/S0021-9509.18.10312-0
Bücke P, Aguilar Pérez M, AlMatter M, Hellstern V, Bäzner H, Henkes H. Functional Outcome and Safety of Intracranial Thrombectomy After Emergent Extracranial Stenting in Acute Ischemic Stroke Due to Tandem Occlusions. Front Neurol. 2018; 9: 940. Published 2018 Nov 20. doi:10.3389/fneur.2018.00940
Anadani M, Spiotta AM, Alawieh A, Turjman F, Piotin M, Haussen DC, Nogueira RG, Papanagiotou P, Siddiqui AH, Lapergue B, Dorn F, Cognard C, Ribo M, Psychogios MN, Labeyrie MA, Mazighi M, Biondi A, Anxionnat R, Bracard S, Richard S, Gory B; TITAN (Thrombectomy In TANdem Lesions) Investigators. Emergent Carotid Stenting Plus Thrombectomy After Thrombolysis in Tandem Strokes: Analysis of the TITAN Registry. Stroke. 2019 Aug; 50(8): 2250–2252. doi: 10.1161/STROKEAHA.118.024733
Gory B, Haussen DC, Piotin M, Steglich-Arnholm H, Holtmannspötter M, Labreuche J, Kyheng M, Taschner C, Eiden S, Nogueira RG, Papanagiotou P, Boutchakova M, Siddiqui AH, Lapergue B, Dorn F, Cognard C, Killer M, Mangiafico S, Ribo M, Psychogios MN, Spiotta AM, Labeyrie MA, Biondi A, Mazighi M, Turjman F; Thrombectomy In TANdem lesions (TITAN) investigators. Impact of intravenous thrombolysis and emergent carotid stenting on reperfusion and clinical outcomes in patients with acute stroke with tandem lesion treated with thrombectomy: a collaborative pooled analysis. Eur J Neurol. 2018 Sep; 25(9): 1115-1120. doi: 10.1111/ene.13633
Writing Group for the BASILAR Group, Zi W, Qiu Z, Wu D, Li F, Liu H, Liu W, Huang W, Shi Z, Bai Y, Liu Z, Wang L, Yang S, Pu J, Wen C, Wang S, Zhu Q, Chen W, Yin C, Lin M, Qi L, Zhong Y, Wang Z, Wu W, Chen H, Yao X, Xiong F, Zeng G, Zhou Z, Wu Z, Wan Y, Peng H, Li B, Hu X, Wen H, Zhong W, Wang L, Jin P, Guo F, Han J, Fu X, Ai Z, Tian X, Feng X, Sun B, Huang Z, Li W, Zhou P, Tu M, Sun X, Li H, He W, Qiu T, Yuan Z, Yue C, Yang J, Luo W, Gong Z, Shuai J, Nogueira RG, Yang Q. Assessment of Endovascular Treatment for Acute Basilar Artery Occlusion via a Nationwide Prospective Registry. JAMA Neurol. 2020 May 1; 77(5): 561-573. doi: 10.1001/jamaneurol.2020.0156
Kang DH, Jung C, Yoon W, Kim SK, Baek BH, Kim JT, Park MS, Kim YW, Hwang YH, Kim YS, Kim BJ, Han MK, Bae HJ. Endovascular Thrombectomy for Acute Basilar Artery Occlusion: A Multicenter Retrospective Observational Study. J Am Heart Assoc. 2018 Jul 7; 7(14): e009419. doi: 10.1161/JAHA.118.009419.
462. Gory B, Mazighi M, Blanc R, Labreuche J, Piotin M, Turjman F, Lapergue B. Mechanical thrombectomy in basilar artery occlusion: influence of reperfusion on clinical outcome and impact of the first-line strategy (ADAPT vs stent retriever). J Neurosurg. 2018 Dec 1; 129(6): 1482-1491. doi: 10.3171/2017.7.JNS171043
Sheng K, Tong M. Therapy for acute basilar artery occlusion: a systematic review and meta-analysis. F1000Res. 2019 Feb 7; 8: 165. doi: 10.12688/f1000research.18042.1
Writing Group for the BASILAR Group, Zi W, Qiu Z, Wu D, Li F, Liu H, Liu W, Huang W, Shi Z, Bai Y, Liu Z, Wang L, Yang S, Pu J, Wen C, Wang S, Zhu Q, Chen W, Yin C, Lin M, Qi L, Zhong Y, Wang Z, Wu W, Chen H, Yao X, Xiong F, Zeng G, Zhou Z, Wu Z, Wan Y, Peng H, Li B, Hu X, Wen H, Zhong W, Wang L, Jin P, Guo F, Han J, Fu X, Ai Z, Tian X, Feng X, Sun B, Huang Z, Li W, Zhou P, Tu M, Sun X, Li H, He W, Qiu T, Yuan Z, Yue C, Yang J, Luo W, Gong Z, Shuai J, Nogueira RG, Yang Q. Assessment of Endovascular Treatment for Acute Basilar Artery Occlusion via a Nationwide Prospective Registry. JAMA Neurol. 2020 May 1; 77(5): 561-573. doi: 10.1001/jamaneurol.2020.0156
Nguyen TN, Qureshi MM, Strambo D, Strbian D, Räty S, Herweh C, Abdalkader M, Olive-Gadea M, Ribo M, Psychogios M, Fischer U, Nguyen A, Kuramatsu JB, Haupenthal D, Köhrmann M, Deuschl C, Kühne Escola J, Yaghi S, Shu L, Puetz V, Kaiser DPO, Kaesmacher J, Mujanovic A, Marterstock DC, Engelhorn T, Klein P, Haussen DC, Mohammaden MH, Abdelhamid H, Souza Viana L, Cunha B, Fragata I, Romoli M, Diana F, Virtanen P, Lappalainen K, Clark J, Matsoukas S, Fifi JT, Sheth SA, Salazar-Marioni S, Marto JP, Ramos JN, Miszczuk M, Riegler C, Jadhav AP, Desai SM, Maus V, Kaeder M, Siddiqui AH, Monteiro A, Masoud HE, Suryadevara N, Mokin M, Thanki S, Siegler JE, Khalife J, Linfante I, Dabus G, Asdaghi N, Saini V, Nolte CH, Siebert E, Meinel TR, Finitsis S, Möhlenbruch MA, Ringleb PA, Berberich A, Nogueira RG, Hanning U, Meyer L, Michel P, Nagel S. Endovascular Versus Medical Management of Posterior Cerebral Artery Occlusion Stroke: The PLATO Study. Stroke. 2023 Jul;54(7):1708-1717. doi: 10.1161/STROKEAHA.123.042674. Epub 2023 May 24. PMID: 37222709.
Brouwer J, Ergezen S, Mulder MJHL, Lycklama A Nijeholt GJ, van Es ACGM, van der Lugt A, Dippel DWJ, Majoie CBLM, Roos YBWEM, Coutinho JM, Emmer BJ; MR CLEAN Registry investigators. Endovascular treatment for isolated posterior cerebral artery occlusion stroke in the MR CLEAN registry. J Neurointerv Surg. 2022 Mar 15: neurintsurg-2021-018505. doi: 10.1136/neurintsurg-2021-018505
Li H, Zhang Y, Zhang L, Li Z, Xing P, Zhang Y, Hong B, Yang P, Liu J. Endovascular Treatment of Acute Ischemic Stroke Due to Intracranial Atherosclerotic Large Vessel
Occlusion: A Systematic Review. Clin Neuroradiol. 2020 Dec; 30(4): 777-787. doi: 10.1007/s00062-019-00839-4
Forbrig R, Lockau H, Flottmann F, Boeckh-Behrens T, Kabbasch C, Patzig M, Mpotsaris A, Fiehler J, Liebig T, Thomalla G, Onur OA, Wunderlich S, Kreiser K, Herzberg M, Wollenweber FA, Prothmann S, Dorn F. Intracranial Rescue Stent Angioplasty After Stent-Retriever Thrombectomy: Multicenter Experience. Clin Neuroradiol. 2019 Sep; 29(3): 445-457. doi: 10.1007/s00062-018-0690-4
Li H, Zhang Y, Zhang L, Li Z, Xing P, Zhang Y, Hong B, Yang P, Liu J. Endovascular Treatment of Acute Ischemic Stroke Due to Intracranial Atherosclerotic Large Vessel Occlusion: A Systematic Review. Clin Neuroradiol. 2020 Dec; 30(4): 777-787. doi: 10.1007/s00062-019-00839-4
Stracke CP, Fiehler J, Meyer L, Thomalla G, Krause LU, Lowens S, Rothaupt J, Kim BM, Heo JH, Yeo LLL, Andersson T, Kabbasch C, Dorn F, Chapot R, Hanning U. Emergency Intracranial Stenting in Acute Stroke: Predictors for Poor Outcome and for Complications. J Am Heart Assoc. 2020 Mar 3; 9(5): e012795. doi: 10.1161/JAHA.119.012795
Luo G, Gao F, Zhang X, Jia B, Huo X, Liu R, Chi MS, Ma G, Peng G, Zhang J, Qi Z, Guo X, Han B, Tong X, Wang B, Song L, Liu L, He Z, Mo D, Ma N, Sun X, Yang M, Miao Z. Intracranial Stenting as Rescue Therapy After Failure of Mechanical Thrombectomy for Basilar Artery Occlusion: Data From the ANGEL-ACT Registry. Front Neurol. 2021 Sep 30; 12: 739213. doi: 10.3389/fneur.2021.739213. PMID: 34659098; PMCID: PMC8514631
Bulwa Z, Del Brutto VJ, Loggini A, Ammar FE, Martinez RC, Christoforidis G, Brorson JR, Ardelt AA, Goldenberg FD. Mechanical Thrombectomy for Patients with In-Hospital Ischemic Stroke: A Case-Control Study. J Stroke Cerebrovasc Dis. 2020 May; 29(5): 104692. doi: 10.1016/j.jstrokecerebrovasdis.2020.104692
Meinel TR, Kniepert JU, Seiffge DJ, Gralla J, Jung S, Auer E, Frey S, Goeldlin M, Mordasini P, Mosimann PJ, Nogueira RG, Haussen DC, Rodrigues GM, Uphaus T, L"Allinec V, Krajíčková D, Alonso A, Costalat V, Hajdu SD, Olivé-Gadea M, Maegerlein C, Pierot L, Schaafsma J, Suzuki K, Arnold M, Heldner MR, Fischer U, Kaesmacher J. Endovascular Stroke Treatment and Risk of Intracranial Hemorrhage in Anticoagulated Patients. Stroke. 2020 Mar; 51(3): 892-898. doi: 10.1161/STROKEAHA.119.026606
Koge J, Tanaka K, Yamagami H, Yoshimoto T, Uchida K, Morimoto T, Toyoda K, Sakai N, Yoshimura S. Mechanical thrombectomy for stroke patients anticoagulated with direct oral anticoagulants versus warfarin. J Neurol Sci. 2021 Aug 15; 427: 117545. doi: 10.1016/j.jns.2021.117545
Paybast S, Mohamadian R, Emami A, Jameie M, Shahrab F, Zamani F, Sharifipour E. Safety and efficacy of endovascular thrombolysis in patients with acute cerebral venous sinus thrombosis: A systematic review. Interv Neuroradiol. 2022 Dec 5:15910199221143418. doi: 10.1177/15910199221143418
Coutinho JM, Zuurbier SM, Bousser MG, Ji X, Canhão P, Roos YB, Crassard I, Nunes AP, Uyttenboogaart M, Chen J, Emmer BJ, Roosendaal SD, Houdart E, Reekers JA, van den Berg R, de Haan RJ, Majoie CB, Ferro JM, Stam J; TO-ACT investigators. Effect of Endovascular Treatment With Medical Management vs Standard Care on Severe Cerebral Venous Thrombosis: The TO-ACT Randomized Clinical Trial. JAMA Neurol. 2020 Aug 1;77(8):966-973. doi: 10.1001/jamaneurol.2020.1022
Saposnik G, Bushnell C, Coutinho JM, Field TS, Furie KL, Galadanci N, Kam W, Kirkham FC, McNair ND, Singhal AB, Thijs V, Yang VXD; American Heart Association Stroke Council; Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; Council on Cardiovascular and Stroke Nursing; and Council on Hypertension. Diagnosis and Management of Cerebral Venous Thrombosis: A Scientific Statement From the American Heart Association. Stroke. 2024 Mar;55(3):e77-e90
Schechter T, Kirton A, Laughlin S, Pontigon AM, Finkelstein Y, MacGregor D, Chan A, deVeber G, Brandão LR. Safety of anticoagulants in children with arterial ischemic stroke. Blood. 2012;119:949–956. doi: 10.1182/blood-2011-06-361535
Medley TL, Miteff C, Andrews I, Ware T, Cheung M, Monagle P, Mandelstam S, Wray A, Pridmore C, Troedson C, Dale RC, Fahey M, Sinclair A, Walsh P, Stojanovski B, Mackay MT. Australian Clinical Consensus Guideline: The diagnosis and acute management of childhood stroke. Int J Stroke. 2019 Jan;14(1):94-106. doi: 10.1177/1747493018799958. Epub 2018 Oct 4. PMID: 30284961;
Monagle P, Chan AKC, Goldenberg NA, Ichord RN, Journeycake JM, Nowak-Göttl U, Vesely SK. Antithrombotic therapy in neonates and children: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e737S-e801S. doi: 10.1378/chest.11-2308. Erratum in: Chest. 2014 Dec;146(6):1694. Dosage error in article text. Erratum in: Chest. 2014 Nov;146(5):1422. PMID: 22315277; PMCID: PMC3278066
Dabbous MK, Sakr FR, Malaeb DN. Anticoagulant therapy in pediatrics. J Basic Clin Pharm. 2014 Mar;5(2):27-33. doi: 10.4103/0976-0105.134947. PMID: 25031496; PMCID: PMC4074692;
Sträter R, Kurnik K, Heller C, Schobess R, Luigs P, Nowak-Göttl U. Aspirin versus low-dose low-molecular-weight heparin: antithrombotic therapy in pediatric ischemic stroke patients: a prospective follow-up study. Stroke. 2001;32:2554–2558
Petricević M, Biocina B, Konosić S, Burcar I, Sirić F, Mihaljević MZ, Ivancan V, Svetina L, Gasparović H. Definition of acetylsalicylic acid resistance using whole blood impedance aggregometry in patients undergoing coronary artery surgery. Coll Antropol. 2013 Sep;37(3):833-9. PMID: 24308225.
Pedersen S.B., Grove E.L., Nielsen H.L., Mortensen J., Kristensen S.D., Hvas A.M. Evaluation of aspirin response by Multiplate whole blood aggregometry and light transmission aggregometry // Platelets. – 2009. - Sep;20(6). – P. 415-20. doi: 10.1080/09537100903100643.
Mueller T, Dieplinger B, Poelz W, Haltmayer M. Utility of the PFA-100 instrument and the novel multiplate analyzer for the assessment of aspirin and clopidogrel effects on platelet function in patients with cardiovascular disease. Clin Appl Thromb Hemost. 2009 Dec;15(6):652-9. doi: 10.1177/1076029608322547. Epub 2008 Sep 19. PMID: 18805846.
Sibbing D., Braun S., Jawansky S., Vogt W., Mehilli J., Schömig A., Kastrati A., von Beckerath N. Assessment of ADP-induced platelet aggregation with light transmission aggregometry and multiple electrode platelet aggregometry before and after clopidogrel treatment // Thromb Haemost. – 2008. - Jan; 99(1). – P. 121-126.
Würtz M., Hvas A.M., Christensen K.H., Rubak P., Kristensen S.D., Grove E.L. Rapid evaluation of platelet function using the Multiplate® Analyzer // Platelets. – 2013. - Nov 18. [Epub ahead of print].
Lvova, O. A. The place of antiplatelet agents in the system of secondary prevention of ischemic stroke in children and young patients / O. A. Lvova, V. V. Gusev // Pharmateca. – 2014. – No. 13(286). – pp. 26-30. – EDN SXUYBX.
Marcia L. Buck. Clopidogrel for Platelet Inhibition in Pediatric Patients PEDIATRIC PHARMACOTHERAPY Volume 16 Number 5, 2010
Dosing of clopidogrel for platelet inhibition in infants and young children: primary results of the platelet inhibition in children on clopidogrel (PICOLO) Trial // Circulation. - 2008. - 117. – P. 553 - 559
Soman T, Rafay MF, Hune S, Allen A, MacGregor D, deVeber G. The risks and safety of clopidogrel in pediatric arterial ischemic stroke. Stroke. 2006 Apr;37(4):1120-2. doi: 10.1161/01.STR.0000209620.44017.97. Epub 2006 Mar 9. PMID: 16527995
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ, Scott RM, Smith ER; American Heart Association Stroke Council; Council on Cardiovascular Disease in the Young. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008 Sep;39(9):2644-91. doi: 10.1161/STROKEAHA.108.189696. Epub 2008 Jul 17. Erratum in: Stroke. 2009 Jan 1;40(1):e8-10. PMID: 18635845
Guekht A, Skoog I, Edmundson S, Zakharov V, Korczyn AD. ARTEMIDA Trial (A Randomized Trial of Efficacy, 12 Months International Double-Blind Actovegin): A Randomized Controlled Trial to Assess the Efficacy of Actovegin in Poststroke Cognitive Impairment. Stroke. 2017 May; 48(5): 1262-1270. doi: 10.1161/STROKEAHA.116.014321. PMID: 28432265; PMCID: PMC5404405
Bereczki D, Fekete I. Vinpocetine for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jan 23; 2008(1): CD000480. doi: 10.1002/14651858.CD000480.pub2. PMID: 18253980; PMCID: PMC7034523
Zhang YS, Li JD, Yan C. An update on vinpocetine: New discoveries and clinical implications. Eur J Pharmacol. 2018 Jan 15; 819: 30-34. doi: 10.1016/j.ejphar.2017.11.041. Epub 2017 Nov 26. PMID: 29183836; PMCID: PMC5766389
Bönöczk P, Panczel G, Nagy Z. Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study. Eur J Ultrasound. 2002 Jun; 15(1-2): 85-91. doi: 10.1016/s0929-8266(02)00006-x. PMID: 12044859.
Zhang W, Huang Y, Li Y, Tan L, Nao J, Hu H, Zhang J, Li C, Kong Y, Song Y. Efficacy and Safety of Vinpocetine as Part of Treatment for Acute Cerebral Infarction: A Randomized, Open-Label, Controlled, Multicenter CAVIN (Chinese Assessment for Vinpocetine in Neurology) Trial. Clin Drug Investig. 2016 Sep; 36(9): 697-704. doi: 10.1007/s40261-016-0415-x. PMID: 27283947
Vas A, Gulyás B, Szabó Z, Bönöczk P, Csiba L, Kiss B, Kárpáti E, Pánczél G, Nagy Z. Clinical and non-clinical investigations using positron emission tomography, near infrared spectroscopy and transcranial Doppler methods on the neuroprotective drug vinpocetine: a summary of evidences. J Neurol Sci. 2002 Nov 15; 203-204: 259-62. doi: 10.1016/s0022-510x(02)00301-5. PMID: 12417394.
Szilágyi G, Nagy Z, Balkay L, Boros I, Emri M, Lehel S, Márián T, Molnár T, Szakáll S, Trón L, Bereczki D, Csiba L, Fekete I, Kerényi L, Galuska L, Varga J, Bönöczk P, Vas A, Gulyás B. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J Neurol Sci. 2005 Mar 15; 229-230: 275-84. doi: 10.1016/j.jns.2004.11.053. Epub 2005 Jan 8. PMID: 15760651
Belova LA, Mashin VV, Abramova VV, Slastyon EY, Belov DV. Éffektivnost" korteksina v ostrom periode polusharnogo ishemicheskogo insul"ta [Efficacy of Korteksin in acute period of hemispheric ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 2018; 118(7): 30-34. Russian. doi: 10.17116/jnevro20181187130. PMID: 30132453.
Mashin VV, Belova LA, Aizatullin IF, Pavlova VA, Slasten EV, Abramova VV, Belov DV. Otsenka éffektivnosti i bezopasnosti primeneniia lekarstvennogo preparata Korteksin v komplekse reabilitatsionnykh meropriiatiĭ po vertikalizatsii u patsientov s ishemicheskim insul"tom v ostrom periode [Evaluation of the efficacy and safety of application of the drug cortexin in the complex rehabilitation of verticalization in patients with ischemic stroke in the acute period]. Zh Nevrol Psikhiatr Im S S Korsakova. 2019; 119(9): 62-67. Russian. doi: 10.17116/jnevro201911909162. PMID: 31626220
Stakhovskaya L.V. et al. Multicenter randomized prospective double-blind placebo-controlled study of the safety and efficacy of Cortexin in the acute and early recovery period of hemispheric ischemic stroke. Bulletin of the Russian Military Medical Academy. 1(37) – 2012
Gusev EI, Skvortsova VI, Dambinova SA, Raevskiy KS, Alekseev AA, Bashkatova VG, Kovalenko AV, Kudrin VS, Yakovleva EV. Neuroprotective effects of glycine for
therapy of acute ischaemic stroke. Cerebrovasc Dis. 2000 Jan-Feb; 10(1): 49-60. doi: 10.1159/000016025. PMID: 10629347
Chen J, Zhuang Y, Zhang ZF, Wang S, Jin P, He C, Hu PC, Wang ZF, Li ZQ, Xia GM, Li G, Wang Y, Wan Q. Glycine confers neuroprotection through microRNA-301a/PTEN Mol Brain. 2016 May 26;9(1):59. doi: 10.1186/s13041-016-0241-3
Agafyina A., Kovalenko A., Rumyantseva S. et al. Efficacy of the neurometabolic protector Cytoflavin in patients with ischemic stroke in the early recovery period (multicenter randomized trial). Vrach. 2006; 1: 60-65.
Sazonov IE, Kudinov AA, Fedotova EP. Izuchenie dozozavisimogo effekta tsitoflavina v terapii ostrogo perioda ishemicheskogo insul"ta [Study cytoflavin dose-dependent effect in the treatment of acute ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 2017; 117(2): 64-67. Russian. doi: 10.17116/jnevro20171172164-67. PMID: 28374695.
Muratov FK, Shermukhamedova FK, Batocyrenov BV, Haritonova TV. Mul"timodal"noe deistvie tsitoflavina pri ostrom mozgovom insul"te, razvivshemsya na fone metabolicheskogo sindroma [Influence of multimodal effect of cytoflavin in the acute brain stroke in patients with metabolic syndrome]. Zh Nevrol Psikhiatr Im S S Korsakova. 2016; 116(12): 44-47. Russian. doi: 10.17116/jnevro201611612144-47. PMID: 28139625.
Odinak MM, Skvortsova VI, Vozniuk IA, Rumiantseva SA, Stakhovskaia LV, Klocheva EG, Novikova LB, Ianishevskiĭ SN, Golokhvastov SIu, Tsygan NV. [Efficacy of cytoflavin in patients in the acute ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 2010; 110(12): 29-36. Russian. PMID: 21311484.
Rumyantseva S.A., Kovalenko A.L., Silina E.V., Stupin V.A., Kabaeva E.N., Chichanovskaya L.L., Nazarov M.V., Tsukurova L.A., Burenichev D.V., Golikov K.V., Salnikov M.V., Belova L.A., Mashin V.V., Mazina N.K., Zhilina E.A., Kolotik-Kameneva O.Y., Sherman M.A. Clinical and morphologic efficacy of a complex antioxidant and energy correction therapy of different duration in brain infarction: results of a multicenter randomized trial. Zh Nevrol Psikhiatr Im S S Korsakova. 2015; 115(8): 45-52. Russian. doi: 10.17116/jnevro20151158145-52. PMID: 26356615
Fedin A.I., Rumyantseva S.A., Piradov M.A. et al. Efficacy of the neurometabolic protector Cytoflavin in cerebral infarction (multicenter randomized trial) New technologies, diagnostic, treatment and prevention methods. 2005; 1(6): 13-19.
Mazin PV, Sheshunov IV, Mazina NK. Metaanaliticheskaia otsenka klinicheskoĭ éffektivnosti tsitoflavina pri nevrologicheskikh zabolevaniiakh [Meta-analytic assessment of parenteral cytoflavin effectiveness in different neurologic disorders]. Zh Nevrol Psikhiatr Im S S Korsakova. 2017; 117(3): 28-39. Russian. doi: 10.17116/jnevro20171173128-39.
Secades JJ, Alvarez-Sabín J, Castillo J, Díez-Tejedor E, Martínez-Vila E, Ríos J, Oudovenko N. Citicoline for Acute Ischemic Stroke: A Systematic Review and Formal Meta-analysis of Randomized, Double-Blind, and Placebo-Controlled Trials. J Stroke Cerebrovasc Dis. 2016 Aug; 25(8): 1984-96. doi: 10.1016/j.jstrokecerebrovasdis.2016.04.010.
Dávalos A, Alvarez-Sabín J, Castillo J, Díez-Tejedor E, Ferro J, Martínez-Vila E, Serena J, Segura T, Cruz VT, Masjuan J, Cobo E, Secades JJ; International Citicoline Trial on acUte Stroke (ICTUS) trial investigators. Citicoline in the treatment of acute ischaemic stroke: an international, randomised, multicentre, placebo-controlled study (ICTUS trial). Lancet. 2012 Jul 28; 380(9839): 349-57. doi: 10.1016/S0140-6736(12)60813-7.
Warach S, Pettigrew LC, Dashe JF, Pullicino P, Lefkowitz DM, Sabounjian L, Harnett K, Schwiderski U, Gammans R. Effect of citicoline on ischemic lesions as measured by diffusion-weighted magnetic resonance imaging. Citicoline 010 Investigators. Ann Neurol. 2000 Nov; 48(5): 713-22.
Odinak M.M., Voznyuk I.A., Piradov M.A., Rumyantseva S.A., Kuznetsov A.N., Yanishevsky S.N., Golokhvastov S.Yu., Tsygan N.V. Annals of Neurology. 2010; 4(1).
Muresanu DF, Heiss WD, Hoemberg V, Bajenaru O, Popescu CD, Vester JC, Rahlfs VW, Doppler E, Meier D, Moessler H, Guekht A. Cerebrolysin and Recovery After Stroke (CARS): A Randomized, Placebo-Controlled, Double-Blind, Multicenter Trial. Stroke. 2016 Jan; 47(1): 151-9. doi: 10.1161/STROKEAHA.115.009416.
Teasell R., Iruthayarajah J., Saikaley M, Longval M. Evidence based review of stroke rehabilitation (EBRSR) 19th Edition. 2019; 209, available at: http://www.ebrsr.com/sites/ default/files/EBRSR%20Handbook%20Chapter%204_Upper%20Extremity%20Post%20Stroke_ ML.pdf.
Association of the Scienti.c Medical Societies in Germany. Rehabilitative Therapie bei Armparese nach Schlaganfall der DGNR. Langversion. 2020; 204, available at: https://www.awmf.org/uploads/tx_szleitlinien/080-001l_S3_Rehabilitative_Therapie_bei_Armparese_nach_Schlaganfall_2020-07.pdf. EAN and EFNR guideline on pharmacological support in early motor rehabilitation after acute ischaemic stroke. Doi: 10.1111/ene.14936
Bornstein NM, Guekht A, Vester J, Heiss WD, Gusev E, Hömberg V, Rahlfs VW, Bajenaru O, Popescu BO, Muresanu D. Safety and efficacy of Cerebrolysin in early post-stroke recovery: a meta-analysis of nine randomized clinical trials. Neurol Sci. 2018 Apr; 39(4): 629-640. doi: 10.1007/s10072-017-3214-0.
Khasanova DR, Kalinin MN. Cerebrolysin as an Early Add-on to Reperfusion Therapy: Risk of Hemorrhagic Transformation after Ischemic Stroke (CEREHETIS), a prospective, randomized, multicenter pilot study. BMC Neurol. 2023 Mar 27;23(1):121. doi: 10.1186/s12883-023-03159-w. PMID: 36973684; PMCID: PMC10041692
Gusev EI, Skvortsova VI, Miasoedov NF, Nezavibat"ko VN, Zhuravleva EIu, Vanichkin AV. Effektivnost" semaksa v ostrom periode polusharnogo ishemicheskogo insul"ta (klinicheskoe i élektrofiziologicheskoe issledovanie) [Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Zh Nevrol Psikhiatr Im S S Korsakova. 1997; 97(6): 26-34. Russian. PMID: 11517472
Gusev E.I., Martynov M.Yu., Kostenko E.V., Petrova L.V., Bobyreva S.N. Efficacy of Semax in the treatment of patients at different stages of ischemic stroke. S.S. Korsakov Journal of Neurology and Psychiatry. Special Issues. 2018;118(3 2):61-68
Stakhovskaya LV, Shamalov NA, Khasanova DR, Melnikova EV, Agafiina AS, Golikov KV, Bogdanov EI, Yakupova AA, Roshkovskaya LV, Lukinykh LV, Lokshtanova TM, Poverennova IE, Shepankevich LA. Rezul"taty randomizirovannogo dvoĭnogo slepogo mul"titsentrovogo platsebo-kontroliruemogo v parallel"nykh gruppakh issledovaniia éffektivnosti i bezopasnosti meksidola pri dlitel"noĭ posledovatel"noĭ terapii u patsientov v ostrom i rannem vosstanovitel"nom periodakh polusharnogo ishemicheskogo insul"ta (ÉPIKA) [Results of a randomized double blind multicenter placebo-controlled, in parallel groups trial of the efficacy and safety of prolonged sequential therapy with mexidol in the acute and early recovery stages of hemispheric ischemic stroke (EPICA)]. Zh Nevrol Psikhiatr Im S S Korsakova. 2017; 117 (3. Vyp. 2): 55-65. Russian. doi: 10.17116/jnevro20171173255-65.
Voznyuk IA, Kolomentsev SV, Morozova EM. The impact of therapy with Mexidol on neurological deficit and functional outcome in patients with ischemic stroke: a systematic review and meta-analysis. S.S. Korsakov Journal of Neurology and Psychiatry. 2023;123(12‑2):49‑60. (In Russ.) https://doi.org/10.17116/jnevro202312312249
Belskaya GN, Krylova LG, Sokolov MA, Izmailov IA. "Possibilities of speech disorder correction in the acute period of ischemic stroke using neuroprotective therapy". S.S. Korsakov Journal of Neurology and Psychiatry. 2015;115(9‑2):60‑63
Belskaya GN, Chuprina SE, Vorobyov AA, Gorozha EN, Butorakina TL, Sokolov MA, Izmailov IA. "Cognitive impairment in stroke: possibilities of pharmacotherapy". S.S. Korsakov Journal of Neurology and Psychiatry. 2016;116(5):33-7
Tanashyan MM, Domashenko MA, Maksimova MYu. "Modern neuroprotection in the complex treatment of patients in the acute and early recovery periods of ischemic stroke". Journal "Nervnye Bolezni". 2017;3:18-22
Kamchatnov PR, Izmailov IA, Sokolov MA. "Results of Cellex administration in patients with cerebrovascular diseases", Journal "Nervnye Bolezni", No. 1, 2018, DOI: 10.24411/2071-5315-2018-11994
Vahedi K, Hofmeijer J, Juettler E, Vicaut E, George B, Algra A, Amelink GJ, Schmiedeck P, Schwab S, Rothwell PM, Bousser MG, van der Worp HB, Hacke W; DECIMAL, DESTINY, and HAMLET Investigators. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007; 6: 215-222.
Yang MH, Lin HY, Fu J, Roodrajeetsing G, Shi SL, Xiao SW. Decompressive hemicraniectomy in patients with malignant middle cerebral artery infarction: a systematic review and meta-analysis. Surgeon. 2015; 13: 230-240.
Alexander P, Heels-Ansdell D, Siemieniuk R, Bhatnagar N, Chang Y, Fei Y, Zhang Y, McLeod S, Prasad K, Guyatt G. Hemicraniectomy versus medical treatment with large MCA infarct: a review and meta-analysis. BMJ Open. 2016; 6: e014390.
Krylov VV, Dreval ON, Dzhinzhikhadze RS, Lazarev VA, Dashyan VG, Nikitin AS, Petrikov SS. Clinical guidelines for the diagnosis and treatment of malignant forms of ischemic stroke in the middle cerebral artery territory. URL: http://ruans.org/Text/Guidelines/ischemic_stroke_severe_form_mca.pdf.
Dominik Lehrieder, Hans-Peter Müller, Jan Kassubek, Nils Hecht, Götz Thomalla, Dominik Michalski, Thomas Gattringer, Katja E. Wartenberg, Jörg Schultze-Amberger, Hagen Huttner, Joji B. Kuramatsu, Silke Wunderlich, Hans-Herbert Steiner, Karin Weissenborn, Suzette Heck, Albrecht Günther, Hauke Schneider, Sven Poli, Christian Dohmen, Johannes Woitzik, Eric Jüttler, Hermann Neugebauer, on behalf of the DESTINY-R (DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY - Registry) Study Group and IGNITE (Initiative of German NeuroIntensive Trial Engagement); Study Group Large diameter hemicraniectomy does not improve long-term outcome in malignant infarction J Neurol. 2023; 270(8): 4080–4089. Published online 2023 May 10. doi: 10.1007/s00415-023-11766-3
Agarwalla PK, Stapleton CJ, Ogilvy CS. Craniectomy in acute ischemic stroke. Neurosurgery. 2014; 74(suppl 1): S151–S162.
Raco A, Caroli E, Isidori A, Salvati M. Management of acute cerebellar infarction: one institution’s experience. Neurosurgery. 2003; 53: 1061–1065.
Mostofi K. Neurosurgical management of massive cerebellar infarct outcome in 53 patients. Surg Neurol Int. 2013; 4: 28.
Krylov VV, Nikitin AS, Dashyan VG, Burov SA, Petrikov SS, Asratyan SA. Surgery of massive ischemic stroke. Moscow: GEOTAR-Media; 2016.
Aaron S, Ferreira JM, Coutinho JM, Canhão P, Conforto AB, Arauz A, Carvalho M, Masjuan J, Sharma VK, Putaala J, Uyttenboogaart M, Werring DJ, Bazan R, Mohindra S, Weber J, Coert BA, Kirubakaran P, Sanchez van Kammen M, Singh P, Aguiar de Sousa D, Ferro JM; DECOMPRESS2 Study Group. Outcomes of Decompressive Surgery for Patients With Severe Cerebral Venous Thrombosis: DECOMPRESS2 Observational Study. Stroke. 2024 May;55(5):1218-1226. doi: 10.1161/STROKEAHA.123.045051
Xu MY. Poststroke seizure: optimising its management. Stroke Vasc Neurol. 2018; 4(1): 48-56.
Beghi E, Carpio A, Forsgren L, Hesdorffer DC, Malmgren K, Sander JW, Tomson T, Hauser WA. Recommendation for a definition of acute symptomatic seizure. Epilepsia. 2010 Apr; 51(4): 671-5.
Holtkamp M, Beghi E, Benninger F, Kälviäinen R, Rocamora R, Christensen H; European Stroke Organisation. European Stroke Organisation guidelines for the management of post-stroke seizures and epilepsy. Eur Stroke J. 2017 Jun; 2(2): 103-115.
Glauser T, Shinnar S, Gloss D, Alldredge B, Arya R, Bainbridge J, Bare M, Bleck T, Dodson WE, Garrity L, Jagoda A, Lowenstein D, Pellock J, Riviello J, Sloan E, Treiman DM. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus in Children and Adults: Report of the Guideline Committee of the American Epilepsy Society. Epilepsy Curr. 2016 Jan-Feb; 16(1): 48-61.
Brigo F, Nardone R, Tezzon F, Trinka E. Nonintravenous midazolam versus intravenous or rectal diazepam for the treatment of early status epilepticus: A systematic review with meta-analysis. Epilepsy Behav. 2015 Aug; 49: 325-36
van Tuijl JH, van Raak EP, de Krom MC, Lodder J, Aldenkamp AP. Early treatment after stroke for the prevention of late epileptic seizures: a report on the problems performing a randomised placebo-controlled double-blind trial aimed at anti-epileptogenesis. Seizure. 2011 May; 20(4): 285-91.
Sales F, Chaves J, McMurray R, Loureiro R, Fernandes H, Villanueva V. Eslicarbazepine acetate in post-stroke epilepsy: Clinical practice evidence from Euro-Esli. Acta Neurol Scand. 2020 Dec; 142 (6): 563-573.
Glauser T, Ben-Menachem E, Bourgeois B, Cnaan A, Guerreiro C, Kälviäinen R, Mattson R, French JA, Perucca E, Tomson T; ILAE Subcommission on AED Guidelines. Updated ILAE evidence review of antiepileptic drug efficacy and effectiveness as initial monotherapy for epileptic seizures and syndromes. Epilepsia. 2013 Mar; 54(3): 551-63.
Werhahn KJ, Trinka E, Dobesberger J, Unterberger I, Baum P, Deckert-Schmitz M, Kniess T, Schmitz B, Bernedo V, Ruckes C, Ehrlich A, Krämer G. A randomized, double-blind comparison of antiepileptic drug treatment in the elderly with new-onset focal epilepsy. Epilepsia. 2015 Mar; 56(3): 450-9.
Zelano J. Poststroke epilepsy: update and future directions. Ther Adv Neurol Disord. 2016 Sep; 9(5): 424-35.
Mauritz M, Hirsch LJ, Camfield P, Chin R, Nardone R, Lattanzi S, Trinka E. Acute symptomatic seizures: an educational, evidence-based review. Epileptic Disord. 2022 Feb 1;24(1):26-49. doi: 10.1684/epd.2021.1376. PMID: 34789447 ;
Chadehumbe MA, Khatri P, Khoury JC, Alwell K, Szaflarski JP, Broderick JP, et al. Seizures are common in the acute setting of childhood stroke: a population-based study. J Child Neurol. 2009;24(1):9-12 ;
Abend NS, Beslow LA, Smith SE, Kessler SK, Vossough A, Mason S, et al. Seizures as a presenting symptom of acute arterial ischemic stroke in childhood. J Pediatr. 2011;159(3):479-83 ;
Singh RK, Zecavati N, Singh J, Kaulas H, Nelson KB, Dean NP, et al. Seizures in acute childhood stroke. J Pediatr. 2012;160(2):291-6.
Fox CK, Glass HC, Sidney S, Lowenstein DH, Fullerton HJ. Acute seizures predict epilepsy after childhood stroke. Ann Neurol. 2013;74(2):249-56 ;
Fox CK, Mackay MT, Dowling MM, Pergami P, Titomanlio L, Deveber G, et al. Prolonged or recurrent acute seizures after pediatric arterial ischemic stroke are associated with increasing epilepsy risk. Dev Med Child Neurol. 2016.
Mitchell AJ, Sheth B, Gill J, Yadegarfar M, Stubbs B, Yadegarfar M, Meader N. Prevalence and predictors of post-stroke mood disorders: A meta-analysis and meta-regression of depression, anxiety and adjustment disorder. Gen Hosp Psychiatry. 2017 Jul; 47: 48-60.
Qin B, Chen H, Gao W, Zhao LB, Zhao MJ, Qin HX, Chen W, Chen L, Yang MX. Efficacy, acceptability, and tolerability of antidepressant treatments for patients with post-stroke depression: a network meta-analysis. Braz J Med Biol Res. 2018; 51(7): e7218.
Gu J, Huang H, Chen K, Huang G, Huang Y, Xu H. Are they necessary? Preventive therapies for post-stroke depression: A meta-analysis of RCTs. Psychiatry Res. 2020 Feb; 284: 112670.
FOCUS Trial Collaboration. Effects of fluoxetine on functional outcomes after acute stroke (FOCUS): a pragmatic, double-blind, randomised, controlled trial. Lancet. 2019 Jan 19; 393(10168): 265-274.
Kalbouneh HM, Toubasi AA, Albustanji FH, Obaid YY, Al-Harasis LM. Safety and Efficacy of SSRIs in Improving Poststroke Recovery: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2022 Jul 5;11(13):e025868. doi: 10.1161/JAHA.122.025868. Epub 2022 Jun 22. PMID: 35730636; PMCID: PMC9333390
Stahl S.M. Prescriber"s guide: Stahl"s essential psychopharmacology. Cambridge University Press, 2020.
Zhou S, Liu S, Liu X, Zhuang W. Selective serotonin reuptake inhibitors for functional independence and depression prevention in early stage of post-stroke: A meta-analysis. Medicine (Baltimore). 2020 Feb; 99(6): e19062.
Bai ZF, Wang LY. Efficacy of sertraline for post-stroke depression: A systematic review protocol of randomized controlled trial. Medicine (Baltimore). 2019 Apr; 98(16): e15299.
Sun Y, Liang Y, Jiao Y, Lin J, Qu H, Xu J, Zhao C. Comparative efficacy and acceptability of antidepressant treatment in poststroke depression: a multiple-treatments metaanalysis. BMJ Open. 2017 Aug 3; 7(8): e016499.
Starkstein SE, Hayhow BD. Treatment of Post-Stroke Depression. Curr Treat Options Neurol. 2019 Jun 25; 21(7): 31.
Lee EJ, Oh MS, Kim JS, Chang DI, Park JH, Cha JK, Heo JH, Sohn SI, Kim DE, Kim HY, Kim J, Seo WK, Lee J, Park SW, Kim YJ, Lee BC; EMOTION investigators. Serotonin transporter gene polymorphisms may be associated with poststroke neurological recovery after escitalopram use. J Neurol Neurosurg Psychiatry. 2018 Mar; 89(3): 271-276.
Jorge RE, Acion L, Moser D, Adams HP Jr, Robinson RG. Escitalopram and enhancement of cognitive recovery following stroke. Arch Gen Psychiatry. 2010 Feb; 67(2): 187-96.
Cipriani A, Furukawa TA, Salanti G, Geddes JR, Higgins JP, Churchill R, Watanabe N, Nakagawa A, Omori IM, McGuire H, Tansella M, Barbui C. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009 Feb 28; 373(9665): 746-58.
Cui M, Huang CY, Wang F. Efficacy and Safety of Citalopram for the Treatment of Poststroke Depression: A Meta-Analysis. J Stroke Cerebrovasc Dis. 2018 Nov; 27(11): 2905-2918
Deng L, Sun X, Qiu S, Xiong Y, Li Y, Wang L, Wei Q, Wang D, Liu M. Interventions for management of post-stroke depression: A Bayesian network meta-analysis of 23 randomized controlled trials. Sci Rep. 2017 Nov 28; 7(1): 16466.
Van de Meent H, Geurts AC, Van Limbeek J. Pharmacologic treatment of poststroke depression: a systematic review of the literature. Top Stroke Rehabil. 2003 Spring; 10(1): 79-92.
Chun HY, Whiteley WN, Dennis MS, Mead GE, Carson AJ. Anxiety After Stroke: The Importance of Subtyping. Stroke. 2018 Mar; 49(3): 556-564.
Lerdal A, Kottorp A, Gay CL, Grov EK, Lee KA. Rasch analysis of the Beck Depression Inventory-II in stroke survivors: a cross-sectional study. J Affect Disord. 2014 Apr; 158: 48-52.
Mitchell AJ, Sheth B, Gill J, Yadegarfar M, Stubbs B, Yadegarfar M, Meader N. Prevalence and predictors of post-stroke mood disorders: A meta-analysis and meta-regression of depression, anxiety and adjustment disorder. Gen Hosp Psychiatry. 2017 Jul; 47: 48-60.
Rafsten L, Danielsson A, Sunnerhagen KS. Anxiety after stroke: A systematic review and meta-analysis. J Rehabil Med. 2018 Sep 28; 50(9): 769-778
Wright F, Wu S, Chun HY, Mead G. Factors Associated with Poststroke Anxiety: A Systematic Review and Meta-Analysis. Stroke Res Treat. 2017; 2017: 2124743.
Mead GE, Hsieh CF, Lee R, Kutlubaev MA, Claxton A, Hankey GJ, Hackett ML. Selective serotonin reuptake inhibitors (SSRIs) for stroke recovery. Cochrane Database Syst Rev. 2012 Nov 14; 11(11): CD009286.
Knapp P, Campbell Burton CA, Holmes J, Murray J, Gillespie D, Lightbody CE, Watkins CL, Chun HY, Lewis SR. Interventions for treating anxiety after stroke. Cochrane Database Syst Rev. 2017 May 23; 5(5): CD008860.
Cui M, Huang CY, Wang F. Efficacy and Safety of Citalopram for the Treatment of Poststroke Depression: A Meta-Analysis. J Stroke Cerebrovasc Dis. 2018 Nov; 27(11): 2905-2918.
Wright F, Wu S, Chun HY, Mead G. Factors Associated with Poststroke Anxiety: A Systematic Review and Meta-Analysis. Stroke Res Treat. 2017; 2017: 2124743.
Knapp P, Campbell Burton CA, Holmes J, Murray J, Gillespie D, Lightbody CE, Watkins CL, Chun HY, Lewis SR. Interventions for treating anxiety after stroke. Cochrane Database Syst Rev. 2017 May 23; 5(5): CD008860
Kim JS, Bashford G, Murphy TK, Martin A, Dror V, Cheung R. Safety and efficacy of pregabalin in patients with central post-stroke pain. Pain. 2011; 152(5): 1018-1023
Campbell BCV, van Zwam WH, Goyal M, Menon BK, Dippel DWJ, Demchuk AM, Bracard S, White P, Dávalos A, Majoie CBLM, van der Lugt A, Ford GA, de la Ossa NP, Kelly M, Bourcier R, Donnan GA, Roos YBWEM, Bang OY, Nogueira RG, Devlin TG, van den Berg LA, Clarençon F, Burns P, Carpenter J, Berkhemer OA, Yavagal DR, Pereira VM, Ducrocq X, Dixit A, Quesada H, Epstein J, Davis SM, Jansen O, Rubiera M, Urra X, Micard E, Lingsma HF, Naggara O, Brown S, Guillemin F, Muir KW, van Oostenbrugge RJ, Saver JL, Jovin TG, Hill MD, Mitchell PJ; HERMES collaborators. Effect of general anaesthesia on functional outcome in patients with anterior circulation ischaemic stroke having endovascular thrombectomy versus standard care: a meta-analysis of individual patient data. Lancet Neurol. 2018 Jan; 17(1): 47-53. doi: 10.1016/S1474-4422(17)30407-6.
Schonenberger, S., et al., Association of General Anesthesia vs Procedural Sedation With Functional Outcome Among Patients With Acute Ischemic Stroke Undergoing Thrombectomy: A Systematic Review and Meta-analysis. JAMA, 2019. 322(13): p. 1283-1293
Küçükdeveci AA, Stibrant Sunnerhagen K, Golyk V, Delarque A, Ivanova G, Zampolini M, Kiekens C, Varela Donoso E, Christodoulou N. Evidence-based position paper on Physical and Rehabilitation Medicine professional practice for persons with stroke. The European PRM position (UEMS PRM Section). Eur J Phys Rehabil Med. 2018 Dec; 54(6): 957-970. doi: 10.23736/S1973-9087.18.05501-6
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Phys Med Rehabil Clin N Am. 2014 May; 25(2): 411-37. doi: 10.1016/j.pmr.2014.01.010. Epub 2014 Mar 14.
Saunders DH, Sanderson M, Hayes S, Johnson L, Kramer S, Carter DD, Jarvis H, Brazzelli M, Mead GE. Physical fitness training for stroke patients. Cochrane Database Syst Rev. 2020 Mar 20; 3(3): CD003316. doi: 10.1002/14651858.CD003316.pub7.
Langhorne P, Collier JM, Bate PJ, Thuy MN, Bernhardt J. Very early versus delayed mobilisation after stroke. Cochrane Database Syst Rev. 2018 Oct 16; 10(10): CD006187. doi: 10.1002/14651858.CD006187.pub3.
Daniels SK, Anderson JA, Willson PC. Valid items for screening dysphagia risk in patients with stroke: a systematic review. Stroke. 2012 Mar; 43(3): 892-7. doi: 10.1161/STROKEAHA.111.640946.
Burgos R, Bretón I, Cereda E, Desport JC, Dziewas R, Genton L, Gomes F, Jésus P, Leischker A, Muscaritoli M, Poulia KA, Preiser JC, Van der Marck M, Wirth R, Singer P, Bischoff SC. ESPEN guideline clinical nutrition in neurology. Clin Nutr. 2018 Feb; 37(1): 354-396. doi: 10.1016/j.clnu.2017.09.003.
Geeganage C, Beavan J, Ellender S, Bath PM. Interventions for dysphagia and nutritional support in acute and subacute stroke. Cochrane Database Syst Rev. 2012 Oct 17; 10: CD000323. doi: 10.1002/14651858.CD000323.pub2.
Ivanova GE, Melnikova EV, Shmonin AA, Verbitskaya EV, Belkin AA, Bodrova RA, Lebedev PV, Maltseva MN, Prokopenko SV, Prosvirnina MS, Sarana AM, Stakhovskaya LV, Suvorov AYu, Khasanova DR, Shamalov NA. Evaluation of the effectiveness of a multidisciplinary team as a new model of rehabilitation care for patients with cerebral stroke. Bulletin of RSMU. 2019; 6: 5-15.
Winstein CJ, Stein J, Arena R, Bates B, Cherney LR, Cramer SC, Deruyter F, Eng JJ, Fisher B, Harvey RL, Lang CE, MacKay-Lyons M, Ottenbacher KJ, Pugh S, Reeves MJ, Richards LG, Stiers W, Zorowitz RD; American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Quality of Care and Outcomes Research. Guidelines for Adult Stroke Rehabilitation and Recovery: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2016 Jun; 47(6): e98-e169. doi: 10.1161/STR.0000000000000098.
Hebert D, Lindsay MP, McIntyre A, Kirton A, Rumney PG, Bagg S, Bayley M, Dowlatshahi D, Dukelow S, Garnhum M, Glasser E, Halabi ML, Kang E, MacKay-Lyons M, Martino R, Rochette A, Rowe S, Salbach N, Semenko B, Stack B, Swinton L, Weber V, Mayer M, Verrilli S, DeVeber G, Andersen J, Barlow K, Cassidy C, Dilenge ME, Fehlings D, Hung R, Iruthayarajah J, Lenz L, Majnemer A, Purtzki J, Rafay M, Sonnenberg LK, Townley A, Janzen S, Foley N, Teasell R. Canadian stroke best practice recommendations: Stroke rehabilitation practice guidelines, update 2015. Int J Stroke. 2016 Jun; 11(4): 459-84. doi: 10.1177/1747493016643553.
Legg LA, Lewis SR, Schofield-Robinson OJ, Drummond A, Langhorne P. Occupational therapy for adults with problems in activities of daily living after stroke. Cochrane Database Syst Rev. 2017 Jul 19; 7(7): CD003585. doi: 10.1002/14651858.CD003585.pub3.
