List of Abbreviations
ICD-10 – International Classification of Diseases, 10th Revision
TBI – traumatic brain injury
mTBI — mild traumatic brain injury
Con – concussion
ATP – adenosine triphosphate
CT – computed tomography
MRI – magnetic resonance imaging
GCS – Glasgow Coma Scale
ICP – intracranial pressure
UCH-L1 — ubiquitin carboxy-terminal hydrolase L1
SRI — scientific research institute
BBB — blood-brain barrier
DAI — diffuse axonal injury
Dura – dura mater
SAH – subarachnoid hemorrhage
Terms and Definitions
Evidence-based medicine — an approach to medical practice aimed at optimizing decision-making by integrating the best available evidence from clinical research with clinical expertise and patient values.
Instrumental diagnostics – diagnostics performed by examining a patient using various devices, apparatuses and instruments.
Laboratory diagnostics – a set of methods aimed at analyzing the test material using various specialized equipment.
Medical intervention — a set of medical examinations and/or procedures performed by a medical worker or other professional authorized to provide medical care, affecting the physical or mental state of a person and having a preventive, diagnostic, therapeutic, rehabilitative, or research orientation.
Working group – two or more people of the same or different professions working together and in a coordinated manner to create clinical guidelines, and bearing joint responsibility for the results of this work.
Condition — changes in the body resulting from the impact of pathogenic and/or physiological factors that require medical care.
Syndrome – a set of symptoms sharing a common etiology and pathogenesis.
Level of evidence certainty – reflects the degree of certainty that the found effect of a medical intervention is true.
Grade of recommendation – reflects not only the certainty in the reliability of the intervention's effect, but also the certainty that following the recommendations will bring more benefit than harm in a specific situation.
Surgical intervention – an invasive procedure that may be used for diagnostic purposes and/or as a method of treating diseases.
Surgical treatment – a method of treating diseases through the division and joining of tissues during a surgical operation.
Recommendation. Treatment and diagnostic measures recommended for use by a majority of experts on these issues. May be considered as treatment options in specific clinical situations (efficacy confirmed by individual randomized trials or cohort clinical studies).
Not recommended – treatment and diagnostic measures that have no positive effect or may cause harm (any level of evidence).
1. Brief information on the disease or condition
1.1 Definition of the disease or condition
Traumatic brain injury (TBI) – injuries to the skull, brain, meninges, blood vessels, and/or cranial nerves accompanied by clinical symptoms and, in most cases, morphological changes. A clear history of trauma is critically important.
Mild TBI (mTBI) – an acutely developed impairment of brain function resulting from traumatic impact, which may be accompanied by brief loss of consciousness (up to 30 minutes) and/or amnesia (up to 24 hours). It includes two nosologies: concussion and mild cerebral contusion.
Cerebral concussion – the mildest clinical form of diffuse transient brain injury, underlying which are metabolic, ionic, neurotransmitter disturbances, and neuroinflammation, characterized by the absence of visible changes on computed tomography (CT).
1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)
Animal experiments, including subprimates and primates, have shown that concussion is caused predominantly by inertial injury under certain parameters of angular and translational acceleration [16,17]. However, it can also occur with impact acceleration [22]. Thus, the acceleration transmitted to the brain at the moment of trauma is a critical component of the pathogenesis of concussion in both indirect (inertial injury) and direct (impact injury) mechanical energy delivery to the head [22]. Light microscopy reveals subcellular changes in the form of perinuclear chromatolysis (tigrolysis), vacuolation, eccentric positioning of neuronal nuclei, elements of chromatolysis, and neurofibrillar swelling. Electron microscopy detects damage to cell membranes, mitochondria, and other organelles [4]. It is believed that the clinical manifestation of concussion is based on asynapsis, predominantly functional. It has been experimentally confirmed that concussion involves damage to the synaptic apparatus and redistribution of tissue fluid; these may be accompanied by ultrastructural abnormalities of neuronal axial cylinders and axons. Previously, it was believed that macroscopic brain damage was absent in concussion [22]. Cerebral contusion differs from concussion by macrostructural damage to the brain parenchyma. Pathomorphologically, mild cerebral contusion is characterized by areas of local brain tissue edema, petechial diapedetic hemorrhages, and limited ruptures of small pial vessels.