Zhang C, Li-Tsang CW, Au RK. Robotic approaches for the rehabilitation of upper limb recovery after stroke: a systematic review and meta-analysis. Int J Rehabil Res. 2017 Mar; 40(1): 19-28. doi: 10.1097/MRR.0000000000000204.
Mitchell C, Bowen A, Tyson S, Butterfint Z, Conroy P. Interventions for dysarthria due to stroke and other adult-acquired, non-progressive brain injury. Cochrane Database Syst Rev. 2017 Jan 25; 1(1): CD002088. doi: 10.1002/14651858.CD002088.pub3.
Russo MJ, Prodan V, Meda NN, Carcavallo L, Muracioli A, Sabe L, Bonamico L, Allegri RF, Olmos L. High-technology augmentative communication for adults with post-stroke aphasia: a systematic review. Expert Rev Med Devices. 2017 May; 14(5): 355-370. doi: 10.1080/17434440.2017.1324291.
Legg LA, Lewis SR, Schofield-Robinson OJ, Drummond A, Langhorne P. Occupational therapy for adults with problems in activities of daily living after stroke. Cochrane Database Syst Rev. 2017 Jul 19; 7(7): CD003585. doi: 10.1002/14651858.CD003585.pub3.
Langhorne P, Collier JM, Bate PJ, Thuy MN, Bernhardt J. Very early versus delayed mobilisation after stroke. Cochrane Database Syst Rev. 2018 Oct 16; 10(10): CD006187. doi: 10.1002/14651858.CD006187.pub3.
Belkin AA. Post-intensive care syndrome (PICS). A.I. Saltanov Intensive Care Issues. 2018; 2: 12-23.
Billinger SA, Arena R, Bernhardt J, Eng JJ, Franklin BA, Johnson CM, MacKay-Lyons M, Macko RF, Mead GE, Roth EJ, Shaughnessy M, Tang A; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; Council on Epidemiology and Prevention; Council on Clinical Cardiology. Physical activity and exercise recommendations for stroke survivors: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Aug; 45(8): 2532-53. doi: 10.1161/STR.0000000000000022.
Billinger SA, Arena R, Bernhardt J, Eng JJ, Franklin BA, Johnson CM, MacKay-Lyons M, Macko RF, Mead GE, Roth EJ, Shaughnessy M, Tang A; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; Council on Epidemiology and Prevention; Council on Clinical Cardiology. Physical activity and exercise recommendations for stroke survivors: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Aug; 45(8): 2532-53. doi: 10.1161/STR.0000000000000022.
Coleman ER, Moudgal R, Lang K, Hyacinth HI, Awosika OO, Kissela BM, Feng W. Early Rehabilitation After Stroke: a Narrative Review. Curr Atheroscler Rep. 2017 Nov 7; 19(12): 59. doi: 10.1007/s11883-017-0686-6.
Hebert D, Lindsay MP, McIntyre A, Kirton A, Rumney PG, Bagg S, Bayley M, Dowlatshahi D, Dukelow S, Garnhum M, Glasser E, Halabi ML, Kang E, MacKay-Lyons M, Martino R, Rochette A, Rowe S, Salbach N, Semenko B, Stack B, Swinton L, Weber V, Mayer M, Verrilli S, DeVeber G, Andersen J, Barlow K, Cassidy C, Dilenge ME, Fehlings D, Hung R, Iruthayarajah J, Lenz L, Majnemer A, Purtzki J, Rafay M, Sonnenberg LK, Townley A,Janzen S, Foley N, Teasell R. Canadian stroke best practice recommendations: Stroke rehabilitation practice guidelines, update 2015. Int J Stroke. 2016 Jun; 11(4): 459-84. doi: 10.1177/1747493016643553.
Coleman ER, Moudgal R, Lang K, Hyacinth HI, Awosika OO, Kissela BM, Feng W. Early Rehabilitation After Stroke: a Narrative Review. Curr Atheroscler Rep. 2017 Nov 7; 19(12): 59. doi: 10.1007/s11883-017-0686-6.
Koog YH, Jin SS, Yoon K, Min BI. Interventions for hemiplegic shoulder pain: systematic review of randomised controlled trials. Disabil Rehabil. 2010; 32(4): 282-91. doi: 10.3109/09638280903127685.
Ratnasabapathy Y, Broad J, Baskett J, Pledger M, Marshall J, Bonita R. Shoulder pain in people with a stroke: a population-based study. Clin Rehabil. 2003 May; 17(3): 304-11. doi: 10.1191/0269215503cr612oa.
Khasanova DR. Stroke. Modern approaches to diagnosis, treatment and prevention: clinical guidelines. Ed. by D.R. Khasanova, V.I. Danilov. Moscow: GEOTAR-Media, 2014; 248. URL: https://www.rosmedlib.ru/book/ISBN9785970428269.html.
Stroke in adults: central paresis of the upper extremity. Clinical guidelines. Moscow, 2017; 105/
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Phys Med Rehabil Clin N Am. 2014 May; 25(2): 411-37. doi: 10.1016/j.pmr.2014.01.010.
Howlett OA, Lannin NA, Ada L, McKinstry C. Functional electrical stimulation improves activity after stroke: a systematic review with meta-analysis. Arch Phys Med Rehabil. 2015 May; 96(5): 934-43. doi: 10.1016/j.apmr.2015.01.013. Epub 2015 Jan 26.
Prenton S, Hollands KL, Kenney LP. Functional electrical stimulation versus ankle foot orthoses for foot-drop: A meta-analysis of orthotic effects. J Rehabil Med. 2016 Oct 5; 48(8): 646-656. doi: 10.2340/16501977-2136.
Veerbeek JM, van Wegen E, van Peppen R, van der Wees PJ, Hendriks E, Rietberg M, Kwakkel G. What is the evidence for physical therapy poststroke? A systematic review and meta-analysis. PLoS One. 2014 Feb 4; 9(2): e87987. doi: 10.1371/journal.pone.0087987.
Norouzi-Gheidari N, Archambault PS, Fung J. Effects of robot-assisted therapy on stroke rehabilitation in upper limbs: systematic review and meta-analysis of the literature. J Rehabil Res Dev. 2012; 49(4): 479-96. doi: 10.1682/jrrd.2010.10.0210.
Mehrholz J, Pohl M, Platz T, Kugler J, Elsner B. Electromechanical and robot-assisted arm training for improving activities of daily living, arm function, and arm muscle strength after stroke. Cochrane Database Syst Rev. 2018 Sep 3; 9(9): CD006876. doi: 10.1002/14651858.CD006876.pub5.
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Phys Med Rehabil Clin N Am. 2014 May; 25(2): 411-37. doi: 10.1016/j.pmr.2014.01.010.
Rosales RL, Efendy F, Teleg ES, Delos Santos MM, Rosales MC, Ostrea M, Tanglao MJ, Ng AR. Botulinum toxin as early intervention for spasticity after stroke or non-progressive brain lesion: A meta-analysis. J Neurol Sci. 2016 Dec 15; 371: 6-14. doi: 10.1016/j.jns.2016.10.005.
Kinnear BZ, Lannin NA, Cusick A, Harvey LA, Rawicki B. Rehabilitation therapies after botulinum toxin-A injection to manage limb spasticity: a systematic review. Phys Ther. 2014 Nov; 94(11): 1569-81. doi: 10.2522/ptj.20130408.
Esquenazi A, Bavikatte G, Bandari DS, Jost WH, Munin MC, Tang SFT, Largent J, Adams AM, Zuzek A, Francisco GE. Long-Term Observational Results from the ASPIRE Study: OnabotulinumtoxinA Treatment for Adult Lower Limb Spasticity. PM R. 2021 Oct; 13(10): 1079-1093. doi: 10.1002/pmrj.12517.
Francisco GE, McGuire JR. Poststroke spasticity management. Stroke. 2012 Nov; 43(11): 3132-6. doi: 10.1161/STROKEAHA.111.639831.
Foley N, Murie-Fernandez M, Speechley M, Salter K, Sequeira K, Teasell R. Does the treatment of spastic equinovarus deformity following stroke with botulinum toxin increase gait velocity? A systematic review and meta-analysis. Eur J Neurol. 2010 Dec; 17(12): 1419-27. doi: 10.1111/j.1468-1331.2010.03084.x.
Khan F, Amatya B, Bensmail D, Yelnik A. Non-pharmacological interventions for spasticity in adults: An overview of systematic reviews. Ann Phys Rehabil Med. 2019 Jul; 62(4): 265-273. doi: 10.1016/j.rehab.2017.10.001. Epub 2017 Oct 16. PMID: 29042299.
Watson JC, Sandroni P. Central Neuropathic Pain Syndromes. Mayo Clin Proc. 2016 Mar; 91(3): 372-85. doi: 10.1016/j.mayocp.2016.01.017. PMID: 26944242
Saunders DH, Sanderson M, Hayes S, Johnson L, Kramer S, Carter DD, Jarvis H, Brazzelli M, Mead GE. Physical fitness training for stroke patients. Cochrane Database Syst Rev. 2020 Mar 20; 3(3): CD003316. doi: 10.1002/14651858.CD003316.pub7.
States RA, Pappas E, Salem Y. Overground physical therapy gait training for chronic stroke patients with mobility deficits. Cochrane Database Syst Rev. 2009 Jul 8; 2009(3): CD006075. doi: 10.1002/14651858.CD006075.pub2.
Billinger SA, Arena R, Bernhardt J, Eng JJ, Franklin BA, Johnson CM, MacKay-Lyons M, Macko RF, Mead GE, Roth EJ, Shaughnessy M, Tang A; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; Council on Epidemiology and Prevention; Council on Clinical Cardiology. Physical activity and exercise recommendations for stroke survivors: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Aug; 45(8): 2532-53. doi: 10.1161/STR.0000000000000022.
Legg LA, Lewis SR, Schofield-Robinson OJ, Drummond A, Langhorne P. Occupational therapy for adults with problems in activities of daily living after stroke. Cochrane Database Syst Rev. 2017 Jul 19; 7(7): CD003585. doi: 10.1002/14651858.CD003585.pub3.
Choi W. Effects of Robot-Assisted Gait Training with Body Weight Support on Gait and Balance in Stroke Patients. Int J Environ Res Public Health. 2022 May 10;19(10):5814. doi: 10.3390/ijerph19105814. PMID: 35627346; PMCID: PMC9141724.
van Heugten C, Gregório GW, Wade D. Evidence-based cognitive rehabilitation after acquired brain injury: a systematic review of content of treatment. Neuropsychol Rehabil. 2012; 22(5): 653-73. doi: 10.1080/09602011.2012.680891.
Poulin V, Korner-Bitensky N, Dawson DR, Bherer L. Efficacy of executive function interventions after stroke: a systematic review. Top Stroke Rehabil. 2012 Mar-Apr; 19(2): 158-71. doi: 10.1310/tsr1902-158.
Cicerone KD, Dahlberg C, Kalmar K, Langenbahn DM, Malec JF, Bergquist TF, Felicetti T, Giacino JT, Harley JP, Harrington DE, Herzog J, Kneipp S, Laatsch L, Morse PA. Evidence-based cognitive rehabilitation: recommendations for clinical practice. Arch Phys Med Rehabil. 2000 Dec; 81(12): 1596-615. doi: 10.1053/apmr.2000.19240.
Akhutina TV, Mikadze YuV, Ivanova MV, Larina OD, Norvils SN, Tsareva IV. Speech therapy diagnostics and rehabilitation of patients with acute brain injury: clinical guidelines. Moscow, 2014; 46.
Bogolepova AN, Vasenina EE, Zakharov VV, Katunina EA, Levin OS, Litvinenko IV, Preobrazhenskaya IS, Fukalov YuA, Shklovsky VM, Tsygan NV, Yakhno NN. Rehabilitation of higher mental functions in patients with focal brain lesions: clinical guidelines. Moscow, 2018; 88.
Bowen A, Hazelton C, Pollock A, Lincoln NB. Cognitive rehabilitation for spatial neglect following stroke. Cochrane Database Syst Rev. 2013 Jul 1;2013(7):CD003586. doi: 10.1002/14651858.CD003586.pub3. Update in: Cochrane Database Syst Rev. 2021 Jul 1; 7: CD003586.
Hebert D, Lindsay MP, McIntyre A, Kirton A, Rumney PG, Bagg S, Bayley M, Dowlatshahi D, Dukelow S, Garnhum M, Glasser E, Halabi ML, Kang E, MacKay-Lyons M, Martino R, Rochette A, Rowe S, Salbach N, Semenko B, Stack B, Swinton L, Weber V, Mayer M, Verrilli S, DeVeber G, Andersen J, Barlow K, Cassidy C, Dilenge ME, Fehlings D, Hung R, Iruthayarajah J, Lenz L, Majnemer A, Purtzki J, Rafay M, Sonnenberg LK, Townley A, Janzen S, Foley N, Teasell R. Canadian stroke best practice recommendations: Stroke rehabilitation practice guidelines, update 2015. Int J Stroke. 2016 Jun;11(4):459-84. doi: 10.1177/1747493016643553.
Thieme H, Morkisch N, Mehrholz J, Pohl M, Behrens J, Borgetto B, Dohle C. Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev. 2018 Jul 11;7(7):CD008449. doi: 10.1002/14651858.CD008449.pub3. PMID: 29993119; PMCID: PMC6513639
Nazarova MA, Piradov MA, Chernikova LA. Visual feedback - mirror therapy in neurorehabilitation. Annals of Clinical and Experimental Neurology. 2012; 6: 36-41
Laver KE, Lange B, George S, Deutsch JE, Saposnik G, Crotty M. Virtual reality for stroke rehabilitation. Cochrane Database Syst Rev. 2017 Nov 20; 11(11): CD008349. doi: 10.1002/14651858.CD008349.pub4
Sorinola IO, Powis I, White CM. Does additional exercise improve trunk function recovery in stroke patients? A meta-analysis. NeuroRehabilitation. 2014 Jan 1; 35(2): 205-13. doi: 10.3233/NRE-141123.
Keller I, Lefin-Rank G. Improvement of visual search after audiovisual exploration training in hemianopic patients. Neurorehabil Neural Repair. 2010 Sep; 24(7): 666-73. doi: 10.1177/1545968310372774
Corbetta D, Sirtori V, Castellini G, Moja L, Gatti R. Constraint-induced movement therapy for upper extremities in people with stroke. Cochrane Database Syst Rev. 2015 Oct 8; 2015(10): CD004433. doi: 10.1002/14651858.CD004433.pub3
Mehrholz J, Pohl M, Platz T, Kugler J, Elsner B. Electromechanical and robot-assisted arm training for improving activities of daily living, arm function, and arm muscle strength after stroke. Cochrane Database Syst Rev. 2018 Sep 3; 9(9): CD006876. doi: 10.1002/14651858.CD006876.pub5
Mehrholz J, Thomas S, Elsner B. Treadmill training and body weight support for walking after stroke. Cochrane Database Syst Rev. 2017 Aug 17; 8(8): CD002840. doi: 10.1002/14651858.CD002840.pub4
Billinger SA, Arena R, Bernhardt J, Eng JJ, Franklin BA, Johnson CM, MacKay-Lyons M, Macko RF, Mead GE, Roth EJ, Shaughnessy M, Tang A; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health; Council on Epidemiology and Prevention; Council on Clinical Cardiology. Physical activity and exercise recommendations for stroke survivors: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Aug; 45(8): 2532-53. doi: 10.1161/STR.0000000000000022.
Lee J, Stone AJ. Combined Aerobic and Resistance Training for Cardiorespiratory Fitness, Muscle Strength, and Walking Capacity after Stroke: A Systematic Review and Meta-Analysis. J Stroke Cerebrovasc Dis. 2020 Jan; 29(1): 104498. doi: 10.1016/j.jstrokecerebrovasdis.2019.104498
Nadler M, Pauls M. Shoulder orthoses for the prevention and reduction of hemiplegic shoulder pain and subluxation: systematic review. Clin Rehabil. 2017 Apr; 31(4): 444-453. doi: 10.1177/0269215516648753
Francisco GE, McGuire JR. Poststroke spasticity management. Stroke. 2012 Nov; 43(11): 3132-6. doi: 10.1161/STROKEAHA.111.639831.
Khan F, Amatya B, Bensmail D, Yelnik A. Non-pharmacological interventions for spasticity in adults: An overview of systematic reviews. Ann Phys Rehabil Med. 2019 Jul; 62(4): 265-273. doi: 10.1016/j.rehab.2017.10.001.
Medici M, Pebet M, Ciblis D. A double-blind, long-term study of tizanidine ("Sirdalud") in spasticity due to cerebrovascular lesions. Curr Med Res Opin. 1989; 11(6):
398-407. doi: 10.1185/03007998909110141.
Stamenova P, Koytchev R, Kuhn K, Hansen C, Horvath F, Ramm S, Pongratz D. A randomized, double-blind, placebo-controlled study of the efficacy and safety of tolperisone in spasticity following cerebral stroke. Eur J Neurol. 2005 Jun; 12(6): 453-61. doi: 10.1111/j.1468-1331.2005.01006.x. PMID: 15885050.
Creamer M, Cloud G, Kossmehl P, Yochelson M, Francisco GE, Ward AB, Wissel J, Zampolini M, Abouihia A, Calabrese A, Saltuari L. Effect of Intrathecal Baclofen on Pain and Quality of Life in Poststroke Spasticity. Stroke. 2018 Sep; 49(9): 2129-2137. doi: 10.1161/STROKEAHA.118.022255
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Phys Med Rehabil Clin N Am. 2014 May; 25(2): 411-37. doi: 10.1016/j.pmr.2014.01.010.
Viana R, Pereira S, Mehta S, Miller T, Teasell R. Evidence for therapeutic interventions for hemiplegic shoulder pain during the chronic stage of stroke: a review. Top Stroke Rehabil. 2012 Nov-Dec; 19(6): 514-22. doi: 10.1310/tsr1906-514. PMID: 23192716.
Corbetta D, Sirtori V, Castellini G, Moja L, Gatti R. Constraint-induced movement therapy for upper extremities in people with stroke. Cochrane Database Syst Rev. 2015 Oct 8; 2015(10): CD004433. doi: 10.1002/14651858.CD004433.pub3.
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: an approach to diagnosis and management. Phys Med Rehabil Clin N Am. 2014 May; 25(2): 411-37. doi: 10.1016/j.pmr.2014.01.010. Epub 2014 Mar 14. PMID: 24787341.
Viana R, Pereira S, Mehta S, Miller T, Teasell R. Evidence for therapeutic interventions for hemiplegic shoulder pain during the chronic stage of stroke: a review. Top Stroke Rehabil. 2012 Nov-Dec; 19(6): 514-22. doi: 10.1310/tsr1906-514.
Corbetta D, Sirtori V, Castellini G, Moja L, Gatti R. Constraint-induced movement therapy for upper extremities in people with stroke. Cochrane Database Syst Rev. 2015 Oct 8;2015(10):CD004433. doi: 10.1002/14651858.CD004433.pub3
Barclay RE, Stevenson TJ, Poluha W, Semenko B, Schubert J. Mental practice for treating upper extremity deficits in individuals with hemiparesis after stroke. Cochrane Database Syst Rev. 2020 May 25; 5(5): CD005950. doi: 10.1002/14651858.CD005950.pub5.
Ang KK, Chua KS, Phua KS, Wang C, Chin ZY, Kuah CW, Low W, Guan C. A Randomized Controlled Trial of EEG-Based Motor Imagery Brain-Computer Interface Robotic Rehabilitation for Stroke. Clin EEG Neurosci. 2015 Oct; 46(4): 310-20. doi: 10.1177/1550059414522229.
Frolov AA, Mokienko OA, Lyukmanov RKh, Chernikova LA, Kotov SV, Turbina LG, Bobrov PD, Biryukova EV, Kondur AA, Ivanova GE, Staritsyn AN, Bushkova YuV, Dzhalagonia IZ, Kurganskaya ME, Pavlova OG, Budilin SYu, Aziatskaya GA, Khyzhnikova AE, Chervyakov AV, Lukyanov AL, et al. Preliminary results of a controlled study on the efficacy of BCI-exoskeleton technology in post-stroke arm paresis. Bulletin of the Russian State Medical University. 2016; 2: 17-25.
Carvalho R, Dias N, Cerqueira JJ. Brain-machine interface of upper limb recovery in stroke patients rehabilitation: A systematic review. Physiother Res Int. 2019 Apr; 24(2): e1764. doi: 10.1002/pri.1764.
Ivanova GE, Krivoborodov GG, Salyukov RV, Bushkov FA, Efremov NS, Kadyrov ZA. Correction of functional disorders of bladder emptying in neurological diseases by intermittent catheterization: clinical guidelines. Moscow, 2016; 40.
Thomas LH, Cross S, Barrett J, French B, Leathley M, Sutton CJ, Watkins C. Treatment of urinary incontinence after stroke in adults. Cochrane Database Syst Rev. 2008 Jan 23; 2008(1): CD004462. doi: 10.1002/14651858.CD004462.pub3.
Panfili Z, Metcalf M, Griebling TL. Contemporary Evaluation and Treatment of Poststroke Lower Urinary Tract Dysfunction. Urol Clin North Am. 2017 Aug; 44(3): 403-414. doi: 10.1016/j.ucl.2017.04.007. PMID: 28716321.
Miller EL, Murray L, Richards L, Zorowitz RD, Bakas T, Clark P, Billinger SA; American Heart Association Council on Cardiovascular Nursing and the Stroke Council. Comprehensive overview of nursing and interdisciplinary rehabilitation care of the stroke patient: a scientific statement from the American Heart Association. Stroke. 2010 Oct; 41(10): 2402-48. doi: 10.1161/STR.0b013e3181e7512b.
B. Blok, J. Pannek, Castro-Diaz, G. del Popolo, J. Groen, R. Hamid, G. Karsenty, T.M. Kessler, R. Boissier, H. Ecclestone, B. Padilla Fernández, T. Gross, L. ‘t Hoen, S. Musco, V. Phé, M.P. Schneider. EAU Guidelines on Neuro-Urology. Transl. by K.A. Shiranov. Moscow; 2016.
Jost WH, Friedman A, Michel O, et al. SIAXI: placebo-controlled, randomized, double-blind study of incobotulinumtoxinA. Neurology 2019;92(17):e1982-e1991. DOI: 10.1212/WNL.0000000000007368
Martinez-Poles J, Nedkova-Hristova V, Escribano-Paredes JB, et al. Incobotulinumtoxin A for sialorrhea in neurological disorders: a real-life experience. Toxins 2018; 10: 217. DOI: 10.3390/toxins10060217
Marvulli R, Mastromauro L, De Venuto G, et al. Efficacy of incobotulinumtoxin type A (Xeomin®) in the management of sialorrhea in neurodegenerative diseases. J Alzheimers Dis Parkinsonism 2017; 7: 1–5. DOI: 10.4172/2161-0460.1000356
Restivo DA, Panebianco M, Casabona A, et al. Botulinum toxin A for sialorrhoea associated with neurological disorders: evaluation of the relationship between effect of treatment and the number of glands treated. Toxins 2018; 10: E55. DOI:10.3390/toxins10020055
Skvortsov DV, Kaurkin SN, Ivanova GE, Suvorov AYu. Target training of walking function based on the parameters of the support and single support period in patients in the early recovery period of cerebral stroke. Clinical Practice. 2023;14(1):31–43. doi: 10.17816/clinpract112483
Skvortsov DV, Kaurkin SN, Ivanova GE, Polyaev BB, Bulatova MA. Targeted gait training in the early recovery period in patients with cerebral stroke (pilot study). Clinical Practice. 2021;12(4):12–22. doi: https://doi.org/10.17816/clinpract77334
Skvortsov, Dmitry V., Sergey N. Kaurkin, and Galina E. Ivanova 2021. "A Study of Biofeedback Gait Training in Cerebral Stroke Patients in the Early Recovery Phase with Stance Phase as Target Parameter" Sensors 2021, no. 21: 7217. https://doi.org/10.3390/s21217217
Szymkowicz, e., Bodet-contentin, l., Marechal, y., & Ehrmann, s. (2023). Eye tracking technology to improve communication with intubated critical care patients: a randomized study.
Bodet-Contentin, L., Szymkowicz, E., Delpierre, E., Chartier, D., Gadrez, P., Muller, G., ... & Ehrmann, S. (2022). Eye tracking communication with intubated critically ill patients: a proof-of-concept multicenter pilot study. Minerva Anestesiologica, 88(9), 690-697.
Bodet -Contentin, L., Messet-Charrière, H., Gissot, V., Renault, A., Muller, G., Aubrey, A., ... & Ehrmann, S. (2022). Assessing oral comprehension with an eye tracking based innovative device in critically ill patients and healthy volunteers: a cohort study. Critical Care, 26(1), 288.
Garry J, Casey K, Cole TK, Regensburg A, McElroy C, Schneider E, Efron D, Chi A. A pilot study of eye-tracking devices in intensive care. Surgery. 2016 Mar;159(3):938-44. doi: 10.1016/j.surg.2015.08.012. Epub 2015 Sep 8. PMID: 26361099.
Kujawa K, Żurek A, Gorączko A, Olejniczak R, Zurek G. Monitoring Eye Movements Depending on the Type of Visual Stimulus in Patients with Impaired Consciousness Due to Brain Damage. International Journal of Environmental Research and Public Health. 2022; 19(10):6280. https://doi.org/10.3390/ijerph19106280
"Gaze shift towards movement onset" as an indicator of semantic perception recovery in severe brain injuries / A.E. Karchevskaya, M.Yu. Kaverina, E.V. Enikolopova, O.A. Krotkova // Cognitive Science in Moscow: New Research : Conference Proceedings, Moscow, June 23–24, 2021 / Edited by E.V. Pechenkova, M.V. Falikman, A.Ya. Koyfman. – Moscow: BukiVedi, Institute of Practical Psychology and Psychoanalysis, 2021. – P. 189-194. – EDN JJGLSA.
Vigasina KD, Sharova EV, Alexandrova EV, Kaverina MYu. Eye-tracking in assessing the functional capabilities of patients with impaired consciousness // Proceedings of the XXIV Scientific School-Conference of Young Scientists on Physiology, Higher Nervous Activity and Neurophysiology. 2020. No. 1. URL: https://cyberleninka.ru/article/n/aytreking-v-otsenke-funktsionalnyh-vozmozhnostey-patsientov-s-ugnetennym-soznaniem.
Vessoyan, K., Smart, E., Steckle, G., & McKillop, M. (2023). A scoping review of eye tracking technology for communication: current progress and next steps. Current Developmental Disorders Reports, 10(1), 20-39.
Sharma, S., Kim, H., Harris, H., Haberstroh, A., Wright, H. H., & Rothermich, K. (2021). Eye tracking measures for studying language comprehension deficits in aphasia: A systematic search and scoping review. Journal of Speech, Language, and Hearing Research, 64(3), 1008-1022.
Wilkinson KM, Mitchell T. Eye tracking research to answer questions about augmentative and alternative communication assessment and intervention. Augment Altern Commun. 2014 Jun;30(2):106-19. doi: 10.3109/07434618.2014.904435. Epub 2014 Apr 23. PMID: 24758526; PMCID: PMC4327869.
Elsahar, Y.; Hu, S.; Bouazza-Marouf, K.; Kerr, D.; Mansor, A. Augmentative and Alternative Communication (AAC) Advances: A Review of Configurations for Individuals with a Speech Disability. Sensors 2019, 19, 1911. https://doi.org/10.3390/s19081911
Kujawa, Katarzyna, et al. "Assessment of language functions in patients with disorders of consciousness using an alternative communication tool." Frontiers in Neurology 12 (2021): 684362.
He, W736., Ji, Y., Wei, X., Wang, F., Xu, F., Lu, C., ... & Wang, K. (2021). Eye movement technique to improve executive function in patients with stroke: A randomized controlled trial. Frontiers in Neurology, 12, 599850.
Kerkhoff G, Reinhart S, Ziegler W, Artinger F, Marquardt C, Keller I. Smooth pursuit eye movement training promotes recovery from auditory and visual neglect: a randomized controlled study. Neurorehabil Neural Repair. 2013 Nov-Dec;27(9):789-98. doi: 10.1177/1545968313491012. PMID: 23797459.
Moon, S. J., Park, C. H., Jung, S. I., Yu, J. W., Son, E. C., Lee, H. N., ... & Jung, T. D. (2022, February). Effects of an eye-tracking linkage attention training system on cognitive function compared to conventional computerized cognitive training system in patients with stroke. In Healthcare (Vol. 10, No. 3, p. 456). MDPI.
Hazelton, C., Pollock, A., Dixon, D., Taylor, A., Davis, B., Walsh, G., & Brady, M. C. (2021). The feasibility and effects of eye movement training for visual field loss after stroke: a mixed methods study. British Journal of Occupational Therapy, 84(5), 278-288.
Aizenshtein AD, Shurupova MA, Ivanova GE. (2022). Application of the eye-tracking method for the rehabilitation of stroke patients with oculomotor disorders: a pilot study. Problems of balneology, physiotherapy, and exercise therapy, 99(3), 37.
Kunka, B., Kosikowski, R., Barlinn, J., & Kozak, K. (2016, October). Brain rehabilitation in clinical trials setup by eye-tracking. In Proceedings of the Fifth International Conference on Telecommunications and Remote Sensing (Vol. 1, pp. 89-94).
Meylan, C., Seidel, D., Gibson, R., & Hazelton, C. (2022). Feasibility study for the use of a low-cost video eye tracker as a tool for eye-movement training. Investigative Ophthalmology & Visual Science, 63(7), 4066-F0030
Belkin AA, et al. Rehabilitation in the critical care unit and intensive care unit (ReabIC). Clinical guidelines of the Union of Rehabilitologists of Russia and the Federation of Anesthesiologists and Reanimatologists // Bulletin of Intensive Care named after A.I. Saltanov. – 2022. – No. 2. – P. 7-40.
Klimov LV, Parfenov VA. Cognitive impairment in the acute period of ischemic stroke // Neurological Journal. – 2006. – Vol. 11. – No. S1. – P. 53-57
Gottesman RF, Hillis AE. Predictors and assessment of cognitive dysfunction resulting from ischaemic stroke // The Lancet Neurology. – 2010. – Vol. 9. – No. 9. – P. 895-905.
Ballard C. et al. Prospective follow-up study between 3 and 15 months after stroke: improvements and decline in cognitive function among dementia-free stroke survivors > 75 years of age // Stroke. – 2003. – Vol. 34. – No. 10. – P. 2440-2444.
Hochstenbach JB, den Otter R, Mulder TW. Cognitive recovery after stroke: a 2-year follow-up // Archives of Physical Medicine and Rehabilitation. – 2003. – Vol. 84. – No. 10. – P. 1499-1504.
Aizenshtein AD, Trofimova AK, Mikadze YuV, Ivanova GE. Methodological problems of using psychometric tests in clinical research practice of cognitive disorders in patients with vascular brain lesions // Bulletin of Restorative Medicine. 2023. No. 1.
Stroke. A guide for physicians. Ed. by L.V. Stakhovskaya, S.V. Kotov. MIA Publishing House, 2014; 400.
Guidelines for management of ischaemic stroke and transient ischaemic attack of the European Stroke Organisation (ESO), 2008 Cerebrovasc Dis 2008; 25: 457-507. URL: http//nsicu.ru/uploads/attachment/file/61/StrokeGuidelinesRussian.pdf (in Russ.) http://www.karger.com/Article/Pdf/131083.
Guidelines for the early management of adults with ischemic stroke of the American Heart Association (AHA) and American Stroke Association (ASA) 2005 Stroke 2005; 36: 916-923. URL: http://stroke.ahajournals.org/content/36/4/916.extract.
Neurology. National Guidelines. Concise edition. Ed. by E.I. Gusev, A.N. Konovalov, A.B. Gekht. Moscow: GEOTAR-Media; 2018; 688.
Estruch R, Ros E, Salas-Salvadó J, Covas MI, Corella D, Arós F, Gómez-Gracia E, Ruiz-Gutiérrez V, Fiol M, Lapetra J, et al; PREDIMED Study Investigators. Primary prevention of cardiovascular disease with a Mediterranean diet supplemented with extra-virgin olive oil or nuts. N Engl J Med. 2018; 378: e34. doi: 10.1056/NEJMoa1800389.
Rees K, Takeda A, Martin N, Ellis L, Wijesekara D, Vepa A, Das A, Hartley L, Stranges S. Mediterranean-style diet for the primary and second- ary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2019; 3: CD009825. doi: 10.1002/14651858. CD009825.pub3
Judd SE, Gutiérrez OM, Newby PK, Howard G, Howard VJ, Locher JL, Kissela BM, Shikany JM. Dietary patterns are associated with incident stroke and contribute to
excess risk of stroke in Black Americans. Stroke. 2013; 44: 3305-3311. doi: 10.1161/STROKEAHA.113.002636
He FJ, Tan M, Ma Y, MacGregor GA. Salt reduction to prevent hypertension and cardiovascular disease: JACC state-of-the-art review. J Am Coll Cardiol. 2020; 75: 632-647. doi: 10.1016/j.jacc.2019.11.055.
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG, et al; DASH- Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet: DASH-Sodium Collaborative Research Group. N Engl J Med. 2001; 344: 3-10. doi: 10.1056/NEJM200101043440101
Turan TN, Nizam A, Lynn MJ, Egan BM, Le NA, Lopes-Virella MF, Hermayer KL, Harrell J, Derdeyn CP, Fiorella D, et al. Relationship between risk factor control and
vascular events in the SAMMPRIS trial. Neurology. 2017; 88: 379-385. doi: 10.1212/WNL.0000000000003534
English C, Janssen H, Crowfoot G, Bourne J, Callister R, Dunn A, Oldmeadow C, Ong LK, Palazzi K, Patterson A, et al. Frequent, short bouts of light-intensity exercises while standing decreases systolic blood pressure: Breaking Up Sitting Time After Stroke (BUST-Stroke) trial. Int J Stroke. 2018; 13: 932-940. doi: 10.1177/1747493018798535
Biswas A, Oh PI, Faulkner GE, Bajaj RR, Silver MA, Mitchell MS, Alter DA. Sedentary time and its association with risk for disease incidence, mortality, and hospitalization in adults: a systematic review and meta-analysis. Ann Intern Med. 2015; 162: 123-132. doi: 10.7326/M14-1651
Rigotti NA, Clair C, Munafò MR, Stead LF. Interventions for smoking cessation in hospitalised patients. Cochrane Database Syst Rev. 2012; 5: CD001837. doi: 10.1002/14651858.CD001837.pub3
Stead LF, Koilpillai P, Fanshawe TR, Lancaster T. Combined pharmacotherapy and behavioural interventions for smoking cessation. Cochrane Database Syst Rev. 2016; 3: CD008286. doi: 10.1002/14651858.CD008286.pub3.
Evans-Hudnall GL, Stanley MA, Clark AN, Bush AL, Resnicow K, Liu Y, Kass JS, Sander AM. Improving secondary stroke self-care among underserved ethnic minority individuals: a randomized clinical trial of a pilot intervention. J Behav Med. 2014; 37: 196-204. doi: 10.1007/s10865-012-9469-2.
Ahmadi M, Laumeier I, Ihl T, Steinicke M, Ferse C, Endres M, Grau A, Hastrup S, Poppert H, Palm F, et al. A support programme for secondary prevention in patients with transient ischaemic attack and minor stroke (INSPiRE-TMS): an open-label, randomised controlled trial. Lancet Neurol. 2020; 19: 49-60. doi: 10.1016/S1474-4422(19)30369-2
Pan B, Jin X, Jun L, Qiu S, Zheng Q, Pan M. The relationship between smoking and stroke: a meta-analysis. Medicine (Baltimore). 2019; 98: e14872. doi: 10.1097/MD.0000000000014872.
Lin MP, Ovbiagele B, Markovic D, Towfighi A. Association of second- hand smoke with stroke outcomes. Stroke. 2016; 47: 2828-2835. doi: 10.1161/STROKEAHA.116.014099.
Bonita R, Duncan J, Truelsen T, Jackson RT, Beaglehole R. Passive smok- ing as well as active smoking increases the risk of acute stroke. Tob Control. 1999; 8: 156-160. doi: 10.1136/tc.8.2.156.
Lee PN, Thornton AJ, Forey BA, Hamling JS. Environmental tobacco smoke exposure and risk of stroke in never smokers: an updated review with meta-analysis. J Stroke Cerebrovasc Dis. 2017; 26: 204-216. doi: 10.1016/j.jstrokecerebrovasdis.2016.09.011
Evans-Hudnall GL, Stanley MA, Clark AN, Bush AL, Resnicow K, Liu Y, Kass JS, Sander AM. Improving secondary stroke self-care among underserved ethnic minority individuals: a randomized clinical trial of a pilot intervention. J Behav Med. 2014; 37: 196-204. doi: 10.1007/s10865-012-9469-2.
Ois A, Gomis M, Rodríguez-Campello A, Cuadrado-Godia E, Jiménez-Conde J, Pont-Sunyer C, Cuccurella G, Roquer J. Factors associated with a high risk of recurrence in patients with transient ischemic attack or minor stroke. Stroke. 2008; 39: 1717-1721. doi: 10.1161/STROKEAHA.107.505438.
Ricci C, Wood A, Muller D, Gunter MJ, Agudo A, Boeing H, van der Schouw YT, Warnakula S, Saieva C, Spijkerman A, et al. Alcohol intake in relation to non-fatal and fatal coronary heart disease and stroke: EPIC-CVD case- cohort study. BMJ. 2018; 361: k934. doi: 10.1136/bmj.k934.
Patra J, Taylor B, Irving H, Roerecke M, Baliunas D, Mohapatra S, Rehm J. Alcohol consumption and the risk of morbidity and mortality for different stroke types a systematic review and meta-analysis. BMC Public Health. 2010; 10: 258. doi: 10.1186/1471-2458-10-258
Marso SP, Daniels GH, Brown-Frandsen K, Kristensen P, Mann JF, Nauck MA, Nissen SE, Pocock S, Poulter NR, Ravn LS, et al; LEADER Steering Committee; LEADER Trial Investigators. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med. 2016; 375: 311-322. doi: 10.1056/NEJMoa1603827.
Wing RR, Lang W, Wadden TA, Safford M, Knowler WC, Bertoni AG, Hill JO, Brancati FL, Peters A, Wagenknecht L; Look AHEAD Research Group. Benefits of modest weight loss in improving cardiovascular risk factors in overweight and obese individuals with type 2 diabetes. Diabetes Care. 2011; 34: 1481-1486. doi: 10.2337/dc10-2415
Kernan WN, Inzucchi SE, Sawan C, Macko RF, Furie KL. Obesity: a stubbornly obvious target for stroke prevention. Stroke. 2013; 44: 278-286. doi: 10.1161/STROKEAHA.111.639922
Kroll ME, Green J, Beral V, Sudlow CL, Brown A, Kirichek O, Price A, Yang TO, Reeves GK; Million Women Study Collaborators. Adiposity and ischemic and hemorrhagic stroke: prospective study in women and meta-analysis. Neurology. 2016; 87: 1473-1481. doi: 10.1212/WNL.0000000000003171
Wing RR, Lang W, Wadden TA, Safford M, Knowler WC, Bertoni AG, Hill JO, Brancati FL, Peters A, Wagenknecht L; Look AHEAD Research Group. Benefits of modest weight loss in improving cardiovascular risk factors in overweight and obese individuals with type 2 diabetes. Diabetes Care. 2011; 34: 1481-1486. doi: 10.2337/dc10-2415
Sjöström L, Peltonen M, Jacobson P, Sjöström CD, Karason K, Wedel H, Ahlin S, Anveden Å, Bengtsson C, Bergmark G, et al. Bariatric surgery and long-term cardiovascular events. JAMA. 2012; 307: 56-65. doi: 10.1001/jama.2011.1914
Fisher DP, Johnson E, Haneuse S, Arterburn D, Coleman KJ, O’Connor PJ, O’Brien R, Bogart A, Theis MK, Anau J, et al. Association between bariatric surgery and macrovascular disease outcomes in patients with type 2 diabetes and severe obesity. JAMA. 2018; 320: 1570-1582. doi: 10.1001/jama.2018.14619
LeBlanc ES, Patnode CD, Webber EM, Redmond N, Rushkin M, O’Connor EA. Behavioral and pharmacotherapy weight loss interventions to prevent obesity-related morbidity and mortality in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2018; 320: 1172-1191. doi: 10.1001/jama.2018.7777
Zonneveld TP, Richard E, Vergouwen MD, Nederkoorn PJ, de Haan R, Roos YB, Kruyt ND. Blood pressure-lowering treatment for preventing recurrent stroke, major vascular events, and dementia in patients with a history of stroke or transient ischaemic attack. Cochrane Database Syst Rev.2018; 7: CD007858. doi: 10.1002/14651858.CD007858.pub2.
PROGRESS Collaborative Group. Randomised trial of perindopril-based blood-pressure lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack. Lancet. 2001; 358: 1033-1041. doi: 10.1016/S0140-6736(01)06178-5.
Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review. Stroke. 2003; 34: 2741-2748. doi: 10.1161/01.STR.0000092488.40085.15
Schrader J, Lüders S, Kulschewski A, Hammersen F, Plate K, Berger J, Zidek W, Dominiak P, Diener HC; MOSES Study Group. Morbidity and Mortality After Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention: principal results of a prospective randomized controlled study (MOSES). Stroke. 2005 Jun;36(6):1218-26. doi: 10.1161/01.STR.0000166048.35740.a9. Epub 2005 May 5. PMID: 15879332.
Mant J, McManus RJ, Roalfe A, Fletcher K, Taylor CJ, Martin U, Virdee S, Greenfield S, Hobbs FD. Different systolic blood pressure targets for people with history of stroke or transient ischaemic attack: PAST-BP (Prevention After Stroke–Blood Pressure) randomised controlled trial. BMJ.2016; 352: i708. doi: 10.1136/bmj.i708.
Bath PM, Scutt P, Blackburn DJ, Ankolekar S, Krishnan K, Ballard C, Burns A, Mant J, Passmore P, Pocock S, et al; PODCAST Trial Investigators. Intensive versus guideline blood pressure and lipid lowering in patients with previous stroke: main results from the pilot ‘Prevention of Decline in Cognition after Stroke Trial’ (PODCAST) randomised controlled trial. PLoS One. 2017; 12: e0164608. doi: 10.1371/journal.pone.0164608
Arterial hypertension in adults. Clinical guidelines 2020. Russian Journal of Cardiology. 2020; 25(3): 3786. doi: 10.15829/1560-4071-2020-3-3786
Bath PM, Scutt P, Blackburn DJ, Ankolekar S, Krishnan K, Ballard C, Burns A, Mant J, Passmore P, Pocock S, et al; PODCAST Trial Investigators. Intensive versus guideline blood pressure and lipid lowering in patients with previous stroke: main results from the pilot ‘Prevention of Decline in Cognition after Stroke Trial’ (PODCAST) randomised controlled trial. PLoS One. 2017; 12: e0164608. doi: 10.1371/journal.pone.0164608.
Yusuf S, Diener HC, Sacco RL, Cotton D, Ounpuu S, Lawton WA, Palesch Y, Martin RH, Albers GW, Bath P, et al; PRoFESS Study Group. Telmisartan to prevent recurrent stroke and cardiovascular events. N Engl J Med. 2008; 359: 1225-1237. doi: 10.1056/NEJMoa0804593.
Mant J, McManus RJ, Roalfe A, Fletcher K, Taylor CJ, Martin U, Virdee S, Greenfield S, Hobbs FD. Different systolic blood pressure targets for people with history of stroke or transient ischaemic attack: PAST-BP (Prevention After Stroke–Blood Pressure) randomised controlled trial. BMJ. 2016; 352: i708. doi: 10.1136/bmj.i708
Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Béjot Y et al. A comparison of two LDL cholesterol targets after ischemic stroke. N Engl J Med. 2020; 382(1): 9. doi: 10.1056/ NEJMoa1910355.
Cholesterol Treatment Trialists Collaboration, Baigent C, Blackwell L, Emberson J, Holland LE, Reith C, Bhala N, Peto R, Barnes EH, Keech A, Simes J, Collins R. Efficacy and safety of more intensive lowering of LDL cholesterol: a metaanalysis of data from 170,000 participants in 26 randomised trials. Lancet 2010; 376: 16701681.
Cholesterol Treatment Trialists Collaboration, Fulcher J, O’Connell R, Voysey M, Emberson J, Blackwell L, Mihaylova B, Simes J, Collins R, Kirby A, Colhoun H, Braunwald E, La Rosa J, Pedersen TR, Tonkin A, Davis B, Sleight P, Franzosi MG, Baigent C, Keech A. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet2 015; 385: 13971405.
Cannon CP, Blazing MA, Giugliano RP, McCagg A, White JA, Theroux P, Darius H, Lewis BS, Ophuis TO, Jukema JW, De Ferrari GM, Ruzyllo W, De Lucca P, Im K, Bohula EA, Reist C, Wiviott SD, Tershakovec AM, Musliner TA, Braunwald E, Califf RM; IMPROVE-IT Investigators. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med 2015; 372: 23872397.
Sabatine MS, Giugliano RP, Keech AC, Honarpour N, Wiviott SD, Murphy SA, Kuder JF, Wang H, Liu T, Wasserman SM, et al; FOURIER Steering Committee and Investigators. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017; 376: 1713–1722. doi: 10.1056/NEJMoa1615664.
Schwartz GG, Steg PG, Szarek M, Bhatt DL, Bittner VA, Diaz R, Edelberg JM, Goodman SG, Hanotin C, Harrington RA, et al; ODYSSEY OUTCOMES Committees and Investigators. Alirocumab and cardiovascular outcomes after acute coronary syndrome. N Engl J Med. 2018; 379: 2097.2107. doi: 10.1056/NEJMoa1801174.
Nave AH, Lange KS, Leonards CO, et al. Lipoprotein (a) as a risk factor for ischemic stroke: a meta-analysis. Atherosclerosis. 2015;242(2):496-503. doi:10.1016/j.atherosclerosis.2015.08.021
Kronenberg F, Mora S, Stroes ESG, Ference BA, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022 Oct 14;43(39):3925-3946. doi: 10.1093/eurheartj/ehac361. PMID: 36036785; PMCID: PMC9639807
Cholesterol Treatment Trialists Collaboration, Baigent C, Blackwell L, Emberson J, Holland LE, Reith C, Bhala N, Peto R, Barnes EH, Keech A, Simes J, Collins R. Efficacy and safety of more intensive lowering of LDL cholesterol: a metaanalysis of data from 170,000 participants in 26 randomised trials. Lancet 2010; 376: 16701681.
Weng TC, Yang YH, Lin SJ, Tai SH. A systematic review and meta-analysis on the therapeutic equivalence of statins. J Clin Pharm Ther. 2010 Apr; 35(2): 139-51. doi: 10.1111/j.1365-2710.2009.01085.x. PMID: 20456733.
Vallejo-Vaz AJ, Fayyad R, Boekholdt SM, Hovingh GK, Kastelein JJ, Melamed S, Barter P, Waters DD, Ray KK. Triglyceride-rich lipoprotein cholesterol and risk of cardiovascular events among patients receiving statin therapy in the TNT trial.Circulation 2018; 138: 770781
Collins R, Reith C, Emberson J, et al. Interpretation of the evidence for the efficacy and safety of statin therapy. Lancet. 2016; 388: 2532-61.
Group HPSC. Randomized trial of the effects of cholesterol-lowering with simvastatin on peripheral vascular and other major vascular outcomes in 20,536 people with peripheral arterial disease and other high-risk conditions. J Vasc Surg. 2007; 45: 645-54; discussion 53-4.
Weng TC, Yang YH, Lin SJ, Tai SH. A systematic review and meta-analysis on the therapeutic equivalence of statins. J Clin Pharm Ther. 2010 Apr; 35(2): 139-51. doi: 10.1111/j.1365-2710.2009.01085.x. PMID: 20456733
Yang Z, Edwards D, Massou E, Saunders CL, Brayne C, Mant J. Statin use and high-dose statin use after ischemic stroke in the UK: a retrospective cohort study. Clin Epidemiol. 2019 Jun 28; 11: 495-508. doi: 10.2147/CLEP.S201983.
Nanna MG, Navar AM, Wang TY, Mi X, Virani SS, Louie MJ, Lee LV, Goldberg AC, Roger VL, Robinson J, Peterson ED. Statin Use and Adverse Effects Among Adults >75 Years of Age: Insights From the Patient and Provider Assessment of Lipid Management (PALM) Registry. J Am Heart Assoc. 2018 May 8; 7(10): e008546. doi: 10.1161/JAHA.118.008546.
Statins After Ischemic Stroke in the Oldest. A Cohort Study Using the Clinical Practice Research Datalink Database. Geert J. Lefeber, Wilma Knol, Patrick C. Souverein, Marcel L. Bouvy, Anthonius de Boer and Huiberdina L. Koek Stroke. 2021; 52: 1244–1252 10.1161/STROKEAHA.120.030755
Bohula EA, Wiviott SD, Giugliano RP, Blazing MA, Park JG, Murphy SA, White JA, Mach F, Van de Werf F, Dalby AJ, et al. Prevention of stroke with the addition of ezetimibe to statin therapy in patients with acute coronary syndrome in IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International Trial). Circulation.2017; 136: 2440-2450. doi: 10.1161/CIRCULATIONAHA.117.029095.
Gazi IF, Daskalopoulou SS, Nair DR, Mikhailidis DP. Effect of ezetimibe in patients who cannot tolerate statins or cannot get to the low density lipoprotein cholesterol target despite taking a statin. Curr Med Res Opin. 2007 Sep;23(9):2183-92. doi: 10.1185/030079907X226267. PMID: 17692154.
Nissen SE, Stroes E, Dent-Acosta RE, Rosenson RS, Lehman SJ, Sattar N, Preiss D, Bruckert E, Ceska R, Lepor N, Ballantyne CM, Gouni-Berthold I, Elliott M, Brennan DM, Wasserman SM, Somaratne R, Scott R, Stein EA; Gauss-3 Investigators. Efficacy and tolerability of evolocumab vs ezetimibe in patients with muscle-related statin intolerance: the GAUSS-3 randomized clinical trial. JAMA 2016; 315: 15801590.
Schreml J, Gouni-Berthold I. Role of anti-PCSK9 antibodies in the treatment of patients with statin intolerance.Curr Med Chem 2018; 25: 15381548.
Sabatine MS, Giugliano RP, Keech AC, Honarpour N, Wiviott SD, Murphy SA, Kuder JF, Wang H, Liu T, Wasserman SM, et al; FOURIER Steering Committee and Investigators. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017; 376: 1713-1722. doi: 10.1056/NEJMoa1615664
Schwartz GG, Steg PG, Szarek M, Bhatt DL, Bittner VA, Diaz R, Edelberg JM, Goodman SG, Hanotin C, Harrington RA, et al; ODYSSEY OUTCOMES Committees and Investigators. Alirocumab and cardiovascular outcomes after acute coronary syndrome. N Engl J Med. 2018; 379: 2097-2107. doi: 10.1056/NEJMoa1801174].
Toth PP, Worthy G, Gandra SR, Sattar N, Bray S, Cheng LI, Bridges I, Worth GM, Dent R, Forbes CA, Deshpande S, Ross J, Kleijnen J, Stroes ESG. Systematic Review and Network Meta-Analysis on the Efficacy of Evolocumab and Other Therapies for the Management of Lipid Levels in Hyperlipidemia. J Am Heart Assoc. 2017 Oct 2; 6(10): e005367.
Benner JS, Tierce JC, Ballantyne CM, Prasad C, Bullano MF, Willey VJ, Erbey J, Sugano DS. Follow-up lipid tests and physician visits are associated with improved adherence to statin therapy. Pharmacoeconomics. 2004; 22(suppl 3): 13-23. doi: 10.2165/00019053-200422003-00003
Keech A, Simes RJ, Barter P, Best J, Scott R, Taskinen MR, Forder P, Pillai A, Davis T, Glasziou P, Drury P, Kesaniemi YA, Sullivan D, Hunt D, Colman P, d’Emden M, Whiting M, Ehnholm C, Laakso M; FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005; 366: 18491861.
Aim-High Investigators, Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, Koprowicz K, McBride R, Teo K, Weintraub W. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy.N Engl J Med 2011; 365: 22552267.
Group HTC, Landray MJ, Haynes R, Hopewell JC, Parish S, Aung T, Tomson J, Wallendszus K, Craig M, Jiang L, Collins R, Armitage J. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 2014; 371: 203212.
Frick MH, Elo O, Haapa K, Heinonen OP, Heinsalmi P, Helo P, Huttunen JK, Kaitaniemi P, Koskinen P, Manninen V, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med. 1987 Nov 12; 317(20): 1237-45. doi: 10.1056/NEJM198711123172001. PMID: 3313041
Lipids and lipoproteins in symptomatic coronary heart disease. Distribution, intercorrelations, and significance for risk classification in 6,700 men and 1,500 women. The Bezafibrate Infarction Prevention (BIP) Study Group, Israel. Circulation1992; 86: 839848.
Antithrombotic Trialists" Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002 Jan 12;324(7329):71-86. doi: 10.1136/bmj.324.7329.71. Erratum in: BMJ 2002 Jan 19;324(7330):141. PMID: 11786451; PMCID: PMC64503.;
CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet. 1996 Nov 16;348(9038):1329-39. doi: 10.1016/s0140-6736(96)09457-3. PMID: 8918275.
Diener, HC, Cunha, L, Forbes, C, Sivenius, J, Smets, P, Lowenthal, A. European Stroke Prevention Study, 2: dipyridamole and acetylsalicylic acid in the secondary prevention of stroke. J Neurol Sci. 1996; 143: 1–13. doi: 10.1016/s0022-510x(96)00308-5;
ESPRIT Study Group; Halkes, PH, van Gijn, J, Kappelle, LJ, Koudstaal, PJ, Algra, A. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial. Lancet. 2006; 367: 1665-1673. doi: 10.1016/S0140-6736(06)68734-5;
Kwok, CS, Shoamanesh, A, Copley, HC, Myint, PK, Loke, YK, Benavente, OR. Efficacy of antiplatelet therapy in secondary prevention following lacunar stroke: pooled analysis of randomized trials. Stroke. 2015; 46: 1014-1023. doi: 10.1161/STROKEAHA.114.008422;
Sacco, RL, Diener, HC, Yusuf, S, Cotton, D, Ounpuu, S, Lawton, WA, Palesch, Y, Martin, RH, Albers, GW, Bath, P, et al; PRoFESS Study Group. Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke. N Engl J Med. 2008; 359: 1238-1251. doi: 10.1056/NEJMoa0805002
SPS3 Investigators; Benavente, OR, Hart, RG, McClure, LA, Szychowski, JM, Coffey, CS, Pearce, LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012; 367: 817-825. doi: 10.1056/NEJMoa1204133.
Johnston, SC, Easton, JD, Farrant, M, Barsan, W, Conwit, RA, Elm, JJ, Kim, AS, Lindblad, AS, Palesch, YY; Clinical Research Collaboration, Neurological Emergencies Treatment Trials Network, and the POINT Investigators. Clopidogrel and aspirin in acute ischemic stroke and high-risk TIA. N Engl J Med. 2018; 379: 215-225. doi: 10.1056/NEJMoa1800410.
Wang, Y, Wang, Y, Zhao, X, Liu, L, Wang, D, Wang, C, Wang, C, Li, H, Meng, X, Cui, L, et al; CHANCE Investigators. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Engl J Med. 2013; 369: 11-19. doi: 10.1056/NEJMoa1215340.
Johnston, SC, Amarenco, P, Denison, H, Evans, SR, Himmelmann, A, James, S, Knutsson, M, Ladenvall, P, Molina, CA, Wang, Y; THALES Investigators. Ticagrelor and aspirin or aspirin alone in acute ischemic stroke or TIA. N Engl J Med. 2020;383:207–217. doi: 10.1056/NEJMoa1916870
Naqvi, IA, Kamal, AK, Rehman, H. Multiple versus fewer antiplatelet agents for preventing early recurrence after ischaemic stroke or transient ischaemic attack. Cochrane Database Syst Rev. 2020; 8: CD009716. doi: 10.1002/14651858.CD009716.pub2
Diener, HC, Bogousslavsky, J, Brass, LM, Cimminiello, C, Csiba, L, Kaste, M, Leys, D, Matias-Guiu, J, Rupprecht, HJ; MATCH Investigators. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. 2004; 364: 331-337. doi: 10.1016/S0140-6736(04)16721-4
SPS3 Investigators; Benavente, OR, Hart, RG, McClure, LA, Szychowski, JM, Coffey, CS, Pearce, LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med. 2012; 367: 817-825. doi: 10.1056/NEJMoa1204133
Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, Janis LS, Lutsep HL, Barnwell SL, Waters MF, Hoh BL, Hourihane JM, Levy EI, Alexandrov AV, Harrigan MR, Chiu D, Klucznik RP, Clark JM, McDougall CG, Johnson MD, Pride GL Jr, Torbey MT, Zaidat OO, Rumboldt Z, Cloft HJ; SAMMPRIS Trial Investigators. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med. 2011 Sep 15;365(11):993-1003. doi: 10.1056/NEJMoa1105335. Epub 2011 Sep 7. Erratum in: N Engl J Med. 2012 Jul 5;367(1):93. PMID: 21899409; PMCID: PMC3552515.
Chimowitz MI, Lynn MJ, Howlett-Smith H, Stern BJ, Hertzberg VS, Frankel MR, Levine SR, Chaturvedi S, Kasner SE, Benesch CG, et al; Warfarin- Aspirin Symptomatic Intracranial Disease Trial Investigators. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. 2005; 352: 1305-1316. doi: 10.1056/NEJMoa043033
Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, Janis LS, Lutsep HL, Barnwell SL, Waters MF, et al; SAMMPRIS Trial Investigators. Stenting versus aggressive medical therapy for intracranial arterial steno- sis. N Engl J Med. 2011; 365: 993-1003. doi: 10.1056/NEJMoa1105335
Chimowitz MI, Lynn MJ, Derdeyn CP, Turan TN, Fiorella D, Lane BF, Janis LS, Lutsep HL, Barnwell SL, Waters MF, et al; SAMMPRIS Trial Investigators. Stenting versus aggressive medical therapy for intracranial arterial steno- sis. N Engl J Med. 2011; 365: 993-1003. doi: 10.1056/NEJMoa1105335
Chaturvedi S, Turan TN, Lynn MJ, Kasner SE, Romano J, Cotsonis G, Frankel M, Chimowitz MI; WASID Study Group. Risk factor status and vas- cular events in patients with symptomatic intracranial stenosis. Neurology. 2007; 69: 2063-2068. doi: 10.1212/01.wnl.0000279338.18776.26.
Liu L, Wong KS, Leng X, Pu Y, Wang Y, Jing J, Zou X, Pan Y, Wang A, Meng X, et al; CHANCE Investigators. Dual antiplatelet therapy in stroke and ICAS: subgroup analysis of CHANCE. Neurology. 2015; 85: 1154–1162. doi: 10.1212/WNL.0000000000001972.
Wong KS, Chen C, Fu J, Chang HM, Suwanwela NC, Huang YN, Han Z, Tan KS, Ratanakorn D, Chollate P, et al; CLAIR Study Investigators. Clopidogrel plus aspirin versus aspirin alone for reducing embolisation in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR study): a ran- domised, open-label, blinded-endpoint trial. Lancet Neurol. 2010; 9: 489-497. doi: 10.1016/S1474-4422(10)70060-0.
Turan TN, Nizam A, Lynn MJ, Egan BM, Le NA, Lopes-Virella MF, Hermayer KL, Harrell J, Derdeyn CP, Fiorella D, et al. Relationship between risk factor control and
vascular events in the SAMMPRIS trial. Neurology. 2017; 88: 379-385. doi: 10.1212/WNL.0000000000003534.
Turan TN, Cotsonis G, Lynn MJ, Chaturvedi S, Chimowitz M; Warfarin- Aspirin Symptomatic Intracranial Disease (WASID) Trial Investigators. Relationship between blood pressure and stroke recurrence in patients with intracranial arterial stenosis. Circulation. 2007; 115: 2969-2975. doi: 10.1161/CIRCULATIONAHA.106.622464.
Yu DD, Pu YH, Pan YS, Zou XY, Soo Y, Leung T, Liu LP, Wang DZ, Wong KS, Wang YL, et al; Chinese Intracranial Atherosclerosis (CICAS) Study Group. High blood pressure increases the risk of poor outcome at dis- charge and 12-month follow-up in patients with symptomatic intracranial large artery stenosis and occlusions: subgroup analysis of the CICAS Study. CNS Neurosci Ther. 2015; 21: 530-535. doi: 10.1111/cns.12400.
Park JM, Kim BJ, Kwon SU, Hwang YH, Heo SH, Rha JH, Lee J, Park MS, Kim JT, Song HJ, et al. Intensive blood pressure control may not be safe in subacute ischemic stroke by intracranial atherosclerosis: a result of randomized trial. J Hypertens. 2018; 36: 1936-1941. doi: 10.1097/HJH.0000000000001784
Derdeyn CP, Chimowitz MI, Lynn MJ, Fiorella D, Turan TN, Janis LS, Montgomery J, Nizam A, Lane BF, Lutsep HL, et al; Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis Trial Investigators. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): the final results of a randomised trial. Lancet. 2014; 383: 333-341. doi: 10.1016/S0140-6736(13)62038-3.
Lutsep HL, Lynn MJ, Cotsonis GA, Derdeyn CP, Turan TN, Fiorella D, Janis LS, Lane BF, Montgomery J, Chimowitz MI; SAMMPRIS Investigators. Does the stenting versus aggressive medical therapy trial support stenting for subgroups with intracranial stenosis? Stroke. 2015; 46: 3282-3284. doi: 10.1161/STROKEAHA.115.009846.
Wabnitz AM, Derdeyn CP, Fiorella DJ, Lynn MJ, Cotsonis GA, Liebeskind DS, Waters MF, Lutsep H, Lopez-Cancio E, Turan TN, et al; SAMMPRIS Investigators. Hemodynamic markers in the anterior circulation as predictors of recurrent stroke in patients with intracranial stenosis [published online December 11, 2018]. Stroke. doi: 10.1161/STROKEAHA.118.020840. https://www.ahajournals.org/doi/10.1161/STROKEAHA.118.020840? url_ver=Z39.88-2003&rfr_id=ori:rid: crossref.org&rfr_dat=cr_pub%20%200pubmed.
EC/IC Bypass Study Group. Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. results of an international randomized trial. N Engl J Med. 1985;313:1191–1200. doi: 10.1056/ NEJM198511073131904
Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Béjot Y, Cabrejo L, Cha JK, Ducrocq G, Giroud M, et al; Treat Stroke to Target Investigators. A comparison of two LDL cholesterol targets after ischemic stroke. N Engl J Med. 2020;382:9. doi: 10.1056/NEJMoa1910355.
Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ; Carotid Endarterectomy Trialists Collaboration. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet. 2004;363:915–924. doi: 10.1016/S0140-6736(04)15785-1
Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, Warlow CP, Barnett HJ; Carotid Endarterectomy Trialists’ Collaboration. Analysis of pooled data from the randomised controlled trials of endarter- ectomy for symptomatic carotid stenosis. Lancet. 2003;361:107–116. doi: 10.1016/s0140-6736(03)12228-3
Powers WJ, Clarke WR, Grubb RL Jr, Videen TO, Adams HP Jr, Derdeyn CP; COSS Investigators. Extracranial-intracranial bypass surgery for stroke prevention in hemodynamic cerebral ischemia: the Carotid Occlusion Surgery Study randomized trial. JAMA. 2011;306:1983–1992. doi: 10.1001/jama.2011.1610.
Markus HS, Harshfield EL, Compter A, Kuker W, Kappelle LJ, Clifton A, van der Worp HB, Rothwell P, Algra A; Vertebral Stenosis Trialists" Collaboration. Stenting for symptomatic vertebral artery stenosis: a preplanned pooled individual patient data analysis. Lancet Neurol. 2019 Jul;18(7):666-673.
Eikelboom J. W., Connolly S. J., Bosch J. et al.; COMPASS Investigators. Rivaroxaban with or without aspirin in stable cardiovascular disease. N Engl J Med 2017;377 (14):1319–1330.
Sharma M, Hart RG, Connolly SJ, Bosch J, Shestakovska O, Ng KKH, Catanese L, Keltai K, Aboyans V, Alings M, Ha JW, Varigos J, Tonkin A, O"Donnell M, Bhatt DL, Fox K, Maggioni A, Berkowitz SD, Bruns NC, Yusuf S, Eikelboom JW. Stroke Outcomes in the COMPASS Trial. Circulation. 2019 Feb 26;139(9):1134-1145.
Cardiovascular consequences of discontinuing low-dose rivaroxaban in people with chronic coronary or peripheral artery disease. Heart 2021;107:1130–1137
Aboyans V, Bauersachs R, Mazzolai L, Brodmann M, Palomares JFR, Debus S, Collet JP, Drexel H, Espinola-Klein C, Lewis BS, Roffi M, Sibbing D, Sillesen H, Stabile E, Schlager O, De Carlo M. Antithrombotic therapies in aortic and peripheral arterial diseases in 2021: a consensus document from the ESC working group on aorta and peripheral vascular diseases, the ESC working group on thrombosis, and the ESC working group on cardiovascular pharmacotherapy. Eur Heart J. 2021 Oct 14;42(39):4013-4024. doi: 10.1093/eurheartj/ehab390
Siegler, J.E.; Dasgupta, S.; Abdalkader, M.; Penckofer, M.; Yaghi, S.; Nguyen, T.N. Cerebrovascular Disease in COVID-19. Viruses 2023, 15, 1598. https://doi.org/10.3390/v15071598
Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on Atrial Fibrillation. Chest. 2010; 137: 263-272. doi: 10.1378/chest.09-1584.
Gage BF, van Walraven C, Pearce L, Hart RG, Koudstaal PJ, Boode BS, Petersen P. Selecting patients with atrial fibrillation for antico- agulation: stroke risk stratification in patients taking aspirin. Circulation. 2004;110:2287–2292. doi: 10.1161/01.CIR.0000145172.55640.93.
Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA. 2001;285:2864– 2870. doi: 10.1001/jama.285.22.2864
Stroke Prevention in Atrial Fibrillation Investigators. Stroke Prevention in Atrial Fibrillation study: final results. Circulation. 1991;84:527–39.
Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the Euro Heart Survey on Atrial Fibrillation. Chest. 2010;137:263–272. doi: 10.1378/chest.09-1584.
Mason PK, Lake DE, DiMarco JP, Ferguson JD, Mangrum JM, Bilchick K, Moorman LP, Moorman JR. Impact of the CHA2DS2-VASc score on anticoagulation recommendations for atrial fibrillation. Am J Med. 2012; 125: 603.e1–603.e6. doi: 10.1016/j.amjmed.2011.09.030.
Olesen JB, Torp-Pedersen C, Hansen ML, Lip GY. The value of the CHA2DS2-VASc score for refining stroke risk stratification in patients with atrial fibrillation with a CHADS2 score 0-1: a nationwide cohort study. Thromb Haemost. 2012;107:1172–1179. doi: 10.1160/TH12-03-0175.
Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, et al; RE-LY Steering Committee and Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361:1139–1151. doi: 10.1056/NEJMoa0905561.
Patel MR, Mahaffey KW, Garg J, Pan G, Singer DE, Hacke W, Breithardt G, Halperin JL, Hankey GJ, Piccini JP, et al; ROCKET AF Investigators. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365:883–891. doi: 10.1056/NEJMoa1009638.
Granger CB, Alexander JH, McMurray JJ, Lopes RD, Hylek EM, Hanna M, Al-Khalidi HR, Ansell J, Atar D, Avezum A, et al; ARISTOTLE Committees and Investigators. Apixaban versus warfarin in patients with atrial fibrilla- tion. N Engl J Med. 2011;365:981–992. doi: 10.1056/NEJMoa1107039.
Giugliano RP, Ruff CT, Braunwald E, Murphy SA, Wiviott SD, Halperin JL, Waldo AL, Ezekowitz MD, Weitz JI, Špinar J, et al; ENGAGE AF-TIMI 48 Investigators. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369:2093–2104. doi: 10.1056/NEJMoa1310907
Healey JS, Connolly SJ, Gold MR, Israel CW, Van Gelder IC, Capucci A, Lau CP, Fain E, Yang S, Bailleul C, et al; ASSERT Investigators. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med. 2012;366:120–129. doi: 10.1056/NEJMoa1105575
Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, et al; RE-LY Steering Committee and Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361:1139–1151. doi: 10.1056/NEJMoa0905561.
Patel MR, Mahaffey KW, Garg J, Pan G, Singer DE, Hacke W, Breithardt G, Halperin JL, Hankey GJ, Piccini JP, et al; ROCKET AF Investigators. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365:883–891. doi: 10.1056/NEJMoa1009638.
Granger CB, Alexander JH, McMurray JJ, Lopes RD, Hylek EM, Hanna M, Al-Khalidi HR, Ansell J, Atar D, Avezum A, et al; ARISTOTLE Committees and Investigators. Apixaban versus warfarin in patients with atrial fibrilla- tion. N Engl J Med. 2011;365:981–992. doi: 10.1056/NEJMoa1107039.
Giugliano RP, Ruff CT, Braunwald E, Murphy SA, Wiviott SD, Halperin JL, Waldo AL, Ezekowitz MD, Weitz JI, Špinar J, et al; ENGAGE AF-TIMI 48 Investigators. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369:2093–2104. doi: 10.1056/NEJMoa1310907
Healey JS, Connolly SJ, Gold MR, Israel CW, Van Gelder IC, Capucci A, Lau CP, Fain E, Yang S, Bailleul C, et al; ASSERT Investigators. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med. 2012;366:120–129. doi: 10.1056/NEJMoa1105575
Ruff CT, Giugliano RP, Braunwald E, Hoffman EB, Deenadayalu N, Ezekowitz MD, Camm AJ, Weitz JI, Lewis BS, Parkhomenko A, et al. Comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. Lancet. 2014;383:955–962. doi: 10.1016/S0140-6736(13)62343-0
Seiffge DJ, Werring DJ, Paciaroni M, Dawson J, Warach S, Milling TJ, Engelter ST, Fischer U, Norrving B. Timing of anticoagulation after re- cent ischaemic stroke in patients with atrial fibrillation. Lancet Neurol. 2019;18:117–126. doi: 10.1016/S1474-4422(18)30356-9.
Paciaroni M, Agnelli G, Corea F, Ageno W, Alberti A, Lanari A, Caso V, Micheli S, Bertolani L, Venti M, et al. Early hemorrhagic transformation of brain infarction: rate, predictive factors, and influence on clinical outcome: results of a prospective multicenter study. Stroke. 2008;39:2249–2256. doi: 10.1161/STROKEAHA.107.510321.
Ahmed N, Steiner T, Caso V, Wahlgren N; ESO-KSU Session Participants. Recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 13-15 November 2016. Eur Stroke J. 2017;2:95–102. doi: 10.1177/2396987317699144.
Kalinin MN, Khasanova DR, Ibatullin MM. Optimal timing for initiation of anticoagulant therapy in patients with ischemic stroke and atrial fibrillation: a post-hoc analysis of the Hemorrhagic Transformation Index. Neurology, Neuropsychiatry, Psychosomatics. 2019;11(2):12-21.
Paciaroni M, Agnelli G, Corea F, Ageno W, Alberti A, Lanari A, Caso V, Micheli S, Bertolani L, Venti M, et al. Early hemorrhagic transformation of brain infarction: rate, predictive factors, and influence on clinical outcome: results of a prospective multicenter study. Stroke. 2008;39:2249–2256. doi: 10.1161/STROKEAHA.107.510321
Steffel J, Verhamme P, Potpara TS, Albaladejo P, Antz M, Desteghe L, Georg Haeusler K, Oldgren J, Reinecke H, Roldan-Schilling V, et al; ESC Scientific Document Group. The 2018 European Heart Rhythm Association practical guide on the use of non-vitamin K antagonist oral an- ticoagulants in patients with atrial fibrillation: executive summary. Europace. 2018; 20: 1231–1242. doi: 10.1093/europace/euy054
Ahmed N, Steiner T, Caso V, Wahlgren N; ESO-KSU Session Participants. Recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 13-15 November 2016. Eur Stroke J. 2017;2:95–102. doi: 10.1177/2396987317699144
Muscari A, Faccioli L, Lega MV, Lorusso A, Masetti M, Pastore Trossello M, Puddu GM, Spinardi L, Zoli M. Predicting hemorrhagic transformation and its timing from maximum cerebral lesion diameter in nonlacunar ischemic strokes. Brain Behav. 2020;10:e01497. doi: 10.1002/brb3.1497
Seiffge DJ, Werring DJ, Paciaroni M, Dawson J, Warach S, Milling TJ, Engelter ST, Fischer U, Norrving B. Timing of anticoagulation after recent ischaemic stroke in patients with atrial fibrillation. Lancet Neurol. 2019 Jan;18(1):117-126. Doi: 10.1016/S1474-4422(18)30356-9.
Hans-Christoph Diener, James Aisenberg, Jack Ansell, Dan Atar, Günter Breithardt, John Eikelboom, Michael D. Ezekowitz, Christopher B. Granger, Jonathan L. Halperin, Stefan H. Hohnloser, Elaine M. Hylek, Paulus Kirchhof, Deirdre A. Lane, Freek W.A. Verheugt, Roland Veltkamp, Gregory Y.H. Lip, Choosing a particular oral anticoagulant and dose for stroke prevention in individual patients with non-valvular atrial fibrillation: part 2, European Heart Journal, Volume 38, Issue 12, 21 March 2017, Pages 860–868
CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST: randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke. Lancet. 1997 Jun 7;349(9066):1641-9.
The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. International Stroke Trial Collaborative Group. Lancet. 1997 May 31;349(9065):1569-81.
Chen ZM, Sandercock P, Pan HC, Counsell C, Collins R, Liu LS, et al.. Indications for early aspirin use in acute ischemic stroke: a combined analysis of 40 000 randomized patients from the Chinese acute stroke trial and the international stroke trial.On behalf of the CAST and IST collaborative groups. Stroke. 2000; 31:1240–1249.
Dans AL, Connolly SJ, Wallentin L et al. Concomitant use of antiplatelet therapy with dabigatran or warfarin in the Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial. Circulation. 2013;127:634–640.
Flaker GC, Gruber M, Connolly SJ et al. Risks and benefits of combining aspirin with anticoagulant therapy in patients with atrial fibrillation: an exploratory analysis of stroke prevention using an oral thrombin inhibitor in atrial fibrillation (SPORTIF) trials. Am Heart J. 2006; 152: 967–973.
SPAF I-III = Hart RG, Pearce LA, McBride R, et al “Factors associated with ischemic stroke during aspirin therapy in atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. The Stroke Prevention in Atrial Fibrillation (SPAF) Investigators” Stroke 1999 Jun; 30(6): 1223-9.
AFASAK 2 = A.L.Gullov, MD, B.G.Koefoed,MD, P.Petersen, DMSc et al “Fixed minidose warfarin and aspirin alone and in combination versus adjusted-dose warfarin for stroke prevention in atrial fibrillation” Arch Intern Med 1998;158:1513-1521 RE-LY (sub-analysis) DOI: 10.1161/CIRCULATIONAHA.112.115386;
Olesen JB, Lip GY, Lindhardsen J, et al. Risks of thromboembolism and bleeding with thromboprophylaxis in patients with atrial fibrillation: A net clinical benefit analysis using a "real world" nationwide cohort study.Thromb Haemost. 2011; 106(4): 739–749. doi:10.1160/TH11-05-0364
Kleindorfer et al 2021 Guideline for the Secondary Prevention of Ischemic Stroke. Stroke. 2021;52:00–00. DOI: 10.1161/STR.0000000000000375
Holmes DR Jr, Kar S, Price MJ, Whisenant B, Sievert H, Doshi SK, Huber K, Reddy VY. Prospective randomized evaluation of the Watchman left atrial appendage closure device in patients with atrial fibrillation versus long- term warfarin therapy: the PREVAIL trial. J Am Coll Cardiol. 2014;64:1–12. doi: 10.1016/j.jacc.2014.04.029.
Holmes DR, Reddy VY, Turi ZG, Doshi SK, Sievert H, Buchbinder M, Mullin CM, Sick P; PROTECT AF Investigators. Percutaneous closure of the left atrial appendage versus warfarin therapy for prevention of stroke in patients with atrial fibrillation: a randomised non-inferiority trial. Lancet. 2009;374:534–542. doi: 10.1016/S0140-6736(09)61343-X.
Reddy VY, Doshi SK, Kar S, Gibson DN, Price MJ, Huber K, Horton RP, Buchbinder M, Neuzil P, Gordon NT, et al; PREVAIL and PROTECT AF Investigators. 5-Year outcomes after left atrial appendage closure: from the PREVAIL and PROTECT AF trials. J Am Coll Cardiol. 2017;70:2964– 2975. doi: 10.1016/j.jacc.2017.10.021.
Reddy VY, Sievert H, Halperin J, Doshi SK, Buchbinder M, Neuzil P, Huber K, Whisenant B, Kar S, Swarup V, et al; PROTECT AF Steering Committee and Investigators. Percutaneous left atrial appendage closure vs warfarin for atrial fibrillation: a randomized clinical trial. JAMA. 2014;312:1988– 1998. doi: 10.1001/jama.2014.15192
Hart RG, Coull BM, Hart D. Early recurrent embolism associated with non- valvular atrial fibrillation: a retrospective study. Stroke. 1983;14:688–693. doi: 10.1161/01.str.14.5.688.
Seiffge DJ, Werring DJ, Paciaroni M, Dawson J, Warach S, Milling TJ, Engelter ST, Fischer U, Norrving B. Timing of anticoagulation after re- cent ischaemic stroke in patients with atrial fibrillation. Lancet Neurol. 2019;18:117–126. doi: 10.1016/S1474-4422(18)30356-9.
Hans-Christoph Diener, James Aisenberg, Jack Ansell, Dan Atar, Günter Breithardt, John Eikelboom, Michael D. Ezekowitz, Christopher B. Granger, Jonathan L. Halperin, Stefan H. Hohnloser, Elaine M. Hylek, Paulus Kirchhof, Deirdre A. Lane, Freek W.A. Verheugt, Roland Veltkamp, Gregory Y.H. Lip, Choosing a particular oral anticoagulant and dose for stroke prevention in individual patients with non-valvular atrial fibrillation: part 2, European Heart Journal 2017; 38(12): 860-868.
Siontis KC, Zhang X, Eckard A, Bhave N, Schaubel DE, He K, Tilea A, Stack AG, Balkrishnan R, Yao X, et al. Outcomes associated with apixaban use in patients with end-stage kidney disease and atrial fibrillation in the United States. Circulation. 2018;138:1519–1529. doi: 10.1161/CIRCULATIONAHA.118.035418
Pan KL, Singer DE, Ovbiagele B, Wu YL, Ahmed MA, Lee M. Effects of non-vitamin K antagonist oral anticoagulants versus warfarin in patients with atrial fibrillation and valvular heart disease: a system- atic review and meta-analysis. J Am Heart Assoc. 2017;6:e005835. doi: 10.1161/JAHA.117.005835.
Avezum A, Lopes RD, Schulte PJ, Lanas F, Gersh BJ, Hanna M, Pais P, Erol C, Diaz R, Bahit MC, et al. Apixaban in comparison with warfarin in patients with atrial fibrillation and valvular heart disease: findings from the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) Trial. Circulation. 2015;132:624–632. doi: 10.1161/CIRCULATIONAHA.114.014807.
Breithardt G, Baumgartner H, Berkowitz SD, Hellkamp AS, Piccini JP, Stevens SR, Lokhnygina Y, Patel MR, Halperin JL, Singer DE, et al; ROCKET AF Steering Committee & Investigators. Clinical characteristics and outcomes with rivaroxaban vs. warfarin in patients with non-valvular atrial fibrillation but underlying native mitral and aortic valve disease participating in the ROCKET AF trial. Eur Heart J. 2014; 35: 3377–3385. doi: 10.1093/eurheartj/ehu305.
Pérez-Gómez F, Alegría E, Berjón J, Iriarte JA, Zumalde J, Salvador A, Mataix L; NASPEAF Investigators. Comparative effects of antiplatelet, anticoagulant, or combined therapy in patients with valvular and nonval- vular atrial fibrillation: a randomized multicenter study. J Am Coll Cardiol. 2004;44:1557–1566. doi: 10.1016/j.jacc.2004.05.084.
Ezekowitz MD, Nagarakanti R, Noack H, Brueckmann M, Litherland C, Jacobs M, Clemens A, Reilly PA, Connolly SJ, Yusuf S, et al. Comparison of dabigatran and warfarin in patients with atrial fibrillation and valvular heart disease: the RE-LY Trial (Randomized Evaluation of Long- Term Anticoagulant Therapy). Circulation. 2016; 134: 589–598. doi: 10.1161/CIRCULATIONAHA.115.020950.
Eikelboom JW, Connolly SJ, Brueckmann M, Granger CB, Kappetein AP, Mack MJ, Blatchford J, Devenny K, Friedman J, Guiver K, et al; RE-ALIGN Investigators. Dabigatran versus warfarin in patients with mechanical heart valves. N Engl J Med. 2013;369:1206–1214. doi: 10.1056/NEJMoa1300615
Hering D, Piper C, Bergemann R, Hillenbach C, Dahm M, Huth C, Horstkotte D. Thromboembolic and bleeding complications following St. Jude Medical valve replacement: results of the German Experience With Low-Intensity Anticoagulation study. Chest. 2005; 127: 53–59. doi: 10.1378/chest.127.1.53
Massel DR, Little SH. Antiplatelet and anticoagulation for patients with prosthetic heart valves. Cochrane Database Syst Rev. 2013: CD003464. doi: 10.1002/14651858.CD003464.pub2
Rodriguez CJ, Bartz TM, Longstreth WT Jr, Kizer JR, Barasch E, Lloyd-Jones DM, Gottdiener JS. Association of annular calcification and aortic valve sclerosis with brain findings on magnetic resonance imaging in community dwelling older adults: the Cardiovascular Health Study. J Am Coll Cardiol. 2011;57:2172–2180. doi: 10.1016/j.jacc.2011.01.034.
Kizer JR, Wiebers DO, Whisnant JP, Galloway JM, Welty TK, Lee ET, Best LG, Resnick HE, Roman MJ, Devereux RB. Mitral annular calcification, aortic valve sclerosis, and incident stroke in adults free of clinical cardiovascular disease: the Strong Heart Study. Stroke. 2005;36:2533–2537. doi: 10.1161/01.STR.0000190005.09442.ad.
Nishimura RA, McGoon MD, Shub C, Miller FA Jr, Ilstrup DM, Tajik AJ. Echocardiographically documented mitral-valve prolapse: long-term follow-up of 237 patients. N Engl J Med. 1985;313:1305–1309. doi: 10.1056/NEJM198511213132101.
Hayek E, Griffin B. Mitral valve prolapse: old beliefs yield to new knowledge. Cleve Clin J Med. 2002;69:889–896. doi: 10.3949/ccjm.69.11.889 483.
Zuppiroli A, Rinaldi M, Kramer-Fox R, Favilli S, Roman MJ, Devereux RB. Natural history of mitral valve prolapse. Am J Cardiol. 1995;75:1028–1032. doi: 10.1016/s0002-9149(99)80718-8
Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021;143:e229]. Circulation. 2021; 143: e72–e227. doi: 10.1161/CIR.0000000000000923.
Makkar RR, Fontana G, Jilaihawi H, Chakravarty T, Kofoed KF, De Backer O, Asch FM, Ruiz CE, Olsen NT, Trento A, et al. Possible subclinical leaflet thrombosis in bioprosthetic aortic valves. N Engl J Med. 2015; 373: 2015– 2024. doi: 10.1056/NEJMoa1509233.
Sundt TM, Zehr KJ, Dearani JA, Daly RC, Mullany CJ, McGregor CG, Puga FJ, Orszulak TA, Schaff HV. Is early anticoagulation with warfarin necessary after bioprosthetic aortic valve replacement? J Thorac Cardiovasc Surg. 2005; 129: 1024–1031. doi: 10.1016/j.jtcvs.2004.11.028
Russo A, Grigioni F, Avierinos JF, Freeman WK, Suri R, Michelena H, Brown R, Sundt TM, Enriquez-Sarano M. Thromboembolic complications after surgical correction of mitral regurgitation incidence, predictors, and clinical implications. J Am Coll Cardiol. 2008;51:1203–1211. doi: 10.1016/j.jacc.2007.10.058.
Colli A, Mestres CA, Castella M, Gherli T. Comparing warfarin to aspirin (WoA) after aortic valve replacement with the St. Jude Medical Epic heart valve bioprosthesis: results of the WoA Epic pilot trial. J Heart Valve Dis. 2007;16:667–671.
Heras M, Chesebro JH, Fuster V, Penny WJ, Grill DE, Bailey KR, Danielson GK, Orszulak TA, Pluth JR, Puga FJ. High risk of thromboemboli early after bioprosthetic cardiac valve replacement. J Am Coll Cardiol. 1995;25:1111– 1119. doi: 10.1016/0735-1097(94)00563-6.
Nuñez L, Gil Aguado M, Larrea JL, Celemín D, Oliver J. Prevention of thromboembolism using aspirin after mitral valve replacement with porcine bioprosthesis. Ann Thorac Surg. 1984;37:84–87. doi: 10.1016/s0003-4975(10)60717-5
Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021;143:e229]. Circulation. 2021; 143: e72–e227. doi: 10.1161/CIR.0000000000000923
Makkar RR, Fontana G, Jilaihawi H, Chakravarty T, Kofoed KF, De Backer O, Asch FM, Ruiz CE, Olsen NT, Trento A, et al. Possible subclinical leaflet thrombosis in bioprosthetic aortic valves. N Engl J Med. 2015; 373: 2015– 2024. doi: 10.1056/NEJMoa1509233.
Sundt TM, Zehr KJ, Dearani JA, Daly RC, Mullany CJ, McGregor CG, Puga FJ, Orszulak TA, Schaff HV. Is early anticoagulation with warfarin necessary after bioprosthetic aortic valve replacement? J Thorac Cardiovasc Surg. 2005; 129: 1024–1031. doi: 10.1016/j.jtcvs.2004.11.028.
Russo A, Grigioni F, Avierinos JF, Freeman WK, Suri R, Michelena H, Brown R, Sundt TM, Enriquez-Sarano M. Thromboembolic complications after surgical correction of mitral regurgitation incidence, predictors, and clinical implications. J Am Coll Cardiol. 2008; 51: 1203–1211. doi: 10.1016/j.jacc.2007.10.058
Colli A, Mestres CA, Castella M, Gherli T. Comparing warfarin to aspirin (WoA) after aortic valve replacement with the St. Jude Medical Epic heart valve bioprosthesis: results of the WoA Epic pilot trial. J Heart Valve Dis. 2007; 16: 667–671.
Heras M, Chesebro JH, Fuster V, Penny WJ, Grill DE, Bailey KR, Danielson GK, Orszulak TA, Pluth JR, Puga FJ. High risk of thromboemboli early after bioprosthetic cardiac valve replacement. J Am Coll Cardiol. 1995;25:1111– 1119. doi: 10.1016/0735-1097(94)00563-6.
Nuñez L, Gil Aguado M, Larrea JL, Celemín D, Oliver J. Prevention of thromboembolism using aspirin after mitral valve replacement with porcine bioprosthesis. Ann Thorac Surg. 1984;37:84–87. doi: 10.1016/s0003-4975(10)60717-5
Infective endocarditis and cardiac implantable electronic device infection. Clinical guidelines 2021. Demin A.A., Kobalava Z.D., Skopin I.I., et al. Russian Journal of Cardiology. 2022;27(10):113-192. (In Russ.)
Eishi K, Kawazoe K, Kuriyama Y, Kitoh Y, Kawashima Y, Omae T. Surgical management of infective endocarditis associated with cerebral complications: multi-center retrospective study in Japan. J Thorac Cardiovasc Surg. 1995;110:1745–1755. doi: 10.1016/S0022-5223(95)70038-2.
Barsic B, Dickerman S, Krajinovic V, Pappas P, Altclas J, Carosi G, Casabé JH, Chu VH, Delahaye F, Edathodu J, et al; International Collaboration on Endocarditis–Prospective Cohort Study Investigators. Influence of the timing of cardiac surgery on the outcome of patients with infective endocarditis and stroke. Clin Infect Dis. 2013;56:209–217. doi: 10.1093/cid/cis878
Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021;143:e229]. Circulation. 2021; 143: e72–e227. doi: 10.1161/CIR.0000000000000923
García-Cabrera E, Fernández-Hidalgo N, Almirante B, Ivanova-Georgieva R, Noureddine M, Plata A, Lomas JM, Gálvez-Acebal J, Hidalgo-Tenorio C, Ruíz-Morales J, et al; Group for the Study of Cardiovascular Infections of the Andalusian Society of Infectious Diseases; Spanish Network for Research in Infectious Diseases. Neurological complications of infective endocarditis: risk factors, outcome, and impact of cardiac surgery: a multicenter observational study. Circulation. 2013; 127: 2272–2284. doi: 10.1161/CIRCULATIONAHA.112.000813
Pöss, J, Desch, S, Eitel, C, de Waha, S, Thiele, H, Eitel, I. Left ventricular thrombus formation after ST-segment-elevation myocardial infarction: insights from a cardiac magnetic resonance multicenter study. Circ Cardiovasc Imaging. 2015; 8: e003417. doi: 10.1161/CIRCIMAGING.115.003417;
Vaitkus, PT, Barnathan, ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol. 1993;22:1004–1009. doi: 10.1016/0735-1097(93)90409-t;
Velangi, PS, Choo, C, Chen, KA, Kazmirczak, F, Nijjar, PS, Farzaneh-Far, A, Okasha, O, Akçakaya, M, Weinsaft, JW, Shenoy, C. Long-term embolic outcomes after detection of left ventricular thrombus by late gadolinium enhancement cardiovascular magnetic resonance imaging: a matched cohort study. Circ Cardiovasc Imaging. 2019;12:e009723. doi: 10.1161/CIRCIMAGING.119.009723
Fleddermann, AM, Hayes, CH, Magalski, A, Main, ML. Efficacy of direct acting oral anticoagulants in treatment of left ventricular thrombus. Am J Cardiol. 2019;124:367–372. doi: 10.1016/j.amjcard.2019.05.009.
Al-Abcha A, Herzallah K, Saleh Y, Mujer M, Abdelkarim O, Abdelnabi M, Almaghraby A, Abela GS. The Role of Direct Oral Anticoagulants Versus Vitamin K Antagonists in the Treatment of Left Ventricular Thrombi: A Meta-Analysis and Systematic Review. Am J Cardiovasc Drugs. 2021 Jul;21(4):435-441.
Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, Kamel H, Kernan WN, Kittner SJ, Leira EC, Lennon O, Meschia JF, Nguyen TN, Pollak PM, Santangeli P, Sharrief AZ, Smith SC Jr, Turan TN, Williams LS. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2021 Jul;52(7):e364-e467. doi: 10.1161/STR.0000000000000375. Epub 2021 May 24. Erratum in: Stroke. 2021 Jul;52(7):e483-e484. PMID: 34024117.
Lee JM, Park JJ, Jung HW, Cho YS, Oh IY, Yoon CH, Suh JW, Chun EJ, Choi SI, Youn TJ, et al. Left ventricular thrombus and subsequent thromboembolism, comparison of anticoagulation, surgical removal, and antiplatelet agents. J Atheroscler Thromb. 2013;20:73–93. doi: 10.5551/jat.13540.
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ, Scott RM, Smith ER; American Heart Association Stroke Council; Council on Cardiovascular Disease in the Young. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008 Sep;39(9):2644-91. doi: 10.1161/STROKEAHA.108.189696. Epub 2008 Jul 17. Erratum in: Stroke. 2009 Jan 1;40(1):e8-10. PMID: 18635845
Johannessen KA, Nordrehaug JE, von der Lippe G. Left ventricular thrombi after short-term high-dose anticoagulants in acute myocardial infarction. Eur Heart J. 1987;8:975–980. doi: 10.1093/oxfordjournals.eurheartj.a062374
Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, Kamel H, Kernan WN, Kittner SJ, Leira EC, Lennon O, Meschia JF, Nguyen TN, Pollak PM, Santangeli P, Sharrief AZ, Smith SC Jr, Turan TN, Williams LS. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2021 Jul;52(7):e364-e467. doi: 10.1161/STR.0000000000000375. Epub 2021 May 24. Erratum in: Stroke. 2021 Jul;52(7):e483-e484. PMID: 34024117.
Amarenco P, Davis S, Jones EF, Cohen AA, Heiss WD, Kaste M, Laouénan C, Young D, Macleod M, Donnan GA; Aortic Arch Related Cerebral Hazard Trial Investigators. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke. 2014;45:1248–1257. doi: 10.1161/STROKEAHA.113.004251.
Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Béjot Y, Cabrejo L, Cha JK, Ducrocq G, Giroud M, et al; Treat Stroke to Target Investigators. A comparison of two LDL cholesterol targets after ischemic stroke. N Engl J Med. 2020;382:9. doi: 10.1056/NEJMoa1910355
Deng X, Gao F, Zhang D, Zhang Y, Wang R, Wang S, Cao Y, Zhao Y, Pan Y, Liu X, et al. Direct versus indirect bypasses for adult ischemic-type moyamoya disease: a propensity score-matched analysis. J Neurosurg. 2018;128:1785–1791. doi: 10.3171/2017.2.JNS162405.
Deng X, Gao F, Zhang D, Zhang Y, Wang R, Wang S, Cao Y, Zhao Y, Pan Y, Ye X, et al. Effects of different surgical modalities on the clinical outome of patients with moyamoya disease: a prospective cohort study. J Neurosurg. 2018; 128: 1327–1337. doi: 10.3171/2016.12.JNS162626.
Jeon JP, Kim JE, Cho WS, Bang JS, Son YJ, Oh CW. Meta-analysis of the surgical outcomes of symptomatic moyamoya disease in adults. J Neurosurg. 2018;128:793–799. doi: 10.3171/2016.11.JNS161688.
Li Q, Gao Y, Xin W, Zhou Z, Rong H, Qin Y, Li K, Zhou Y, Wang J, Xiong J, et al. Meta-analysis of prognosis of different treatments for symptomatic moyamoya disease. World Neurosurg. 2019;127:354–361. doi: 10.1016/j.wneu.2019.04.062.
Sun H, Wilson C, Ozpinar A, Safavi-Abbasi S, Zhao Y, Nakaji P, Wanebo JE, Spetzler RF. Perioperative complications and long-term outcomes after bypasses in adults with moyamoya disease: a systematic review and meta-analysis. World Neurosurg. 2016;92:179–188. doi: 10.1016/j.wneu.2016.04.083.
Kim H, Jang DK, Han YM, Sung JH, Park IS, Lee KS, Yang JH, Huh PW, Park YS, Kim DS, et al. Direct bypass versus indirect bypass in adult moy- amoya angiopathy with symptoms or hemodynamic instability: a meta- analysis of comparative studies. World Neurosurg. 2016;94:273–284. doi: 10.1016/j.wneu.2016.07.009.
Jang DK, Lee KS, Rha HK, Huh PW, Yang JH, Park IS, Ahn JG, Sung JH, Han YM. Bypass surgery versus medical treatment for symptomatic moyamoya disease in adults. J Neurosurg. 2017;127:492–502. doi: 10.3171/2016.8.JNS152875
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ, Scott RM, Smith ER; American Heart Association Stroke Council; Council on Cardiovascular Disease in the Young. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008 Sep;39(9):2644-91. doi: 10.1161/STROKEAHA.108.189696. Epub 2008 Jul 17. Erratum in: Stroke. 2009 Jan 1;40(1):e8-10. PMID: 18635845
Kent DM, Dahabreh IJ, Ruthazer R, Furlan AJ, Reisman M, Carroll JD, Saver JL, Smalling RW, Jüni P, Mattle HP, et al. Device closure of patent foramen ovale after stroke: pooled analysis of completed randomized trials. J Am Coll Cardiol. 2016;67:907–917. doi: 10.1016/j. jacc.2015.12.023.
Lee PH, Song JK, Kim JS, Heo R, Lee S, Kim DH, Song JM, Kang DH, Kwon SU, Kang DW, et al. Cryptogenic stroke and high-risk patent foramen ovale: the DEFENSE-PFO trial. J Am Coll Cardiol. 2018;71:2335–2342. doi: 10.1016/j.jacc.2018.02.046.
Mas JL, Derumeaux G, Guillon B, Massardier E, Hosseini H, Mechtouff L, Arquizan C, Béjot Y, Vuillier F, Detante O, et al; CLOSE Investigators. Patent foramen ovale closure or anticoagulation vs. antiplatelets after stroke. N Engl J Med. 2017;377:1011–1021. doi: 10.1056/NEJMoa1705915.
Saver JL, Carroll JD, Thaler DE, Smalling RW, MacDonald LA, Marks DS, Tirschwell DL; RESPECT Investigators. Long-term outcomes of patent foramen ovale
closure or medical therapy after stroke. N Engl J Med. 2017; 377: 1022–1032. doi: 10.1056/NEJMoa1610057.
Søndergaard L, Kasner SE, Rhodes JF, Andersen G, Iversen HK, Nielsen-Kudsk JE, Settergren M, Sjöstrand C, Roine RO, Hildick-Smith D, et al; Gore REDUCE Clinical Study Investigators. Patent foramen ovale closure or antiplatelet therapy for cryptogenic stroke. N Engl J Med. 2017;377:1033–1042. doi: 10.1056/NEJMoa1707404.
Turc G, Lee JY, Brochet E, Kim JS, Song JK, Mas JL; CLOSE and DEFENSE-PFO Trial Investigators. Atrial septal aneurysm, shunt size, and recurrent stroke risk in patients with patent foramen ovale. J Am Coll Cardiol. 2020;75:2312–2320. doi: 10.1016/j.jacc.2020.02.068
Kent DM, Ruthazer R, Weimar C, Mas JL, Serena J, Homma S, Di Angelantonio E, Di Tullio MR, Lutz JS, Elkind MS, et al. An index to identify stroke-related vs incidental patent foramen ovale in cryptogenic stroke. Neurology. 2013;81:619–625
Stam J, De Bruijn SF, DeVeber G. Anticoagulation for cerebral sinus thrombosis. Cochrane Database Syst Rev. 2002;(4):CD002005.
Miranda B, Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F, Scoditti U; ISCVT Investigators. Venous thromboembolic events after cerebral vein thrombosis. Stroke. 2010;41:1901–1906.
Ferro JM. et al. Safety and Efficacy of Dabigatran Etexilate vs Dose-Adjusted Warfarin in Patients With Cerebral Venous Thrombosis: A Randomized Clinical Trial. JAMA Neurol. Published online September 03, 2019. doi:10.1001/jamaneurol.2019.2764.
Ferro JM, Bousser MG, Canhão P, Coutinho JM, Crassard I, Dentali F, di Minno M, Maino A, Martinelli I, Masuhr F, de Sousa DA, Stam J; European Stroke Organization. European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis - Endorsed by the European Academy of Neurology. Eur Stroke J. 2017 Sep;2(3):195-221. doi: 10.1177/2396987317719364. Epub 2017 Jul 21. PMID: 31008314; PMCID: PMC6454824.
Ferro JM. et al. Safety and Efficacy of Dabigatran Etexilate vs Dose-Adjusted Warfarin in Patients With Cerebral Venous Thrombosis: A Randomized Clinical Trial. JAMA Neurol. Published online September 03, 2019. doi:10.1001/jamaneurol.2019.2764
Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14:361–367. doi: 10.1016/S1474-4422(15)70018-9.
Markus HS, Levi C, King A, Madigan J, Norris J; Cervical Artery Dissection in Stroke Study (CADISS) Investigators. Antiplatelet therapy vs anticoagulation therapy in cervical artery dissection: the Cervical Artery Dissection in Stroke Study (CADISS) randomized clinical trial final results. JAMA Neurol. 2019;76:657–664. doi: 10.1001/jamaneurol.2019.0072
Redekop GJ. Extracranial carotid and vertebral artery dissection: a review. Can J Neurol Sci. 2008;35:146–152. doi:10.1017/s0317167100008556.
Moon K, Albuquerque FC, Cole T, Gross BA, McDougall CG. Stroke prevention by endovascular treatment of carotid and vertebral artery dissections. J Neurointerv Surg. 2017;9:952–957. doi: 10.1136/neurintsurg-2016-012565.
Spanos K, Karathanos C, Stamoulis K, Giannoukas AD. Endovascular treatment of traumatic internal carotid artery pseudoaneurysm. Injury. 2016; 47: 307–312. doi: 10.1016/j.injury.2015.09.015
Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, Kamel H, Kernan WN, Kittner SJ, Leira EC, Lennon O, Meschia JF, Nguyen TN, Pollak PM, Santangeli P, Sharrief AZ, Smith SC Jr, Turan TN, Williams LS. 2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2021 Jul;52(7):e364-e467. doi: 10.1161/STR.0000000000000375.