1.3 Epidemiology of the Disease or Condition
TBI is the leading cause of mortality among individuals under 45 years of age [11]. According to the Sklifosovsky Research Institute for Emergency Medicine, the number of hospitalized patients with TBI in Moscow is 13,000–15,000 per year. Men are predominantly affected, with a mean age under 43 years, and 15% to 25% of patients have polytrauma [9].
Mild traumatic brain injury (mTBI) dominates the structure of craniocerebral trauma, accounting for 60%–95% of all injured patients [5]. The prevalence ratio of mTBI to severe TBI is 22:1. The ratio of concussion to mild contusion is approximately 4:1. Mortality in mTBI is low (0.04%–0.29%) and almost exclusively caused by intracranial hematomas [11]. Causes of mTBI in the population include motor vehicle accidents, domestic, criminal, sports, and occupational injuries [8].
Most studies note that traumatic brain injury is more common among children, young people under 30, and elderly patients. Men sustain TBI predominantly. In various studies on TBI, the proportion of men ranges from 70% to 81%. The male-to-female ratio in different countries ranges from 1.2:1 in Sweden to 2.7:1 in Spain. In developing countries, this ratio is 4.8:1.
1.4 Features of Coding the Disease or Condition
S06.0 – Concussion
1.5 Classification of the disease or condition
The classification of TBI is based on its biomechanics, type, category, nature, form, severity of injuries, clinical phase, course period, and injury outcome [7].
By biomechanics, TBI is classified into: 1) impact-countercoup, 2) acceleration-deceleration, 3) mixed.
By type of injury: 1) focal, 2) diffuse, 3) mixed.
By the genesis of brain injury in TBI, a distinction is made between: 1) primary injuries that occur as a direct result of traumatic factors – focal contusions and lacerations of the brain, diffuse axonal injuries, primary intracranial hematomas, and combinations thereof; 2) secondary intracranial injuries resulting from factors such as blood-brain barrier disruption, increased brain volume or swelling due to edema, hyperemia or venous congestion, elevated intracranial pressure, brain displacement and deformation, delayed hematomas (epi-subdural, intracerebral), impaired hemato- and cerebrospinal fluid circulation due to subarachnoid or intraventricular hemorrhage, intracranial infection, etc. b) secondary extracranial factors: arterial hypotension, hypoxemia, hypercapnia, anemia, etc. [Reilly P., Bullock R., 2005]. Secondary factors can be prevented or treated, which depends on timely and correct diagnosis, organization, and quality of neurosurgical care.
By clinical forms: 1) concussion, 2) mild cerebral contusion, 3) moderate cerebral contusion, 4) severe cerebral contusion, 5) diffuse axonal injury, 6) brain compression, 7) head compression.
According to the course of traumatic brain disease [Likhterman L.B. et al., 2012]:
1) acute, 2) intermediate, 3) remote.
Note. Acute period – the time interval from the moment of mechanical energy impact on the brain with a sudden disorder of its integrative-regulatory and local functions until the stabilization of impaired general cerebral and systemic functions at a certain level, or the death of the patient. The duration of the acute period ranges from 2 to 10 weeks, depending on the clinical form of TBI. Approximate durations of the acute period of TBI are: for concussion – up to 2 weeks, for mild contusion – up to 3 weeks, for moderate contusion – up to 4–5 weeks, for severe contusion – up to 6–8 weeks, for diffuse axonal injury – up to 8–10 weeks, for brain compression – from 3 to 10 weeks (depending on background conditions).
Intermediate period – the time interval from the stabilization of systemic, general cerebral, and focal functions impaired by the trauma until their complete or partial recovery or stable compensation. Duration of the intermediate period: for mild TBI – up to 2 months, for moderate TBI – up to 4 months, for severe TBI – up to 6 months.