VITATOPS Trial Study Group. B vitamins in patients with recent transient ischaemic attack or stroke in the VITAmins TO Prevent Stroke (VITATOPS) trial: a randomised, double-blind, parallel, placebo-controlled trial. Lancet Neurol. 2010; 9: 855–865. doi: 10.1016/S1474-4422(10)70187-3.
Toole JF, Malinow MR, Chambless LE, Spence JD, Pettigrew LC, Howard VJ, Sides EG, Wang CH, Stampfer M. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA. 2004;291:565–575. doi: 10.1001/jama.291.5.565
Toole JF, Malinow MR, Chambless LE, Spence JD, Pettigrew LC, Howard VJ, Sides EG, Wang CH, Stampfer M. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for
Stroke Prevention (VISP) randomized controlled trial. JAMA. 2004; 291: 565–575. doi: 10.1001/jama.291.5.565.
Yap S, Naughten E. Homocystinuria due to cystathionine beta-synthase deficiency in Ireland: 25 years’ experience of a newborn screened and treated population with reference to clinical outcome and biochemical control. J Inherit Metab Dis. 1998; 21: 738–747. doi: 10.1023/a:1005445132327.
Yap S, Naughten ER, Wilcken B, Wilcken DE, Boers GH. Vascular complications of severe hyperhomocysteinemia in patients with homocystinuria due to cystathionine beta-synthase deficiency: effects of homocysteine-lowering therapy. Semin Thromb Hemost. 2000;26:335–340. doi:10.1055/s-2000-8100
Toole JF, Malinow MR, Chambless LE, Spence JD, Pettigrew LC, Howard VJ, Sides EG, Wang CH, Stampfer M. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA. 2004;291:565–575.
Roach ES, Golomb MR, Adams R, Biller J, Daniels S, Deveber G, Ferriero D, Jones BV, Kirkham FJ, Scott RM, Smith ER; American Heart Association Stroke Council; Council on Cardiovascular Disease in the Young. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke. 2008 Sep;39(9):2644-91. doi: 10.1161/STROKEAHA.108.189696. Epub 2008 Jul 17. Erratum in: Stroke. 2009 Jan 1;40(1):e8-10. PMID: 18635845.
Chevalet P, Barrier JH, Pottier P, Magadur-Joly G, Pottier MA, Hamidou M, Planchon B, El Kouri D, Connan L, Dupond JL, et al. A randomized, multicenter, controlled trial using intravenous pulses of methylprednisolone in the initial treatment of simple forms of giant cell arteritis: a one year followup study of 164 patients. J Rheumatol. 2000;27:1484–1491.
Diamantopoulos AP, Haugeberg G, Lindland A, Myklebust G. The fasttrack ultrasound clinic for early diagnosis of giant cell arteritis significantly reduces permanent visual impairment: towards a more effective strategy to improve clinical outcome in giant cell arteritis? Rheumatology (Oxford). 2016;55:66–70. doi: 10.1093/rheumatology/kev289.
Mazlumzadeh M, Hunder GG, Easley KA, Calamia KT, Matteson EL, Griffing WL, Younge BR, Weyand CM, Goronzy JJ. Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial. Arthritis Rheum. 2006;54:3310–3318. doi: 10.1002/art.22163
Saraya T, Shimura C, Wada H, Aoshima M, Goto H. Evidence for vascular spread of varicella zoster-associated vasculopathy. Ann Intern Med. 2006; 144:535–537. doi: 10.7326/0003-4819-144-7-200604040-00022.
Carod-Artal FJ, Gascon J. Chagas disease and stroke. Lancet Neurol. 2010;9:533–542. doi: 10.1016/S1474-4422(10)70042-9.
Lima-Costa MF, Matos DL, Ribeiro AL. Chagas disease predicts 10-year stroke mortality in community-dwelling elderly: the Bambui Cohort Study of Aging. Stroke. 2010;41:2477–2482. doi: 10.1161/ STROKEAHA.110.588061.
de Sousa AS, Xavier SS, Rodriguez de Freitas GR, Hasslocher-Moreno A. Prevention strategies of cardioembolic ischemic stroke in Chagas’ disease. Arq Bras Cardiol. 2008;91:306–310. doi: 10.1590/s0066-782x2008001700004.
Misra UK, Kalita J, Maurya PK. Stroke in tuberculous meningitis. J Neurol Sci. 2011;303:22–30. doi: 10.1016/j.jns.2010.12.015.
Anderson NE, Somaratne J, Mason DF, Holland D, Thomas MG. Neurological and systemic complications of tuberculous meningitis and its treatment at Auckland City Hospital, New Zealand. J Clin Neurosci. 2010;17:1114–1118. doi: 10.1016/j.jocn.2010.01.006.
Cordato DJ, Djekic S, Taneja SR, Maley M, Beran RG, Cappelen-Smith C, Griffith NC, Hanna IY, Hodgkinson SJ, Worthington JM, et al. Prevalence of positive syphilis serology and meningovascular neurosyphilis in patients admitted with stroke and TIA from a culturally diverse population (2005-09). J Clin Neurosci. 2013; 20: 943–947. doi: 10.1016/j.jocn.2012. 08.011.
Mishra AK, Arvind VH, Muliyil D, Kuriakose CK, George AA, Karuppusami R, Benton Carey RA, Mani S, Hansdak SG. Cerebrovascular injury in cryptococcal meningitis. Int J Stroke. 2018;13:57–65. doi: 10.1177/1747493017706240
Genthard HF, Aberg JA, Eron JJ, Hoy JF, Telenti A, Benson CA, Burger DM, Cahn P, Gallant JE, Glesby MJ, et al; International Antiviral Society-USA Panel. Antiretroviral treatment of adult HIV infection: 2014 recommendations of the International Antiviral Society-USA Panel. JAMA. 2014;312:410–425. doi: 10.1001/jama.2014.8722.
Connor M. Human immunodeficiency virus (HIV) and stroke: targets for intervention. Infect Disord Drug Targets. 2010;10:76–83. doi:10.2174/187152610790963483.
Cutfield NJ, Steele H, Wilhelm T, Weatherall MW. Successful treatment of HIV associated cerebral vasculopathy with HAART. J Neurol NeurosurgPsychiatry. 2009;80:936–937. doi: 10.1136/jnnp.2008.165852.
Benjamin LA, Allain TJ, Mzinganjira H, Connor MD, Smith C, Lucas S, Joekes E, Kampondeni S, Chetcuti K, Turnbull I, et al. The role of human immunodeficiency virus-associated vasculopathy in the etiology of stroke. J Infect Dis. 2017;216:545–553. doi: 10.1093/infdis/jix340
Edwards HB, Mallick AA, O"Callaghan FJK. Immunotherapy for arterial ischaemic stroke in childhood: a systematic review. Arch Dis Child. 2017 May;102(5):410-415. doi: 10.1136/archdischild-2016-311034. Epub 2016 Nov 18. PMID: 27864289.
Steinlin M, Bigi S, Stojanovski B, Gajera J, Regényi M, El-Koussy M, Mackay MT; Swiss NeuroPediatric Stroke Registry. Focal Cerebral Arteriopathy: Do Steroids Improve Outcome? Stroke. 2017 Sep;48(9):2375-2382. doi: 10.1161/STROKEAHA.117.016818. Epub 2017 Jul 21. PMID: 28733481
Beelen J, Benseler SM, Dropol A, Ghali B, Twilt M. Strategies for treatment of childhood primary angiitis of the central nervous system. Neurol Neuroimmunol Neuroinflamm. 2019 May 3;6(4):e567. doi: 10.1212/NXI.0000000000000567. PMID: 31355303; PMCID: PMC6624095.
Fonkem E, Dayawansa S, Stroberg E, Lok E, Bricker PC, Kirmani B, Wong ET, Huang JH. Neurological presentations of intravascular lymphoma (IVL): meta-analysis of 654 patients. BMC Neurol. 2016;16:9. doi:10.1186/s12883-015-0509-8.
Patil A, Shree R, Naheed D, Goyal MK, Mehta S, Ahuja CK, Radotra BD, Lal V. Pearls & oysters: paraneoplastic cerebral vasculitis: rare cause of spontaneous convexity
subarachnoid hemorrhage. Neurology. 2018; 90: e815–e817. doi: 10.1212/WNL.0000000000005025.
Quinones E, Potes LI, Silva N, Lobato-Polo J. Lymphomatoid granulomatosis of the brain: a case report. Surg Neurol Int. 2016;7(suppl 23):S612–S616. doi: 10.4103/2152-7806.189732
Miyakis S, Lockshin MD, Atsumi T, Branch DW, Brey RL, Cervera R, Derksen RH, DE Groot PG, Koike T, Meroni PL, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006;4:295–306. doi: 10.1111/j.1538-7836.2006.01753.x.
Andreoli L, Chighizola CB, Banzato A, Pons-Estel GJ, Ramire de Jesus G, Erkan D. Estimated frequency of antiphospholipid antibodies in patients with pregnancy morbidity, stroke, myocardial infarction, and deep vein thrombosis: a critical review of the literature. Arthritis Care Res (Hoboken). 2013;65:1869–1873. doi: 10.1002/acr.22066
Pengo V, Denas G, Zoppellaro G, Jose SP, Hoxha A, Ruffatti A, Andreoli L, Tincani A, Cenci C, Prisco D, et al. Rivaroxaban vs warfarin in high-risk patients with antiphospholipid syndrome. Blood. 2018;132:1365–1371. doi: 10.1182/blood-2018-04-848333.
Ordi-Ros J, Sáez-Comet L, Pérez-Conesa M, Vidal X, Riera-Mestre A, Castro-Salomó A, Cuquet-Pedragosa J, Ortiz-Santamaria V, Mauri-Plana M, Sola C, et al. Rivaroxaban versus vitamin K antagonist in antiphospholipid syndrome: a randomized noninferiority trial. Ann Intern Med. 2019;171:685–694. doi: 10.7326/M19-0291.
Dufrost V, Risse J, Reshetnyak T, Satybaldyeva M, Du Y, Yan XX, Salta S, Gerotziafas G, Jing ZC, Elalamy I, et al. Increased risk of thrombosis in antiphospholipid syndrome patients treated with direct oral anticoagulants: results from an international patient-level data meta-analysis. Autoimmun Rev. 2018;17:1011–1021. doi: 10.1016/j.autrev.2018.04.009
Lamy C, Hamon JB, Coste J and Mas JL. Ischemic stroke in young women: Risk of recurrence during subsequent pregnancies. French Study Group on Stroke in Pregnancy.Neurology2000; 55: 269–274.
Coppage KH, Hinton AC, Moldenhauer J, Kovilam O, Barton JR and Sibai BM. Maternal and perinatal outcome in women with a history of stroke. Am J Obstet Gynecol2004; 190: 1331–1334.
Crovetto F, Ossola MW, Spadaccini G, Duiella SF, Somigliana E and Fedele L. Ischemic stroke recurrence during pregnancy: A case series and a review of the literature.Arch Gynecol Obstet2012; 286: 599–604
Viscoli CM, Brass LM, Kernan WN, Sarrel PM, Suissa S, Horwitz RI. A clinical trial of estrogen-replacement therapy after ischemic stroke. N Engl J Med. 2001;345:1243–1249.
Caso V, Falorni A, Bushnell CD, Acciarresi M, Remohí J, Sprigg N, Gerli S. Pregnancy, Hormonal Treatments for Infertility, Contraception, and Menopause in Women After Ischemic Stroke: A Consensus Document. Stroke. 2017 Feb; 48(2): 501-506. doi: 10.1161/STROKEAHA.116.013964.
Cherry N, Gilmour K, Hannaford P, Heagerty A, Khan MA, Kitchener H, et al. Oestrogen therapy for prevention of reinfarction in postmenopausal women: a randomised placebo controlled trial. Lancet. 2002; 360: 2001–2008.
Swartz RH, Ladhani NNN, Foley N, Nerenberg K, Bal S, Barrett J, Bushnell C, Chan WS, Chari R, Dowlatshahi D, Amrani ME, Gandhi S, Gubitz G, Hill MD, James A, Jeerakathil T, Jin A, Kirton A, Lanthier S, Lausman A, Leffert LR, Mandzia J, Menon B, Pikula A, Poppe A, Potts J, Ray J, Saposnik G, Sharma M, Smith EE, Bhogal S, Smitko E, Lindsay MP; Heart and Stroke Foundation Canadian Stroke Best Practice Advisory Committees. Canadian stroke best practice consensus statement: Secondary stroke prevention during pregnancy. Int J Stroke. 2018 Jun;13(4):406-419. doi: 10.1177/1747493017743801.
Shanmugalingam R, Reza Pour N, Chuah SC, et al. Vertebral artery dissection in hypertensive disorders of pregnancy: A case series and literature review. BMC Preg Childbirth2016; 16: 164
Schisterman EF, Silver RM, Lesher LL, et al. Preconception low-dose aspirin and pregnancy outcomes: Results from the EAGeR randomised trial.Lancet2014; 384: 29–36
Henderson JT, Whitlock EP, O’Connor E, Senger CA, Thompson JH and Rowland MG. Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: A systematic evidence review for the U.S. Preventive Services Task Force.Ann Intern Med2014; 160: 695–703.
Kozer E, Nikfar S, Costei A, Boskovic R, Nulman I and Koren G. Aspirin consumption during the first trimester of pregnancy and congenital anomalies: A meta-analysis. Am J Obstet Gynecol2002; 187: 1623–1630.
Norgard B, Puho E, Czeizel AE, Skriver MV and Sorensen HT. Aspirin use during early pregnancy and the risk of congenital abnormalities: A populationbased case-control study. Am J Obstet Gynecol2005; 192: 922–923
Visser J, Ulander VM, Helmerhorst FM, et al. Thromboprophylaxis for recurrent miscarriage in women with or without thrombophilia. HABENOX: A randomised multicentre trial.Thromb Haemost2011; 105: 295–301
Xu Z, Fan J, Luo X, et al. Anticoagulation regimens during pregnancy in patients with mechanical heart valves: A systematic review and meta-analysis. Can J Cardiol2016; 32: 1248.e1–e9
Tektonidou MG, Andreoli L, Limper M, et al. EULAR recommendations for the manage-ment of antiphospholipid syndrome in adults. Ann Rheum Dis. 2019 Oct;78(10):1296-1304. doi: 10.1136/annrheumdis-2019-215213. Epub 2019 May 15. PMID: 31092409
Rodger MA, Hague WM, Kingdom J, et al. Antepartum dalteparin versus no antepartum dalteparin for the prevention of pregnancy complications in pregnant women with thrombophilia (TIPPS): A multinational open-label randomised trial.Lancet2014; 384: 1673–1683.
Chan WS, Rey E, Kent NE, et al. Venous thromboembolism and antithrombotic therapy in pregnancy. J Obstet Gynaecol Can2014; 36: 527–553
Bell AD, Roussin A, Cartier R, et al. The use of antiplatelet therapy in the outpatient setting: Canadian Cardiovascular Society guidelines.Can J Cardiol2011; 27: S1–59.
Datta P, Rewers-Felkins K, Kallem RR, Baker T and Hale TW. Transfer of low dose aspirin into human milk. J Hum Lact2017; 33: 296–299
Arterial hypertension in adults: clinical guidelines. Russian Journal of Cardiology. 2020;25(3):3786. (In Russ.) doi: 10.15829/1560-4071-2020-3-3786
Diagnosis and treatment of cardiovascular diseases during pregnancy 2018. National guidelines. Stryuk R.I., Bunin Yu.A., Guryeva V.M., et al. Russian Journal of Cardiology. 2018;23(3):91-134. (In Russ.)
Easterling T. et al. Oral antihypertensive regimens (nifedipine retard, labetalol, and methyldopa) for management of severe hypertension in pregnancy: an open-label, randomised controlled trial. The Lancet 2019; 394 (10203): 1011-1021.
Weitz C. et al. Treatment of hypertension in pregnancy with methyldopa: a randomized double blind study. International Journal of Gynecology & Obstetrics. 1987; 25 (1): 35-40.
Williams B et al. 2018 Practice guidelines for the management of arterial hypertension of the European Society of Cardiology and the European Society of Hypertension. Blood pressure 2018; 27(6): 314-340.
Bateman BT, Hernandez-Diaz S, Fischer MA, et al. Statins and congenital malformations: Cohort study. BMJ2015; 350: h1035.
Zarek J and Koren G. The fetal safety of statins: A systematic review and meta-analysis. J Obstet Gynaecol Can 2014; 36: 506–509.
Winterfeld U, Allignol A, Panchaud A, et al. Pregnancy outcome following maternal exposure to statins: A multicentre prospective study.BJOG2013; 120: 463–471
Scott CA, Bewley S, Rudd A, et al. Incidence, risk factors, management, and outcomes of stroke in pregnancy. Obstet Gynecol2012; 120: 318–324
Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, Warlow CP, Barnett HJ; Carotid Endarterectomy Trialists’ Collaboration. Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet. 2003;361:107–116. doi: 10.1016/s0140-6736(03)12228-3
Bonati LH, Kakkos S, Berkefeld J, de Borst GJ, Bulbulia R, Halliday A, van Herzeele I, Koncar I, McCabe DJ, Lal A, Ricco JB, Ringleb P, Taylor-Rowan M, Eckstein HH. European Stroke Organisation guideline on endarterectomy and stenting for carotid artery stenosis. Eur Stroke J. 2021 Jun;6(2):I-XLVII. doi: 10.1177/23969873211012121. Epub 2021 May 11. PMID: 34414302; PMCID: PMC8370069
Brott TG, Hobson RW 2nd, Howard G, Roubin GS, Clark WM, Brooks W, Mackey A, Hill MD, Leimgruber PP, Sheffet AJ, Howard VJ, Moore WS, Voeks JH, Hopkins LN, Cutlip DE, Cohen DJ, Popma JJ, Ferguson RD, Cohen SN, Blackshear JL, Silver FL, Mohr JP, Lal BK, Meschia JF; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010 Jul 1;363(1):11-23. doi: 10.1056/NEJMoa0912321
Barnett HJM, Taylor DW, Haynes RB, Sackett DL, Peerless SJ, Ferguson GG, Fox AJ, Rankin RN, Hachinski VC, Wiebers DO. et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453
De Rango P, Brown MM, Chaturvedi S, Howard VJ, Jovin T, Mazya MV, Paciaroni M, Manzone A, Farchioni L, Caso V. Summary of Evidence on Early Carotid Intervention for Recently Symptomatic Stenosis Based on Meta-Analysis of Current Risks. Stroke. 2015 Dec;46(12):3423-36. doi: 10.1161/STROKEAHA.115.010764
AbuRahma AF, Avgerinos ED, Chang RW, Darling RC 3rd, Duncan AA, Forbes TL, Malas MB, Murad MH, Perler BA, Powell RJ, Rockman CB, Zhou W. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. J Vasc Surg. 2022 Jan;75(1S):4S-22S. doi: 10.1016/j.jvs.2021.04.073. Epub 2021 Jun 19. PMID: 34153348
Naylor R, Rantner B, Ancetti S, de Borst GJ, De Carlo M, Halliday A, Kakkos SK, Markus HS, McCabe DJH, Sillesen H, van den Berg JC, Vega de Ceniga M, Venermo MA, Vermassen FEG, Esvs Guidelines Committee, Antoniou GA, Bastos Goncalves F, Bjorck M, Chakfe N, Coscas R, Dias NV, Dick F, Hinchliffe RJ, Kolh P, Koncar IB, Lindholt JS, Mees BME, Resch TA, Trimarchi S, Tulamo R, Twine CP, Wanhainen A, Document Reviewers, Bellmunt-Montoya S, Bulbulia R, Darling RC 3rd, Eckstein HH, Giannoukas A, Koelemay MJW, Lindström D, Schermerhorn M, Stone DH. Editor"s Choice - European Society for Vascular Surgery (ESVS) 2023 Clinical Practice Guidelines on the Management of Atherosclerotic Carotid and Vertebral Artery Disease. Eur J Vasc Endovasc Surg. 2023 Jan;65(1):7-111. doi: 10.1016/j.ejvs.2022.04.011. Epub 2022 May 20. PMID: 35598721
Rantner B, Eckstein HH, Ringleb P, Woelfle KD, Bruijnen H, Schmidauer C, Fraedrich G. American Society of Anesthesiology and Rankin as predictive parameters for the outcome of carotid endarterectomy within 28 days after an ischemic stroke. J Stroke Cerebrovasc Dis. 2006 May-Jun;15(3):114-20. doi: 10.1016/j.jstrokecerebrovasdis.2006.03.004.
Wölfle KD, Pfadenhauer K, Bruijnen H, Becker T, Engelhardt M, Wachenfeld-Wahl C, Schulze-Hamma E, Loeprecht H, Wohlgemuth WA. Early carotid endarterectomy in patients with a nondisabling ischemic stroke: results of a retrospective analysis. Vasa. 2004 Feb;33(1):30-5. doi: 10.1024/0301-1526.33.1.30
Karkos CD, McMahon G, McCarthy MJ, Dennis MJ, Sayers RD, London NJ, Naylor AR. The value of urgent carotid surgery for crescendo transient ischemic attacks. J Vasc Surg. 2007 Jun;45(6):1148-54. doi: 10.1016/j.jvs.2007.02.005.
Dorigo W, Pulli R, Nesi M, Alessi Innocenti A, Pratesi G, Inzitari D, Pratesi C. Urgent carotid endarterectomy in patients with recent/crescendo transient ischaemic attacks or acute stroke. Eur J Vasc Endovasc Surg. 2011 Mar;41(3):351-7. doi: 10.1016/j.ejvs.2010.11.026
Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, Bajwa TK, Whitlow P, Strickman NE, Jaff MR, et al; Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy Investigators. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004;351:1493–1501. doi: 10.1056/NEJMoa040127.
Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, Brooks W, Mackey A, Hill MD, Leimgruber PP, Sheffet AJ, et al; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363:11–23. doi: 10.1056/NEJMoa0912321
Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, Bajwa TK, Whitlow P, Strickman NE, Jaff MR, Popma JJ, Snead DB, Cutlip DE, Firth BG, Ouriel K; Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy Investigators. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004 Oct 7;351(15):1493-501. doi: 10.1056/NEJMoa040127
Massop D, Dave R, Metzger C, Bachinsky W, Solis M, Shah R, Schultz G, Schreiber T, Ashchi M, Hibbard R; SAPPHIRE Worldwide Investigators. Stenting and angioplasty with protection in patients at high-risk for endarterectomy: SAPPHIRE Worldwide Registry first 2,001 patients. Catheter Cardiovasc Interv. 2009 Feb 1;73(2):129-36. doi: 10.1002/ccd.21844.
Kang JL, Chung TK, Lancaster RT, Lamuraglia GM, Conrad MF, Cambria RP. Outcomes after carotid endarterectomy: is there a high-risk population? A National Surgical Quality Improvement Program report. J Vasc Surg. 2009 Feb;49(2):331-8, 339.e1; discussion 338-9. doi: 10.1016/j.jvs.2008.09.018.
Bangalore S, Kumar S, Wetterslev J, Bavry AA, Gluud C, Cutlip DE, Bhatt DL. Carotid artery stenting vs carotid endarterectomy: meta-analysis and diversity-adjusted trial sequential analysis of randomized trials. Arch Neurol. 2011 Feb;68(2):172-84. doi: 10.1001/archneurol.2010.262
Zhu F, Bracard S, Anxionnat R, Derelle AL, Tonnelet R, Liao L, Mione G, Humbertjean L, Lacour JC, Hossu G, Anadani M, Richard S, Gory B. Impact of Emergent Cervical Carotid Stenting in Tandem Occlusion Strokes Treated by Thrombectomy: A Review of the TITAN Collaboration. Front Neurol. 2019 Mar 11; 10: 206. doi: 10.3389/fneur.2019.00206
Kataoka H, Miyamoto S, Ogasawara K, Iihara K, Takahashi JC, Nakagawara J, Inoue T, Mori E, Ogawa A; JET-2 Investigators. Results of Prospective Cohort Study on Symptomatic Cerebrovascular Occlusive Disease Showing Mild Hemodynamic Compromise [Japanese Extracranial-Intracranial Bypass Trial (JET)-2 Study]. Neurol Med Chir (Tokyo). 2015;55(6):460-8. doi: 10.2176/nmc.oa.2014-0424. Epub 2015 Jun 2. PMID: 26041628; PMCID: PMC4628197;
Cai S, Fan H, Peng C, Wu Y, Yang X. The comparison of STA-MCA bypass and BMT for symptomatic internal carotid artery occlusion disease: a systematic review and meta-analysis of long-term outcome. Chin Neurosurg J. 2021 Apr 5;7(1):17. doi: 10.1186/s41016-021-00236-2. PMID: 33814006; PMCID: PMC8020543;
Nguyen VN, Motiwala M, Parikh K, Miller LE, Barats M, Nickele CM, Inoa V, Elijovich L, Goyal N, Hoit DA, Arthur AS, Morcos JJ, Khan NR. Extracranial-Intracranial Cerebral Revascularization for Atherosclerotic Vessel Occlusion: An Updated Systematic Review of the Literature. World Neurosurg. 2023 May;173:199-207.e8. doi: 10.1016/j.wneu.2023.02.003. Epub 2023 Feb 8. PMID: 36758795
Giuseppe, E., et al. (2016). "Role of and Indications for Bypass Surgery After Carotid Occlusion Surgery Study (COSS)?" Stroke 47(1): 282-290
Chernyavsky M.A., Irtyuga O.B., Yanishevskiy S.N., Alieva A.S., Samochernikh K.A., Abramov K.B., Vavilova T.V., Lukyanchikov V.A., Kurapeyev D.I., Vanyurkin A.G., Chernova D.V., Shelukhanov N.K., Kozlenok A.V., Kavteladze Z.A., Malevanniy M.V., Vinogradov R.A., Khafizov T.N., Ivanova G.E., Zhukovskaya N.V., Fokin A.A., Ignatyev I.M., Karpenko A.A., Ignatenko P.V., Astapov D.A., Semenov V.Yu., Porkhanov V.A., Krylov V.V., Usachev D.Yu., Svetlikov A.V., Alekyan B.G., Akchurin R.S., Chernyavsky A.M., Konradi A.O., Shlyakhto E.V. Russian consensus on the diagnosis and treatment of patients with carotid artery stenosis. Russian Journal of Cardiology. 2022;27(11):5284. (In Russ.) https://doi.org/10.15829/1560-4071-2022-5284
Langhorne P, Ramachandra S. Organised inpatient (stroke unit) care for stroke: network meta-analysis. Cochrane Database of Systematic Reviews 2020, Issue 4. Art. No.: CD000197. DOI: 10.1002/14651858.CD000197.pub4.
Alberts MJ, Hademenos G, Latchaw RE, Jagoda A, Marler JR, Mayberg MR, Starke RD, Todd HW, Viste KM, Girgus M, Shephard T, Emr M, Shwayder P, Walker MD. Recommendations for the establishment of primary stroke centers: Brain Attack Coalition. JAMA.2000; 283: 3102–3109.
Alberts MJ, Latchaw RE, Selman WR, Shephard T, Hadley MN, Brass LM, Koroshetz W, Marler JR, Booss J, Zorowitz RD, Croft JB, Magnis E, Mulligan D, Jagoda A, O’Connor R, Cawley CM, Connors JJ, Rose-DeRenzy JA, Emr M, Warren M, Walker MD; Brain Attack Coalition. Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition. Stroke.2005;36:1597–1616.
Effectiveness of Primary and Comprehensive Stroke Centers. PERFECT Stroke: A Nationwide Observational Study From Finland. Atte Meretoja, Risto O. Roine, Markku Kaste, Miika Linna, Susanna Roine, Merja Juntunen, Terttu Erilä, Matti Hillbom, Reijo Marttila, Aimo Rissanen, Juhani Sivenius, and Unto Häkkinen. Stroke. 2010;41:1102–1107
Zhai YK, Zhu WJ, Hou HL, Sun DX, Zhao J. Efficacy of telemedicine for thrombolytic therapy in acute ischemic stroke: a meta-analysis. J Telemed Telecare. 2015;21(3):123–30.
Kepplinger J, Barlinn K, Deckert S, Scheibe M, Bodechtel U, Schmitt J. Safety and efficacy of thrombolysis in telestroke: A systematic review and meta-analysis. Neurology. 2016;87(13):1344–51.
Baratloo A, Rahimpour L, Abushouk AI, Safari S, Lee CW, Abdalvand A. Effects of Telestroke on Thrombolysis Times and Outcomes: A Meta-analysis. Prehospital Emerg Care. 2018;22(4):472–84.
Boden-Albala B, Stillman J, Roberts ET, Quarles LW, Glymour MM, Chong J, Moats H, Torrico V, Parides MC. Comparison of acute stroke preparedness strategies to decrease emergency department arrival time in a multiethnic cohort: the Stroke Warning Information and Faster Treatment Study. Stroke. 2015;46:1806–1812. doi: 10.1161/STROKEAHA.114.008502
Meretoja A, Strbian D, Mustanoja S, Tatlisumak T, Lindsberg PJ, Kaste M. Reducing in-hospital delay to 20 minutes in stroke thrombolysis. Neurology. 2012 Jul 24;79(4):306-13. doi: 10.1212/WNL.0b013e31825d6011. Epub 2012 May 23. PMID: 22622858
Rudd M. et al. A systematic review of stroke recognition instruments in hospital and prehospital settings. Emergency Medicine Journal. 2016;33(11):818-822.
Brandler ES, Sharma M, Sinert RH, Levine SR. Prehospital stroke scales in urban environments: a systematic review. Neurology 2014; 82: 2241–2249.
Zhelev Z, Walker G, Henschke N, Fridhandler J, Yip S. Prehospital stroke scales as screening tools for early identification of stroke and transient ischemic attack. Cochrane Database of Systematic Reviews 2019, Issue 4. Art. No.: CD011427. DOI: 10.1002/14651858.CD011427.pub2
Ojike, N, Ravenell, J, Seixas, A, Masters-Israilov, A, Rogers, A, Jean-Louis, G, Ogedegbe, G, McFarlane, SI. Racial disparity in stroke awareness in the US: an analysis of the 2014 National Health Interview Survey. J Neurol Neurophysiol. 2016;7:365;
Ekundayo, OJ, Saver, JL, Fonarow, GC, Schwamm, LH, Xian, Y, Zhao, X, Hernandez, AF, Peterson, ED, Cheng, EM. Patterns of emergency medical services use and its association with timely stroke treatment: findings from Get With The Guidelines–Stroke. Circ Cardiovasc Qual Outcomes. 2013;6:262–269. doi: 10.1161/CIRCOUTCOMES.113.000089
Ekundayo OJ, Saver JL, Fonarow GC, Schwamm LH, Xian Y, Zhao X, Hernandez AF, Peterson ED, Cheng EM. Patterns of emergency medical services use and its association with timely stroke treatment: findings from Get With The Guidelines–Stroke.Circ Cardiovasc Qual Outcomes. 2013;6:262–269;
Mochari-Greenberger H, Xian Y, Hellkamp AS, Schulte PJ, Bhatt DL, Fonarow GC, Saver JL, Reeves MJ, Schwamm LH, Smith EE. Racial/ethnic and sex differences in emergency medical services transport among hospitalized US Stroke patients: analysis of the national Get With The Guidelines-Stroke Registry. J Am Heart Assoc. 2015;4:e002099;
Boden-Albala B, Stillman J, Roberts ET, Quarles LW, Glymour MM, Chong J, Moats H, Torrico V, Parides MC. Comparison of acute stroke preparedness strategies to decrease emergency department arrival time in a multiethnic cohort: the Stroke Warning Information and Faster Treatment Study. Stroke. 2015;46:1806–1812. doi: 10.1161/STROKEAHA.114.008502.
Berglund A, Svensson L, Sjostrand C, et al. Higher prehospital priority level of stroke improves thrombolysis frequency and time to stroke unit: the hyper acute stroke alarm (HASTA) study. Stroke 2012; 43: 2666–2670.
Provost C, Soudant M, Legrand L, Ben Hassen W, Xie Y, Soize S, Bourcier R, Benzakoun J, Edjlali M, Boulouis G, Raoult H, Guillemin F, Naggara O, Bracard S, Oppenheim C. Magnetic Resonance Imaging or Computed Tomography Before Treatment in Acute Ischemic Stroke. Stroke. 2019 Mar;50(3):659-664. doi: 10.1161/STROKEAHA.118.023882.
Aghaebrahim A, Granja MF, Agnoletto GJ, Aguilar-Salinas P, Cortez GM, Santos R, Monteiro A, Camp W, Day J, Dellorso S, Naval N, Chmayssani M, Stromberg R, Rill MC, Sauvageau E, Hanel R. Workflow Optimization for Ischemic Stroke in a Community-Based Stroke Center. World Neurosurg. 2019 Sep;129:e273-e278. doi: 10.1016/j.wneu.2019.05.127.
Meretoja A, Strbian D, Mustanoja S, Tatlisumak T, Lindsberg PJ, Kaste M. Reducing in-hospital delay to 20 minutes in stroke thrombolysis. Neurology. 2012 Jul 24;79(4):306-13. doi: 10.1212/WNL.0b013e31825d6011.
Spokoyny I, Raman R, Ernstrom K, Demaerschalk BM, Lyden PD, Hemmen TM, Guzik AK, Chen JY, Meyer BC. Pooled assessment of computed tomography interpretation by vascular neurologists in the STRokE DOC telestroke network. J Stroke Cerebrovasc Dis. 2014;23:511–515. doi: 10.1016/j.jstrokecerebrovasdis.2013.04.023.
Puetz V, Bodechtel U, Gerber JC, Dzialowski I, Kunz A, Wolz M, Hentschel H, Schultheiss T, Kepplinger J, Schneider H, Wiedemann B, Wojciechowski C, Reichmann H, Gahn G, von Kummer R. Reliability of brain CT evaluation by stroke neurologists in telemedicine. Neurology. 2013;80:332–338. doi: 10.1212/WNL.0b013e31827f07d0.
Sulter G, Elting JW, Langedijk M, Maurits NM, De Keyser J.Admitting acute ischemic stroke patients to a stroke care monitoring unit versus a conventional stroke unit: a randomized pilot study. Stroke. 2003;34:101–104.
Cavallini A, Micieli G, Marcheselli S, Quaglini S. Role of monitoring in management of acute ischemic stroke patients. Stroke. 2003;34:2599–2603.
Kummer BR, Lerario MP, Hunter MD, Wu X, Efraim ES, Salehi Omran S, Chen ML, Diaz IL, Sacchetti D, Lekic T, Kulick ER, Pishanidar S, Mir SA, Zhang Y, Asaeda G, Navi BB, Marshall RS, Fink ME. Geographic Analysis of Mobile Stroke Unit Treatment in a Dense Urban Area: The New York City METRONOME Registry. J Am Heart Assoc. 2019 Dec 17;8(24):e013529. doi: 10.1161/JAHA.119.013529;
Zhao H, Coote S, Easton D, Langenberg F, Stephenson M, Smith K, Bernard S, Cadilhac DA, Kim J, Bladin CF, Churilov L, Crompton DE, Dewey HM, Sanders LM, Wijeratne T, Cloud G, Brooks DM, Asadi H, Thijs V, Chandra RV, Ma H, Desmond PM, Dowling RJ, Mitchell PJ, Yassi N, Yan B, Campbell BCV, Parsons MW, Donnan GA, Davis SM. Melbourne Mobile Stroke Unit and Reperfusion Therapy: Greater Clinical Impact of Thrombectomy Than Thrombolysis. Stroke. 2020 Mar;51(3):922-930. doi: 10.1161/STROKEAHA.119.027843;
Ebinger M, Siegerink B, Kunz A, Wendt M, Weber JE, Schwabauer E, Geisler F, Freitag E, Lange J, Behrens J, Erdur H, Ganeshan R, Liman T, Scheitz JF, Schlemm L, Harmel P, Zieschang K, Lorenz-Meyer I, Napierkowski I, Waldschmidt C, Nolte CH, Grittner U, Wiener E, Bohner G, Nabavi DG, Schmehl I, Ekkernkamp A, Jungehulsing GJ, Mackert BM, Hartmann A, Rohmann JL, Endres M, Audebert HJ; Berlin_PRehospital Or Usual Delivery in stroke care (B_PROUD) study group. Association Between Dispatch of Mobile Stroke Units and Functional Outcomes Among Patients With Acute Ischemic Stroke in Berlin. JAMA. 2021 Feb 2;325(5):454-466. doi: 10.1001/jama.2020.26345.
Czap AL, Singh N, Bowry R, Jagolino-Cole A, Parker SA, Phan K, Wang M, Sheth SA, Rajan SS, Yamal JM, Grotta JC. Mobile Stroke Unit Computed Tomography Angiography Substantially Shortens Door-to-Puncture Time. Stroke. 2020 May;51(5):1613-1615. doi: 10.1161/STROKEAHA.119.028626.
James C. Grotta, M.D., Jose-Miguel Yamal, Ph.D., Stephanie A. Parker, M.H.A., Suja S. Rajan, Ph.D., Nicole R. Gonzales, M.D., William J. Jones, M.D., Anne W. Alexandrov, Ph.D., Babak B. Navi, M.D., May Nour, M.D., Ph.D., Ilana Spokoyny, M.D., Jason Mackey, M.D., David Persse, M.D., et al. Prospective, Multicenter, Controlled Trial of Mobile Stroke Units. N Engl J Med 2021; 385:971-981 DOI: 10.1056/NEJMoa2103879
Lin CB, Peterson ED, Smith EE, Saver JL, Liang L, Xian Y, Olson DM, Shah BR, Hernandez AF, Schwamm LH, Fonarow GC. Emergency medical service hospital prenotification is associated with improved evaluation and treatment of acute ischemic stroke. Circ Cardiovasc Qual Outcomes. 2012;5:514–522
Nielsen VM, DeJoie-Stanton C, Song G, Christie A, Guo J, Zachrison KS. The association between presentation by ems and ems prenotification with receipt of intravenous tissue-type plasminogen activator in a state implementing stroke systems of care. Prehosp Emerg Care. 2020 May-Jun;24(3):319-325
Saver JL, Fonarow GC, Smith EE, Reeves MJ, Grau-Sepulveda MV, Pan W, Olson DM, Hernandez AF, Peterson ED, Schwamm LH. Time to treatment with intravenous tissue plasminogen activator and outcome from acute ischemic stroke. JAMA. 2013;309:2480–2488;
Higashida R, Alberts MJ, Alexander DN, Crocco TJ, Demaerschalk BM, Derdeyn CP, Goldstein LB, Jauch EC, Mayer SA, Meltzer NM, Peterson ED, Rosenwasser RH, Saver JL, Schwamm L, Summers D, Wechsler L, Wood JP; American Heart Association Advocacy Coordinating Committee. Interactions within stroke systems of care: a policy statement from the American Heart Association/American Stroke Association. Stroke. 2013 Oct;44(10):2961-84.
Alasheev AM, Hubert GJ, Santo GC, Vanhooren GT, Zvan B, Campos ST, et al. Recommendations on telestroke in Europe. Zhurnal Nevrol i psikhiatrii im SS Korsakova. 2020;120(3):33.
Pedragosa A, Alvarez-Sabin J, Molina CA, Sanclemente C, Martín MC, Alonso F, et al. Impact of a telemedicine system on acute stroke care in a community hospital. J Telemed Telecare. 2009;15(5):260–3.
Audebert, H. J., Schultes, K., Tietz, V., Heuschmann, P. U., Bogdahn, U., Haberl, R. L., & Schenkel, J. (2009). Long-term effects of specialized stroke care with telemedicine support in community hospitals on behalf of the Telemedical Project for Integrative Stroke Care (TEMPiS). Stroke; a Journal of Cerebral Circulation, 40(3), 902–908. Doi: 10.1161/STROKEAHA.108.529255.
Demaerschalk, B. M., Boyd, E. L., Barrett, K. M., Gamble, D. M., Sonchik, S., Comer, M. M., Wieser, J., Hentz, J. G., Fitz-Patrick, D., & Chang, Y. H. H. (2018). Comparison of Stroke Outcomes of Hub and Spoke Hospital Treated Patients in Mayo Clinic Telestroke Program. Journal of Stroke and Cerebrovascular Diseases, 27(11), 2940–2942. Doi: 10.1016/j.jstrokecerebrovasdis.2018.06.024
Eichberg DG, Basil GW, Di L, Shah AH, Luther EM, Lu VM, Perez-Dickens M, Komotar RJ, Levi AD, Ivan ME. Telemedicine in Neurosurgery: Lessons Learned from a Systematic Review of the Literature for the COVID-19 Era and Beyond. Neurosurgery. 2020 Dec 15;88(1):E1-E12. doi: 10.1093/neuros/nyaa306. PMID: 32687191; PMCID: PMC7454774.
Angileri, F. F., Cardali, S., Conti, A., Raffa, G., & Tomasello, F. (2012). Telemedicine-assisted treatment of patients with intracerebral hemorrhage. Neurosurgical Focus, 32(4), E6. doi: 10.3171/2012.1.FOCUS11356
Jeyaraj D. Pandain, Peter D. Panagos, Ivy A. Sebastian, Gisele Sampaio Silva, Karen L. Furie, Liping Liu, Mayowa O. Owolabi, Valeria Caso, Suhail A. Alrukn and World Stroke Organization and American Stroke Association Writing Group. Stroke. 2022;53:1043–1050. DOI: 10.1161/STR.0000000000000394
Gusev E.I., Martynov M.Yu., Boyko A.N., Voznyuk I.A., Lashch N.Yu., Siverttseva S.A., Spirin N.N., Shamalov N.A. Novel coronavirus infection (COVID-19) and nervous system involvement: mechanisms of neurological disorders, clinical manifestations, organization of neurological care. S.S. Korsakov Journal of Neurology and Psychiatry. 2020;120(6):7-16. (In Russ.)
Gusev, E.I., Martynov, M.Y., Boyko, A.N. et al. The Novel Coronavirus Infection (COVID-19) and Nervous System Involvement: Mechanisms of Neurological Disorders, Clinical Manifestations, and the Organization of Neurological Care. Neurosci Behav Physi 51, 147–154 (2021). https://doi.org/10.1007/s11055-021-01050-0
Ivanova G.E., Bogolepova A.N., Levin O.S., Shamalov N.A., Khasanova D.R., Yanishevskiy S.N., Zakharov V.V., Khatkova S.E., Stakhovskaya L.V. Main directions of treatment and rehabilitation of neurological manifestations of COVID-19. Expert panel resolution. S.S. Korsakov Journal of Neurology and Psychiatry. 2021;121(6):145–151. (In Russ.) https://doi.org/10.17116/jnevro2021121061145
Shamalov N.A., Klimov L.V., Soldatov M.A., Kiseleva T.V., Shamalova V.N., Marskaya N.A., Lyang O.V. Acute cerebrovascular accidents in patients with COVID-19 novel coronavirus infection. Neurology, Neuropsychiatry, Psychosomatics. 2024;16(1):82–86. (In Russ.) DOI: 10.14412/2074-2711-2024-1-82-86
Hubert, Gordian J.a; Corea, Francescob; Schlachetzki, Felixc. The role of telemedicine in acute stroke treatment in times of pandemic. Current Opinion in Neurology 34(1):p 22-26, February 2021. | DOI: 10.1097/WCO.0000000000000887
Alexander Merkin, Sofya Akinfieva, Oleg N. Medvedev, Rita Krishnamurthi, Alexey Gutsaluk, Ulf-Dietrich Reips, Rufat Kuliev, Evgeny Dinov, Igor Nikiforov, Nikolay Shamalov, Polina Shafran, Lyudmila Popova, Dmitry Burenchev, Valery Feigin; A Pilot Study of Application of the Stroke Riskometer Mobile App for Assessment of the Course and Clinical Outcomes of COVID-19 among Hospitalized Patients. Cerebrovasc Dis Extra 22 December 2023; 13 (1): 47–55. https://doi.org/10.1159/000529277
Ivanova G.E., Bogolepova A.N., Levin O.S., Shamalov N.A., Khasanova D.R., Yanishevskiy S.N., Zakharov V.V., Khatkova S.E., Stakhovskaya L.V. Main directions of treatment and rehabilitation of neurological manifestations of COVID-19. Expert panel resolution. S.S. Korsakov Journal of Neurology and Psychiatry. 2021;121(6):145–151. (In Russ.)
https://www.consultant.ru/document/cons_doc_LAW_358669/8dda8df191569ec5e1a83da4ada25e7d0f29aa19/
Shamalov N.A., Klimov L.V., Soldatov M.A., Kiseleva T.V., Shamalova V.N., Marskaya N.A., Lyang O.V. Acute cerebrovascular accidents in patients with COVID-19 novel coronavirus infection. Neurology, Neuropsychiatry, Psychosomatics. 2024;16(1):82–86. (In Russ.) DOI: 10.14412/2074-2711-2024-1-82-86.
Suponeva N.A., Arestova A.S., Melnik E.A., et al. Validation of the Medical Research Council sum score (MRC sum score) for use in Russian-speaking patients with chronic inflammatory demyelinating polyneuropathy. Neuromuscular Diseases. 2023;13(1):68–74. (In Russ.) DOI: 10.17650/2222-8721-2023-13-1-68-74
Suponeva N.A., Yusupova D.G., Ilyina K.A., Melchenko D.A., Butkovskaya A.A., Zhirova E.S., Taratukhina A.S., Zimin A.A., Zaitsev A.B., Klochkov A.S., Lyukmanov R.Kh., Kotov-Smolenskiy A.M., Khizhnikova A.E., Gatina G.A., Kutlubaev M.A., Piradov M.A. Validation of the Modified Ashworth Scale in Russia. Annals of Clinical and Experimental Neurology. 2020;14(1):89–96. (In Russ.) DOI: 10.25692/ACEN.2020.1.10
Suponeva N.A., Yusupova D.G., Zhirova E.S., Melchenko D.A., Taratukhina A.S., Butkovskaya A.A., Ilyina K.A., Zaitsev A.B., Zimin A.A., Klochkov A.S., Lyukmanov R.Kh., Kalinkina M.E., Piradov M.A., Kotov-Smolenskiy A.M., Khizhnikova A.E. Validation of the Modified Rankin Scale (mRS) in Russia. Neurology, Neuropsychiatry, Psychosomatics. 2018;10(4):36-39. (In Russ.)
Piradov M.A., Suponeva N.A., Ryabinkina Yu.V., Sergeev D.V., Legostaeva L.A., Yazeva E.G., Yusupova D.G., Luneva I.E., Domashenko M.A., Samorukov V.Yu., Zaitsev A.B., Zimin A.A., Polekhina N.V., Bundhun P., Ramchandani N.M., Ilyina K.A. Full Outline of UnResponsiveness (FOUR) scale: linguo-cultural adaptation of the Russian-language version. Annals of Clinical and Experimental Neurology. 2019;13(3):5–12. (In Russ.) DOI: 10.25692/ACEN.2019.3.7
Trinka E, Hofler J, Zerbs A. Causes of status epilepticus. Epilepsia. 2012;53 Suppl4:127‐138. doi:10.1111/j.1528-1167.2012.03622.x Trinka E et al, 2012.
Guekht A, Bornstein NM. Seizures after stroke. Handb Clin Neurol. 2012;108:569‐583. doi:10.1016/B978-0-444-52899-5.00016-2.
Khomutov VE, Sumskiĭ LI, Lebedeva AV, Kaĭmovskiĭ IL, Magomedov RA, GuekhtAB. ZhNevrolPsikhiatrIm S SKorsakova. 2013;113(4 Pt 2):36-40.
Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol. 2000;57(11):1617-1622. doi:10.1001/archneur.57.11.1617.
Freiman S, Hauser WA, Rider F, Yaroslavskaya S, Sazina O, Vladimirova E, Kaimovsky I, Shpak A, Gulyaeva N, Guekht A. Post-stroke seizures, epilepsy, and mortality in a prospective hospital-based study. Front Neurol. 2023 Dec 1;14:1273270. doi: 10.3389/fneur.2023.1273270. PMID: 38107633; PMCID: PMC10722584.
Sinkin MV, Kaimovsky IL, Komoltsev IG, Trifonov IS, Shtekleyn AA, TsygankovaME, Guekht AB Electroencephalography in acute stroke. ZhNevrolPsikhiatrIm S S Korsakova.2020;120 8. Vyp. 2:10-16. doi: 10.17116/jnevro202012008210.
Flink R, Pedersen B, Guekht AB, et al. Guidelines for the use of EEG methodologyin the diagnosis of epilepsy. International League Against Epilepsy: commission report.Commission on European Affairs: Subcommission on European Guidelines. Acta Neurol Scand.2002;106(1):1‐7. doi:10.1034/j.1600-0404.2002.01361.
Xu MY. Stroke and Vascular Neurology 2019;4:e000175. doi:10.1136/svn-2018-000175
Herman ST, Abend NS, Bleck TP, et al. Consensus statement on continuous EEG incritically ill adults and children, part I: indications. J Clin Neurophysiol. 2015;32(2):87‐95.doi:10.1097/WNP.0000000000000166.
Koubeissi MZ, ed. Seizures in cerebrovascular disorders. New York: SpringerScience+Business Media, 2015.
Lapalme-Remis S, Cascino GD. Imaging for Adults With Seizures and Epilepsy.Continuum (Minneap Minn). 2016;22 (5, Neuroimaging):1451-1479.doi:10.1212/CON.0000000000000370.
Bernasconi A, Cendes F, Theodore WH, et al. Recommendations for the use ofstructural magnetic resonance imaging in the care of patients with epilepsy: A consensus reportfrom the International League Against Epilepsy Neuroimaging Task Force. Epilepsia.2019;60(6):1054-1068. doi:10.1111/epi.15612.
Zhao Y, Li X, Zhang K, Tong T, Cui R. The Progress of Epilepsy after Stroke. CurrNeuropharmacol. 2018;16(1):71-78. doi:10.2174/1570159X15666170613083253.
Khan SA, Naz A, Qamar Masood M, Shah R. Meta-Analysis of Inclisiran for the Treatment of Hypercholesterolemia. Am J Cardiol. 2020 Nov 1;134:69-73. doi: 10.1016/j.amjcard.2020.08.018. Epub 2020 Aug 15. PMID: 32892993.
Ziganshina LE, Abakumova T, Nurkhametova D, Ivanchenko K. Cerebrolysin for acute ischaemic stroke. Cochrane Database Syst Rev. 2023 Oct 11;10(10):CD007026. doi: 10.1002/14651858.CD007026.pub7. PMID: 37818733; PMCID: PMC10565895.
Guzeva V.I. Manual of Pediatric Neurology. Guzeva V.I. et al. Meditsinskoe Informatsionnoe Agentstvo; 2023. p. 379-430. (In Russ.)
Sellers D, Bryant E, Hunter A, Campbell V, Morris C. The Eating and Drinking Ability Classification System for cerebral palsy: A study of reliability and stability over time. J Pediatr Rehabil Med. 2019;12(2):123-131. doi: 10.3233/PRM-180581. PMID: 31227668.
Group PSW. Stroke in Childhood: Clinical Guidelines for the diagnosis, managment and rehabilitation. In: Unit CEE, editor. UK: Royal College of Physicians; 2004.
Andrade A, Bigi S, Laughlin S, Parthasarathy S, Sinclair A, Dirks P, Pontigon AM, Moharir M, Askalan R, MacGregor D, deVeber G. Association Between Prolonged Seizures and Malignant Middle Cerebral Artery Infarction in Children With Acute Ischemic Stroke. Pediatr Neurol. 2016 Nov;64:44-51. doi: 10.1016/j.pediatrneurol.2016.08.015. Epub 2016 Aug 27. PMID: 27663488
Andrade A, Bigi S, Laughlin S, Parthasarathy S, Sinclair A, Dirks P, Pontigon AM, Moharir M, Askalan R, MacGregor D, deVeber G. Association Between Prolonged Seizures and Malignant Middle Cerebral Artery Infarction in Children With Acute Ischemic Stroke. Pediatr Neurol. 2016 Nov;64:44-51. doi: 10.1016/j.pediatrneurol.2016.08.015. Epub 2016 Aug 27. PMID: 27663488.
Kuznetsova A.A., Shchederkina I.O., Sinkin M.V., Gorev V.V. Epileptic seizures and epilepsy in children with a history of acute cerebrovascular accident. L.O. Badalyan Neurological Journal. 2023;4(1):29-42. (In Russ.) https://doi.org/10.46563/2686-8997-2023-4-1-29-42 https://elibrary.ru/xaxojw
Besha A, Adamu Y, Mulugeta H, Zemedkun A, Destaw B. Evidence-based guideline on management of status epilepticus in adult intensive care unit in resource-limited settings: a review article. Ann Med Surg (Lond) 2023;85:2714–20. https://doi.org/10.1097/MS9.0000000000000625.
Brigo F, Bragazzi NL, Bacigaluppi S, Nardone R, Trinka E. Is intravenous lorazepam really more effective and safe than intravenous diazepam as first-line treatment for convulsive status epilepticus? A systematic review with meta-analysis of randomized controlled trials. Epilepsy Behav 2016;64:29–36. https://doi.org/10.1016/J.YEBEH.2016.09.020.
Moura LMVR, Donahue MA, Yan Z, Smith LH, Hsu J, Newhouse JP, et al. Comparative Effectiveness and Safety of Seizure Prophylaxis Among Adults After Acute Ischemic Stroke. Stroke 2023a;54:527–36. https://doi.org/10.1161/STROKEAHA.122.039946.
Consoli D, Bosco D, Postorino P, Galati F, Plastino M, Perticoni GF, et al. Levetiracetam versus carbamazepine in patients with late poststroke seizures: a multicenter prospective randomized open-label study (EpIC Project). Cerebrovasc Dis 2012;34:282–9. https://doi.org/10.1159/000342669.
Brigo F, Lattanzi S, Zelano J, Bragazzi NL, Belcastro V, Nardone R, et al. Randomized controlled trials of antiepileptic drugs for the treatment of post-stroke seizures: A systematic review with network meta-analysis. Seizure 2018;61:57–62. https://doi.org/10.1016/J.SEIZURE.2018.08.001.
Gilad R, Sadeh M, Rapoport A, Dabby R, Boaz M, Lampl Y. Monotherapy of lamotrigine versus carbamazepine in patients with poststroke seizure. Clin Neuropharmacol 2007;30:189–95. https://doi.org/10.1097/WNF.0B013E3180333069.
Zhang YJ, Lu XM, Li PW, Guo CA, Wan DJ. Oxcarbazepine versus Carbamazepine for the Treatment of Post-Stroke Epilepsy: A Systematic Review and Meta-Analysis. Turk Neurosurg 2022;32:176–84. https://doi.org/10.5137/1019-5149.JTN.34664-21.3.
Alvarez-Sabín J, Montaner J, Padró L, Molina CA, Rovira R, Codina A, et al. Gabapentin in late-onset poststroke seizures. Neurology 2002;59:1991–3. https://doi.org/10.1212/01.WNL.0000038388.57824.B6.
Doğan EA, Genç E, Genç BO, Erdoğan Ç. Efficacy, tolerability, and retention rates of zonisamide in older adult patients with focal-onset epilepsy: Experiences from two tertiary epilepsy centers. Epilepsy Behav 2017;76:19–23. https://doi.org/10.1016/J.YEBEH.2017.08.040.
Ghatan S, McGoldrick P, Palmese C, La Vega-Talbott M, Kang H, Kokoszka MA, Goodman RR, Wolf SM. Surgical management of medically refractory epilepsy due to early childhood stroke. J Neurosurg Pediatr. 2014 Jul;14(1):58-67. doi: 10.3171/2014.3.PEDS13440. Epub 2014 May 9. PMID: 24866497.
Marchi A, Pennaroli D, Lagarde S, McGonigal A, Bonini F, Carron R, Lépine A, Villeneuve N, Trebuchon A, Pizzo F, Scavarda D, Bartolomei F. Epileptogenicity and surgical outcome in post stroke drug resistant epilepsy in children and adults. Epilepsy Res. 2019 Sep;155:106155. doi: 10.1016/j.eplepsyres.2019.106155. Epub 2019 Jun 21. PMID: 31252221.
Moura LMVR, Yan Z, Donahue MA, Smith LH, Schwamm LH, Hsu J, et al. No short-term mortality from benzodiazepine use post-acute ischemic stroke after accounting for bias. J Clin Epidemiol 2023b;154:136–45. https://doi.org/10.1016/J.JCLINEPI.2022.12.013.
Oddo M, Crippa IA, Mehta S, Menon D, Payen JF, Taccone FS, et al. Optimizing sedation in patients with acute brain injury. Crit Care 2016;20. https://doi.org/10.1186/S13054-016-1294-5.
Xu H, Guan M, Chen YF, Qin H, Huang S. Efficacy and safety of pregabalin vs carbamazepine in patients with central post-stroke pain. Neurol Res 2024;46:291–6. https://doi.org/10.1080/01616412.2024.2302269.
Bayes J, Peng W, Adams J, Sibbritt D. The effect of the Mediterranean diet on health outcomes in post-stroke adults: a systematic literature review of intervention trials. Eur J Clin Nutr. 2023 May;77(5):551-560. doi: 10.1038/s41430-022-01212-4. Epub 2022 Sep 20. PMID: 36127392.
Feng Q, Fan S, Wu Y, Zhou D, Zhao R, Liu M, Song Y. Adherence to the dietary approaches to stop hypertension diet and risk of stroke: A meta-analysis of prospective studies. Medicine (Baltimore). 2018 Sep;97(38):e12450. doi: 10.1097/MD.0000000000012450. PMID: 30235731; PMCID: PMC6160167.
Messas E, Goudot G, Halliday A, Sitruk J, Mirault T, Khider L, Saldmann F, Mazzolai L, Aboyans V. Management of carotid stenosis for primary and secondary prevention of stroke: state-of-the-art 2020: a critical review. Eur Heart J Suppl. 2020 Dec 6;22(Suppl M):M35-M42. doi: 10.1093/eurheartj/suaa162.;
Kapila V, Jetty P, Basile VS, Dubois L. Management of transient ischemic attack or nondisabling stroke related to extracranial internal carotid artery stenosis. CMAJ. 2019 Apr 15;191(15):E418-E422. doi: 10.1503/cmaj.180735.
Tsivgoulis G, Safouris A, Kim DE, Alexandrov AV. Recent Advances in Primary and Secondary Prevention of Atherosclerotic Stroke. J Stroke. 2018 May;20(2):145-166. doi: 10.5853/jos.2018.00773. Epub 2018 May 31. Erratum in: J Stroke. 2018 Sep;20(3):417. doi: 10.5853/jos.2018.00773.e1.
Tanne JH. Study shows what INR level is best for preventing stroke in patients with atrial fibrillation. BMJ. 2003 Sep 20;327(7416):638. PMCID: PMC196415.
Gurol ME, Sposato LA. Advances in Neurocardiology: Focus on Anticoagulation for Valvular Heart Disease With and Without Atrial Fibrillation. Stroke. 2022 Dec;53(12):3763-3768. doi: 10.1161/STROKEAHA.122.039310.
Turpie AG, Gent M, Laupacis A, Latour Y, Gunstensen J, Basile F, Klimek M, Hirsh J. A comparison of aspirin with placebo in patients treated with warfarin after heart-valve replacement. N Engl J Med. 1993 Aug 19;329(8):524-9. doi: 10.1056/NEJM199308193290802,
Whitlock RP, Sun JC, Fremes SE, Rubens FD, Teoh KH. Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e576S-e600S. doi: 10.1378/chest.11-2305,
Meschengieser SS, Fondevila CG, Frontroth J, Santarelli MT, Lazzari MA. Low-intensity oral anticoagulation plus low-dose aspirin versus high-intensity oral anticoagulation alone: a randomized trial in patients with mechanical prosthetic heart valves. J Thorac Cardiovasc Surg. 1997 May;113(5):910-6. doi: 10.1016/S0022-5223(97)70264-2.
Diener HC, Chutinet A, Easton JD, Granger CB, Kleine E, Marquardt L, Meyerhoff J, Zini A, Sacco RL. Dabigatran or Aspirin After Embolic Stroke of Undetermined Source in Patients With Patent Foramen Ovale: Results From RE-SPECT ESUS. Stroke. 2021 Mar;52(3):1065-1068. doi: 10.1161/STROKEAHA.120.031237,
Kasner SE, Swaminathan B, Lavados P, Sharma M, Muir K, Veltkamp R, Ameriso SF, Endres M, Lutsep H, Messé SR, Spence JD, Nedeltechev K, Perera K, Santo G, Olavarria V, Lindgren A, Bangdiwala S, Shoamanesh A, Berkowitz SD, Mundl H, Connolly SJ, Hart RG; NAVIGATE ESUS Investigators. Rivaroxaban or aspirin for patent foramen ovale and embolic stroke of undetermined source: a prespecified subgroup analysis from the NAVIGATE ESUS trial. Lancet Neurol. 2018 Dec;17(12):1053-1060. doi: 10.1016/S1474-4422(18)30319-3. Epub 2018 Sep 28. Erratum in: Lancet Neurol. 2018 Dec;17(12):e1. doi: 10.1016/S1474-4422(18)30395-8.
Mazlumzadeh M, Hunder GG, Easley KA, Calamia KT, Matteson EL, Griffing WL, Younge BR, Weyand CM, Goronzy JJ. Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial. Arthritis Rheum. 2006 Oct;54(10):3310-8. doi: 10.1002/art.22163. PMID: 17009270.
de Boysson H, Liozon E, Larivière D, Samson M, Parienti JJ, Boutemy J, Maigné G, Martin Silva N, Ly K, Touzé E, Bonnotte B, Aouba A, Sacré K, Bienvenu B. Giant Cell Arteritis-related Stroke: A Retrospective Multicenter Case-control Study. J Rheumatol. 2017 Mar;44(3):297-303. doi: 10.3899/jrheum.161033.
Beyer SE, Dicks AB, Shainker SA, Feinberg L, Schermerhorn ML, Secemsky EA, Carroll BJ. Pregnancy-associated arterial dissections: a nationwide cohort study. Eur Heart J. 2020 Nov 21;41(44):4234-4242. doi: 10.1093/eurheartj/ehaa497. Erratum in: Eur Heart J. 2021 Jul 31;42(29):2863. doi: 10.1093/eurheartj/ehab406,
Baffour FI, Kirchoff-Torres KF, Einstein FH, Karakash S, Miller TS. Bilateral internal carotid artery dissection in the postpartum period. Obstet Gynecol. 2012 Feb;119(2 Pt 2):489-492. doi: 10.1097/AOG.0b013e318242d8d4,
Waidelich JM, Bullough AS, Mhyre JM. Internal carotid artery dissection: an unusual cause of postpartum headache. Int J Obstet Anesth. 2008 Jan;17(1):61-5. doi: 10.1016/j.ijoa.2007.04.003,
Abisaab J, Nevadunsky N, Flomenbaum N. Emergency department presentation of bilateral carotid artery dissections in a postpartum patient. Ann Emerg Med. 2004 Nov;44(5):484-9. doi: 10.1016/j.annemergmed.2004.03.031. Erratum in: Ann Emerg Med. 2005 Jan;45(1):84
Order of the Ministry of Health of the Russian Federation No. 168n dated March 15, 2022, "On approval of the procedure for dispensary observation of adults." (In Russ.)
Sadeghi-Hokmabadi E, Taheraghdam A, Hashemilar M, Rikhtegar R, Mehrvar K, Mehrara M, Mirnour R, Hassasi R, Aliyar H, Farzi M, Hasaneh Tamar S. Simple In-Hospital Interventions to Reduce Door-to-CT Time in Acute Stroke. Int J Vasc Med. 2016;2016:1656212. doi: 10.1155/2016/1656212. Epub 2016 Jul 10. PMID: 27478641; PMCID: PMC4958441.
Naylor R, Rantner B, Ancetti S et al. European Society for Vascular Surgery (ESVS) 2023 Clinical Practice Guidelines on the Management of Atherosclerotic Carotid and Vertebral Artery Disease. Eur J Vasc Endovasc Surg. 2023 Jan;65(1):7-111. doi: 10.1016/j.ejvs.2022.04.011. Epub 2022 May 20. PMID: 35598721.
Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995 May 10;273(18):1421-8. PMID: 7723155.
Halliday A, Harrison M, Hayter E et al.; Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. 10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis (ACST-1): a multicentre randomised trial. Lancet. 2010 Sep 25;376(9746):1074-84. doi: 10.1016/S0140-6736(10)61197-X. PMID: 20870099; PMCID: PMC2956884
Appendix A1. Working Group Composition
Akhjigitov Renat Gayyasovich, Candidate of Medical Sciences, Deputy Director of the Solovyov Research and Practical Center for Psychoneurology of the Moscow Healthcare Department.
Bagrat G. Alekyan, MD, DSc, Academician of the Russian Academy of Sciences, Chief Specialist of the Russian Ministry of Health for X-ray Endovascular Diagnostics and Treatment, Professor at the Department of Cardiovascular Surgery, Federal State Autonomous Educational Institution of Higher Education I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Member of the Presidium of the National Stroke Association.
Andrey M. Alasheev, MD, DSc, Chief Freelance Neurologist of the Russian Ministry of Health in the Ural Federal District, Head of the Neurological Department for Patients with Acute Cerebrovascular Accidents, Sverdlovsk Regional Clinical Hospital No. 1, Member of WSO and ESO.
Vera V. Alferova, MD, DSc, Leading Researcher at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the All-Russian Society of Neurologists.
Asiyat S. Alieva, MD, Head of the Research Laboratory of Lipid Metabolism Disorders and Atherosclerosis, Head of the Center for Atherosclerosis and Lipid Metabolism Disorders, Almazov National Medical Research Centre, Cardiologist.
Irina N. Balashova, PhD in Psychology, Associate Professor at the Department of Pedagogy and Psychology, Faculty of Postgraduate Education, Highest Category Speech Therapist, First Pavlov State Medical University of St. Petersburg of the Russian Ministry of Health, Head of the St. Petersburg City Association of Speech Therapists.
Andrey A. Belkin, Doctor of Medical Sciences, Professor at the Departments of Anesthesiology and Intensive Care, Physical Rehabilitation Medicine and Nervous Diseases, Ural State Medical University; Director of the Brain Institute Clinic; Chief freelance specialist of the Russian Ministry of Health for rehabilitation in the Ural Federal District.
Elena S. Berdnikovich – PhD in Pedagogy, Senior Researcher, Head of the Psychological and Speech Therapy Group, Highest Category Speech Therapist, Research Center of Neurology.
Madina D. Bogatyreva, MD, PhD, Head of the Neurological Department for Patients with Acute Cerebrovascular Accidents, Regional Vascular Center, Stavropol Regional Clinical Hospital, Chief Freelance Neurologist of the Ministry of Health of the Russian Federation in the North Caucasian Federal District, Chief Freelance Neurologist of the Ministry of Health of Stavropol Krai.
Rezeda A. Bodrova, MD, DSc, Associate Professor, Head of the Department of Rehabilitology and Sports Medicine, Kazan State Medical Academy – branch of the Russian Medical Academy of Continuous Professional Education of the Russian Ministry of Health, Chief Freelance Specialist in Medical Rehabilitation of the Ministry of Health of the Republic of Tatarstan, Head of the Medical and Rehabilitation Center of City Clinical Hospital No. 7 named after M.N. Sadykov, Kazan, Member of the Presidium of the Union of Rehabilitation Therapists of Russia (SRR), President of the SRR in the Republic of Tatarstan, Honored Doctor of the Russian Federation.
Sergey A. Boytsov, MD, DSc, Professor, Academician of the Russian Academy of Sciences, General Director of the National Medical Research Center for Cardiology of the Ministry of Health of the Russian Federation, Chief Specialist Cardiologist of the Ministry of Health of the Russian Federation, Member of the Presidium of the Russian Society of Neurologists, Vice-President of the Russian Society of Cardiology.
Tatyana V. Vavilova, MD, DSc, Professor, Chief Freelance Specialist in Clinical Laboratory Diagnostics of the Ministry of Health of the Russian Federation, Head of the Department of Laboratory Medicine and Genetics, Almazov National Medical Research Centre.
Igor A. Voznyuk, MD, DSc, Professor, Chief freelance neurologist of the Healthcare Committee of Saint Petersburg, Chief freelance neurologist of the Russian Ministry of Health in the Northwestern Federal District, Professor at the Department of Neurology, Deputy Chief Medical Officer for Neurology at Pavlov First Saint Petersburg State Medical University.
Alla B. Gekht, Doctor of Medical Sciences, Professor, Corresponding Member of the Russian Academy of Sciences, Director of the Z.P. Solovyov Scientific and Practical Psychoneurological Center of the Moscow Healthcare Department; Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation; Member of the Presidium of the National Stroke Association; Scientific Secretary of the All-Russian Society of Neurologists.
Sergey Yu. Golokhvastov, MD, PhD, Senior Lecturer at the Department of Nervous Diseases, Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation.
Ilya L. Gubsky, MD, PhD, Senior Research Fellow at the Federal Center for Brain Research and Neurotechnologies of the Federal Medical-Biological Agency (FMBA of Russia).
Leonid V. Gubsky, MD, DSc, Chief Research Fellow at the Federal Center for Brain Research and Neurotechnologies of the Federal Medical-Biological Agency (FMBA of Russia).
Valentina I. Guzeva, MD, DSc, Professor, Head of the Department of Neurology, Neurosurgery and Medical Genetics, Saint Petersburg State Pediatric Medical University, Chief freelance pediatric neurologist of the Ministry of Health of the Russian Federation.
Viktoria V. Guzeva, MD, DSc, Professor, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Saint Petersburg State Pediatric Medical University of the Ministry of Health of the Russian Federation.
Oksana V. Guzeva, MD, DSc, Professor, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Saint Petersburg State Pediatric Medical University of the Ministry of Health of the Russian Federation.
Vadim V. Gusev, MD, PhD, Associate Professor, Head of the Department of Neurology and Neurosurgery, Ural State Medical University of the Ministry of Health of the Russian Federation.
Evgeny I. Gusev, MD, DSc, Academician of the Russian Academy of Sciences, Head of the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, President of the National Stroke Association, Chairman of the All-Russian Society of Neurologists.
Vladimir G. Dashyan, MD, DSc, Professor at the Department of Neurosurgery and Neuroreanimation, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Member of the Association of Neurosurgeons of Russia.
Natalya A. Devyatova, Medical Psychologist at the Medical Rehabilitation Department No. 1, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia.
Dmitry A. Demin, Neurologist at the Federal Centre of Cardiovascular Surgery of the Ministry of Health of the Russian Federation (Astrakhan).
Natalya V. Zhukovskaya, MD, PhD, Head of the Neurological Department for Acute Cerebrovascular Pathology Patients, Leningrad Regional Clinical Hospital, Chief freelance neurologist of the Healthcare Committee of the Leningrad Region.
Dmitry V. Zhuravlev, MD, PhD, Senior Research Fellow at the Department for the Study of Paroxysmal States and Dissomnias in Borderline Mental Disorders, Z.P. Solovyov Scientific and Practical Psychoneurological Center of the Moscow Healthcare Department.
Galina E. Ivanova, MD, DSc, Professor, Head of the Medical Rehabilitation Research Center, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia, Head of the Department of Medical and Social Stroke Rehabilitation, Research Institute of Cerebrovascular Pathology and Stroke, Head of the Department of Medical Rehabilitation, Faculty of Additional Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of Russia, Chairman of the Dissertation Council at Pirogov Russian National Research Medical University, Chief freelance specialist in medical rehabilitation of the Ministry of Health of Russia, Chairman of the Presidium of the All-Russian Public Organization for the Promotion of Medical Rehabilitology "Union of Rehabilitologists of Russia", Secretary General of the Russian Association for Sports Medicine and Rehabilitation of Patients and Persons with Disabilities.
Olga B. Irtyuga, MD, PhD, Associate Professor at the Department of Cardiology, Institute of Medical Education, Head of the Research Laboratory of Congenital and Acquired Heart Defects, Almazov National Medical Research Centre of the Ministry of Health of the Russian Federation.
Sergey N. Kaurkin, MD, PhD, Head of the Department of Early Medical Rehabilitation, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia, Associate Professor at the Department of Medical Rehabilitation, Faculty of Additional Professional Education, Institute of Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation.
Tatyana V. Kiseleva, Researcher at the Department of Vascular Diseases of the Nervous System, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia.
Leonid V. Klimov, MD, PhD, Senior Research Fellow at the Department of Vascular Diseases of the Nervous System, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia.
Sergey V. Kolomentsev, MD, PhD, Head of the Neurological Department of the Clinic of Nervous Diseases, Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation.
Ivan A. Koltsov, MD, PhD, Senior Research Fellow at the Research Laboratory of Cerebral Vascular Diseases, Pirogov Russian National Research Medical University of the Ministry of Health of Russia, Senior Research Fellow at the Department of Neuroimmunology, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia.
Alexander N. Konovalov, MD, DSc, Professor, Academician of the Russian Academy of Sciences, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Board Member of the National Stroke Association, President of the Association of Neurosurgeons of Russia.
Vladimir V. Krylov, MD, DSc, Professor, Academician of the Russian Academy of Sciences, Chief freelance neurosurgeon of the Ministry of Health of the Russian Federation, Head of the Department of Fundamental Neurosurgery, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Chief Research Fellow at the Sklifosovsky Research Institute of Emergency Medicine of the Moscow Healthcare Department.
Alexandra A. Kuznetsova, Head of the Center for the Treatment of Cerebrovascular Pathology in Children and Adolescents, Morozovskaya Children's City Clinical Hospital of the Moscow Healthcare Department, Junior Research Fellow at the Z.P. Solovyov Scientific and Practical Psychoneurological Center of the Moscow Healthcare Department.
Tatyana A. Kuzminova, PhD in Pedagogy, Senior Physical Rehabilitation Specialist at the Medical Rehabilitation Research Center, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia, Associate Professor at the Department of Medical Rehabilitation, Faculty of Additional Professional Education, Institute of Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Associate Professor at the Department of Adaptive Physical Culture and Sports Medicine, Moscow State Academy of Physical Culture.
Alexey A. Kulesh, MD, DSc, Professor at the Department of Neurology and Medical Genetics, Academician E.A. Wagner Perm State Medical University, Head of the Neurological Department for Acute Cerebrovascular Pathology Patients, Regional Vascular Center, City Clinical Hospital No. 4, Perm.
Stanislav S. Kucherenko, MD, DSc, Professor at the Department of Neurology and Psychiatry with Clinic, Almazov National Medical Research Centre of the Ministry of Health of the Russian Federation, Head of the Neurological Department, L.G. Sokolov North-Western Scientific and Clinical Center of the FMBA of Russia, Chief freelance neurologist of the Northwestern Federal District of the FMBA of Russia.
Olga D. Larina – Senior Research Fellow at the Laboratory of Neuropsychology, Speech Therapy and Neurolinguistics, Medical Rehabilitation Research Center, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia, Speech Therapist at the Consultative and Diagnostic Department with Day Hospital, Federal Center for Brain Research and Neurotechnologies of the FMBA of Russia, Associate Professor at the Department of Speech Therapy, Moscow State Pedagogical University, Member of the Expert Council for Certification and Accreditation of the Ministry of Health of the Russian Federation, Deputy Chairman of the Accreditation Subcommission for the Accreditation of Medical Speech Therapists, Pirogov Russian National Research Medical University of the Ministry of Health of Russia, Member of the Committees on Education, Medical Speech Therapy and Neuropsychology of the All-Russian Public Organization for the Promotion of Medical Rehabilitology "Union of Rehabilitologists of Russia".
Anna V. Lebedeva, MD, DSc, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the All-Russian Society of Neurologists, Member of the Russian Anti-Epilepsy League.
Andrey L. Lukyanov, MD, PhD, Head of the Resuscitation and Intensive Care Unit for Acute Cerebrovascular Pathology Patients, City Clinical Hospital No. 31 of the Moscow Healthcare Department.
Viktor A. Lukyanchikov, MD, DSc, Leading Research Fellow at the Research Center of Neurology, Professor at the Department of Fundamental Neurosurgery, Faculty of Additional Professional Education, Institute of Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation.
Vasily A. Lukshin, MD, DSc, Leading Researcher, Head of the Department of Reconstructive Surgery of Main Arteries of the Head, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko of the Russian Ministry of Health, Professor at the Department of Neurosurgery with Neuroscience Courses, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko of the Russian Ministry of Health.
Olga A. Lvova, MD, DSc, Associate Professor, Senior Researcher, Ural State Medical University of the Russian Ministry of Health.
Olga V. Lyang, MD, DSc, Associate Professor, Professor at the Department of Hospital Therapy with a Course of Clinical Laboratory Diagnostics, Peoples' Friendship University of Russia named after Patrice Lumumba, Head of the Department of Clinical Laboratory Diagnostics, Senior Researcher at the Department of Vascular Diseases of the Nervous System, Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia.
Marina Yu. Maksimova, MD, DSc, Professor, Head of the 2nd Neurology Department, Research Center of Neurology, Professor at the Department of Neurology, Faculty of General Medicine, Research and Educational Institute of Clinical Medicine named after N.A. Semashko, Russian University of Medicine of the Russian Ministry of Health.
Azamat R. Maremkulov, MD, PhD, Associate Professor at the Department of Medical Rehabilitation, Faculty of Advanced Training and Professional Retraining of Specialists, Kuban State Medical University of the Russian Ministry of Health; Head of the Inpatient Department of Medical Rehabilitation for Patients with Central Nervous System Disorders; Head of the Rehabilitation and Recovery Center, Regional Clinical Hospital No. 2 of the Ministry of Health of Krasnodar Krai.
Nataliia A. Marskaya, Researcher at the Department of Vascular Diseases of the Nervous System Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia.
Mikhail Yu. Martynov, MD, DSc, Professor, Corresponding Member of the Russian Academy of Sciences, First Deputy General Director of the Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia; Professor at the Department of Neurology, Neurosurgery, and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation; Scientific Secretary of the All-Russian Society of Neurologists; Board Member of the National Stroke Association.
Elena V. Melnikova, MD, DSc, Chief Freelance Specialist of the Ministry of Health of the Russian Federation for Medical Rehabilitation in the Northwestern Federal District, Professor at the Department of Neurology and Neurosurgery, Pavlov First Saint Petersburg State Medical University of the Ministry of Health of the Russian Federation.
Yuri V. Mikadze - PhD in Psychology, Professor at the Department of Neuro- and Pathopsychology, Faculty of Psychology, Lomonosov Moscow State University; Head of the Laboratory of Neuropsychology, Speech Therapy, and Neurolinguistics, Research Center of Neurology and Neurotechnologies of the FMBA of Russia.
Violetta R. Mkrtchyan, MD, DSc, Associate Professor, Head of the Department of Borderline Mental Disorders in Individuals with Central Nervous System Diseases and Older Age, Solovyov Research and Practical Psychoneurological Center of the Moscow Healthcare Department.
Andrey S. Nikitin, MD, PhD, Associate Professor at the Department of Neurosurgery and Neuroreanimation, A.I. Evdokimov Moscow State University of Medicine and Dentistry of the Ministry of Health of the Russian Federation, Member of the Association of Neurosurgeons of Russia.
Miroslav M. Odinak, MD, DSc, Corresponding Member of the Russian Academy of Sciences, Professor at the Department, S.M. Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation.
Olga S. Orlova – Doctor of Pedagogical Sciences, Professor, Academician of the Ya.A. Kamensky International Slavic Academy of Education, Professor at the Department of Speech Therapy, Moscow State Pedagogical University; Chief Researcher, National Medical Research Center for Otorhinolaryngology of the FMBA of Russia (Department of Phoniatrics); Chief Researcher, Laboratory of Neuropsychology, Speech Therapy, and Neurolinguistics, Research Center for Medical Rehabilitation, Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia; Member of the Expert Council for Certification and Accreditation of the Russian Ministry of Health; Chair of the Accreditation Subcommissions for Medical Speech Therapists, Pirogov Russian National Research Medical University of the Russian Ministry of Health; Vice-President of the Association of Phoniatrists and Phonopedists of Russia; Member of the Presidium, Head of the Committee on Medical Speech Therapy and Neuropsychology of the All-Russian Public Organization for the Promotion of Medical Rehabilitology "Union of Rehabilitologists of Russia".
Inna V. Okhrim, MD, PhD, Associate Professor, Associate Professor at the Department of Neurology, Neurosurgery, and Medical Genetics, Saint Petersburg State Pediatric Medical University of the Ministry of Health of the Russian Federation.
Nikolay A. Pavlov, Candidate of Medical Sciences, Leading Researcher at the Department of Neurology, Neurosurgery and Medical Genetics, N.I. Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the All-Russian Society of Neurologists.
Vladimir A. Parfenov, MD, DSc, Professor, Head of the Department of Nervous Diseases, Director of the Clinic of Nervous Diseases, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation; Board Member of the National Stroke Association; Member of the Presidium of the Moscow and All-Russian Societies of Neurologists.
Sergey S. Petrikov, MD, DSc, Professor, Corresponding Member of the Russian Academy of Sciences, Director of the Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department; Professor at the Department of Neurosurgery and Neuroreanimation, A.I. Evdokimov Moscow State University of Medicine and Dentistry of the Ministry of Health of the Russian Federation; President of the Interregional Public Organization "Association of Neuroanesthesiologists and Neurointensivists".
Mikhail A. Piradov, MD, DSc, Academician of the Russian Academy of Sciences, Professor, Director of the Research Center of Neurology, Vice-President of the Russian Academy of Sciences, Member of the Presidium of the All-Russian Society of Neurologists, Member of the Presidium of the National Stroke Association.
Natalia A. Polunina - MD, PhD, Associate Professor at the Department of Fundamental Neurosurgery, Faculty of Postgraduate Education, Institute of Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation; Researcher at the Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department.
Aleksey Yu. Polushin, MD, PhD, Neurologist, Head of the Department of Chemotherapy and Bone Marrow Transplantation for Oncological and Autoimmune Diseases, Head of the Research Laboratory of Neuro-oncology and Autoimmune Diseases at the R.M. Gorbacheva Research Institute of Pediatric Oncology, Hematology and Transplantology; Associate Professor at the Department of Neurology, Pavlov First Saint Petersburg State Medical University of the Ministry of Health of Russia, Saint Petersburg.
Boris B. Polyaev, MD, PhD, Head of the Department of Medical Rehabilitation for Patients with Central Nervous System Disorders, Federal Center of Brain Research and Neurotechnologies of the FMBA of Russia,
Associate Professor at the Department of Medical Rehabilitation, Faculty of Postgraduate Education, Pirogov Russian National Research Medical University.
Natalia I. Pryanikova – Head of the Medical Speech Therapy Department, Research Institute of Rehabilitology, Federal Research and Clinical Center of Intensive Care and Rehabilitology; Highest-Category Speech Therapist at the Early Rehabilitation Department.
Flora K. Rieder, MD, PhD, Head of the Department of Epidemiology, Prevention, and Care Organization for Borderline Mental Disorders, Solovyov Research and Practical Psychoneurological Center of the Moscow Healthcare Department.
Alexander V. Savello, MD, DSc, Professor, Deputy Head of the Department of Neurosurgery, S.M. Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation; Chief Specialist in X-ray Endovascular Diagnostics and Treatment of the Ministry of Defense of the Russian Federation; Board Member of the Academician F.A. Serbinenko Association of Endovascular Neurosurgeons.
Yaroslav B. Skiba, MD, PhD, Researcher at the Research Laboratory of Neuro-oncology and Autoimmune Diseases, Head of the Laboratory of Clinical Pharmacology and Pain Therapy, A.V. Valdman Institute of Pharmacology, Pavlov First Saint Petersburg State Medical University of the Ministry of Health of the Russian Federation.
Alexander A. Skoromets, MD, DSc, Academician of the Russian Academy of Sciences, Head of the Department of Neurology, Pavlov First Saint Petersburg State Medical University of the Ministry of Health of the Russian Federation; Member of the Presidium of the National Stroke Association; Member of the Presidium of the All-Russian Society of Neurologists.
Dmitry V. Skrypnik, MD, DSc, Head of the Department of Cardiology, A.I. Evdokimov Moscow State University of Medicine and Dentistry of the Russian Ministry of Health; Chief Specialist for X-ray Endovascular Diagnostics and Treatment of the Moscow Healthcare Department; Head of the Department of X-ray Endovascular Diagnostics and Treatment, I.V. Davydovsky City Clinical Hospital of the Moscow Healthcare Department.
Mikhail A. Soldatov, Senior Research Fellow, Department of Vascular Diseases of the Nervous System, Federal Center of Brain Research and Neurotechnologies, Federal Medical-Biological Agency of Russia.
Viktor A. Sorokoumov, MD, PhD, Professor, Department of Neurology, Pavlov First Saint Petersburg State Medical University of the Ministry of Health of the Russian Federation.
Alexander E. Talypov – MD, PhD, Leading Research Fellow, Sklifosovsky Research Institute for Emergency Medicine of the Moscow Healthcare Department; Professor, Department of Fundamental Neurosurgery, Faculty of Additional Professional Education, Institute of Continuous Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation.
Marine M. Tanashyan - Corresponding Member of the Russian Academy of Sciences, Professor, MD, PhD, Honored Scientist of the Russian Federation, Deputy Director for Science, Head of the 1st Neurological Department, Research Center of Neurology; Head of the Neurology Course, Department of Multifunctional Clinical Training, Faculty of Fundamental Medicine, Lomonosov Moscow State University; Professor, Department of Neurology, Russian University of Medicine of the Ministry of Health of the Russian Federation.
Lyudmila V. Timchenko, Head of the Neurological Department for Patients with Acute Cerebrovascular Accidents, Research Institute - Ochapovsky Regional Clinical Hospital No. 1 of the Ministry of Health of Krasnodar Krai, Chief Freelance Specialist Neurologist of the Ministry of Health of the Russian Federation in the Southern Federal District.
Olga V. Tikhomirova, MD, PhD, Head of the Department of Clinical Neurology and Sleep Medicine, Chief Research Fellow, Nikiforov All-Russian Center of Emergency and Radiation Medicine of the Emergencies Ministry of Russia, Chief Freelance Neurologist of the Emergencies Ministry of Russia.
Dmitry Yu. Usachev, MD, PhD, Professor, Academician of the Russian Academy of Sciences, Professor, Director of the Burdenko National Medical Research Center of Neurosurgery of the Ministry of Health of the Russian Federation, President of the Association of Neurosurgeons of Russia, Head of the Department of Neurosurgery, Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation.
Anatoly I. Fedin, MD, PhD, Professor of the Department of Neurology, Faculty of Additional Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the All-Russian Society of Neurologists, Member of the Board of the National Stroke Association.
Mikhail S. Fiedler, Expert Analyst, Department of Analytical Work, Directorate for Implementation of Functions of the National Medical Research Center for Neurology; Assistant, Department of Neurology, Neurosurgery and Medical Genetics, Faculty of General Medicine, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation.
Tatiana V. Kharitonova, Candidate of Medical Sciences, Senior Research Fellow, Saint Petersburg I.I. Dzhanelidze Research Institute of Emergency Medicine.
Dmitry S. Khan — Head of the Neurological Department for Patients with Acute Cerebrovascular Accidents, Primorsky Krai Clinical Hospital No. 1, Vladivostok; Chief Freelance Specialist for Acute Cerebrovascular Accidents of the Ministry of Health of Primorsky Krai, Chief Freelance Neurologist of the Ministry of Health of Russia in the Far Eastern Federal District.
Natalia V. Khalo, Candidate of Medical Sciences, Head of the Primary Vascular Department for Patients with Acute Cerebrovascular Accidents, Krasnoyarsk Interdistrict Clinical Hospital No. 20 named after I.S. Berzon; Chief Freelance Specialist for the Treatment of Cerebrovascular Pathology of the Ministry of Health of Krasnoyarsk Krai, Chief Freelance Specialist Neurologist of the Ministry of Health of Russia in the Siberian Federal District.
Dina R. Khasanova, MD, PhD, Professor, Professor of the Department of Neurology, Kazan State Medical University of the Ministry of Health of the Russian Federation; Chief Freelance Neurologist of the Ministry of Health of the Russian Federation in the Volga Federal District, Member of the Board of the National Stroke Association, Member of the Board of the All-Russian Society of Neurologists.
Maria G. Khlyustova - Leading Speech Therapist, Laboratory of Neuropsychology, Speech Therapy and Neurolinguistics, Research Center of Medical Rehabilitation; Speech Therapist, Medical Rehabilitation Department, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia.
Nikolay V. Tsygan, MD, PhD, Associate Professor, Deputy Head of the Department and Clinic of Nervous Diseases, Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation; Leading Research Fellow, Petersburg Nuclear Physics Institute named after B.P. Konstantinov of the National Research Centre "Kurchatov Institute".
Svetlana E. Chuprina, Candidate of Medical Sciences, Head of the Neurological Department for Patients with Cerebrovascular Accidents, Voronezh Regional Clinical Hospital No. 1; Chief Freelance Specialist Neurologist of the Ministry of Health of Voronezh Oblast, Chief Freelance Specialist Neurologist of the Ministry of Health of Russia in the Central Federal District, Chief Freelance Specialist in Medical Rehabilitation of the Ministry of Health of Russia in the Central Federal District.
Nikolay A. Shamalov, MD, PhD, Professor, Chief Freelance Specialist Neurologist of the Ministry of Health of the Russian Federation, Chief Freelance Neurologist of the Moscow Healthcare Department, Director of the Institute of Cerebrovascular Pathology and Stroke, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency; Executive Secretary of the National Stroke Association.
Rafiz K. Shikhkerimov, MD, PhD, Professor of the Department of Clinical Medicine, Reaviz Moscow Medical University; Neurologist, City Polyclinic No. 166 of the Moscow Healthcare Department, Neurologist, Polyclinic No. 4 of the Directorate of the President of the Russian Federation, Member of the Interregional Association of Botulinum Therapy Specialists (IABTS).
Evgeny V. Shlyakhto, MD, PhD, Professor, Academician of the Russian Academy of Sciences, General Director, Almazov National Medical Research Centre of the Ministry of Health of Russia; President of the Russian Society of Cardiology; Chief Freelance Cardiology Specialist of the Ministry of Health of Russia for the Northwestern, Southern, North Caucasian, Volga Federal Districts, and Zaporozhye and Kherson Oblasts; Honored Scientist of the Russian Federation.
Ivan A. Schukin, Candidate of Medical Sciences, Associate Professor of the Department of Neurology, Neurosurgery and Medical Genetics, Faculty of General Medicine, Pirogov Russian National Research Medical University of the Ministry of Health of Russia; Senior Research Fellow, Department of Neuroimmunology, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency of Russia.
Stanislav N. Yanishevsky, MD, PhD, Professor, Head of the Research Laboratory of Neurology and Neurorehabilitation, Professor of the Department of Neurology and Clinic, Almazov National Medical Research Centre; President of the Association "Society of Neurologists of Saint Petersburg and Leningrad Oblast".
All members of the working group declared no financial or non-financial conflicts of interest regarding the topic of the developed clinical guidelines. Working group member(s) who reported circumstances that might lead to a conflict of interest were excluded from the discussion of sections related to the conflict of interest area.
Appendix A2. Methodology for Developing Clinical Guidelines
Target audience of these clinical guidelines:
Neurologists.
Anesthesiologists-resuscitators.
Radiologists.
Neurosurgeons.
Physical and rehabilitation medicine physicians.
Exercise therapy physicians.
Medical speech therapists.
Ergo-rehabilitation specialists.
Exercise therapy instructors-methodologists.
Cardiologists.
General practitioners (family physicians).
General practitioners.
Urologists
Table 1
Scale for assessing levels of evidentiary certainty (LEC)
for diagnostic methods (diagnostic interventions)
LoE | Definition |
|---|---|
1 | Systematic reviews of studies with reference standard control or systematic reviews of randomized clinical trials with meta-analysis |
2 | Individual studies with reference-method control, or individual randomized controlled trials and systematic reviews of studies of any design except randomized controlled trials incorporating meta-analysis |
3 | Studies without consecutive reference standard control or studies with a reference standard not independent of the test method, or non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case report |
5 | Only justification of mechanism of action or expert opinion is available |
Table 2
Scale for assessing levels of evidence (LoE) for prevention, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, therapeutic, and rehabilitative interventions)
LoE | Definition |
|---|---|
1 | Systematic review of RCTs incorporating meta-analysis |
2 | Individual RCTs and systematic reviews of studies of any design except RCTs incorporating meta-analysis |
3 | Non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case reports or case series, case-control studies |
5 | Only justification of the mechanism of action of the intervention (preclinical studies) or expert opinion is available |
Table 3
Scale for assessing levels of recommendation grades (RG) for prevention, diagnostic, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, diagnostic, therapeutic, and rehabilitative interventions)
GoR | Definition |
|---|---|
A | Strong recommendation (all considered efficacy criteria (outcomes) are important, all studies are of high or acceptable methodological quality, and their conclusions on the outcomes of interest are consistent) |
B | Conditional recommendation (not all considered efficacy criteria (outcomes) are important, not all studies are of high or acceptable methodological quality, and/or their conclusions on the outcomes of interest are inconsistent) |
C | Weak recommendation (lack of evidence of proper quality; all considered efficacy criteria [outcomes] are unimportant, all studies have low methodological quality, and their conclusions regarding outcomes of interest are inconsistent) |
Procedure for updating clinical guidelines
The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based data regarding the diagnosis, treatment, prevention, and rehabilitation of specific conditions, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every six months.
Appendix A3. Reference Materials
Order of the Ministry of Health of the Russian Federation No. 1740n dated December 29, 2012, "On Approval of the Standard of Specialized Medical Care for Cerebral Infక్షన్" [Note: Cerebral Infarction]
Order of the Ministry of Health of the Russian Federation No. 928n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to Patients with Acute Cerebrovascular Accidents."
Appendix A3-1. Methods used for early medical rehabilitation of patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A01.23.003 Palpation in pathology of the central nervous system and brain | Examination with assessment of muscle tone, skin condition, skin and muscle turgor, subcutaneous adipose tissue, bone and joint projections, tissue compressibility, evaluation of subcutaneous vascular formations, facial, masticatory and oral muscles, and tongue | 2.25 Medical gloves 129880 Single-use isolation gown 302900 Non-woven non-sterile wipe | 10 minutes | 1 | 1 |
A01.23.004 Examination of sensory and motor spheres in pathology of the central nervous system and brain | Assessment of deep and superficial sensation, assessment of muscle strength and range of motion in the limbs and joints | 2.25 Medical gloves 300820 Neurological reflex hammer (with a needle and brush, cotton ball), 341840 Tongue depressor, Test tubes (containers) with water of different temperatures, a kit for assessing taste sensation, tuning fork, | 10 minutes | 1 | 1 |
A14.30.014 Pain intensity assessment | Pain syndrome assessment for communicative patients using a visual analogue scale (VAS pain scale) For non-communicative patients, the following is used Behavioral Pain Scale (BPS), assessment of tenderness in soft tissues, joints, and mucous membranes. | Scales, pen, paper, 2.25 Medical gloves electronic devices (smart) | 10 minutes | 1 | 1 |
A02.04.003 Measurement of joint mobility (goniometry) | Assessment of the range of motion in the joints of the upper and lower limbs | 181060 Manual goniometer Pen, paper, electronic devices (smart) | 10 minutes | 1 | 1 |
A23.30.004 Formulation of a functional diagnosis | Determination of the state of functioning and restriction of activity and participation formulation of a rehabilitation diagnosis, goals and objectives of rehabilitation measures, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 1 | 1 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 1 | 1 |
A13.23.001 Medical and speech therapy examination for dysphagia | Examination of swallowing function. Selection of the optimal degree of liquid thickening and food consistency. Performing the V-VST test | Speech therapy probe Set of speech therapy tongue depressors Disposable gloves Liquid thickener Test containers (disposable cups, measuring cups) Disposable plastic spoon Water | 20 minutes | 0,35 | 2 |
A13.23.002 Medical-speech therapy evaluation for aphasia | Assessment of all types of speech, praxis, and gnosis | Methodological manuals for speech assessment | 20 minutes | 0,35 | 2 |
Appendix A3-2. Methods used by MDRC specialists for medical rehabilitation interventions in patients with ischemic stroke
Nomenclature of medical services | What is performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A01.23.001 Collection of anamnesis and complaints in central nervous system pathology and brain | Collection of complaints, life and disease (condition) anamnesis. Review of medical documents, including electronic media. | PC, MFP, telephony, voice recorder, pencils, pen, paper, electronic devices (smartphone) | 15 minutes | 1 | 1 |
A01.23.003 Palpation in pathology of the central nervous system and brain | Examination with assessment of muscle tone, skin, skin and muscle turgor, subcutaneous adipose tissue, presence of tenderness in soft tissues, in bone and joint projections, tissue mobility, assessment of subcutaneous vascular formations | 2.25 Medical gloves 290200 Adaptive electric bed 4-section 129880 Disposable isolation gown 302900 Non-woven non-sterile wipe | 15 minutes | 1 | 3 |
A01.23.004 Sensory and motor sphere examination in pathology of the central nervous system and brain | Assessment of deep and superficial sensitivity | 2.25 Medical gloves 300820 Neurological hammer (with needle and brush, cotton ball), 341840 Tongue depressor, Test tubes (containers) with water of different temperatures, kit for gustatory sensitivity assessment, tuning fork, pencils, pen, paper | 15 minutes | 1 | 3 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) For non-communicative patients, it is used Behavioral Pain Scale (BPS) | Scales, pen, paper, electronic devices (smart) | 5 minutes | 0,3 | 3 |
A02.04.003 Joint mobility assessment (goniometry) | Examination with assessment of range of motion in limb joints | 181060 Manual goniometer Pen, paper, electronic devices (smart) | 10 minutes | 0,3 | 3 |
A02.02.005 Assessment of dynamic strength of a single muscle | Assessment of upper and lower limb muscle strength (severity of paresis), handgrip dynamometry | Medical Research Council (MRC) Scale for Muscle Strength 103800 Handheld electronic dynamometer Pen, paper, electronic devices (smart) | 5 minutes | 0,3 | 3 |
A23.30.007 Determination of the cardiovascular system reaction type to physical activity | Assessment of heart rate, blood pressure | 290200 Adaptive electric bed 4-section 239410 Aneroid mechanical sphygmomanometer Pen, paper, electronic devices (smart) | 5 minutes | 0,5 | 3 |
23.30.006 Determination of the activity regimen | Assessment of achieving the patient's activity level sufficient for self-care and mobility | 239410 Aneroid mechanical sphygmomanometer Pen, paper, electronic devices (smart) | 5 minutes | 1 | 3 |
A23.30.038 Study of recovery response | Assessment of blood pressure, heart rate | 239410 Aneroid mechanical sphygmomanometer Pen, paper, electronic devices (smart) | 5 minutes | 1 | 3 |
A23.30.004 Formulation of a functional diagnosis | Determination of the state of functioning and activity limitations formulation of a rehabilitation diagnosis, goals and objectives of rehabilitation measures, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, multidisciplinary unit, pen, paper, | 5 minutes | 1 | 3 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and activity limitations, formulation of an individual medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, multidisciplinary unit, pen, paper, | 5x5 minutes | 0,3 | 3 |
A23.30.011 Determination of rehabilitation prognosis | Determination of the prospect of achieving the intended goals and objectives of medical rehabilitation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, multidisciplinary unit, pen, paper, | 10 minutes | 0,3 | 2 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment (personal items used in minimal bodily self-care), training in the use of adapted items. For patients with cognitive impairments, sensory impairments, and upper limb motor impairments. | 2.25 Gloves 290200 Adaptive electric bed 4-section Personal protective equipment: Disposable gloves 129880 Disposable isolation gown 184150 Bedside table 184150 Bedside cabinet High-back upholstered armchair 189290 Reclining armchair Functional armchair 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis Material for making adaptive grips (foam rubber, foamed polyethylene, etc. (plastic polymer)) | 30 | 0,3 | 5 |
A23.30.017 Postural correction | Assessment of body and limb positions in space, application of postural positioning, selection of postural methods for correcting swallowing disorders during meals, prevention of secondary complications (pressure ulcers, contractures), selection of orthoses | 290200 Adaptive electric bed 4-section 189290 Reclining armchair 239410 Aneroid mechanical sphygmomanometer Pen, paper, 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis Other equipment: set of soft modules for the physical therapy room | 4x10 minutes | 0,1 | 7 |
A19.23.002.014 Individual physical therapy session for diseases of the central nervous system and brain | Formation of movements, patterns, and locomotions (turning in bed/on the couch, sitting up in/on the bed) | 116940 Powered massage table/couch (Bobath table) 149390 Pulse oximeter 136940 Wipe for cleaning/disinfecting medical devices Other equipment: set of weights set of soft modules for the physical therapy room full-length mirror wall bars gymnastic bench | 20 minutes | 0,1 | 5 |
A14.30.001 Passive mobilization | Assessment of voluntary movements, active movements, and performance of contact kinesiotherapy manipulations with the patient (methods) | 290200 Adaptive electric bed 4-section 116940 Powered massage table/couch (Bobath table) 102930 Continuous passive motion device for hip/knee joint 149460 Continuous passive motion device for ankle joint 208810 Passive shoulder exercise device 208810 Passive shoulder exercise device 110440 Continuous passive motion device for hand/wrist joint 136940 Wipe for cleaning/disinfecting medical devices | 20 minutes | 0,1 | 5 |
A19.23.002.021 Mechanotherapy using pneumatically driven mechanotherapy devices for central nervous system and brain disorders | Performing the procedure, monitoring efficacy and safety | 140790 Exercise bike | 30 minutes | 0,1 | 5 |
A19.23.002.003 Physical therapy for aphasia, dysarthria | Correction of breathing patterns, neck and facial muscle tone, performance of contact kinesiotherapy manipulations with the patient (methods) | 2.25 Medical gloves 136940 Wipe for cleaning/disinfection of medical devices, mirror | 10 minutes | 0,1 | 5 |
A19.23.002.004 Individual physical therapy session for aphasia, dysarthria | Correction of breathing patterns, performance of contact manipulations with the patient (kinesiotherapy methods), | 136940 Wipe for cleaning/disinfecting medical devices mirror Set of sensory panels | 10 minutes | 0,1 | 5 |
A19.23.006 Dynamic proprioceptive correction | Performance of neuromuscular stimulation of the foot support zones | Corvit plantar pressure stimulation device | 20 minutes | 0,1 | 7 |
A13.30.001 Self-care training | Training in simple (bodily) forms or elements of self-care, for example, wiping the face with a handkerchief, cleaning hands with wipes, grasping and using personal items, brushing teeth, combing hair; training in social communication. | 290200 Adaptive electric bed 4-section Mirror 136940 Wipe for cleaning/disinfecting medical devices 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside table | 10 minutes | 0,1 | 5 |
A21.30.006 Ergotherapy | Movement training and skill practice focused on forms and elements of self-care. | 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis Other equipment: adapted kitchen and dining tableware standard kitchen and dining tableware | 10 minutes | 0,1 | 7 |
A14.30.003 Feeding a severely ill patient orally and/or via nasogastric tube | Performing the feeding procedure, monitoring efficacy and safety of swallowing during food and fluid intake | Other equipment: adapted kitchen and dining tableware standard kitchen and dining tableware Set of speech therapy tongue depressors | 30 minutes | Speech therapist -0.1 Nurse – 0.4 | 10 |
A23.30.013 Use of games in the rehabilitation process | Development of general and speech activity skills Restoration of control and self-control skills Activation of speech function Activation of everyday vocabulary Organization of voluntary activity Improvement of emotional state Music therapy | 175960 Psychological status assessment system Set of games (dominoes, lotto, checkers, etc.) Visual and didactic material Methodological manuals (schemes for neuropsychological assessment of higher mental functions, exercise books, reading books) Tablets of various sizes Equipment for recording and playing sound (music) | 30 | 0,1 | 5 |
A21.23.006 Training patient relatives in tactics and methods for restoring cognitive functions in patients | Briefing and training of relatives in the rules and measures of interaction with a patient having cognitive impairments. | Visual and didactic material Methodological manuals (schemes for neuropsychological assessment of higher mental functions, exercise books, reading books) | 30 | 0,1 | 2 |
A13.30.007 Oral hygiene training | Briefing, training, demonstration | Other equipment: Specialized stands for social and domestic adaptation Specialized kit for domestic adaptation of non-ambulatory patients, including a toothbrush, comb, aids for dressing assistance | 5 | 0,1 | 2 |
A14.07.008 Individual oral and dental hygiene training, selection of oral hygiene products and items | Briefing, training, demonstration Selection of toothpastes, denture care products, etc. | Other equipment: Specialized stands for social and domestic adaptation Specialized kit for domestic adaptation of non-ambulatory patients, including a toothbrush | 15 | 0,1 | 2 |
A14.08.002 Tracheostomy care | Monitoring and care of a tracheostomy, using a speaking valve. | Disposable medical syringe 149390 Pulse oximeter Medical suction unit Dressing material Antiseptics Tracheostomy filter 1 set Handouts for independent practice on swallowing training and articulation gymnastics | 10 minutes | 0,025 | 10 |
A13.23.007 Medical and speech-language tonal-rhythmic procedure | Listening to and recognition of non-verbal sounds, melodies, songs with lyrics, poetic and prose stimuli Development of diaphragmatic speech breathing Expansion of voice modulation capabilities Expansion of the vocal range in terms of loudness, pitch, and stability. Restoration of voice production Restoration of voice guidance Correction of tempo-rhythm disorders of speech function. Correction of disorders of the prosodic aspect of speech. Playback of melodies, songs with lyrics, poetic and prose stimuli Synchronization of speech and movement Improvement of emotional state. | Workstation with a personal computer and access to the Internet information and communication network Voice recorder Tablets of various sizes 342050 Mobile audiovisual system Visual and didactic material Methodological manuals (diagrams, exercise collections, readers) | 10/30 minutes | 0,05 | 5 |
A13.23.008 Medical and speech-language procedure using interactive information technologies | Hand-eye coordination training Unblocking of the expressive aspect of speech Activation of nominal and verbal vocabulary Restoration of oral phrasal speech Restoration of written speech: copying, writing from memory, dictation Restoration of phoneme-grapheme analysis and synthesis of word structure Restoration of arithmetic skills Restoration of memory Restoration of time orientation Voice correction Correction of sound pronunciation Overcoming optic-spatial disorders Rehabilitative training in the use of augmentative and alternative communication means | Workstation with a personal computer and access to the Internet information and communication network Video camera Voice recorder Headphones Microphone Tablets of various sizes 342050 Mobile audiovisual system 343660 Equipment for biofeedback training based on EMG parameters 324120 Virtual system, unsupported, clinical Neurointerface with consumables Set of sensory panels Communication systems (stationary, mobile) Computer programs for speech and voice rehabilitation Visual and didactic material Functional armchair Computer desk | 10/45 minutes | 0,05 | 10 |
Appendix A3-3. Methods used by MDRC specialists to monitor the development of complications in patients with ischemic stroke
Nomenclature of Medical Services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A01.23.003 Palpation in pathology of the central nervous system and brain | Examination with assessment of muscle tone, skin condition, skin and muscle turgor, subcutaneous adipose tissue, presence of tenderness in soft tissues, bone and joint projections, tissue mobility, assessment of subcutaneous vascular structures | 2.25 Medical gloves 129880 Single-use isolation gown 302900 Non-woven non-sterile wipe | 5 minutes | 1 | 10 |
A14.30.014 Pain intensity assessment | Pain syndrome assessment for communicative patients using a visual analogue scale (VAS pain scale) For non-communicative patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, 2.25 Medical gloves electronic devices (smart) | 5 minutes | 1 | 10 |
A02.04.003 Measurement of joint mobility (goniometry) | Examination with assessment of the range of motion in the joints of the extremities | 181060 Manual goniometer Pen, paper, electronic devices (smart) | 5 minutes | 0,3 | 2 |
A02.30.005 Orthostatic test | Assessment of cardiovascular system response to exertion (verticalization) | Aneroid mechanical blood pressure monitor, functional bed, tilt table, Pen, paper, electronic devices (smart) | 15 minutes | 0,1 | 2 |
A23.30.006 Determination of motor regimen | Assessment of achieving a patient activity level sufficient for self-care and transfer | Aneroid mechanical blood pressure monitor | 5 minutes | 0,1 | 3 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, opinions/recommendations of the multidisciplinary rehabilitation team specialists, PC, multifunction device | 15 minutes | 0,5 | 2 |
A13.29.013 Microenvironment adaptation procedures | Maintenance of circadian rhythm, prevention of post-intensive care syndrome, | earplugs, soft modular positioning aids, light-blocking eye mask, | 24 hours | 1 | 10 |
A23.30.017 Postural correction | Correction of body and limb positions, - use of postural bolsters/rolls, - selection of postural correction methods - prevention of secondary complications (pressure ulcers, contractures), selection of orthoses | 290200 Adaptive electric functional bed 4-section 189290 Recliner chair with adjustable backrest angle 239410 Aneroid mechanical blood pressure monitor 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis (other equipment: set of soft modules for the exercise therapy gym) | 24 hours | 1 | 10 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Development of movements, patterns, and locomotion (turning in bed/on a couch, sitting up in/on a bed) | 290200 Adaptive electric bed 4-section 116940 Massage table/couch, mains-powered (Bobath table) 239410 Aneroid mechanical blood pressure monitor, 149390 Pulse oximeter Other equipment: set of weight cuffs set of soft modules for the exercise therapy gym | 30 minutes | 0,5 | 10 |
A14.30.001 Passive mobilization | Development of voluntary movements, active movements, and contact kinesitherapy maneuvers with the patient (techniques). | 239410 Aneroid mechanical blood pressure monitor 290200 Adaptive electric bed 4-section 116940 Massage table/couch, mains-powered (Bobath table) 102930 Continuous passive motion device for hip/knee joint 149460 Continuous passive motion device for ankle joint 208810 Passive motion device for shoulder 208810 Passive motion device for shoulder 110440 Continuous passive motion device for hand/wrist joint | 20 minutes | 0,3 | 10 |
A19.23.002.021 Mechanotherapy using pneumatic mechanotherapy devices for central nervous system and brain diseases | Prevention of contractures, maintenance of muscle tone and body schema, preservation of range of motion, disuse syndrome, increased exertion tolerance, trophic disorders, | 147070 Tilt table 140790 Cycle ergometer 209580 Mobile patient lift and transfer system with hard seat | 30 minutes | 0,3 | 10 |
A21.30.006 Occupational therapy | Patient training in simple (bodily) forms or elements of self-care, e.g., wiping the face with a handkerchief, cleaning hands with wipes, grasping and using personal items; training in social communication. | Disposable gloves personal protective equipment, Items and polymer materials for microenvironment adaptation | 30 minutes | 0,3 | 10 |
A14.07.007 Assessment of swallowing competency | Examination of bulbar reflexes (swallowing, cough, pharyngeal) | Disposable gloves 341840 Spatula | 15 minutes | 0,1 | 1 |
A13.23.001 Medical and speech therapy examination for dysphagia | Performance of functional tests to assess swallowing function Indirect assessment of aspiration risks (fibrobronchoscopy) | Colored food stimulus of 3 consistencies (water, nectar, pudding), syringe (spoon) for administering the food stimulus: Specialized thickening product, methylene blue solution, 20 ml syringe, disposable cups - 4 pcs, disposable dessert spoon - 1 pc, fork - 1 pc, sterile gauze pads, disposable cap, disposable cape, PC, multifunction device, telephony, dictaphone, pencils, pen, paper, clipboard, electronic devices (smartphone) | 60 minutes | 1 | 1 |
A13.23.001 Medical and speech therapy examination for dysphagia | Visual assessment of the laryngeal mucosa and swallowing functions (VVT test under endoscopic control) | Colored food stimulus of 3 consistencies (water, nectar, pudding), syringe (spoon) for administering the food stimulus: Specialized thickening product methylene blue solution - 20 ml syringe - disposable cups - 4 pcs - disposable dessert spoon - 1 pc fork – 1 pc - sterile gauze wipes - disposable gloves PC, multifunction printer, telephony, voice recorder, pencils, pen, paper, clipboard, electronic devices (smartphone) | 60 minutes | 0,1 | 2 |
A13.23.003 Medical-speech therapy assessment for dysarthria | 1. Assessment of respiratory function 2. Voice assessment | Respiratory spirometer Mouthpieces Stopwatch Rhythmometer (metronome) Tongue depressor Speech therapy flashlight Speech therapy mirror Disposable gloves Paper Pen | 20 min | 1 | 3 |
A13.23.002 Medical-speech therapy evaluation for aphasia (express assessment) | Assessment of the receptive language side Assessment of the expressive language side | Express assessment chart Diagnostic album for oral language express assessment, Diagnostic album for written language express assessment, Pen, pencil, paper, voice recorder, video camera | 10 minutes | 0,1 | 3 |
Appendix A3-4. Methods used for the correction of speech disorders and prevention of cognitive impairment in patients with ischemic stroke
Nomenclature of Medical Services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
B05.069.006 Development of an individual speech therapy rehabilitation program | Selection of illustrative and didactic material taking into account the patient's social and communicative potential. Selection of stimuli for swallowing training | PC, multifunction printer (color), Laminator Laminating pouches, pen, paper recordings with sound and speech stimuli real objects, anatomical models specialized thickeners | 20 minutes | 0, 5 | 10 |
A17.24.010 Multifunctional electrical muscle stimulation | Neuromuscular stimulation of the oral and articulation area | Catheter for pharyngeal muscle electrical stimulation Neuromuscular stimulation device | 15 minutes | 0,2 | 10 |
A17.30.035.001 Biofeedback-assisted electrical stimulation | Neuromuscular stimulation of the oral and articulation area | Neuromuscular stimulation device with biofeedback (BFB) | 15 minutes | 0,2 | 10 |
09.PZZ.17.001.008 Kinesio taping | Speech correction using kinesio taping | Disposable gloves Kinesio tape Tape scissors | 10 minutes | 0,2 | 10 |
A21.01.002 Medical facial massage | Improvement of muscle tone, sensitivity, and range of motion | Disposable gloves Massage oil | 15 min | 0,2 | 10 |
A21.01.003 Medical neck massage | Improvement of muscle tone and sensitivity | Disposable gloves Massage oil | 5 min | 0,2 | 10 |
A21.01.003.001 Collar zone massage | Improvement of muscle tone and sensitivity | Disposable gloves Massage oil | 5 min | 0,2 | 10 |
A21.01.004 Medical upper extremity massage | Improvement of muscle tone, sensitivity, and range of motion | Disposable gloves Massage oil | 5 min | 0,2 | 10 |
A21.01.005 Medical scalp massage | Improvement of muscle tone and sensitivity, | Disposable gloves | 5 min | 0,2 | 10 |
A21.01.004.005 Hand and forearm massage | Improvement of muscle tone, sensitivity, and range of motion | Disposable gloves Massage oil | 5 min | 0,2 | 10 |
A24.01.005 Skin cryomassage | Improvement of muscle tone and sensitivity | Disposable gloves Ice cubes Ice cube trays Gel freezing sticks Gel pads Towel Fabric napkin Metal teaspoon and dessert spoon Refrigerator cooler | 5 min | 0,2 | 5 |
09.PZZ.11.005.008 Vibrotherapy | Improvement of muscle tone, sensitivity, and range of motion | Disposable gloves Vibrostimulator with translingual attachments | 5 min | 0,2 | 10 |
A13.23.006 Medical speech therapy procedure for dysarthria | Restoration of speech articulation, improvement of speech intelligibility, normalization of muscle tone involved in swallowing, phonation, and speech, restoration of lower diaphragmatic breathing, voice restoration Restoration of the prosodic aspect of speech (tempo, rhythm, intonation) Restoration of sound pronunciation | Training devices for developing speech inhalation and exhalation: Respiratory spirometer "Artificial candle" trainer Breathing tubes Weather vane Plastic cocktail straws Glass Speech therapy probe Tongue depressor Tongue navigator Speech therapy mirror Rhythmograph (metronome) Musical instruments Computer discs with recorded speech samples and tasks Visual didactic material Voice recorder Headphones Feedback device with white noise, echo effect, and metronome Computer programs | 40 | 0,1 | 10 |
A13.23.005 Medical speech therapy procedure for aphasia | Restoration of receptive speech Restoration of expressive speech Restoration of written speech: reading and writing Restoration of counting operations Restoration of body schema Restoration of spatio-temporal representations Restoration of oral-articulatory and manual praxis Restoration of visual and object agnosia/gnosis, Restoration of auditory-verbal memory capacity Restoration of formal and abstract thinking Restoration of discourse Restoration of communication and social skills | Stimulus illustrative didactic material: Sets of images by lexical groups, thematic pictures, series of thematic pictures, Set of facial images; Stimulus lexical material: workbooks Texts Poems Letter, number, and syllable box Models, Communication boards, Communication buttons, Sets of pictograms Magnetic board Magnet sets Magnetic alphabet Markers Eraser Interactive whiteboard Discs with a sound library of verbal stimuli Specialized computer programs Computer Voice recorder Stereo headphones Pen for right- and left-handed use Pencils Markers Paper - 10 sheets per 1 session | 40 minutes | 0,5 | 10 |
A13.29.013 Microenvironment adaptation procedures Occupational therapist | Adaptation of the patient's microenvironment (personal items used in minimal bodily self-care), training in the use of adapted items. | Material for making adaptive handles (foam rubber, expanded polyethylene, etc.) Modified writing instruments | 20 | 0,5 | 10 |
A23.30.013 Application of games in the rehabilitation process | Overcoming general and speech inactivity Restoration of control and self-control skills Disinhibition of speech function Actualization of everyday vocabulary Organization of voluntary activity Improvement of emotional state | 175960 (manual nomenclature) Psychological status assessment system Set of games (dominoes, lotto, checkers, etc.) Visual didactic material Methodological manuals (schemes for neuropsychological examination of higher mental functions, exercise collections, reading books) Tablets of various sizes Equipment for recording and listening to sound (music) | 30 | 0,1 | 7 |
A21.23.006 Training of the patient's relatives in tactics and methods of restoring cognitive functions in patients | Briefing and training of relatives on the rules and measures of interaction with a patient having cognitive impairments. | 175960 Psychological status assessment system Visual didactic material Methodological manuals (schemes for neuropsychological examination of higher mental functions, exercise collections, reading books) Tablets of various sizes Equipment for recording and listening to sound (music) | 30 | 0,1 | 2 |
A13.23.007 Medical speech therapy tonal-rhythmic procedure | Listening to and recognition of non-speech sounds, melodies, songs with words, poetic and prosaic stimuli Development of diaphragmatic speech breathing Expansion of voice modulation capabilities Expansion of voice range in loudness, pitch, and stability. Restoration of voice production Restoration of voice leading Restoration of tempo-rhythm disorders of speech function. Restoration of impairments of the prosodic aspect of speech. Reproduction of melodies, songs with words, poetic and prosaic stimuli Synchronization of speech and movements Improvement of emotional state. | Workplace with a personal computer. Voice recorder Tablets of various sizes 342050 (equipment nomenclature) Mobile audiovisual complex Visual didactic material Methodological manuals (schemes, exercise collections, reading books) | 30 min | 0,03 | 7 |
A13.23.008 Medical speech therapy procedure using interactive information technologies | Hand-eye movement synchronization Unblocking of the expressive aspect of speech Actualization of nominative and verbal vocabulary Restoration of oral phrasal speech Restoration of written speech: copying, writing from memory, dictation writing Restoration of sound-letter analysis and synthesis of word structure Restoration of calculation Restoration of memory Restoration of time orientation Voice correction Correction of sound pronunciation Overcoming optic-spatial disorders Rehabilitative training in the use of augmentative and alternative communication devices | Workstation with a personal computer Video camera Voice recorder Headphones Microphone Tablets of various sizes 342050 Mobile audiovisual complex 343660 Equipment for training with biofeedback based on EMG parameters 324120 Clinical virtual system, unsupported Neurointerface with consumable materials Set of sensory panels Communication systems (stationary, mobile) Computer programs for speech and voice restoration Visual didactic material Functional chair Computer desk | 45 minutes | 0,3 | 10 |
Appendix: A3-5. Methods used by MDRC specialists to improve personal activities of daily living skills in patients with ischemic stroke
Nomenclature of Medical Services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A23.30.006 Determination of motor regimen | Assessment of achieving a patient activity level sufficient for self-care and transfer | Aneroid mechanical blood pressure monitor, dynamometer, goniometer, pain assessment VAS | 5 minutes | 0,3 | 3 |
A23.30.038 Assessment of the recovery response | Assessment of heart rate, blood pressure, and saturation response | Aneroid mechanical blood pressure monitor, pen, paper, electronic devices (smartphone), pulse oximeter | 5 minutes | 0,3 | 3 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 0,3-0,7 | 3 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Development of movements, patterns, and locomotion (turning in bed/on a couch, sitting up in/on a bed) | Adaptive electrically powered bed 4-section Mains-powered massage table/couch (Bobat table) Aneroid mechanical blood pressure monitor, Pulse oximeter Other equipment: set of weights set of soft modules for the exercise therapy gym | 30 minutes | 0,2 | 10 |
A19.23.002.021 Mechanotherapy using pneumatic mechanotherapy devices for central nervous system and brain diseases | Maintenance of muscle strength, preservation of range of motion, prevention of disuse syndrome, prevention of thromboembolic and trophic complications, preservation of body schema, overcoming neglect syndrome | Aneroid mechanical blood pressure monitor Standing frame Cycle ergometer Mobile patient lift and transfer system with a rigid seat | 30 minutes | 0,3 | 10 |
A14.30.016 Patient education in self-care during transfers in bed and/or chair | Mastering transfer skills, fall prevention, development of supporting function of postural muscles, expansion of the motor regime | Standard hospital bed with electric drive Attendant-propelled wheelchair, foldable Attendant-propelled wheelchair with drive, foldable | 10 minutes | 0,1 | 10 |
A14.30.016.1 Independent position changes (turning in bed; transition to a sitting position, into a chair, standing up) using support surfaces (chair back, cane, walker) | Mastering the skills of turning in bed and sitting up, posture maintenance, prevention of falls and trophic disorders, expansion of the motor regime | Standard hospital bed with electric drive Attendant-propelled wheelchair, foldable Attendant-propelled wheelchair with drive, foldable | 10 minutes | 0,1 | 10 |
A14.30.018 Patient education in self-care during transfers using an assistive support | Training in self-care skills in supine, sitting, and standing positions, using necessary assistive devices for rehabilitation (ADR) | Medical gloves Aneroid mechanical blood pressure monitor Standard wheeled walker, foldable Standard wheeled walker, non-foldable Electrically powered stair-climbing simulator Standard motorized treadmill, multi-point cane | 10 minutes | 0,1 | 10 |
A14.30.017 Patient education on walking with crutches | Training in self-care skills using necessary assistive devices for rehabilitation (ADR) | Assistive devices for rehabilitation (crutches) | 10 minutes | 0,05 | 5 |
A19.23.004 Correction of motor function disorders using computer technology | Use of robotic devices for upper limb function training using computer technology and gaming or virtual environments. Use of robotic devices for stance foundation | Robotic biofeedback trainers for gait restoration with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton Robotic system for locomotor therapy and lower limb rehabilitation with body weight support Virtual reality equipment Other equipment (software): Neurointerface | 10 minutes | 0,1 | 10 |
A13.30.001 Self-care training | Patient training in simple (bodily) forms or elements of self-care, e.g., wiping the face with a handkerchief, cleaning hands with wipes, grasping and using personal items; training in social communication. | Disposable gloves Personal protective equipment Items and polymer materials for microenvironment adaptation | 10 minutes | 0,2 | 10 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment (personal items used in minimal bodily self-care), training in the use of adapted items | Disposable gloves Personal protective equipment, Items and polymer materials for microenvironment adaptation, soft modules | 10 minutes | 0,2 | 10 |
A13.23.004 Medical-speech therapy procedure for dysphagia | Performance of training exercises using speech therapy maneuvers Neuromuscular stimulation of the oral and articular area Swallowing correction using thickeners | Speech therapy probe Set of speech therapy tongue depressors Liquid thickener Catheter for electrical stimulation of pharyngeal muscles Device for neuromuscular stimulation of the palate, pharynx, and larynx with a set of electrodes for intrapharyngeal stimulation | 30 min | 0.1 | 10 |
A14.07.008 Individual training in oral cavity and dental hygiene, selection of oral hygiene products and items | Training in oral cavity care techniques | Disposable gloves Speech therapy probe Tongue depressor | 10 minutes | 1 | 2 |
A13.23.005 Medical speech therapy procedure for aphasia at the first stage of medical rehabilitation | Restoration of all types of speech, reading, writing, counting, and other cognitive functions | Visual didactic material Speech therapy mirror Metronome Musical instruments Computer discs with speech samples and tasks Pen, notebook | 40 minutes | 0,35 | 10 |
A13.23.008 Medical speech therapy procedure using interactive information technologies | Restoration of the receptive aspect of speech Restoration of the expressive aspect of speech | Specialized hardware-software systems | 40 minutes | 0,15 | 5 |
A19.23.002.005 Electromyography biofeedback training in aphasia, dysarthria | Consolidation of acquired communication, phonation, and articulation skills | Biofeedback device Visual and didactic material Computer discs with speech samples and tasks | 30 minutes | 0,15 | 5 |
A19.23.002.006 Electroencephalography biofeedback training in aphasia, dysarthria | Consolidation of acquired communication, phonation, and articulation skills | Biofeedback device Visual and didactic material Computer discs with speech samples and tasks | 30 minutes | 0,15 | 5 |
A19.23.002.008 Hemodynamic parameter (blood pressure) biofeedback training in aphasia, dysarthria | Restoration of speech, phonation, and articulation | Biofeedback device Visual and didactic material Computer discs with speech samples and tasks | 30 minutes | 0,15 | 5 |
A19.23.002.007 Spirographic parameter biofeedback training in aphasia, dysarthria | Restoration of speech, phonation, and articulation | Biofeedback device Visual and didactic material Computer discs with speech samples and tasks | 30 minutes | 0,15 | 5 |
Appendix A3-6. Methods used for early mobilization of ischemic stroke patients after assessing individual exercise tolerance
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A02.30.005 Orthostatic test | Assessment of cardiovascular system response to exercise in the vertical position | Aneroid mechanical blood pressure monitor, stopwatch | 5 minutes | 0,1 | 3 |
A23.30.018 Martinet-Kushelevsky test | Execution of a low-load test by the patient and assessment of cardiovascular system response to active load | Aneroid mechanical blood pressure monitor, stopwatch | 5 minutes | 0,1 | 3 |
A23.09.001 Stange test | Assessment of inspiratory breath-holding time | Stopwatch | 5 minutes | 0,1 | 3 |
A23.09.002 Genchi test | Assessment of expiratory breath-holding time | Stopwatch | 5 minutes | 0,1 | 3 |
A23.30.006 Determination of motor regimen | Determination of achieving a level of patient activity sufficient for self-care and transfer | Pen, paper, electronic devices | 5 minutes | 0,1 | 3 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team (MDRT) specialists, PC, MFP, pen, paper | 5 minutes | 0,1 | 3 |
A19.23.006 Dynamic proprioceptive correction | Neuromuscular stimulation of foot support zones | 136210 Standard electric hospital bed 239410 Aneroid mechanical blood pressure monitor 116940 Powered massage table/couch (Bobath table), 216810 Pneumatic massager | 20 minutes | 0,1 | 10 |
Verticalization | Transferring the patient from a supine to a vertical position | 147070 Standing frame | 30 minutes | 0,1 | 10 |
A19.30.006.002 Hardware statokinetic loads | Application of mechanotherapy equipment | Biofeedback training devices for gait and balance training | 30 minutes | 0,1 | 10 |
A19.23.003.008 Linear acceleration biofeedback training for central nervous system and brain disorders | Training of movement patterns and locomotor skills | Standard motorized treadmill Robotic biofeedback training device for gait restoration with an integrated synchronized electrical stimulation system Robotic system for locomotor therapy and lower limb rehabilitation Manually operated training device for gait function on a treadmill/elliptical trainer | 0,1 | 10 | |
A19.23.002.025 Physiotherapy exercise using apparatus and training devices for central nervous system and brain disorders | Performing the procedure, monitoring efficacy and safety | Gymnastic equipment (weights, sticks, dumbbells, fitballs, resistance bands) | 30 minutes | 0,1 | 10 |
A19.23.003.006 Linear movement speed biofeedback training for central nervous system and brain disorders | Performing the procedure, monitoring efficacy and safety | 140790 Medical robotic ergometer with biofeedback 110440 Continuous passive motion device for hand/wrist joint | 30 minutes | 0,1 | 10 |
A17.02.001 Muscle electrical stimulation | Prescription, administration of the procedure, monitoring of the patient's condition during the procedure | Multifunctional physiotherapeutic system for electrotherapy 173300 Portable electromagnetic deep tissue stimulator 181480 Transcutaneous electrical neuromuscular stimulation physiotherapeutic system | 20 minutes | 0,1 | 10 |
A23.30.012 Monitoring the effectiveness of exercise therapy sessions | Monitoring the reaction of the cardiovascular and respiratory systems to physical exertion | Mechanical aneroid sphygmomanometer, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
Appendix A3-7. Methods used for verticalization of patients with ischemic stroke after assessing individual exercise tolerance
Nomenclature of Medical Services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A01.23.004 Examination of sensory and motor spheres in pathology of the central nervous system and brain | Assessment of deep and superficial sensibility | 2.25 Medical gloves 300820 Neurological reflex hammer (with a needle and brush, cotton ball), 341840 Tongue depressor, Test tubes (containers) with water of different temperatures, a kit for assessing taste sensation, tuning fork, pencils, pen, paper | 5 minutes | 0,3-0,7 | 3 |
A14.30.014 Pain intensity assessment | Pain syndrome assessment for communicative patients using a visual analogue scale (VAS pain scale) For non-communicative patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, electronic devices (smartphone) | 5 minutes | 0,3-0,1 | 3 |
A 23.30.006 Determination of motor mode | Assessment of achieving a patient activity level sufficient for self-care and transfer | 239410 Mechanical aneroid sphygmomanometer, Pen, paper, electronic devices (smart) | 5 minutes | 0,3-0,1 | 3 |
A23.30.007 Determination of the cardiovascular system reaction type to physical exertion | Assessment of heart rate, blood pressure | 290200 Adaptive electric bed 4-section 239410 Mechanical aneroid sphygmomanometer, Pen, paper, electronic devices (smart) | 5 minutes | 0,3-0,1 | 3 |
A23.30.009 Drawing up an exercise therapy course plan | Selection of exercise therapy means and methods | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical records, functional diagnostics, telephony, voice recorder, pen, paper, electronic devices (smartphone) | 10 minutes | 0,3-0,7 | 3 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Movement training (turning in bed/sitting up in/on the bed) | 290200 Adaptive electric bed 4-section 239410 Mechanical aneroid sphygmomanometer, 149390 Pulse oximeter | 30 minutes | 0,1 | 10 |
A19.23.002.021 Mechanotherapy using pneumatic mechanotherapy devices for central nervous system and brain diseases | Transferring the patient from a supine to a vertical position | 2.25 Medical gloves 239410 Aneroid mechanical blood pressure monitor 147070 Tilt table 209450 Mobile patient lift and transfer system, mains-powered | 30 minutes | 0,1 | 10 |
A23.30.012 Monitoring the effectiveness of exercise therapy sessions | Monitoring the reaction of the cardiovascular and respiratory systems to physical exertion | Mechanical aneroid sphygmomanometer, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
Appendix A3-8. Methods used for positioning patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 0,3-0,7 | 3 |
A23.30.006 Determination of motor regimen | Assessment of achieving a patient activity level sufficient for self-care and transfer | Aneroid mechanical blood pressure monitor, dynamometer, goniometer, pain assessment VAS | 5 minutes | 0,3 | 3 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) For non-communicative patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, electronic devices (smartphone) | 5 minutes | 0,3-0,1 | 4/3 |
A02.04.003 Joint range of motion measurement (goniometry) | Examination with assessment of the range of motion in the joints of the extremities | 181060 Manual goniometer Pen, paper, electronic devices (smart) | 10 minutes | 0,3-0,1 | 4/3 |
A23.30.004 Formulation of a functional diagnosis | Determination of the state of functioning and restriction of activity and participation formulation of a rehabilitation diagnosis, goals and objectives of rehabilitation measures, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 0,3-0,7 | 4/3 |
A23.30.007 Determination of the cardiovascular system reaction type to physical exertion | Assessment of heart rate, blood pressure | 290200 Adaptive electric bed 4-section 239410 Mechanical aneroid sphygmomanometer, Pen, paper, electronic devices (smart) | 5 minutes | 0,3-0,1 | 4/3 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment (personal items used in basic self-care), training in the use of adapted items. For patients with cognitive impairments, sensory deficits, and upper extremity motor impairments. | 2.25 Gloves 290200 Adaptive electric bed 4-section Personal protective equipment: Disposable gloves 129880 Single-use isolation gown 184150 Bedside table 184150 Bedside cabinet High-back upholstered armchair 189290 Recliner chair with adjustable backrest angle Functional armchair 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis Material for making adaptive grips (foam rubber, expanded polyethylene, etc. (plastic polymer)) | 30 | 0,1/0,07 | 10/14 |
A23.30.017 Postural correction | Giving the body and limbs physiological positions, applying postural positioning, prevention of secondary complications (pressure ulcers, contractures) | Adaptive electrically powered bed 4-section Mains-powered massage table/couch (Bobat table) Mechanical aneroid sphygmomanometer, Pulse oximeter Other equipment: set of weight cuffs set of soft modules for the exercise therapy gym 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis (other equipment: set of soft modules for the exercise therapy hall) | 20 minutes | 0,1 | 10 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Performing passive-active movements in the upper and lower extremities, turns in bed | 290200 Adaptive electric bed 4-section 116940 Massage table/couch, mains-powered (Bobath table) 239410 Mechanical aneroid sphygmomanometer, 149390 Pulse oximeter 136940 Wipe for cleaning/disinfection of medical devices Other equipment: set of weight cuffs set of soft modules for the exercise therapy gym | 30 minutes | 0,2 | 10 |
Appendix A3-9. Methods used to train ischemic stroke patients and their family members in proper handling of the paretic limb
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) For unresponsive patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, 2.25 Medical gloves electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
A23.30.017 Postural correction | Correction of body and limb positions, - application of postural positioning, - selection of postural correction methods - prevention of secondary complications (pressure ulcers, contractures), selection of orthoses | 290200 Adaptive motor-driven functional bed 4-section 189290 Recliner chair with adjustable backrest 239410 Mechanical aneroid sphygmomanometer, 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis (other equipment: set of soft modules for the physical therapy room) | 24 hours | 1 | 10 |
A14.30.001 Passive mobilization | Development of voluntary movements, active movements, and performing contact kinesiotherapy manipulations with the patient (methods). | 239410 Aneroid mechanical blood pressure monitor 290200 Adaptive electric bed 4-section 116940 Massage table/couch, mains-powered (Bobat table) 102930 Continuous passive motion device for hip/knee joint 149460 Continuous passive motion device for ankle joint 208810 Passive shoulder exercise device 208810 Passive shoulder exercise device 110440 Continuous passive motion device for hands/wrist joint | 20 minutes | 0,3 | 10 |
A19.23.001 Physical therapy exercises aimed at reducing spasticity | Assessment of tone in spastic limbs, selection of special exercises, and their safe execution | 2.25 Medical gloves 129880 Single-use isolation gown 239410 Aneroid mechanical blood pressure monitor 136210 Standard hospital bed with electric drive 116940 Massage table/couch, mains-powered (Bobat table) 136940 Wipe for cleaning/disinfection of medical devices | 30 minutes | 0,5 | 10 |
A19.23.003 Correction of motor function disorders using biofeedback | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A23.30.012 Monitoring the effectiveness of physical therapy sessions | Monitoring the response of the cardiovascular and respiratory systems to physical exertion | Aneroid mechanical blood pressure monitor, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
A14.30.015 Training family members in patient transfer and/or positioning techniques in bed | Instruction/training/demonstration | 116940 Massage table/couch, mains-powered (Bobat table) 157500 Mechanical patient transfer system 184150 Bedside cabinet 184150 Bedside table | 20 minutes | 0,5 | 10 |
A13.30.001 Self-care training | Training in simple (bodily) forms or elements of self-care, for example, wiping the face with a handkerchief, cleaning hands with wipes, grasping and using personal items; social communication training. | 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis | 20 minutes | 0,3 | 10 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment (personal items used in minimal bodily self-care), training in the use of adapted items | 290200 Adaptive electric bed 3-section bed Disposable gloves Personal protective equipment 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table Material for making adaptive grips (foam rubber, expanded polyethylene) | 20 minutes | 0,3 | 10 |
Appendix A3-10. Methods used for correction of shoulder subluxation in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) For unresponsive patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, 2.25 Medical gloves electronic devices (smartphone) | 5 minutes | 1 | 10 |
A23.30.009 Drawing up a physical therapy course plan | Selection of physical therapy means and methods | ICF, conclusions/recommendations of multidisciplinary team specialists, medical commission, functional diagnostic unit, telephony, voice recorder, pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 3 |
A19.23.002.014 Individual physical therapy session for diseases of the central nervous system and brain | Development of movements, patterns, and locomotions - turning in bed/on couches, sitting up | 109670 Knee/ankle/foot orthosis Other equipment: set of weights, set of soft modules for the physical therapy room, full-length mirror | 10 minutes | 0,1 | 3 |
A23.30.017 Postural correction | Assessment of body and limb positions in space, application of postural alignments, selection of postural methods for correcting swallowing disorders during meals, prevention of secondary disorders (pressure ulcers, contractures), selection of orthoses | 290200 Adaptive electric bed 4-section 239410 Mechanical aneroid sphygmomanometer, Pen, paper, (other equipment: set of soft modules for the physical therapy room) 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis | 20 minutes | 0,1 | 10 |
A19.30.012 Physical therapy exercises using suspension systems | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,1 | 10 |
A23.30.012 Monitoring the effectiveness of physical therapy sessions | Monitoring the response of the cardiovascular and respiratory systems to physical exertion | Aneroid mechanical blood pressure monitor, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 2 |
A13.30.001 Self-care training | 2.25 Medical gloves 239410 Aneroid mechanical blood pressure monitor 136210 Standard hospital bed with electric drive 207820 Attendant-propelled wheelchair, foldable 208340 Attendant-propelled wheelchair with drive, foldable 116940 Massage table/couch, mains-powered (Bobat table) 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table 136940 Wipe for cleaning/disinfection of medical devices | 20 minutes | 0,1 | 2 |
Appendix A3-11. Methods used for functional electrical stimulation of muscles in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) For unresponsive patients, the following is used Behavioral Pain Scale (BPS) | Scales, pen, paper, electronic devices (smartphones) | 5 minutes | 0,1-0,3 | 3 |
A17.02.001 Muscle electrical stimulation | Prescription, administration, and monitoring of the patient's condition during the procedure | 335360 Multifunctional electrotherapy physiotherapy system | 20 minutes | 0,5 | 10 |
A17.13.001 Medicinal drug electrophoresis for microcirculation disorders | Prescription, administration, and monitoring of the patient's condition during the procedure | 335360 Multifunctional electrotherapy physiotherapy system | 20 minutes | 0,5 | 10 |
A17.13.002 Sinusoidal modulated current therapy (SMT therapy) for microcirculation disorders | Prescription, administration, and monitoring of the patient's condition during the procedure | 335360 Multifunctional electrotherapy physiotherapy system | 20 minutes | 0,5 | 10 |
A17.13.003 Supratonal frequency current therapy (ultratonotherapy) for microcirculation disorders | Prescription, administration, and monitoring of the patient's condition during the procedure | 335360 Multifunctional electrotherapy physiotherapy system 173300 Portable electromagnetic deep tissue stimulator | 20 minutes | 0,3-0,5 | 10 |
Appendix A3-12. Methods used for hardware-based (electromechanical and robotic) rehabilitation to improve arm function in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A23.30.023.001 Performing a single-bout physical exertion test of varying intensity | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,1 | 3 |
A19.30.012 Physical therapy exercises using suspension systems | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,3 | 10 |
A19.30.011 Biofeedback training based on ground reaction | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,1-0,3 | 10 |
A19.23.003.013 Biofeedback training based on hemodynamic parameters (blood pressure) in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5-0,7 | 10 |
A19.23.003.012 Biofeedback training based on muscle mechanogram parameters in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5-0,7 | 10 |
A19.23.003.010 Biofeedback training based on electroencephalography in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5-0,7 | 7 |
A19.23.003 Correction of motor function impairment using biofeedback | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,3 | 10 |
A19.23.003.001 Biofeedback training based on dynamographic parameters (force) in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.003.004 Biofeedback training based on goniographic parameters (joint angle) in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.003.005 Biofeedback training based on kinesiological pattern in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,1-0,3 | 10 |
A19.23.003.006 Biofeedback training based on linear displacement velocity in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.003.007 Biofeedback training based on angular displacement velocity in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.003.008 Biofeedback training based on linear acceleration in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.003.009 Biofeedback training based on angular acceleration in central nervous system and brain disorders | Performing the procedure, monitoring effectiveness and safety | 140790 Robotic medical cycle ergometer with biofeedback | 30 minutes | 0,5 | 10 |
A19.23.002.017 Robotic mechanotherapy in central nervous system and brain disorders | Administration Robotic devices featuring feedback and utilizing a gaming or virtual environment. Use of robotic devices to establish the foundation for using the arm in daily life | 207630 Robotic biofeedback gait training device with built-in synchronized electrical stimulation system, rehabilitation exoskeleton 147350 Robotic system for lower limb locomotor therapy and rehabilitation with body weight support 147370 Rehabilitation system with automatically controlled treadmill 122810 Manually operated treadmill/elliptical trainer device for gait function training 324120 Clinical virtual reality rehabilitation system, unsupported | 30 minutes | 0,5 | 10 |
A19.23.002.023 Mechanotherapy using motor-driven mechanotherapy devices in central nervous system and brain disorders | Use of robotic devices to establish the foundation for using the arm in daily life | 156650 External electrical stimulation system for gait improvement 102930 Continuous passive motion device for the hip/knee joint 149460 Continuous passive motion device for the ankle joint 208810 Passive motion device for the shoulder 208810 Passive motion device for the shoulder 110440 Continuous passive motion device for the hands/wrist joint 158620 Rehabilitation coordination training device 147360 Standard motorized treadmill 140790 Exercise bike 261950 Powered stair-climber exercise machine 261940 Non-powered stair-climber exercise machine 181010 Stationary vibration platform machine 213860 Non-powered parallel bars for gait training 156650 External electrical stimulation system for gait improvement | 30 minutes | 0,5 | 10 |
A23.30.012 Monitoring the effectiveness of physical therapy sessions | Monitoring the response of the cardiovascular and respiratory systems to physical exertion | Aneroid mechanical blood pressure monitor, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
Appendix A3-13. Methods used for the prevention of contractures, reduction of pain, and restoration of limb motor function in ischemic stroke patients with early spasticity
Nomenclature of Medical Services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A14.30.014 Pain intensity assessment | Assessment of pain syndrome for responsive and unresponsive patients using pain assessment scales | Scales, pen, paper, electronic devices (smartphone) Visual Analog Scale (VAS) for pain Behavioral Pain Scale (BPS) | 5 minutes | 0,1 | 3 |
A02.03.007 Measurement of major anatomical circumferences | Measurement of limb segment volumes in the presence of edema | 2.25 Medical gloves Measuring tape | 5 minutes | 0,1 | 1 |
A01.23.003 Palpation in pathology of the central nervous system and brain | Assessment of spastic muscle tone and muscle turgor using scales and calculation of botulinum toxin dose | Ashworth Scale (MAS) | 5 minutes | 0,1 | 3 |
A02.04.003 Measurement of joint mobility (goniometry) | Assessment of velocity-dependent range of motion in limb joints, | Tardieu Scale | 15 minutes | 0,05 | 2 |
A19.23.002.012 Procedures aimed at reducing spasticity | Use of postural positioning, correct patient positioning, kinesiotaping, and thermal procedures | tapes, orthoses, splints, Other equipment: set of weight cuffs set of soft modules | 30 minutes | 0,1 | 5 |
A17.30.037 Variable electrostatic field therapy | Use of stimulating factors for pain management and muscle tone reduction | Hivamat, infinitotherapy, Darsonvalization, ultratony therapy, | 10 minutes | 0,05 | 5 |
A24.01.005.003 Local cryotherapy | Use of cooling for pain management and muscle tone reduction | Cryo-kit, local cryotherapy devices | 5 minutes | 0,05 | 5 |
A21.03.002 Massage session in a massage chair/couch | Performance of medical massage techniques for pain management and muscle tone reduction | 182590 Physiotherapy massager Medical massage kit Massage couch | 20 minutes | 0,05 | 5 |
A19.23.001 Therapeutic exercise aimed at spasticity reduction | Formation of movement sequences in the limbs in the presence of spasticity. | 2.25 Medical gloves | 30 minutes | 0,05 | 5 |
A19.23.002.025 Physiotherapy exercise using apparatus and training devices for central nervous system and brain disorders | Practice of global limb movements and fine motor skills of the hands in the presence of spasticity. | 159790 Rehabilitation finger and hand exerciser 110440 Continuous passive motion device for hand/wrist joint 349710 Biofeedback-based passive hand mobilization device ARAT AMADEO ARMEO Artromot arm table, shoulder wheel Biofeedback devices and apparatus | 30 minutes | 0,05 | 5 |
I.m. botulinum toxin type A injection, including under ultrasound guidance | Administration of botulinum toxin therapy drugs into spastic muscles | syringes, ultrasound machine, botulinum toxin preparations | 20 | 0,05 | 1 |
Appendix A3-14. Methods used for active physical rehabilitation of ischemic stroke patients following botulinum toxin therapy
Nomenclature of Medical Services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Formation of movement sequences in the limbs in the presence of spasticity, including muscle stretching techniques within the physiological range. Motor function training | 2.25 Medical gloves 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis 136540 Standard wheeled non-folding walker 136520 Standard folding support walker 136530 Standard non-folding support walker 197850 Multi-point cane 116940 Powered table/couch | 30 minutes | 0,05 | 5 |
A19.23.005 Passive movements in joints within the physiological range without stretching | Formation of joint range of motion in the limbs. Prevention of learned non-use syndrome | 2.25 Medical gloves | 20 minutes | 0,05 | 5 |
A21.30.006 Occupational therapy | Scoring of cognitive activity and motor function using scales. Selection of rehabilitation assistive devices. Selection (fabrication) of limb orthoses. Adaptation of personal care items and training in their use. | COPM scale FIM scale Devices for fine motor skills and coordination recovery with functional assessment using biofeedback, polymeric materials, modeling clay. Specialized kit for item adaptation. Specialized stands for socio-domestic adaptation. Material for fabricating adaptive grips. Drawing material. | 30 min | 0,05 | 2 |
Appendix A3-15. Methods used for the complex therapy of post-stroke spasticity in ischemic stroke patients
Nomenclature of Medical Services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A14.30.014 Pain intensity assessment assessment of motor response | assessment of muscle contraction in response to a magnetic stimulus or M-wave in non-responsive patients | TMS, MS, rTMS | 5 | 0,05 | 10 |
A17.30.036 Pulsed low-frequency electromagnetic field therapy | Restoration of contractility in paretic muscles | Multimodal neuromiostimulation physical therapy system (MS) | 30 minutes | 0,05 | 10 |
A22.30.006 Vibrational therapy | Mechanical impact on spastic muscles by vibration method | 182590 Physiotherapeutic massager 216810 Pneumatic massager 181010 Stationary vibration platform trainer | 15 minutes | 0,05 | 10 |
Appendix A3-16. Methods used for the correction of neuropathic pain syndrome in patients with ischemic stroke
Nomenclature of medical services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
10A01.23.004 Examination of sensory and motor systems in pathology of the central nervous system and brain | Assessment of neuropathic pain | VAS scale LANSS scale McGill Pain Questionnaire Pain intensity questionnaires | 10 minutes | 0,05 | 2 |
Instrumental assessment of peripheral nerve status | Assessment of peripheral nerve trunks in neuropathic pain syndrome | Ultrasound examination ENMG | 20 min. | 0,05 | 1 |
A23.30.004 Formulation of a functional diagnosis | Determination of the state of functioning and restriction of activity and participation formulation of a rehabilitation diagnosis, goals and objectives of rehabilitation measures, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 0,05 | 1 |
A23.30.010 Determination of rehabilitation potential | Analysis of the state of functioning and restriction of activity and participation, development of an individual (personalized) medical rehabilitation program, maintenance of medical documentation | ICF, conclusions/recommendations of multidisciplinary rehabilitation team specialists, medical commission, medical and physical training unit, pen, paper, | 5 minutes | 0,05 | 1 |
Psychocorrection, counseling | ?? | ?? | ?? | ?? |
Appendix A3-17. Methods used for neurodevelopmental Bobath therapy in patients with ischemic stroke
Nomenclature of Medical Services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A19.23.002.014 Individual exercise therapy session for central nervous system and brain diseases | Formation of postural tonic reactions and movement stereotypes | 158620 Rehabilitation coordination training device Set of weights Metronome Tabletop mirror Wall-mounted mirror Full-length mirror Set of soft modules for exercise therapy room Wall bars Gymnastic bench Biofeedback equipment for the assessment and restoration of balance and equilibrium 147070 Tilt table | 30 minutes | 0,1 | 10 |
A19.30.014 Balanstherapy | Active verticalization training and balance control | 181010 Stationary vibration platform trainer | 30 minutes | 0,3 | 10 |
A19.30.011 Biofeedback training based on support reaction | Support and balance skills training and improvement of functional outcome | 228380 Stabilography system | 30 minutes | 0,3 | 10 |
A19.23.001 Active joint gymnastics with stretching | Application of active exercises with the formation of neurodevelopmental movement patterns | Set of weights Metronome Tabletop mirror Wall-mounted mirror Full-length mirror Set of soft modules for exercise therapy room Wall bars Gymnastic bench | 20 minutes | 0,3 | 10 |
A19.23.002.004 Individual exercise therapy session for aphasia, dysarthria | Training of neurodevelopmental patterns and locomotion | 147070 Mobile body weight support frame for walking 147370 Rehabilitation system with computer-controlled treadmill 122810 Manually operated treadmill/elliptical gait training device 147350 Robotic system for lower limb locomotor therapy and rehabilitation with body weight support 261940 Non-powered stair climber trainer | 30 minutes | 0,5 | 10 |
Appendix A3-18. Methods used for training to increase activities of daily living in patients with ischemic stroke
Nomenclature of Medical Services | Actions performed when applying the method | Nomenclature of medical equipment and consumables | Procedure duration | Frequency of procedures | Number of procedures (course) Stage 1 / Stage 2 |
A23.30.012 Monitoring the effectiveness of physical therapy sessions | Monitoring the reaction of the cardiovascular and respiratory systems to physical exertion | Mechanical aneroid sphygmomanometer, stopwatch. Pen, paper, electronic devices (smartphone) | 5 minutes | 0,1 | 10 |
A19.23.003.006 Linear movement speed biofeedback training for central nervous system and brain disorders | Training of movement patterns and locomotor skills to increase activities of daily living and restore personal skills | 147350 Robotic system for locomotor therapy and lower limb rehabilitation with body weight support 122810 Manually operated treadmill/elliptical gait training device 349710 Biofeedback-based passive hand mobilization device | 30 minutes | 0,1 | 9 |
A19.23.003.008 Linear acceleration biofeedback training for central nervous system and brain disorders | Training of movement patterns and locomotor skills | 159790 Rehabilitation finger and hand exerciser 110440 Continuous passive motion device for hand/wrist joint 349710 Biofeedback-based passive hand mobilization device 156650 External electrical stimulation system for gait improvement 102930 Continuous passive motion device for hip/knee joint 149460 Continuous passive motion device for ankle joint 208810 Passive shoulder exercise trainer (passive cyclic exercise trainer for the elbow joint) 110440 Continuous passive motion device for hand/wrist joint | 30 minutes | 0,1 | 9 |
A19.23.004 Correction of motor function impairment using computer technologies | Correction to increase activities of daily living | 158620 Rehabilitation coordination training device 207630 Robotic biofeedback trainer for gait restoration with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton | 30 minutes | 0,1 | 9 |
A14.30.017 Patient training in crutch transfer | Training in crutch transfer techniques | Crutches 213860 Non-powered parallel bars gait training device | 10 minutes | 0,5 | 2 |
A14.30.018 Patient training in self-care during transfer using an assistive device | Training in personal skills, increasing the patient's level of independence | Cane Walkers 213860 Non-powered parallel bars gait training device 136540 Standard wheeled non-folding walker 136520 Standard folding support walker 136530 Standard non-folding support walker 197850 Multi-point cane | 30 minutes | 0,1 | 9 |
A19.23.002.17 Robotic mechanotherapy for central nervous system and brain disorders | Conducting a session to increase the patient's daily activity and restore personal skills | 147350 Robotic system for locomotor therapy and lower limb rehabilitation with body weight support 122810 Manually operated treadmill/elliptical gait training device | 30 minutes | 0,1 | 9 |
A05.23.007 Stabilometry | Assessment of postural reaction and balance training | 228380 Stabilography system 228390 Platform for stabilography system | 20 minutes | 0,1 | 9 |
A19.30.011 Biofeedback training based on postural reaction | Correction of static balance and balance training | 207630 Robotic biofeedback training device for gait recovery with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton 207630 Robotic biofeedback training device for gait recovery with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton | 30 minutes | 0,1 | 9 |
A19.30.006.001 Training and functional assessment on exercise equipment | Assessment of exercise tolerance, training of personal skills and their correction | 147360 Standard motorized treadmill 140790 Motorized medical ergometer | 30 minutes | 0,1 | 9 |
A19.23.004 Correction of motor function impairment using computer technologies (virtual reality) | Training of personal skills and their correction | 324120 Clinical virtual reality rehabilitation system, unsupported 343660 Virtual reality rehabilitation system using mechanotherapy/electrical stimulation | 60 minutes | 0,5 | 9 |
Appendix A3-19. Methods used for body-weight-supported gait training using robotic and mechanical devices in patients with ischemic stroke, lower limb paresis, and balance and weight-bearing impairment
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.003.006 Biofeedback training based on linear displacement velocity in central nervous system and brain disorders | Formation and consolidation of balance control and weight-bearing function skills | 122810 Manually operated treadmill/elliptical gait training device | 30 minutes | 0,05 | 5 |
A19.30.011 Biofeedback training based on ground reaction | Weight-bearing function training during stair climbing | 261950 Motorized stair-climbing simulator | 30 minutes | 0,05 | 5 |
A19.23.002.023 Mechanotherapy using motor-driven mechanotherapy devices in central nervous system and brain disorders | Conducting a session aimed at practicing cyclic movements during walking | 147350 Robotic system for locomotor therapy and lower limb rehabilitation with body weight support 156650 External electrical stimulation system to improve gait | 30 minutes | 0,05 | 7 |
A19.23.002.017 Robotic mechanotherapy in central nervous system and brain disorders | Gait pattern correction with body weight reduction | 207630 Robotic biofeedback training device for gait recovery with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton 147350 Robotic system for locomotor therapy and lower limb rehabilitation with body weight support | 30 minutes | 0,05 | 5 |
Appendix A3-20. Methods used for cognitive rehabilitation in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A21.30.006 Occupational therapy | Training the patient in basic self-care and daily living skills | 156900 Patient room furniture Wrist orthosis 280370 Elbow orthosis 302530 Shoulder orthosis 208830 Elbow/wrist/hand orthosis 302580 Hand orthosis 106470 Bedside cabinet 184150 Overbed table 184150 Modeling clay Drawing materials Fine motor skills module Audio (music) listening equipment Mechanically height-adjustable activity table Kitchen furniture (floor cabinet, wall cabinet, wall shelf, kitchen table, dining table) Adapted kitchen and dining tableware Standard kitchen and dining tableware Hotplate or electric stove Microwave oven Sewing, embroidery, and minor clothing repair kit Mirror | 30 minutes | 0,05 | 9 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment, including the use of reminder devices and home safety measures | 4-section bed Disposable gloves Personal protective equipment Wrist orthosis 280370 Elbow orthosis 302530 Shoulder orthosis 208830 Elbow/wrist/hand orthosis 302580 Hand orthosis 106470 Bedside cabinet 184150 Overbed table 184150 Material for making adaptive grips (foam rubber, expanded polyethylene) Height-adjustable utility cabinet Computer desk Refrigerator Handwashing sink Toilet Washbasin Shower Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids | 30 minutes | 0,05 | 9 |
Appendix A3-21. Methods used to train compensatory cognitive skills in patients with AI
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A21.30.006 Occupational therapy | Training the patient in basic self-care and daily living skills | 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table Modeling clay Drawing materials Fine motor skills module Audio (music) listening equipment Mechanically height-adjustable activity table Kitchen furniture (floor cabinet, wall cabinet, wall shelf, kitchen table, dining table) Adapted kitchen and dining tableware Standard kitchen and dining tableware Hotplate or electric stove Microwave oven Sewing, embroidery, and minor clothing repair kit Mirror | 30 minutes | 0,05 | 9 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment, including the use of reminder devices and home safety measures. | 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table Material for making adaptive grips (foam rubber, expanded polyethylene) Height-adjustable utility cabinet Computer desk Refrigerator Handwashing sink Toilet Washbasin Shower Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids | 30 minutes | 0,05 |
Appendix A3-22. Methods used for the rehabilitation of AI patients with neglect syndrome
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A21.30.006 Occupational therapy | Sensory retraining; Training in bimanual self-care skills | Device for continuous passive motion of the hands/wrist joint Devices for fine motor skills and coordination recovery with functional assessment using biofeedback Modeling clay Specialized kit for object adaptation Specialized stands for social and domestic adaptation Mirror Bolsters Material for making adaptive grips Mechanically adjustable occupational therapy table Drawing materials Fine motor skills module Products for activities in the adaptive kitchen Wheelchair | 30 minutes | 0,05 | 9 |
Appendix A3-23. Methods used to restore independent mobility, communication, and self-care in patients with AI
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A14.30.015 Training of the patient's family members in patient transfer and/or positioning techniques in bed | Demonstration to family members of techniques for transferring the patient in bed, and moving them into a wheelchair and bedside armchair | 208710 Attendant-propelled wheelchair, non-folding 189290 High-back bedside armchair with removable armrests | 20 minutes | 0,07 | 2 |
A14.30.018 Patient self-help training for transfers using an assistive support | Selection of an assistive support and training in its use for independent mobility | 136540 Standard wheeled walker, non-folding 136520 Standard support walker, folding 136530 Standard support walker, non-folding 197850 Multi-point cane | 20 minutes | 0,07 | 2 |
A19.23.002.025 Exercise therapy using apparatuses and exercise machines in central nervous system diseases | Patient lifting and transfer | 209440 Mobile battery-powered patient lifting and transfer system | 30 minutes | 0,07 | 5 |
A13.30.001 Self-care training | Training the patient in basic washing, hair-combing, and dressing skills | 220280 Commode chair Wheelchair, Shirt-donning aids, Sock-donning aid, Tights-donning aid, Object grip thickening attachment. Specialized kit for daily living adaptation Specialized stands for social and domestic adaptation Mechanically adjustable occupational therapy table | 30 minutes | 0,05 | 7 |
A21.30.006 Occupational therapy | Development of bimanual skills in daily living | 3-section bed 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table Material for making adaptive grips (foam rubber, expanded polyethylene) Height-adjustable utility cabinet Computer desk Refrigerator Handwashing sink 220280 Commode chair Washbasin Shower Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids | 30 minutes | 0,07 | 7 |
Appendix A3-24. Methods used to perform mirror therapy in patients with AI
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.004 Correction of motor function impairment using computer technologies | Training and mastering motor skills for hand and finger grasping | Tabletop mirror, SensoRehab - "Sensor Glove" technology | 30 minutes | 0,05 | 5 |
Individual exercise therapy | Training and mastering motor skills for hand and finger grasping | Tabletop mirror | 10 minutes | 0,07 | 5 |
Appendix A3-25. Methods used for applying virtual reality technology in patients with AI
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A 19.23.004 Correction of motor function impairment using computer technologies | Practice of coordinated, precise, and targeted movements. Formulation of an action plan in accordance with the task. | 324120 Virtual reality rehabilitation system, unsupported, clinical 343660 Virtual reality rehabilitation system using mechanotherapy/electrostimulation | 30 minutes | 0,07 | 5 |
Appendix A3-26. Methods used for balance training in stroke patients with a high risk of falls
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.30.011 Biofeedback training based on ground reaction | Practice of static balance and postural reaction | 158620 Rehabilitation device for coordination training | 15 minutes | 0,05 | 5 |
A19.30.014 Balneotherapy | Practice of static balance and postural control | 158620 Rehabilitation device for coordination training | 15 minutes | 0,05 | 5 |
A19.30.013 Simulated walking with stabilization | Training in stair ascent and descent | 261950 Stair-climbing simulator (motorized) 261940 Stair-climbing simulator | 15 minutes | 0,05 | 5 |
A05.23.007 Stabilometry | Assessment of the effectiveness of static balance and postural reaction control | 228380 Stabilography system 228390 Platform for stabilography system | 30 minutes | 0,01 | 2 |
A19.23.003.005 Hardware statokinetic loads | Development of sustained weight-bearing function in various postures | 158620 Rehabilitation device for coordination training | 30 minutes | 0,05 | 5 |
Appendix A3-27. Methods used for upper extremity motor function recovery in stroke patients
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A13.29.001.001 Functional occupational therapy | Execution of tasks with restriction of movements of the unaffected limb | 110440 Continuous passive motion device for the hands/wrist joint 159790 Rehabilitation trainer for fingers and hands 349710 Trainer for passive hand mobilization with biofeedback Tabletop mirror | 20 minutes | 0,05 | 5 |
Appendix A3-28. Methods used for fine motor skill recovery of the upper extremity using robotic complexes in stroke patients
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.002.017 Robotic mechanotherapy in central nervous system and brain disorders | Restoration of global hand and finger functions using robotic technologies | 110440 Trainer for continuous passive mobilization of hands/wrist joint 349710 Trainer for passive hand mobilization with biofeedback | 20 minutes | 0,05 | 5 |
Appendix A3-29. Methods used to increase exercise tolerance in stroke patients
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.002.013 Terrain cure (walking therapy) | Use of walking, including with body weight support, for the prevention of deconditioning syndrome in patients | 147070 Mobile frame for body weight support during walking 122810 Manually operated treadmill/elliptical gait training device 156650 External electrical stimulation system to improve gait | 30 minutes | 0,05 | 5 |
A19.23.003.006 Training with biofeedback based on linear movement velocity in central nervous system and brain disorders | Restoration of proper gait pattern in patients using functional electrical stimulation, biofeedback control, and functional exoprosthetics of motor acts | 207630 Robotic biofeedback training device for gait recovery with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton | 20 minutes | 0,05 | 5 |
A19.23.003.13 Training with biofeedback based on hemodynamic parameters (blood pressure) in central nervous system and brain disorders | Inclusion of robotic cyclic trainers with automated hemodynamic monitoring of physical exertion into the comprehensive medical rehabilitation program | 140790 Bicycle ergometer | 20 minutes | 0,05 | 5 |
Appendix A3-30. Methods used for the selection of assistive rehabilitation devices in stroke patients
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A13.29.013 Microenvironment adaptation procedures | Use of shoulder and shoulder-elbow orthoses for upper extremity mobilization, as well as prevention and reduction of humeral head subluxation and hemiplegic shoulder pain | 208830 Shoulder orthosis 208850 Shoulder/elbow orthosis | 30 | 0,05 | 7 |
A14.30.016 Patient education in self-care for transfers in bed and/or wheelchair | Application of physical therapy and occupational therapy technologies to instruct the patient on the rules and methods of transferring from the bed to various types of wheelchairs, a high-back chair with adjustable tilt and removable armrests, a commode chair for eating, performing activities of daily living, hygiene procedures, and elimination, as well as transferring back from the chairs to the bed | 274560 Transport wheelchair, foldable 208340 Attendant-controlled wheelchair, foldable 189290 Reclining backrest chair 220280 Commode chair | 20 minutes | 0,05 | 5 |
Appendix A3-31. Physical therapy methods used to improve functional outcomes in stroke patients
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.002. Physical therapy for central nervous system and brain disorders | Performance of physical exercises for targeted practice of specific movements and integrating them into activities of daily living | Other equipment: set of weights, set of soft modules for the physical therapy gymnasium | 30 minutes | 0,05 | 5 |
A19.30.007 Physical therapy using exercise equipment | Execution of lower limb locomotor function recovery exercises according to an individually tailored program prescribed to the robotic system under conditions of complete or partial body weight support of the patient | 147350 Robotic system for locomotor therapy and lower limb rehabilitation with body weight support | 30 minutes | 0,05 | 5 |
A19.30.013 Simulated walking with stabilization | Application of specially designed exercises aimed at restoring walking skills using software-integrated functional electrical stimulation or a system of external robotic fixation of the lower extremities | 207630 Robotic biofeedback training device for gait recovery with an integrated synchronized electrical stimulation system, rehabilitation exoskeleton | 30 minutes | 0,05 | 5 |
A19.23.002.013 Terrain cure (terraintreatment) | Training sessions to improve gait pattern, speed, and safety using a treadmill that allows individual adjustment of movement speed and resistance force of the walking belt | 147360 Standard motorized treadmill | 30 minutes | 0,05 | 5 |
Appendix A3-32. Methods used in strength training in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.002. Physical therapy for central nervous system and brain disorders | Independent performance of special exercises for muscle strength training under the supervision of a medical exercise instructor or physical therapist (kinesiotherapist) | Other equipment: set of weights, dumbbells, therabands, gymnastic sticks, set of soft modules for the physical therapy gymnasium | 20 minutes | 0,05 | 5 |
A19.23.003.001 Training with dynamographic biofeedback (based on force) for central nervous system and brain disorders | Performance of specially selected strength exercises and physical tasks with a gradual transition from assisted mode to strength and endurance training, with simultaneous monitoring of dynamogram parameters | 110440 Trainer for continuous passive mobilization of hands/wrist joint 349710 Trainer for passive hand mobilization with biofeedback 140790 Bicycle ergometer 147370 Rehabilitation system with automatically controlled treadmill | 20 minutes | 0,05 | 5 |
A19.23.003.012 Training with muscle mechanogram biofeedback for central nervous system and brain disorders | Performance of specially selected strength exercises and physical tasks with a gradual transition from assisted mode to strength and endurance training, with simultaneous monitoring of mechanogram parameters | 140790 Cycle ergometer 122810 Manually operated treadmill/elliptical gait training device 349710 Trainer for passive hand mobilization with biofeedback | 20 minutes | 0,05 | 5 |
Appendix A3-33. Methods used to increase exercise tolerance in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A23.30.007 Determination of the cardiovascular system reaction type to physical exertion | Assessment of heart rate and blood pressure | 290200 Adaptive electric bed 4-section 239410 Mechanical aneroid sphygmomanometer, Pen, paper, electronic devices (smartphone) | 5 minutes | 0,3-0,1 | 4/3 |
A19.23.003.006 Training with linear movement speed biofeedback for central nervous system and brain disorders | 30 minutes | 0,05 | 5 | ||
A19.30.007 Medical gymnastics using exercise machines | 30 minutes | 0,05 | 5 | ||
A19.23.002.016 Mechanotherapy for central nervous system and brain disorders | Performance of cyclic exercises during walking | 147360 Standard motorized treadmill 140790 Cycle ergometer 261950 Motorized stair-climbing simulator 122810 Manually operated device for gait training on a treadmill/elliptical trainer | 30 minutes | 0,05 | 5 |
Appendix A3-34. Methods used for the treatment of developing contractures of the elbow and wrist joints in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A02.04.003 Joint mobility assessment (goniometry) | Examination with assessment of the range of motion in extremity joints | 181060 Manual goniometer Pen, paper, electronic devices (smartphone) | 10 minutes | 0,3-0,1 | 4/3 |
A21.01.004 Upper extremity massage | 30 minutes | 0,05 | 5 | ||
A15.02.001 Application of a bandage for muscle disorders (brace) | Application of an elastic bandage or kinesio tape | 20 minutes | 0,05 | 5 | |
A23.30.017 Postural correction | Positioning the body and extremities in physiological positions, application of postural alignments, prevention of secondary complications (pressure ulcers, contractures) | Adaptive motorized bed 4-section Powered massage table/couch (Bobat table) Mechanical aneroid blood pressure monitor, Pulse oximeter Other equipment: set of weights set of soft modules for the physical therapy gymnasium 106470 Hand orthosis 208850 Shoulder/elbow orthosis 106470 Hand orthosis 109670 Knee/ankle/foot orthosis (other equipment: set of soft modules for the physical therapy room) | 20 minutes | 0,1 | 5 |
A13.29.013 Microenvironment adaptation procedures | Adaptation of the patient's microenvironment (personal items used in minimal bodily self-care), training in the use of adapted items | 290200 Adaptive electric bed 3-section bed Disposable gloves Personal protective equipment 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside cabinet 184150 Bedside table Material for making adaptive grips (foam rubber, expanded polyethylene) | 20 minutes | 0,3 | 10 |
Appendix A3-35. Methods used to increase safety and enhance activity in daily living in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.30.012 Physical therapy exercises using suspension systems | 147350 Robotic system for locomotor therapy and lower extremity rehabilitation with body weight support | 30 minutes | 0,05 | 5 | |
147350 Robotic system for locomotor therapy and lower extremity rehabilitation with body weight support |
Appendix A3-35. Methods used in generalized or multifocal spasticity in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A14.30.014 Pain intensity assessment | Assessment of pain syndrome using a separator mark (VAS pain scale) | VAS scale Pen Paper Clipboard | 5 minutes | 0.1 | 2 |
Appendix A3-36. Methods used to improve instrumental activities of daily living skills in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A21.30.006 Occupational therapy | Patient training in self-care skills in lying, sitting, and standing positions using necessary assistive devices | 280370 Wrist orthosis 302530 Elbow orthosis 208830 Shoulder orthosis 302580 Elbow/wrist/hand orthosis 106470 Hand orthosis 184150 Bedside table Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids Computer desk Refrigerator Handwashing sink Toilet Washbasin Shower Audio (music) listening equipment Mechanically height-adjustable activity table Kitchen furniture (floor cabinet, wall cabinet, wall shelf, kitchen table, dining table) Adapted kitchen and dining tableware Standard kitchen and dining tableware Hotplate or electric stove Microwave oven Height-adjustable utility cabinet Wheelchair, walkers | 30 minutes | 0,07 | 7 |
A13.29.013 Procedures for microenvironment adaptation | Adaptation of the patient's microenvironment, including household appliances and personal items, to improve self-care learning, training in the use of adapted items | Material for making adaptive grips (foam rubber, expanded polyethylene) Height-adjustable utility cabinet Computer desk Refrigerator Handwashing sink Toilet Washbasin Shower Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids | 10 minutes | 0,05 | 5 |
A13.29.014 Procedures for macroenvironment adaptation | Training in the use of assistive devices and technologies for activities of daily living and occupational tasks | 106470 Bedside cabinet 184150 Bedside table Material for making adaptive grips (foam rubber, expanded polyethylene) Height-adjustable utility cabinet Computer desk Refrigerator Handwashing sink Toilet Washbasin Shower Specialized kit for daily living adaptation of immobile patients, including a toothbrush, hairbrush, and dressing assistance aids | 20 minutes | 0,05 | 3 |
Appendix A3-37. Methods used for the diagnosis and treatment of post-stroke shoulder pain in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 | |
A23.30.009 Elaboration of a therapeutic exercise program | Design of an individual exercise session plan | Physical therapy specialist workstation equipped with a personal computer and Internet access | 30 minutes | 0,1 | 1 | |
A21.23002 Reflexology in diseases of the central nervous system | Application of meridian and diagnostic methods to identify biologically active trigger points and performing an acupuncture session | 299040 Disposable sterile acupuncture needles | 15 minutes | 0,01 | 7 | |
A17.30.019 Variable magnetic field therapy | Application of a variable magnetic field targeting metabolic and trophic tissue processes to achieve anti-edematous, anti-inflammatory, and analgesic effects | 285040 Professional deep electromagnetic tissue stimulation system | 10 minutes | 0,01 | 7 | |
A17.30.034 Medicinal ultraphonophoresis | Utilizing the effects of ultrasound on biochemical and biophysical processes to achieve analgesic, anti-inflammatory, and antispasmodic effects, and to improve peripheral nerve conduction | 182600 Physiotherapy ultrasound system 275460 Universal gel for ultrasound examinations, electrophysiological studies, and therapy | 5 minutes | 0,01 | 7 | |
A21.01.004.002 Medical massage of the upper extremity | Other: talc, massage oil | 0,03 | 10 minutes | 5 | ||
A21.01.009.001 Massage of the lower extremity and lower back | Other: talc, massage oil | 0,03 | 10 minutes | 5 | ||
Appendix A3-38. Methods used to improve motor control and restore sensorimotor limb function in ischemic stroke patients with spastic hemiparesis
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.001 Active articular gymnastics with stretching | Active movements with muscle stretching within the physiological range | 116940 Mains-powered massage table/couch (Bobath table) Other equipment: set of weights set of soft modules for the physical therapy gymnasium | 10 minutes | 0,05 | 5 |
A19.23.002.012 Procedures aimed at reducing spasticity | Performance of goal-oriented movements with a high number of repetitions | 116940 Mains-powered massage table/couch (Bobath table) Other equipment: set of weights set of soft modules for the physical therapy gymnasium | 30 minutes | 0,05 | 5 |
A19.23.002.025 Therapeutic exercise using equipment and trainers in diseases of the central nervous system and brain | Performance of stimulating movements for the sensorimotor function of the upper extremity | 208810 Passive shoulder exercise device 110440 Continuous passive motion device for hands/wrist joint | 30 minutes | 0,05 | 5 |
A19.23.003 Correction of motor function impairments using biofeedback | Limb movement training with patient monitoring through task execution on a monitor screen | Robotic trainer with biofeedback | 30 minutes | 0,05 | 5 |
A19.23.004 Correction of motor function impairment using computer technologies | Correction of pathological (deficient) limb movement | Virtual reality rehabilitation system with mechanized support | 30 minutes | 0,05 | 5 |
A19.23.003 Correction of motor function impairments using biofeedback | Robotic trainer with biofeedback | 30 minutes | 0,05 | 5 | |
A19.23.002.017 Robotic mechanotherapy for diseases of the central nervous system and brain | Use of robotic devices for upper extremity function training with feedback and the application of a gaming or virtual environment | Biofeedback trainers Disinfectant | 30 minutes | 0,05 | 5 |
A19.23.002.023 Mechanotherapy using motor-driven mechanotherapeutic devices in diseases of the central nervous system and brain | Individual session: conducting the session, patient condition monitoring | Training on the THERA-Vital, MOTOmed, or Velokinez cycle ergometer | 30 minutes | 0,05 | 5 |
A19.23.002.012 Procedures aimed at reducing spasticity | Use of robotic devices to reduce upper limb muscle spasticity | Robotic trainers Disinfectant | 30 minutes | 0,05 | 5 |
A19.30.006 Mechanotherapy | Individual session: conducting the session, patient condition monitoring, dosed rhythmic repeated physical exercises on special apparatuses or devices | Mechanical exercise machines Disinfectant | 30 minutes | 0,05 | 5 |
A19.23.002.014 Individual therapeutic exercise session for diseases of the central nervous system and brain | Individual therapeutic exercise session for diseases of the central nervous system and brain (PNF, Bobath, Vojta) | Adaptive motorized bed Medical gloves Personal protective equipment Bobath couch | 30 minutes | 0,05 | 5 |
A21.30.006 Occupational therapy | Training in self-care skills Training in simple meal preparation and household cleaning Training in the performance of job duties | Elbow/wrist/hand orthosis Device for continuous passive motion of the hands/wrist joint Devices for fine motor skills and coordination recovery with functional assessment using biofeedback Modeling clay Specialized kit for object adaptation Specialized stands for social and domestic adaptation Mirror Bolsters Material for making adaptive grips Mechanically adjustable occupational therapy table Drawing materials Fine motor skills module Products for activities in the adaptive kitchen | 20 minutes | 0,05 | 5 |
Appendix A3-39. Transcutaneous electrical nerve stimulation (TENS) as an adjuvant method in the motor rehabilitation of patients with post-stroke arm paresis
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A17.30.006 Transcutaneous electrical nerve stimulation (TENS) | Utilizing the capacity of electric current to affect upper extremity muscles in order to restore strength and range of motion | 335360 Multifunctional electrotherapy physical therapy system 152210 Electrophysiotherapy and electrosurgery equipment | 15 minutes | 0,01 | 7 |
A14.30.014 Pain intensity assessment | Pain assessment for responsive patients using a visual analogue scale (VAS pain scale) | Scales, pen, paper, 2.25 Medical gloves electronic devices (smartphone) | 3 minutes | 0,01 | 1 |
Appendix: A3-40. Method of low-frequency passive neuromuscular electrical stimulation (NMES) or EMG-NMES of the wrist and finger flexors and extensors as an adjuvant method in the restoration of hand and finger movements in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A17.30.035 Electrical stimulation | Performing the procedure | Exam table Disposable gloves Personal protective equipment Electrical stimulation device Electrodes | 20 minutes | 0,05 | 5 |
A17.30.035.001 Biofeedback-assisted electrical stimulation | Performing the procedure | Exam table Disposable gloves Personal protective equipment Biofeedback electrical stimulation device Electrodes | 30 minutes | 0,05 | 5 |
Appendix A3-41. Methods using kinesthetic movement imagery technology with a brain-computer interface and a hand exoskeleton in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A19.23.003.010 Biofeedback training based on electroencephalography in central nervous system and brain disorders | Use of the brain-computer interface | Brain-computer interface device with biofeedback Electroencephalograph Robotic orthosis Computer monitor Software EEG cap Water-based gel Syringe Water-based scrub Disinfectant Cotton swabs Disposable wipes | 30 minutes | 0,05 | 5 |
A19.23.002.17 Robotic mechanotherapy for diseases of the central nervous system and brain | Use of the brain-computer interface using myography | Brain-computer interface device with biofeedback Robotic orthosis Myograph Electrodes Computer monitor Software Disinfectant | 30 minutes | 0,07 | 5 |
A19.23.004 Correction of motor function disorders using computer technologies | Preparation: explanation of the exercise technique Performing the procedure with biofeedback: - fixation of the arm with a robotic orthosis - placement of electrodes for EEG recording, corrective settings when performing the task methodology | Brain-computer interface device with biofeedback Robotic orthosis Myograph Electrodes Computer monitor Software Disinfectant | 40 minutes | 0,09 | 5 |
Appendix A3-42. Methods used for prescribing intermittent urinary catheterization in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A01.28.001 Collection of anamnesis and complaints in pathology of the kidneys and urinary system | Initial consultation | 2.25 Medical gloves | 10 minutes | 0,07 | 1 |
A01.28.002 Visual examination in pathology of the kidneys and urinary system | Initial consultation | 2.25 Medical gloves | 3 minutes | 0,07 | 1 |
A01.28.003 Palpation in pathology of the kidneys and urinary system | Initial consultation | 2.25 Medical gloves, 187160 Mobile examination/therapeutic procedure light 227960 Vaginal speculum, single-use 151550 Mechanical gynaecological examination/therapeutic procedure table 116940 Mains-powered massage table/couch | 3 minutes | 0,07 | 1 |
A01.28.004 Percussion in pathology of the kidneys and urinary system | Initial consultation | 2.25 Medical gloves, disposable gloves | 3 minutes | 0,07 | 1 |
A25.28.001 Prescription of medicinal products for diseases of the kidneys and urinary tract | Prescription of drugs for the treatment of urinary incontinence, infection suppression, and care products | 5 minutes | 0,07 | 1 |
Appendix A3-43. Methods used to determine residual urine volume in patients with ischemic stroke
Nomenclature of medical services | Procedure performed when using the method | Nomenclature of medical equipment, consumables | Procedure duration | Procedure frequency | Number of procedures (course) Phase 1 / Phase 2 |
A04.28.002.005 Ultrasound examination of the urinary bladder with determination of residual urine | Ultrasound examination using an ultrasound machine | 2.25 Medical gloves Ultrasound scanner | 20 minutes | 0,09 | 1 |
A04.28.002.005 Ultrasound examination of the urinary bladder with determination of residual urine | Ultrasound examination of residual urine using an ultrasound imaging system | 2.25 Medical gloves 146290 Bladder volume ultrasound imaging system | 10 minutes | 0,09 | 1 |
A11.28.007 Urinary bladder catheterization | Genital hygiene/antisepsis Insertion of a urethral catheter into the urinary bladder Evacuation of urine from the urinary bladder Removal of the urethral catheter | 2.25 Medical gloves, skin antiseptic 16.4 Urological catheters and related devices | 15 minutes | 0,07 | 10 |
Appendix A3-44. Methods used for the treatment of urinary incontinence in patients with acute ischemic stroke
Nomenclature Order 804n | Procedure | Equipment used (equipment, consumables) Order 788n | Procedure duration | Frequency of procedures | Number of procedures (course) |
A14.30.007 Perineal and external genitalia care for a severely ill patient | Perineal sanitation Changing the urine collection device | 2.25 Medical gloves, Skin antiseptic Diaper Pad Gauze wipes 16.1 Urethral barriers for the treatment of urinary incontinence in women Care products for patients with urinary incontinence (external catheters, urine collection bags, catheters, pads) | 15 minutes | 0,07 | 3 |
A14.28.001 Assisting a severely ill patient with urination | Assisting the patient onto a bedpan/commode, use of urine collection devices | 2.25 Medical gloves Urinal Bedpan/commode | 20 minutes | 0,07 | 1 |
A14.28.004 Assistance with urinary incontinence | Perineal sanitation, Changing the external catheter | 2.25 Medical gloves, Skin antiseptic External catheter Gauze wipes | 15 minutes | 0,07 | 1 |
A14.28.003 Cystostomy and urostomy care | Sanitation of the skin around the fistula tract | 2.25 Medical gloves, Skin antiseptic Gauze wipes Aseptic dressing | 15 minutes | 0,07 | 2 |
A14.28.002 Urinary catheter care | Cleansing the genitalia and indwelling urethral catheter with antiseptic or soapy water | 2.25 Medical gloves, Skin antiseptic Gauze wipes | 10 minutes | 0,07 | 5 |
A11.28.014 Collection of urine for laboratory testing | Collection of urine for laboratory testing | 2.25 Medical gloves, Skin antiseptic 5.2 In vitro diagnostic specimen containers/vessels Gauze wipes | 15 minutes | 0,07 | 2 |
A19.28.001.004 Electromyography-biofeedback training for kidney and urinary tract diseases | Preparing the patient for biofeedback therapy | 2.25 Medical gloves, Skin antiseptic Gauze wipes | 10 minutes | 0,07 | 3 |
A19.28.001.004 Electromyography-biofeedback training for kidney and urinary tract diseases | Placement of cutaneous or intracavitary sensors | 2.25 Medical gloves Ultrasound gel Skin electrodes Vaginal probe Vaginal probe 233780 Perineal electrostimulation system for urinary/fecal incontinence control | 30 minutes | 0,07 | 3 |
A19.28.001.004 Electromyography-biofeedback training for kidney and urinary tract diseases | Perineal sanitation after biofeedback therapy | 2.25 Medical gloves Skin antiseptic, Gauze wipes | 10 minutes | 0,07 | 3 |
Appendix B. Physician Action Algorithms
Fig. 1. Algorithm for deciding on reperfusion therapy in patients taking DOACs
Fig. 2. Algorithm for deciding on intravenous thrombolysis based on the time elapsed from symptom onset: * – automated mismatch assessment; ischemic core volume (rCBF < 30% (CTP) or ADC < 620 mm2/s (DWI)) < 70 ml; ratio of critical hypoperfusion zone volume (Tmax > 6 s (perfusion CT or MRI)) to core volume > 1.2; mismatch zone volume > 10 ml
Fig. 3. Algorithm for blood pressure correction in ischemic stroke. * – except when necessary based on comorbid pathology (e.g., aortic dissection, pulmonary edema, preeclampsia or eclampsia)
Fig. 4. Algorithm for diagnosing the main causes of ischemic stroke and ESUS
Fig. 5. Algorithm for initial antithrombotic therapy in ischemic stroke and TIA: *ABCD2 score risk
Appendix C. Patient Information
Information for the patient, patient's relatives, and caregivers
A stroke is an acute brain condition caused by the rupture or blockage of a blood vessel supplying blood to the brain.
Signs of a stroke include sudden weakness in the facial muscles or limbs, especially on one side of the body, sensory disturbances also frequently on one side, and difficulty speaking or understanding speech. In severe cases, loss of consciousness may occur.
The condition can be recognized on the spot immediately. The "FAST" test is used for this purpose. Ask the person to:
"F" (Face) – Smile. The smile may be uneven, the corner of the mouth on one side may point downward instead of upward, and the face may be drooping.
"A" (Arms) – Raise both arms. The arms may not rise equally, or one may not rise at all.
"S" (Speech) – Speak a simple sentence. Speech may be slurred, or the instruction may not be understood.
It is very important to note that all these symptoms occur SUDDENLY (ACUTELY)! If the person has difficulty performing any of these tasks, you must immediately call an ambulance, describe the symptoms, and inform the arriving paramedics of the time of symptom onset. Before the ambulance arrives, make the patient comfortable, with the head and shoulders elevated to prevent flexion, loosen restrictive clothing, and ensure a sufficient supply of fresh air. Do not give anything by mouth; treatment for a stroke patient is carried out exclusively in a hospital in a specialized department.
Following the inpatient treatment course upon discharge, the patient is advised to continue treatment, which includes medications to prevent a recurrent stroke. The patient must strictly follow all recommendations of the physician supervising them for the required period. If any new symptoms appear, seek medical attention immediately.
Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools
Appendix G1. National Institutes of Health Stroke Scale [101] for assessing neurological deficit severity in stroke patients
Original title: National Institutes of Health Stroke Scale
Source:
Adams, H. P., Davis, P. H., Leira, E. C., Chang, K-C., Bendixen, B. H., Clarke, W. R., Woolson, R. F., Hansen, M. D. (1999). Baseline NIH Stroke Scale score strongly predicts outcome after stroke: a report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology, 53, 126 -31.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess the severity of neurological deficit in stroke patients
Content:
1a. Level of consciousness. The examiner must assign the appropriate score even if assessment is difficult due to an endotracheal tube, language barrier, orotracheal trauma, or bandage. A score of three is given only if the patient has no motor response to painful stimuli (except for reflexive posturing). Ask the patient two or three general questions regarding the circumstances of their hospital admission. Based on the responses received, evaluate the results. Remember that the patient should not be helped.
0 = alert, responsive immediately to examination.
1 = drowsy, responsive to minor stimulation.
2 = stuporous, requires repeated stimulation to respond, or unresponsive requiring more intense stimulation to elicit a non-stereotypic motor response.
3 = comatose, response only via reflex motor acts, spontaneous movements, or complete unresponsiveness, atonia, areflexia.
1b. Level of consciousness. Questions. Ask the patient: "What month is it now? How old are you?" Close but incorrect answers are not counted. Patients with aphasia and/or decreased level of alertness who cannot answer the two questions correctly will receive 2 points. Patients who cannot speak due to endotracheal intubation, orotracheal trauma, severe dysarthria, a language barrier, or for other reasons (other than aphasia) will receive 1 point. Only the first attempt is scored; verbal and non-verbal assistance from the physician is not permitted.
0 = correct answer to both questions.
1 = correct answer to one question.
2 = incorrect answer to both questions.
1c. Level of consciousness. Commands. The patient must be asked to close and open their eyes, and to squeeze and release the hand of the non-paretic arm. If the patient's arm cannot be used for this assessment, another command may be substituted. If the patient cannot understand the commands, the task may be demonstrated to them. Patients with trauma, amputation, or another physical defect should be assessed using a single-step command. Only the first attempt is scored. Questions are also asked only once.
0 = both commands performed correctly.
1 = one command performed correctly.
2 = neither command performed correctly.
1. Gaze movements. Only horizontal eye movements are considered. Spontaneous or reflex (oculocephalic reflex) eye movements are assessed. Caloric testing is not permitted. If the patient has conjugate gaze deviation that the patient can overcome independently or with the help of triggering the oculocephalic reflex, a score of 1 is given. If the patient has an isolated paralysis of eye muscles innervated by the III, IV, or VI cranial nerve pairs, a score of 1 is given. Eye movements must be tested in all patients, including those with aphasia. Patients with ocular trauma, a bandage, preexisting blindness, or other visual acuity or visual field disorders must be examined by eliciting the oculocephalic reflex. To detect partial gaze paresis, it is recommended to establish eye contact with the patient and move from side to side relative to the patient.
0 = normal.
1 = partial gaze palsy, overcome voluntarily or by eliciting the oculocephalic reflex.
2 = forced deviation of the eyes not overcome by eliciting the oculocephalic reflex.
2. Visual fields. Visual fields (upper and lower quadrants) are tested separately. Finger counting or the sudden appearance of a visual stimulus (the examiner's finger) in the patient's visual field may be used if necessary. During testing, the patient must look at the examiner's face; however, if they track the movement of the fingers, this can be assessed as a normal positive reaction. In the presence of unilateral blindness or enucleation, visual fields are assessed in the healthy eye. In the presence of a clearly demarcated visual field defect in the form of upper- or lower-quadrant hemianopia, a score of 1 is given. If the patient is blind for any other reasons, a score of 3 is given. Synchronous bilateral stimulation must also be performed. If differences are revealed as a result (reduced visual field towards the affected eye), a score of 1 is given, and the test results are used to answer question No. 11. Two points correspond to cases of complete hemianopia, and the presence of any partial visual field disorder, including quadrant hemianopia, corresponds to 1 point.
0 = normal.
1 = partial hemianopia.
2 = complete hemianopia.
3 = bilateral hemianopia (blindness, including cortical blindness).
3. Facial palsy. Using verbal and non-verbal techniques, ask the patient to show their teeth, raise their eyebrows, close their eyes, and squeeze their eyes shut. Demonstration of these commands by the physician is permitted. Assess the symmetry of the grimace in response to a painful stimulus in patients who cannot understand you. If there is a facial bandage, orotracheal intubation, or other barriers, they should be removed (as far as possible) for the duration of the assessment.
0 = normal.
1 = minor paralysis, facial asymmetry in the form of flattening of the nasolabial fold, asymmetry when smiling.
2 = partial paralysis (partial or complete paralysis of the lower facial muscles).
3 = complete paralysis of the lower and upper facial muscles on one or both sides (complete absence of movement in the upper and lower facial muscles).
5a. Motor function in the upper extremities (left arm). The patient's limbs must be positioned as follows: arms extended (palms down) at an angle of 90° (if the patient is sitting) or 45° (if the patient is supine). Each limb is assessed in turn, starting with the non-paretic arm. Demonstration of the maneuver by the physician is permitted in patients with aphasia. Painful stimuli are not allowed. In the case of limb amputation or shoulder joint pathology, the examiner must enter UN (untestable) in the appropriate box. Clearly count aloud to ten and demonstrate the count on your fingers so that the patient can see it. Start counting as soon as you release the patient's limb.
0 = limb holds the 90° or 45° position for 10 seconds without downward drift.
1 = limb drifts down before the full 10 seconds, but does not hit the bed or other support.
2 = limb cannot sustain the raised position (drifts down to the bed or other support within 10 seconds), but has some effort against gravity.
3 = limb falls to the bed with no effort against gravity, minimal movement is present.
4 = no active movement.
UN = limb amputation or shoulder joint injury.
5b. Motor function in the upper extremity (right arm).
6a. Motor function in the lower extremities (left leg). Limbs are positioned accordingly: at an angle of 30° in the supine position. Demonstration of the maneuver by the physician is permitted in patients with aphasia. Painful stimuli are not allowed. Each limb is assessed in turn, starting with the non-paretic leg. Only in the case of limb amputation or hip joint pathology, the examiner must enter UN (untestable) in the appropriate box. Clearly count aloud to five and demonstrate the count on your fingers so that the patient can see it. Start counting as soon as you release the patient's limb.
0 = leg holds the 30° position for 5 seconds without downward drift.
1 = leg drifts down before the full 5 seconds, but does not hit the bed or other support.
2 = leg cannot sustain the raised position (drifts down to the bed or other support within 5 seconds), but has some effort against gravity.
3 = leg falls to the bed with no effort against gravity, minimal movement is present.
4 = no active movement.
UN = limb amputation or hip joint injury.
6b. Motor function in the lower extremity (right leg).
4. Limb ataxia. Unilateral cerebellar symptoms are assessed. The test is performed with eyes open. If there is any visual defect, test in the unaffected visual field. Ataxia will be absent in a patient who does not understand what is required or is paralyzed. In case of joint damage or limb amputation, UN (untestable) is assigned. Ask the patient to perform finger-nose, finger-finger, and heel-shin tests with both limbs. In case of blindness, the finger-finger test must be omitted. A patient with aphasia will often be able to perform the test normally if the examiner moves the limb beforehand.
0 = absent.
1 = present in one limb.
2 = present in two limbs.
5. Sensory loss. Only sensory loss due to the current condition is considered. The examiner must test as many areas of the patient's body as possible (face; arms, except hands; legs, except feet; trunk). Patients in a stupor and/or with aphasia are assigned 1 point; patients with brainstem stroke and bilateral sensory loss are assigned 2 points. If the patient does not respond to external stimuli and has tetraplegia, 2 points are assigned, just as when the level of consciousness is impaired to a coma.
0 = normal; no sensory loss.
1 = moderate sensory loss; the patient feels pinprick as less sharp or as dull on the affected side.
2 = severe to total sensory loss; the patient feels nothing (is not aware of being touched) in the face, arm, and leg.
6. Aphasia. The patient is asked to describe the attached picture, list the objects depicted on a sheet of paper, and read sentences from the attached list. If the patient is blind, they must name objects by taking them in their hand, repeat something after the examiner, or say something independently. An intubated patient should be asked to reply in writing. Three points should be assigned only if the patient does not respond to any command and does not answer questions. Mild aphasia is scored 1 point. To correctly choose between 1 and 2 points, use the provided materials; it is assumed that a patient who skips more than 2/3 of the items provided for this or completes a small number of simple commands will receive 2 points. In a comatose state, 3 points are assigned.
0 = no aphasia; normal.
1 = mild to moderate aphasia.
2 = severe aphasia.
3 = mute, global aphasia.
7. Dysarthria. If the patient's condition is assessed as normal, they should be able to speak adequately when responding to the examiner's request to read something or repeat words from the attached list. If signs of severe aphasia are observed in the patient, articulation clarity is assessed during spontaneous speech. Only if the patient is intubated or there is some other physical barrier to speech, the patient's condition is scored 9 points and the examiner must provide a clear written explanation of the reason why the patient's condition cannot be assessed. Do not tell the patient the reason for testing them.
Use the provided word list for all patients and do not inform them that you are performing a speech clarity test. As a rule, unclear pronunciation of one or more words is considered normal. Zero points are given to patients who read all words distinctly. Patients with aphasia or those who cannot read are evaluated based on the quality of their spontaneous speech or their repetition of words spoken aloud by the examiner. Two points are given when the patient is completely incomprehensible or remains mute.
0 = normal.
1 = mild to moderate dysarthria; the patient slurs at least some words and, at worst, can be understood with some difficulty.
2 = severe dysarthria; the patient's speech is so slurred as to be unintelligible in the absence of or out of proportion to any dysphasia, or is mute/anarthric.
UN = patient intubated or has other physical barrier to speech.
8. Extinction or inattention (formerly termed «neglect»). The information obtained during the previous tests is sufficient to detect neglect (inattention). If simultaneous bilateral visual stimulation cannot be performed due to severe visual impairment, but the response to cutaneous stimuli is normal, the patient's condition is considered normal. If the patient has aphasia but clearly shows attentive tracking of voice from both sides, the condition is considered normal. The presence of visual spatial neglect or anosognosia is regarded as abnormal. Since abnormalities are scored only when present, this item must always be tested.
It can be assumed that significant variability in examiner opinions is possible when scoring this item, as all neurologists use somewhat different methods for testing neglect. Therefore, to increase the reliability of the study, perform only simultaneous bilateral visual and tactile stimulation. For unilateral neglect of stimuli in both modalities, score inattention as 2; for unilateral neglect of stimuli in one modality, score as 1. If the patient is conscious but demonstrates any other pronounced type of neglect, score the level of inattention as 1.
0 = no abnormalities.
1 = depressed response (extinction, inattention) to simultaneous bilateral stimulation in one of the listed modalities (visual, tactile, auditory, spatial).
2 = marked unilateral extinction or extinction of stimuli in more than one modality; the patient does not recognize (fails to distinguish) their own hand or other landmarks on one side only.
Key (Interpretation): maximum score is 42. Absence of neurological deficit corresponds to 0 points.
Notes: scale items must be scored in order. Instructing the patient is not permitted, even if it contradicts normal clinical practice. The patient's first response is recorded. Only the patient's actual response is evaluated, not their (in your opinion) potential actions. All existing symptoms must be noted, including those that may have resulted from prior strokes.
To examine speech output, the patient is asked to describe events in a picture, name objects, and read sentences and words presented by the evaluating physician.
Appendix G2. PedNIHSS - Pediatric National Institutes of Health Stroke Scale
Russian Name: Pediatric National Institutes of Health Stroke Scale
Original Name: The Pediatric National Institutes of Health (NIH) Stroke Scale (PedNIHSS)
Source:
Beslow LA, Kasner SE, Smith SE, Mullen MT, Kirschen MP, Bastian RA, Dowling MM, Lo W, Jordan LC, Bernard TJ, Friedman N, DeVeber G, Kirton A, Abraham L, Licht DJ, Jawad AF, Ellenberg JH, Lautenbach E, Ichord RN. Concurrent validity and reliability of retrospective scoring of the Pediatric National Institutes of Health Stroke Scale. Stroke. 2012 Feb;43(2):341-5. doi: 10.1161/STROKEAHA.111.633305. Epub 2011 Nov 10. PMID: 22076000; PMCID: PMC3265644.
Shchederkina I.O., Vitkovskaya I.P., Koltunov I.E., et al. Stroke in children. Formation of a pediatric stroke registry: international and regional experience. Russian Journal of Pediatric Neurology 2018; 13(1):7—19.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for assessing the severity of neurological deficit in pediatric stroke patients
Content:
Sign | Points | Definition of Scale Score Values | ||||
|---|---|---|---|---|---|---|
1. Level of Consciousness: a) level of alertness | 0 | Alert | ||||
1 | Drowsy (lethargic, sleepy, but responds even to minor stimulus-command, question) | |||||
2 | Stupor (requires repeated, strong, or painful stimulation to make a movement or become temporarily accessible for contact) | |||||
3 | Coma (inaccessible for verbal contact, responds to stimuli only with reflex motor or vegetative reactions) | |||||
For children older than 2 years, this item is assessed as in adults. The examiner must elicit a response even if communication barriers are present, such as a language barrier, endotracheal tube, or oropharyngeal trauma. In children aged 4 months to 2 years, the score for this item must be multiplied by 3. Items 1b and 1c are not assessed in this age group. | ||||||
1. Level of Consciousness: b) answers to the questions "How old are you?" "Where is mom (or another close family member)?" | 0 | Correct answers to both questions | ||||
1 | Correct answer to one question | |||||
2 | Incorrect answers to both questions | |||||
The answer must be exact. Approximate answers are not counted. In aphasia or stupor, if the patient does not understand the meaning of the question, the item is scored 2 points. If the patient cannot speak due to endotracheal intubation, oropharyngeal trauma, severe dysarthria of any etiology, a language barrier, or for any other reason (not due to aphasia), the item is scored 1 point. Only the initial response is evaluated. Do not help the patient verbally or non-verbally. The primary family member must be present. The answer to the first question is considered correct if the child, according to their age (development), answers non-verbally by showing the corresponding number of years on their fingers. For the second question, the designation familiar to the child for the family member (mom, dad, etc.) should be used. The answer is counted if the child correctly points to or gazes intently at the named close person. | ||||||
1. Level of Consciousness: c) following commands: The patient is asked to close and open the eyes (first command), and show the nose (touch the nose) with the non-paretic hand (second command) | 0 | Performs both commands correctly | ||||
1 | Performs one command correctly | |||||
2 | Performs neither command correctly | |||||
The second command can be replaced with any other one-step command if the hands cannot be used. The response is scored even if an attempt was made but the patient could not complete it due to weakness. If the patient does not respond to verbal commands, they must be reinforced with pantomime. If executed, the result is scored as correct. Only the initial response is evaluated. | ||||||
2. Eye movements (tracking a toy, reflex hammer, or other object) | 0 | Normal | ||||
1 | Partial gaze palsy (no fixed ocular deviation) | |||||
2 | Fixed ocular deviation | |||||
Only horizontal eye movements are tested. Voluntary or reflexive (oculocephalic) movements are evaluated. Caloric testing is not performed. If the patient exhibits head and eye deviation to one side that can be overcome voluntarily or reflexively, the sign is scored as 1 point. With an isolated peripheral ophthalmoparesis (3rd, 4th, or 6th cranial nerve), the sign is scored as 1 point. In patients with eye trauma, eye patches, or baseline blindness, eye movements are tested using reflexive maneuvers. In partial gaze palsy, it is necessary to establish "eye-to-eye" contact and move from side to side relative to the patient | ||||||
3. Visual fields | 0 | No impairment | ||||
1 | Partial hemianopia | |||||
2 | Complete hemianopia | |||||
Visual fields (superior and inferior quadrants) are tested by confrontation, counting fingers (in children over 6 years old) or threatening gestures (in children from 4 months to 6 years old) from the periphery to the center of the gaze. Appropriate prompts can be given to patients, but if they look in the direction of the moving fingers, this can be considered normal. If one eye is blind or missing, the other eye is tested. A score of 1 is given only if a clear asymmetry (including quadrantanopia) is detected. If the patient is blind (for any reason), a score of 3 is given. Simultaneous bilateral stimulation is also assessed here, and if hemi-inattention is present, a score of 1 is given and the result is used in the "Hemi-inattention (neglect)" section. | ||||||
4. Facial palsy | 0 | No | ||||
1 | Mild (asymmetry) | |||||
2 | Moderate (complete or near-complete paralysis of the lower facial muscles) | |||||
3 | Complete (absence of movement in both upper and lower facial muscle groups) | |||||
The patient is asked (verbally or via pantomime) to show teeth, raise eyebrows, and close eyes tightly. If the patient cannot follow commands, a noxious stimulus is applied and the symmetry of the grimace is assessed. If there are any physical obstacles to assessing the sign (e.g., a facial bandage), they should be temporarily removed if possible. | ||||||
5a. Left arm motor function The patient is asked to hold the arm for 10 seconds at 90° of shoulder flexion if sitting, and at 45° of shoulder flexion if lying down | 0 | Arm does not drift | ||||
1 | The patient initially holds the arm in the specified position, then the arm begins to drift downward | |||||
2 | The arm begins to fall immediately, but the patient still offers some resistance against gravity | |||||
3 | The arm falls immediately; the patient is completely unable to overcome gravity | |||||
4 | No active movement | |||||
9 | See explanation below | |||||
5b. Right arm motor function The patient is asked to hold the arm for 10 seconds at 90° of shoulder flexion if sitting, and at 45° of shoulder flexion if lying down | 4 | No active movement | ||||
9 | See explanation below | |||||
2 | The arm begins to fall immediately, but the patient still offers some resistance against gravity | |||||
3 | The arm falls immediately; the patient is completely unable to overcome gravity | |||||
4 | No active movement | |||||
9 | See explanation below | |||||
6a. Left leg motor function The supine patient is asked to hold for 5 seconds the leg flexed at the hip joint and elevated at an angle of 30° | 0 | The leg does not drop for 5 seconds | ||||
1 | The patient initially holds the leg in the specified position, then the leg begins to drop | |||||
2 | The leg begins to fall immediately, but the patient still holds it up somewhat against gravity | |||||
3 | The leg falls immediately; the patient is completely unable to overcome gravity | |||||
4 | No active movement | |||||
9 | See explanation below | |||||
6b. Movements in the right leg The supine patient is asked to hold for 5 seconds the leg flexed at the hip joint and elevated at an angle of 30° | 0 | The leg does not drop for 5 seconds | ||||
1 | The patient initially holds the leg in the specified position, then the leg begins to drop | |||||
2 | The leg begins to fall immediately, but the patient still holds it up somewhat against gravity | |||||
3 | The leg falls immediately; the patient is completely unable to overcome gravity | |||||
4 | No active movement | |||||
9 | See explanation below | |||||
For items 5 and 6. If the child cannot perform the tasks due to lack of comprehension, limb strength is assessed by observing spontaneous movements or by passively positioning the respective limb according to the specified parameters (excluding the time limit). For patients with aphasia, use persistent verbal or gestural commands, but not painful stimuli. Each limb is tested separately, starting with the non-paretic arm. In the case of limb amputation, shoulder or hip joint arthrodesis, or immobilization, a score of "9" may be assigned; the reason for assigning a score of "9" must be documented. | ||||||
7. Limb ataxia coded as "U" in complete paralysis) | 0 | No | ||||
1 | Present in either the upper or the lower limb | |||||
2 | Present in both the upper and the lower limb | |||||
9 | See explanation below | |||||
This item is assessed to detect possible unilateral cerebellar involvement. Finger-nose (FN) and heel-shin (HS) tests are used. | ||||||
The patient is tested with eyes open. Ataxia is scored only if it is out of proportion to the degree of paresis. Ataxia is absent in complete limb paralysis or failure to understand the task. In case of limb amputation or arthrodesis, a score of "9" is assigned; the reason for assigning a score of "9" must be documented. In blindness, the FN test is performed from the position of maximum arm extension. In children under 5 years of age or with insufficient comprehension of the task, the FN test is replaced by touching a toy, and the HS test by kicking or pushing a toy or the examiner's hand with the foot. | ||||||
8. Sensory Tested using a pin | 0 | Normal | ||||
1 | Mildly decreased | |||||
2 | Significantly reduced | |||||
Assessed either by the patient's verbal response or by behavioral reaction to pain (grimacing or withdrawing the limb). In children too young for verbal contact, with aphasia, or in stupor, the item is graded based on behavioral reactions as "normal response", "slightly reduced response", and "significantly reduced response". Sensory loss is considered pathological if it is detected in different parts of the body (arm, leg, trunk, face). A score of 2 is assigned only if there is a clear reduction in (or absence of) response to a pinprick. In patients with aphasia or stupor, the item may be scored as "0" or "1". The item is scored as "2" in bilateral sensory loss (brainstem stroke), in tetraparesis, and in a comatose patient (scored as "3" on item 1a). | ||||||
9. Language | 0 | No aphasia | ||||
1 | Mild to moderate aphasia (naming errors, paraphasias). The patient has an obvious reduction in speech fluency and comprehension without significant limitation of expression. Discussion of presented materials is severely hindered, but the examiner can understand the patient's responses. | |||||
2 | Severe aphasia. Communication with the patient is severely hindered. To understand the patient, the listener is forced to guess and repeat questions. From the patient's words, the examiner cannot understand what is depicted in the pictures. | |||||
3 | Global aphasia (mutism) | |||||
For children 6 years of age and older. The patient is presented with an event picture to describe, cards with objects to name, and sentences and words to read (if it is known that the child could read before the illness). If visual impairment hinders test performance, the patient is asked to identify and describe an object placed in their hand, repeat a phrase, or talk about an event. If the patient is intubated, they are asked to write their answers. If the patient is in a coma, a score of "3" is assigned. For children aged 2 to 6 years: the item is assessed based on observation of speech activity during the examination. For children from 4 months to 2 years: the item is assessed based on auditory concentration and orienting reactions. | ||||||
10. Dysarthria | 0 | Normal articulation | ||||
1 | Mild to moderate dysarthria (slurs some words) | |||||
2 | Severe dysarthria (pronounces words almost unintelligibly or worse) | |||||
9 | ||||||
The patient is not told that articulation is being examined. The patient is asked to read or repeat words. With normal articulation, the patient speaks clearly and has no difficulty pronouncing complex sound combinations or tongue twisters. In aphasia, articulation is assessed in spontaneous speech. If articulation cannot be examined (intubation, facial trauma), a score of "9" is assigned and an appropriate note is made. | ||||||
11. Extinction and inattention (neglect) | 0 | No neglect | ||||
1 | Gives no response to visual, tactile, or auditory stimuli on one side | |||||
2 | Profound hemi-inattention (neglect) in more than one modality | |||||
Sensory hemi-inattention is defined as a perceptual disturbance on one half of the body (usually the left) when stimuli are applied bilaterally simultaneously in the absence of hemihypesthesia. Visual hemi-inattention is defined as a perceptual disturbance of objects in the left half of the visual field in the absence of left-sided hemianopia. For children 2 years of age and older. As a rule, data from previous sections are sufficient. If visual hemi-inattention cannot be examined due to visual impairment, and perception of painful stimuli is intact, the score is 0. If the patient has aphasia but non-verbally demonstrates attention to stimuli of various modalities, a score of "0" is assigned. Anosognosia indicates hemi-inattention. The conclusion "unable to examine" cannot be applied to this item. For children from 4 months to 2 years: if either motor or sensory deficit is detected during a general neurological examination, a score of 1 is assigned; if both motor and sensory deficits are detected, a score of 2 is assigned. | ||||||
Total score | ||||||
Interpretation: 1–4 points: minor stroke, 5–15 points: moderate stroke, 16–20 points: moderately severe stroke, 21–42 points: severe stroke.
The table and figure below present the stimulus material for PedNIHSS.
Table. PedNIHSS scale – Language testing
Repetition | The patient must repeat the following words/phrases after the examiner: — Stop. — Stop, then move. — If it rains, we will play at home. — The President of Russia lives in Moscow. |
Pronunciation | The patient is asked to read the words and sentences in Figure 24.3a |
Object naming | The patient is presented with Figure 24.3b with objects to name: clock, pencil, skateboard (skate, board), shirt, ball, bicycle |
Speech fluency and word retrieval | The patient is asked to describe the picture (Figure 24.3c) |
Appendix G3. Medical Research Council Scale
Russian title: Medical Research Council Scale
Original title: The Medical Research Council (MRC) Scale for Muscle Strength
Source:
Medical Research Council Scale, R. Van der Ploeg, et al 1984.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess muscle strength
Content:
Score | Range of motion |
|---|---|
5 | Muscle strength is intact (the examiner cannot flex/extend the limb) |
4 | Muscle strength is reduced, but contraction is sufficient, full range of motion against gravity and against full resistance |
3 | Moderate reduction in muscle strength (cannot overcome additional resistance applied by the examiner) |
2 | Marked muscle weakness (full range of motion with gravity eliminated, incomplete range of motion against gravity, unable to overcome resistance) |
1 | Severe weakness (faint muscle contraction) |
0 | Paralysis (no movement) |
Key (interpretation): muscle strength of the tested muscles is scored according to the data presented in the table.
Notes:
If the patient has marked cognitive deficits or speech disorders, it is necessary to observe the patient's limb movements and assess accordingly. Alternative communication sources can also be used.
This scale can be used to assess the strength of any muscle. The testing of all muscles is based on the principles of manual muscle testing. The specialist should know the position of the tested body part and which movement allows the tested muscle to be loaded to the maximum extent. The specialist ensures that agonist muscles are, as far as possible, "excluded" from the movement and the tested muscle is maximally "engaged" in the work.
Appendix G4. Modified Ashworth Scale
Russian title: Modified Ashworth Scale for clinical assessment of increased muscle tone in stroke patients
Original title: Modified Ashworth Scale (MAS)
Source:
Suponeva N.A., Yusupova D.G., Ilyina K.A., Melchenko D.A., Butkovskaya A.A., Zhirova E.S., Taratukhina A.S., Zimin A.A., Zaitsev A.B., Klochkov A.S., Lyukmanov R.Kh., Kotov-Smolenskiy A.M., Khizhnikova A.E., Gatina G.A., Kutlubaev M.A., Piradov M.A. Validation of the Modified Ashworth Scale in Russia. Annals of Clinical and Experimental Neurology. 2020;14(1):89–96. (In Russ.) DOI: 10.25692/ACEN.2020.1.10
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for clinical assessment of increased muscle
tone in stroke patients
Content:
Score | Description |
|---|---|
0 | No increase in muscle tone. |
1 | Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part(s) is moved in flexion or extension. |
1+ | Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the range of motion. |
2 | More marked increase in muscle tone through most of the range of motion, but affected part(s) easily moved. |
3 | Considerable increase in muscle tone, passive movement difficult. |
4 | Affected part(s) rigid in flexion or extension. |
Notes:
General information:
1. The patient should lie supine;
2. When testing a flexor muscle, place the limb in maximum flexion and take it to maximum extension in 1 second (say to yourself "one thousand and one");
3. When testing an extensor muscle, place the limb in maximum extension and take it to maximum flexion in 1 second (say to yourself "one thousand and one");
4. Determine the score using the rules below.
Before performing the assessment, ask the patient to relax.
Key (interpretation):
0 — no increase in muscle tone;
1 — slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion when the affected part is moved in flexion or extension;
1+ — slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the range of motion;
2 — more marked increase in muscle tone through most of the range of motion, but affected parts easily moved;
3 — considerable increase in muscle tone, passive movement difficult;
4 — affected parts rigid in flexion or extension.
The maximum score of 4 corresponds to a considerable increase in muscle tone. No increase in muscle tone corresponds to 0 points.
Appendix G5. Richmond Agitation–Sedation Scale
Russian title: Richmond Agitation-Sedation Scale
Original title: Richmond Agitation Sedation Scale (RASS)
Source:
Sessler CN, Gosnell MS, Grap MJ, Brophy GM, O’Neal PV, Keane KA, Tesoro EP, Elswick RK. The Richmond Agitation-Sedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002; 166 (10): 1338–1344.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess a patient's psychomotor agitation or the depth of sedation
Content:
+4 Combative | Overtly combative, violent, immediate danger to staff |
|---|---|
>+3 Very agitated | Pulls or removes tube(s) or catheter(s); aggressive |
+2 Agitated | Frequent non-purposeful movement, frequent dyssynchrony with ventilator |
+1 Restless | Anxious but movements not aggressive, vigorous, or purposeful |
0 Alert and calm | |
-1 Drowsy | Not fully alert, but has sustained awakening to voice (eye opening and contact) > 10 seconds |
-2 Light sedation | Briefly awakens to voice with eye contact < 10 seconds |
-3 Moderate sedation | Movement or eye opening to voice (but no eye contact) |
-4 Deep sedation | No response to voice, but movement to physical stimulation |
-5 Unarousable | No response to voice or physical stimulation |
Notes and interpretation:
RASS Assessment Procedure
1. Observe patient:
– if patient is alert, calm, and attentive – score 0;
– if patient exhibits behavior characterized by restlessness or agitation – score +1 to +4 using the criteria listed above in the description.
2. If patient is not alert, speak to patient in a loud voice and call by name to open eyes and look at you. Repeat as necessary. Ask patient to look at you.
– if patient has eye contact and sustains it for > 10 seconds – score -1;
– if patient has eye contact, but it is not sustained for 10 seconds – score -2;
– if patient moves in response to voice, except for eye contact – score -3.
3. If patient does not respond to voice, physically stimulate patient by shaking shoulder and/or rubbing sternum.
– if patient responds to physical stimulation with any movement – score -4;
– if patient does not respond to voice or physical stimulation – score -5.
The scale score depends on the patient's hearing and vision acuity and is not suitable for patients with severe impairments. The scale is most commonly used during mechanical ventilation to avoid excessive or insufficient sedative effects from medications.
If RASS is -4 or -5, the patient is unconscious; reassess later.
Appendix G6. Rivermead Mobility Index
Russian title: Rivermead Mobility Index for assessing patient walking and mobility
Original title: Rivermead Mobility Index (RMI)
Source:
Antonucci, G., Aprile, T., & Paolucci, S. (2002). Rasch Analysis of the Rivermead Mobility Index: A study using mobility measures of first-stroke inpatients. Arch Phys Med Rehabil, 83, 1442-1449.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess a patient's walking and mobility
Content:
№ | Skill | Question |
|---|---|---|
0 | Patient is immobile | What movements does the patient make during the day? |
1 | Turning in bed | Can you turn from your back onto your side without assistance? |
2 | Moving from lying to sitting | Can you sit up independently on the edge of the bed from a lying position? |
3 | Maintaining balance while sitting | Can you sit on the edge of the bed without support for 10 seconds? |
4 | Moving from sitting to standing | Can you stand up (from any chair) in less than 15 seconds and maintain a standing position near the chair for about 15 seconds (using your hands or assistive devices if required)? |
5 | Standing without support | Observe whether the patient can stand unsupported for 10 seconds |
6 | Transfers | Can you transfer from bed to chair and back without any assistance? |
7 | Walking indoors, including with assistive devices if necessary. | Can you walk 10 meters using assistive devices if needed, but without the help of another person? |
8 | Ascending stairs | Can you climb one flight of stairs without assistance? |
9 | Walking outdoors (on flat surfaces) | Can you walk outdoors on the sidewalk without assistance? |
10 | Walking indoors without assistive devices | Can you walk 10 meters indoors without a cane, brace, or the help of another person? |
11 | Picking up objects from the floor | If you drop something on the floor, can you walk 5 meters, pick up the dropped item, and return? |
12 | Walking outdoors (on uneven surfaces) | Can you walk outdoors on uneven surfaces (grass, gravel, snow, etc.) without assistance? |
13 | Taking a bath | Can you get in and out of a bath (shower) without supervision and wash yourself independently? |
14 | Climbing up and down 4 steps | Can you climb up 4 steps and descend without holding onto the handrail, using assistive devices if necessary? |
15 | Running | Can you run 10 meters without a limp in 4 seconds (fast walking is allowed)? |
Key (interpretation): the index value can range from 0 (inability to independently perform any voluntary movements) to 15 (ability to run 10 meters).
Notes: the index value corresponds to the score assigned to the question to which the physician can give a positive response regarding the patient.
Appendix G7. Modified Rankin Scale
Russian title: Modified Rankin Scale
Original title: The Modified Rankin Scale (mRS)
Source:
Suponeva N.A., Yusupova D.G., Zhirova E.S., Melchenko D.A., Taratukhina A.S., Butkovskaya A.A., Ilyina K.A., Zaitsev A.B., Zimin A.A., Klochkov A.S., Lyukmanov R.Kh., Kalinkina M.E., Piradov M.A., Kotov-Smolenskiy A.M., Khizhnikova A.E. Validation of the Modified Rankin Scale (mRS) in Russia. Neurology, Neuropsychiatry, Psychosomatics. 2018;10(4):36-39. (In Russ.)
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess general disability and the approximate degree of the patient's dependence on assistance from others
Content:
Score | Description |
|---|---|
0 | No symptoms |
1 | Despite the presence of symptoms of the disease, there are no signs of disability; the patient is able to carry out all usual duties and activities |
2 | Slight disability; the patient is unable to carry out all previous activities, but looks after own affairs without assistance |
3 | Moderate disability; requires some help, but is able to walk without assistance |
4 | Moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance |
5 | Severe disability; bedridden, incontinent and requiring constant nursing care and attention |
6 | Dead |
Key (interpretation):
0 points correspond to no symptoms at all.
1 point corresponds to no significant disability despite symptoms; able to carry out all usual duties and activities.
2 points correspond to slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance.
3 points correspond to moderate disability; requiring some help, but able to walk without assistance.
4 points correspond to moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance.
5 points correspond to severe disability; bedridden, incontinent and requiring constant nursing care and attention.
Notes: the evaluator should not attempt to separate disability due to stroke from disability due to other causes.
Appendix G8. Full Outline of UnResponsiveness (FOUR) Score
Russian title: Full Outline of UnResponsiveness Score for assessing the level of consciousness in intensive care unit patients
Original title: Full Outline of UnResponsiveness Score (FOUR)
Source:
Wijdicks E.F., Bamlet W.R., Maramattom B.V., Manno E.M., McClelland R.L. Validation of a new coma scale: the FOUR score. Ann Neurol 2005; 58: 585–593. DOI:10.1002/ana.20611. PMID: 16178024
Piradov M.A., Suponeva N.A., Ryabinkina Yu.V., Sergeev D.V., Legostaeva L.A., Yazeva E.G., Yusupova D.G., Luneva I.E., Domashenko M.A., Samorukov V.Yu., Zaitsev A.B., Zimin A.A., Polekhina N.V., Bundhun P., Ramchandani N.M., Ilyina K.A. [Full Outline of UnResponsiveness (FOUR) scale: linguocultural adaptation of the Russian version]. Annals of Clinical and Experimental Neurology 2019; 13(3): 000–000. DOI: 10.25692/ACEN.2019.3.7
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess the level of consciousness in intensive care unit patients
Content:
Eye Response (E) subscale
Score | Criterion |
|---|---|
4 | Spontaneous eye opening, patient tracks an object or blinks on command |
3 | Patient's eyes are open, but do not track an object |
2 | Patient's eyes are closed, but open in response to a loud voice |
1 | Patient's eyes are closed, but open in response to a painful stimulus |
0 | Patient's eyes remain closed despite a painful stimulus |
Motor Response (M) subscale
Score | Criterion |
|---|---|
4 | At the doctor's request, the patient shows a thumbs-up, makes a fist, or shows a V-sign with two raised fingers |
3 | Localizes pain |
2 | Flexion withdrawal response to pain |
1 | Extension response to pain |
0 | No response to pain or generalized myoclonic status epilepticus |
Brainstem Reflexes (B) subscale
Score | Criterion |
|---|---|
4 | Pupillary and corneal reflexes preserved |
3 | One pupil dilated and unreactive to light |
2 | Either pupillary or corneal reflex absent |
1 | Both pupillary and corneal reflexes absent |
0 | Pupillary, corneal, and cough reflexes absent |
Respiration (R) subscale
Score | Criterion |
|---|---|
4 | Regular, patient not intubated |
3 | Cheyne–Stokes, patient not intubated |
2 | Irregular, patient not intubated |
1 | Respiratory rate higher than the ventilator-set rate |
0 | Respiratory rate matches the ventilator-set rate or apnea is recorded |
Notes and interpretation:
Eye response (E). Assess the best response after at least three attempts to achieve the highest level of alertness. A score of E4 indicates at least three voluntary movements. If the patient's eyes are closed, open them and assess tracking of a finger or other object. In the presence of eyelid edema or facial trauma, detecting tracking with one eye open is sufficient. If horizontal tracking is absent, vertical tracking must be checked. Alternatively, recording blinking twice on command is sufficient. This helps identify locked-in syndrome, in which patients are conscious. A score of E3 indicates the absence of voluntary tracking. A score of E2 indicates the patient opens the eye to a loud voice. A score of E1 indicates eye opening in response to a painful stimulus. A score of E0 indicates the patient's eyes remain closed despite a painful stimulus.
Motor response (M). Score the best response of the upper extremities. A score of M4 indicates the patient can perform at least one of three movements with either hand (thumbs up, fist clasp, or the 'peace sign' with two raised fingers). A score of M3 indicates the patient localizes pain by touching the physician's hand in response to a painful stimulus over the temporomandibular joint or supraorbital nerve notch. A score of M2 indicates any flexion response of the arms to pain. A score of M1 indicates an extension response to pain. A score of M0 indicates no response to pain or generalized myoclonic status epilepticus.
Brainstem reflexes (B). Score the best response. Check pupillary and corneal reflexes. The corneal reflex is preferably tested by instilling 2–3 drops of sterile normal saline onto the cornea from a distance of 10–15 mm (this minimizes corneal trauma during repeated testing). Sterile cotton-tipped applicators can also be used. The cough reflex is assessed during tracheal suctioning. It should be tested only if both reflexes mentioned above are absent. A score of B4 indicates both pupillary and corneal reflexes are present. A score of B3 indicates one pupil is wide and fixed to light. A score of B2 indicates either the pupillary or corneal reflex is absent. A score of B1 indicates both reflexes are absent. A score of B0 indicates absence of pupillary, corneal, and cough reflexes (the latter tested via tracheal suctioning).
Respiration (R). Assess the spontaneous breathing pattern in a non-intubated patient. A score of R4 indicates regular breathing. A score of R3 indicates Cheyne-Stokes breathing. A score of R2 indicates irregular breathing. In mechanically ventilated patients, assess the airway pressure waveform during the patient's spontaneous breaths or ventilator triggering in response to an inspiratory effort (score of R1). To determine spontaneous breathing efforts in a ventilated patient, evaluate the breathing pattern displayed on the ventilator monitor. Ventilator settings should not be changed during the assessment, but evaluation is recommended at a normal PaCO2 level. A score of R0 indicates the patient's respiratory rate matches the ventilator set rate, and a standard apnea test may be required.
Appendix G9. Glasgow Coma Scale
Russian title: Glasgow Coma Scale for assessing the level of consciousness in intensive care unit patients
Original title: The Glasgow Coma Scale (GCS)
Source: https://www.glasgowcomascale.org
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: Intended to assess the degree of impaired consciousness and coma. The scale consists of three tests evaluating eye opening (E), verbal (V), and motor (M) responses.
Content:
Eye Opening (E) subscale.
Criterion | Response to stimulus | Points |
|---|---|---|
Spontaneous | No stimulus required | 4 |
To normal or loud voice | To sound | 3 |
To nailbed pressure | To pressure | 2 |
Absent with auditory and painful stimuli, in the absence of other factors hindering eye opening | No response | 1 |
Factor present that interferes with eye opening | Not testable | Not testable |
Verbal Response (V) subscale.
Criterion | Response to stimulus | Points |
|---|---|---|
States name, oriented in space and time | Oriented | 5 |
Disoriented, but able to converse freely | Disoriented | 4 |
Utters single words | Inappropriate words | 3 |
Produces incomprehensible sounds | Incomprehensible sounds | 2 |
Makes no sounds in the absence of interfering factors | No response | 1 |
Factors present that interfere with verbal communication | Not testable | Not testable |
Motor Response (M) subscale.
Criterion | Response to stimulus | Points |
|---|---|---|
Performs a two-step command according to the physician's instructions | Obeys commands | 6 |
Raises arm above clavicle when the physician applies pressure to the trapezius muscle or supraorbital notch | Localizes pain | 5 |
Rapid elbow flexion in response to pain, predominant signs of normal flexion | Normal flexion | 4 |
Elbow flexion in response to pain, predominant signs of abnormal flexion | Abnormal flexion | 3 |
Elbow extension | Extension | 2 |
Patient's arms and legs do not move in response to pain in the absence of interfering factors | No response | 1 |
Presence of limb paresis or another factor preventing movement | Not testable | Not testable |
Notes.
The obtained assessment results are recorded as an alphanumeric code (e.g., E2V3M4).
Presenting the Glasgow Coma Scale results with a breakdown of each individual category was deemed the most correct approach. Interpreting the total Glasgow Coma Scale score as representing a specific level of impaired consciousness is not valid and is not recommended.
Principles of patient assessment using the GCS:
1. Check. Assess whether there are factors hindering communication, ability to respond, or other injuries.
2. Observation. Observe eye opening, speech content, and movements of the right and left limbs.
3. Stimulation. Auditory stimulus: response to a normal or loud voice. Pain stimulus: pressure on the nail bed, trapezius muscle, or supraorbital notch.
4. Assessment. Score the best response.
Interpretation:
15 points – clear consciousness
10–14 points – moderate and deep obtundation
8–10 points – stupor
6–7 points – moderate coma
4–5 points – terminal coma
3 points – brain death
Appendix G10. Pediatric Glasgow Coma Scale
Russian title: Pediatric Glasgow Coma Scale (for children under 4 years of age)
Original title (if applicable):
Source:
Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974,
Morray JP et al: Coma scale for use in brain-injured children. Critical Care Medicine 12:1018, 1984. doi: 10.1097/00003246-198412000-00002 [152, 153]
Type: rating scale
Purpose: to assess the level of consciousness
Content (template):
Eye opening | Verbal response | Motor response |
|---|---|---|
1 - none | 1 – absent | 1 - absent |
2 - to pain | 2 - does not calm when crying, agitated | 2 - abnormal extension to pain |
3 - to sound | 3 - calms down briefly when crying, moans | 3 – abnormal flexion to pain |
4 - spontaneous | 4 - child can be soothed when crying, interactive impaired | 4 - withdrawal to pain |
5 - child smiles, responds to sound, tracks objects, interactive | 5 - localization of pain | |
6 - follows commands |
Key (interpretation):
Scores are summed up. Possible result from 3 to 15.
15 points – alert
13–14 points – mild obtundation
11–12 points – moderate obtundation
9–10 points – stupor
7–8 points – moderate coma
4–6 points – deep coma
3 points – terminal coma
Appendix G11. Sepsis-related Organ Failure Assessment scale for dynamic evaluation of organ dysfunction in patients with sepsis admitted to intensive care units
Russian title: Sepsis-related Organ Failure Assessment scale for dynamic evaluation of organ dysfunction in patients with sepsis admitted to intensive care units
Original title: Sequential Organ Failure Assessment (SOFA)
Source:
Bell D, Sequential Organ Failure Assessment score. Reference article, Radiopaedia.org (Accessed on 13 Sep 2024) https://doi.org/10.53347/rID-75603
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess organ failure, mortality risk, and sepsis in patients in the intensive care unit.
Content:
Score | Lungs | Coagulation | Liver | Cardiovascular system | Central nervous system | Kidneys |
|---|---|---|---|---|---|---|
PaO2/FiO2 | Platelets | Bilirubin | BP, Inotropes | By Glasgow | Creatinine or urine output | |
1 | <400 | <150 | 20–32 | MAP < 70 without inotropes | 13–14 | 110–170 |
2 | <300 | <100 | 33–101 | Dopamine < mcg/kg/min, or Dobutamine | 10–12 | 171–299 |
3 | <200 | <50 | 102–204 | Dopamine > 5 mcg/kg/min, or epinephrine < 0.1 mcg/min | 0–9 | 300–440 and/or urine output per 24 hours < 500 ml |
4 | <100 | <20 | >204 | Dopamine > 15 mcg/kg/min, or epinephrine > 0.1 mcg/min | <6 | > 440 and/or urine output per 24 hours < 200 ml |
Key (interpretation): The SOFA scale is based on the assessment of dysfunction in six organ systems: respiratory, cardiovascular, hepatic, coagulation, renal, and neurological, ranging from mild dysfunction (0 points) to severe failure (4 points). The total SOFA score is the sum of the scores of all 6 parameters. The higher the total score, the more pronounced the multiple organ dysfunction.
A total score of 12 or less suggests multiple organ dysfunctions, 13–17 points suggests progression from dysfunction to failure, and a score around 24 indicates a high probability of death.
Notes:
– PaO2 – partial pressure of oxygen in arterial blood, mmHg;
– FiO2 – fraction of inspired oxygen, % (0.21–1.00);
– PaO2/FiO2 – oxygenation index, mmHg;
– platelets – × 109/L;
– bilirubin – µmol/L;
– MAP – mean arterial pressure. Formula for calculating mean arterial pressure: Mean BP = Diastolic BP + (Systolic BP – Diastolic BP) / 3;
– adrenergic drugs prescribed for at least 1 hour at a dose of mcg/kg/min;
– CNS – score on the Glasgow Coma Scale;
– creatinine – µmol/L.
Appendix G12. Alberta Stroke Program Early CT Score (ASPECTS)
Alberta Stroke Program Early CT Score (ASPECTS)
Russian title: Scale for standardization of detection and description of the extent of hypodense areas of ischemic brain injury in the middle cerebral artery territory on computed tomography scans
Original title:
Alberta stroke Program early CT score (ASPECTS)
Source:
Sair H, Hacking C, Sharma R, et al. Alberta stroke programme early CT score (ASPECTS). Reference article, Radiopaedia.org (Accessed on 13 Sep 2024) https://doi.org/10.53347/rID-4936
Andropova P.L., Gavrilov P.V., Savintseva Z.I. ASPECTS scale: inter-rater agreement among radiologists. Diagnostic Radiology and Radiotherapy. 2022;13(1):7-13.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for standardizing the detection
and description of the extent of hypodense areas of ischemic brain injury
in the middle cerebral artery territory on computed tomography scans
Content:
Key: in the absence of changes, the scale score is 10 points. One point is subtracted for each area showing signs of early ischemic changes. A score of 0 points indicates diffuse involvement of the entire middle cerebral artery territory.
Notes: ASPECTS is a 10-point topographic non-contrast head CT scale used in patients with ischemic stroke in the middle cerebral artery (MCA) territory. The scale is not valid for assessing lesions in the vertebrobasilar system.
The middle cerebral artery territory on two axial slices (one at the level of the thalamus and basal ganglia, and the other rostrally, immediately above the basal ganglia) is divided into 10 regions.
Assessed regions:
C – caudate nucleus,
L – lentiform nucleus,
IC – internal capsule,
I – insular cortex,
M1 – anterior MCA cortex or opercular area,
M2 – middle MCA cortex or anterior temporal area,
M3 – posterior MCA cortex,
M4 – anterior superior MCA territory,
M5 – middle superior MCA territory,
M6 – posterior superior MCA territory.
Regions M1–M3 are at the level of the basal ganglia, and regions M4–M6 are at the ventricular level immediately above the basal ganglia.
Appendix G13. Paradoxical Embolism Risk Score
Russian title: The Risk of Paradoxical Embolism Score for determining the probability of a causal relationship between patent foramen ovale and cryptogenic stroke
Original title: The Risk of Paradoxical Embolism (The RoPE) Score
Source:
Kent DM, Saver JL, Ruthazer R, Furlan AJ, Reisman M, Carroll JD, Smalling RW, Jüni P, Mattle HP, Meier B, Thaler DE. Risk of Paradoxical Embolism (RoPE)-Estimated Attributable Fraction Correlates With the Benefit of Patent Foramen Ovale Closure: An Analysis of 3 Trials. Stroke. 2020 Oct;51(10):3119-3123. doi: 10.1161/STROKEAHA.120.029350. Epub 2020 Sep 14. PMID: 32921262; PMCID: PMC7831886.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for determining the probability of a causal relationship between patent foramen ovale and cryptogenic stroke
Content:
RoPE score parameters | Score |
|---|---|
No history of hypertension | +1 |
No history of diabetes mellitus | +1 |
No history of stroke/TIA | +1 |
Non-smoker | +1 |
Cortical infarct on neuroimaging | +1 |
Age, years: | |
18–29 | +5 |
30–39 | +4 |
40–49 | +3 |
50–59 | +2 |
60–69 | +1 |
70 and over | 0 |
Key: the highest probability is observed when the scale score is above 5 points (6 points – 62%, 7 points – 72%, 8 points – 84%, 9–10 points – 88%). Conversely, the risk of recurrent stroke within 2 years decreases with an increasing scale score: from 20% at 0–3 points to 2% at 9–10
Notes: points. The maximum score is 10 points.
Appendix G14. CHA2DS2-VASc scale for assessing the risk of thromboembolic complications in patients with atrial fibrillation/atrial flutter
Russian title: Scale for assessing the risk of thromboembolic complications in patients with atrial fibrillation/atrial flutter
Original title: The CHA2DS2-VASc score
Source:
Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ (2001). "Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation". JAMA. 285 (22): 2864–70. doi:10.1001/jama.285.22.2864.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for predicting the risk of ischemic stroke and systemic thromboembolism in patients with atrial fibrillation
Content:
Scoring system for risk factors of stroke and systemic thromboembolism in patients with atrial fibrillation.
CHA2DS2-VASc criteria | Score |
|---|---|
Heart failure / left ventricular dysfunction | 1 |
Arterial hypertension | 1 |
Age ³75 years | 2 |
Diabetes mellitus | 1 |
Stroke / TIA / thromboembolism | 2 |
Vascular disease (myocardial infarction, peripheral arterial disease, or aortic plaque) | 1 |
Age 65–74 years | 1 |
Female sex | 1 |
Key:
Risk of stroke within one year
Score | Stroke rate (% per year) |
|---|---|
0 | 0.0 |
1 | 1.3 |
2 | 2.2 |
3 | 3.2 |
4 | 4.0 |
5 | 6.7 |
6 | 9.8 |
7 | 9.6 |
8 | 6.7 |
9 | 15.2 |
Appendix G15. HAS-BLED bleeding risk score in patients with atrial fibrillation
Russian title: Bleeding risk score in patients with atrial fibrillation for predicting the risk of major bleeding within one year
Original title (if applicable): The HAS-BLED Score
Source:
Vázquez E, Sánchez-Perales C. The HAS-BLED score and renal failure. Chest. 2011 May;139(5):1248-1249. doi: 10.1378/chest.10-2961. PMID: 21540225.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify)
Purpose: for predicting the risk of major bleeding within one year
Content:
HAS-BLED criterion | Score |
|---|---|
Hypertension (SBP >160 mmHg) | 1 |
Abnormal renal and liver function (1 point each) | 1 or 2 |
Stroke | 1 |
History of bleeding | 1 |
Labile INR | 1 |
Elderly age (over 65 years) | 1 |
Drugs or alcohol (1 point each) | 1 or 2 |
Key: ≥ 3 points – high bleeding risk,
1–2 points – low bleeding risk.
Notes: maximum 9 points
Appendix G16. Modified Treatment in Cerebral Infarction (mTICI) Scale
Russian title: Modified Treatment in Cerebral Infarction (mTICI) scale for assessing blood flow restoration on cerebral angiograms after endovascular revascularization in patients with acute ischemic stroke.
Original title: Modified treatment in cerebral infarction (mTICI) Score
Source:
Coulthard A, Worsley C, Alhusseiny K, et al. Modified treatment in cerebral infarction (mTICI) score. Reference article, Radiopaedia.org (Accessed on 13 Sep 2024) https://doi.org/10.53347/rID-43526
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess blood flow restoration on cerebral angiograms after endovascular revascularization in patients with acute ischemic stroke
Content:
Grade | Angiographic characteristics of blood flow restoration grades |
|---|---|
0 | No perfusion |
1 | Antegrade reperfusion past the initial occlusion, with minimal or slow filling of the distal branches |
2a | Antegrade reperfusion in less than half of the target occluded artery's vascular territory (e.g., in one major branch of the middle cerebral artery and its corresponding territory) |
2b | Antegrade reperfusion in more than half of the target occluded artery's vascular territory (e.g., in two major branches of the middle cerebral artery and their corresponding territories) |
2c | Nearly complete perfusion except for slow flow or distal emboli in a small number of distal cortical vessels |
3 | Complete antegrade reperfusion of the occluded target artery with no occlusion of any distal branches |
Key (interpretation):
0 — no perfusion;
1 — antegrade reperfusion past the initial occlusion with limited filling of distal branches and minimal or slow distal reperfusion;
2a — antegrade reperfusion of less than half of the previously ischemic territory of the occluded target artery (one major MCA branch and its territory);
2b — antegrade reperfusion of more than half of the previously ischemic territory of the occluded target artery (two major MCA branches and their territories);
2c — near-complete reperfusion with slow flow in distal branches or distal embolization in isolated distal branches;
3 — complete antegrade reperfusion of the previously ischemic territory of the occluded target artery with no visible occlusion in all distal branches.
Appendix G17. ABCD2 score for stroke risk assessment after transient ischemic attack
Russian title: Stroke risk assessment scale following transient ischemic attack (TIA)
Original title: The ABCD2 Score (Age, Blood pressure, Clinical features, Duration of symptoms, Diabetes mellitus)
Source:
Rothwell PM, Giles MF, Flossmann E, et al. A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet. 2005 Jul 2-8;366(9479):29-36. PubMed.
Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007 Jan 27;369(9558):283-92. PubMed.
Chandratheva A, Mehta Z, Geraghty OC, Marquardt L, et al. Population-based study of risk and predictors of stroke in the first few hours after a TIA. Neurology. 2009 Jun 2;72(22):1941-7. PubMed.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: to assess stroke risk following a transient ischemic attack (TIA)
Content:
Characteristics | Numeric scoring |
|---|---|
Age over 60 years | 1 |
Diabetes mellitus | 1 |
Systolic BP > 140 mmHg or diastolic BP > 90 mmHg | 1 |
Duration | = > 60 minutes (2 points), 10–59 minutes (1 point) |
Speech disturbance without other focal symptoms | 1 |
Focal symptoms | 2 |
Key. ABCD2 risk groups: low risk = 0–3 points; moderate risk = 4–5 points; high risk = 6–8 points.
Risk of stroke within 2, 7, and 90 days after TIA
according to the ABCD2 risk category
Risk group | Stroke within 2 days | Stroke within 7 days | Stroke within 90 days |
|---|---|---|---|
Low (0–3 points) | 1,0 % | 1,2 % | 3,1 % |
Moderate (4–5 points) | 4,1 % | 5,9 % | 9,8 % |
High (6–8 points) | 8,1 % | 12 % | 18 % |
Appendix G18. Bleeding risk score
Russian title: Bleeding risk scale for assessing bleeding risk
Original title: IMPROVE Bleeding Risk Score
Source (official website of the developers, validation publication):
Validation of the IMPROVE bleeding risk assessment model in surgical patients: Results from the DissolVE-2 Study. Zhang, Zhu et al., Thrombosis Research, Volume 223, 69 - 77
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for bleeding risk assessment
Content (template):
Parameter | Score |
|---|---|
Age, years | |
≥85 | 3,5 |
40–84 | 1,5 |
<40 | 0 |
Sex | |
Masculine | 1 |
Feminine | 0 |
Renal function | |
GFR ≥ 60 mL/min/1.73 m2 | 0 |
GFR 30–59 mL/min/1.73 m2 | 1 |
GFR < 30 mL/min/1.73 m2 | 2,5 |
Liver function | |
INR ≤ 1.5 | 0 |
INR > 1.5 | 2,5 |
Platelet count | |
≥50 ∙ 109/L | 0 |
<50 ∙ 109/L | 4 |
Admission to step-down unit or ICU | 2,5 |
Central venous catheter | 2 |
Active gastric or duodenal ulcer | 4,5 |
Bleeding within the previous 3 months | 4 |
Rheumatic disease | 2 |
Active cancer | 2 |
Key: score ≥ 7 points – increased bleeding risk, < 7 points – low risk.
Appendix G19. Los Angeles Motor Scale (LAMS).
Russian title: Los Angeles Motor Scale for prehospital screening of proximal occlusion
Original title: The Los Angeles Motor Scale (LAMS)
Source: Llanes JN, Kidwell CS, Starkman S, Leary MC, Eckstein M, Saver JL. The Los Angeles Motor Scale (LAMS): a new measure to characterize stroke severity in the field. Prehosp Emerg Care. 2004 Jan-Mar;8(1):46-50. doi: 10.1080/312703002806. PMID: 14691787.
Type (underline):
- rating scale
- index
- questionnaire
- other (specify):
Purpose: for prehospital screening of proximal occlusion
Content:
Criterion | Score |
|---|---|
Facial asymmetry | none = 0 present = 1 |
Upper extremity weakness | none = 0 drifts down = 1 falls rapidly = 2 |
Grip strength | normal = 0 weaker on one side = 1 no grip on one side = 2 |
Key: total score ≥4 indicates a high probability of proximal occlusion.
Total score <3 indicates a low probability of proximal occlusion.
Appendix G20. Montreal Cognitive Assessment (MoCA test)
Russian title: Montreal Cognitive Assessment
Original title: The Montreal Cognitive Assessment (MoCA-test)
Source: www.mocatest.org
Type (underline):
- rating scale
- index
- questionnaire
- other (specify): surveys
Purpose: detection (screening) and assessment of the severity of cognitive impairment
Content:
The Montreal Cognitive Assessment (MoCA) was designed as a rapid screening instrument for mild cognitive dysfunction. It assesses different cognitive domains: attention and concentration, executive functions, memory, language, visuoconstructive skills, conceptual thinking, calculations, and orientation. Time to administer the MoCA is approximately 10 minutes. The total possible score is 30 points; a score of 26 and above is considered normal. A score of 25 and below indicates cognitive impairment.
1. Alternating Trail Making:
The examiner instructs the subject as follows: "Please draw a line, going from a number to a letter in ascending order. Begin here [point to (1)] and draw a line from 1, then to A, then to 2 and so on. End here [point to (E)]".
Scoring: Allocate one point if the subject successfully draws the line in the following sequence: 1-A-2-B-3-C-4-D-5-E, without any intersecting lines. Any error that is not immediately self-corrected by the subject earns 0 points.
2. Visuoconstructive Skills (Cube):
Administration: The examiner gives the following instructions, pointing to the cube: "Copy this drawing as accurately as possible in the space below it".
Scoring: One point is allocated for a correctly executed drawing:
- Drawing must be three-dimensional;
- All lines are drawn;
- No extra lines are added;
- Lines are relatively parallel and their length is similar (a rectangular prism is acceptable).
A point is not awarded if any of the above-mentioned criteria are not met.
3. Visuoconstructive Skills (Clock):
Administration: Indicate the right third of the space on the sheet and give the following instructions: "Draw a clock. Put in all the numbers and set the time to 10 past 11".
Scoring: One point is allocated for each of the following three criteria:
- Contour (1 point): The clock face must be a circle with only minor distortion (e.g., slight imperfection in closing the circle);
- Numbers (1 point): All clock numbers must be present, with no extra numbers; numbers must be in the correct order and placed in the appropriate quadrants on the clock face; Roman numerals are acceptable; numbers can be placed outside the clock face contour;
- Hands (1 point): There must be two hands jointly indicating the correct time; the hour hand must clearly be shorter than the minute hand; the hands must be centered with their junction close to the center.
No point is allocated for this item if any of the above-mentioned criteria are not met.
4. Naming:
Administration: Beginning on the left, point to each figure and say: "Name this animal".
Scoring: One point is allocated for each of the following responses: (1) camel or dromedary, (2) lion, (3) rhinoceros.
5. Memory:
Administration: The examiner reads a list of 5 words at a rate of one word per second, giving the following instructions: "This is a memory test. I am going to read a list of words that you will have to remember. Listen carefully. When I am through, tell me as many words as you can remember. It doesn't matter in what order you say them". Mark a check in the allocated space for each word the subject names on the first trial. When the subject indicates that they have finished (named all words) or can recall no more words, read the list a second time with the following instructions: "I am going to read the same list for a second time. Try to remember and repeat as many words as you can, including the words you said the first time". Mark a check in the allocated space for each word the subject repeats on the second trial. At the end of the second trial, inform the subject that they will be asked to recall these words again: "I will ask you to recall those words again at the end of the test".
Scoring: No points are allocated for either the first or second trials.
6. Attention:
Forward Digit Span:
Administration: Give the following instructions: "I am going to say some numbers and when I am through, repeat them exactly as I said them". Read a five-number sequence at a rate of one digit per second.
Backward Digit Span:
Administration: Give the following instructions: "I am going to say some numbers, but when I am through, you must repeat them in the reverse order". Read a three-number sequence at a rate of one digit per second.
Scoring: Allocate one point for each correctly repeated sequence (N.B.: the correct response for the backward recall is 2-4-7).
Vigilance:
Administration: The examiner reads a list of letters at a rate of one letter per second, after the following instructions: "I will read you a sequence of letters. Every time I say the letter A, tap your hand once. If I say a different letter, do not tap your hand".
Scoring: One point is allocated if there are zero errors or only one error (an error is considered when the patient taps the hand upon hearing a different letter or fails to tap upon hearing the letter A).
Serial 7 Subtraction:
Administration: The examiner gives the following instructions: "Now I will ask you to subtract 7 from 100, and then keep subtracting 7 from your answer until I tell you to stop". Repeat the instructions if necessary.
Scoring: This item is evaluated out of 3 points. Allocate 0 points for no correct subtractions, 1 point for one correct calculation, 2 points for two to three correct calculations, and 3 points if the subject successfully makes four or five correct calculations. Count each correct 7-subtraction starting from 100. Each subtraction is evaluated independently; thus, if a participant gives an incorrect answer but then continues to subtract 7 accurately from that number, give a point for each accurate subtraction. For example, a participant may answer "92-85-78-71-64" where "92" is incorrect, but all subsequent values are subtracted correctly. This is a single error, and 3 points are allocated for this item.
7. Sentence Repetition:
Administration: The examiner gives the following instructions: "I am going to read you a sentence.
Repeat this, exactly as I say (pause): I know that Ivan is the only one who can help today". Following the response, say: "Now I will read you another sentence. Repeat it, exactly as I say (pause): The cat always hid under the couch when the dogs were in the room"
Scoring: Assign 1 point for each correctly repeated sentence. Repetition must be exact. Listen carefully for errors due to word omissions (e.g., omitting "only", "always") and substitutions/additions (e.g., "Ivan is the only one who helped today"; substitution of "hides" for "hid", use of plural form, etc.).
8. Verbal fluency:
Administration: The examiner gives the following instructions: "Name as many words as you can that begin with a specific letter of the alphabet that I will tell you now. You can name any type of word, except proper nouns (such as Peter or Moscow), numbers, or words that begin with the same sound but have different suffixes, for example, love, lover, to love. I will stop you after one minute. Are you ready? (Pause) Now name as many words as you can think of that begin with the letter S. (Time 60 sec). Stop."
Scoring: One point is awarded if the subject names 11 words or more in 60 seconds. Record the answers at the bottom or side of the page.
9. Abstraction:
Administration: The examiner asks the subject to explain what each pair of words has in common, starting with an example: "Tell me what an orange and an apple have in common." If the patient answers in a concrete manner, say only one more time: "Tell me in what other way they are alike." If the subject does not give the correct answer (fruit), say, "Yes, and they are also both fruits." Do not give any other instructions or explanations.
After the practice trial, say: "Now, tell me what a train and a bicycle have in common." After the response, give the second task by asking: "Now, tell me what a ruler and a watch have in common." Do not give any other instructions or prompts.
Scoring: Only the last two pairs of words are scored. 1 point is given for each correct answer.
The following answers are considered correct:
Train-bicycle = modes of transport, means of travel, you can ride on both;
Ruler-watch = measuring instruments, used for measuring.
The following answers are not considered correct:
Train-bicycle = they have wheels;
Ruler-watch = they have numbers on them.
10. Delayed recall:
Administration: The examiner gives the following instructions: "I previously read a list of words to you and asked you to remember them. Tell me as many words as you can recall". Make a mark for each correctly recalled word without a cue in the designated space.
Scoring: 1 point is awarded for each word recalled without any cues.
Optional: After the delayed free recall attempt, provide the subject with a cue in the form of a semantic category clue for each uncalled word. Make a mark in the designated area if the subject recalled the word using a category cue or a multiple-choice cue. Prompt all words that the subject did not recall in this manner. If the subject does not recall a word after the category cue, you should give him/her a multiple-choice cue using the following instructions: "Which of the words do you think was mentioned, NOSE, FACE, or HAND?" Use the following category cues and/or multiple-choice cues for each word:
FACE category cue: body part; multiple choice: nose, face, hand
VELVET category cue: type of fabric; multiple choice: jeans, cotton, velvet
CHURCH category cue: type of building; multiple choice: church, school, hospital
DAISY category cue: type of flower; multiple choice: rose, tulip, daisy
RED category cue: color; multiple choice: red, blue, green
Scoring: No points are given for cued word recall. Cues are used for informational clinical purposes only and may provide the test interpreter with additional information about the type of memory impairment. In memory impairment due to retrieval deficits, performance improves with cueing. In memory deficits due to encoding impairment, test performance does not improve after cueing.
11. Orientation:
Administration: The examiner gives the following instructions: "Tell me today's date". If the subject does not give a complete answer, give the appropriate prompt: "Name the (year, month, exact date, and day of the week)". Then say: "Now, tell me this place and the city it is located in."
Scoring: One point is awarded for each correctly named item. The subject must name the exact date and exact location (name of the hospital, clinic, outpatient clinic). No point is awarded if the patient makes an error in the day of the week or date.
Total score: Sum all scores in the right-hand column. Add one point if the patient has 12 years of education or less, up to a maximum possible score of 30 points.