Remote period – the period of clinical recovery, or the maximally achievable rehabilitation of impaired functions, or the onset and/or progression of new pathological conditions resulting from the sustained TBI. Duration of the remote period: in case of clinical recovery – up to 2 years, in case of a progressive course – unlimited [18].
By the nature of TBI (closed/open; penetrating/non-penetrating; isolated/polytrauma/combined).
By the substrate of injury: (DAI/contusion foci/meningeal hematomas; bone structure injuries; presence or absence of subarachnoid hemorrhage; as well as a detailed description of soft tissue and extracranial structure injuries (chest/abdominal cavity; cervical spine; skeletal injury, pelvis).
By the presence of soft tissue injuries, a distinction is made between closed severe TBI (with soft tissue damage up to the aponeurosis) and open severe TBI (with soft tissue damage deeper than the aponeurosis).
By the presence of dural (dura mater) injuries, a distinction is made between penetrating (dura mater is damaged) and
non-penetrating (dura mater is intact) severe TBI.
By the type of TBI, distinctions are made: isolated injury (if extracranial injuries are absent), polytrauma or concomitant injury (if mechanical energy simultaneously causes extracranial injuries), and combined injury (if different types of energy – mechanical and thermal, radiation, or chemical – act simultaneously).
1.6 Clinical presentation of the disease or condition
Cerebral concussion is characterized by impaired consciousness following trauma lasting from several seconds to several minutes, retrograde, con-, and anterograde amnesia for a short period of time (from several minutes to 1 hour) (30%–50% of cases) [1,10], and the presence of predominantly subjective symptoms.
Impairments of consciousness are noted in approximately 90% of patients with concussions. At the same time, 70% experience a brief loss of consciousness at the moment of trauma [2,5]. There may be headache (up to 90%), non-systemic dizziness (about 70-75%), nausea, vomiting (predominantly single episode, about 35%), general weakness (about 75%), rapid fatigue (30%), tinnitus (10%), photophobia (10%), autonomic symptoms (pallor (60%) or hyperemia (5%) of the skin and mucous membranes, palmar and plantar hyperhidrosis (30%), dermographism disturbance (20%), arterial hypertension (25%), arterial hypotension (20%), tachycardia (40%), bradycardia (10%)), as well as sleep disturbance (up to 30%), pain on eye movement, convergence disorder (25%), and emotional lability.
In most patients, recovery after mild TBI occurs in a short time frame (within 1-2 weeks), however, in 5-50% of victims, more prolonged (up to several months or years) physical, cognitive, emotional, and behavioral disorders may be observed, which are termed persistent post-concussion syndrome [26,43,44]. In general, patients with pronounced acute and subacute symptoms, female gender, older age group, low level of education, those injured as a result of traffic accidents, and those with a prior history of psychiatric illnesses are most susceptible to developing post-traumatic syndrome [21].
Concussion slightly increases the risk of developing epi-syndrome, whereas brain contusion, hemorrhage, and skull fractures increase the risk by more than 2 times. A seizure occurring immediately after the traumatic event (1-2% of cases) is the result of impaired inhibitory processes in the cortex and does not affect the outcome of TBI or the likelihood of subsequent development of post-traumatic epilepsy [24].
The regression time of clinical symptoms in the vast majority of victims with concussion averages 4-5 days, and the period of temporary disability usually does not exceed two weeks. With prolonged persistence of symptoms and complaints (more than 7 days), additional examination and determination of causes are necessary. The regression time of neurological symptoms of mild brain contusion with an unremarkable history is usually 7-14 days, and temporary disability is up to 3 weeks [5].
2. Diagnostics, medical indications and contraindications for diagnostic methods
Criteria for establishing the diagnosis of the disease or condition:
1) anamnesic data: presence of a fact of trauma with loss/impairment of consciousness according to the description of the victim or witnesses.
2) physical examination: presence of wounds and abrasions on the scalp or facial area, signs of skull bone fracture.
3) thorough neurological examination upon admission and dynamically.
4) instrumental examination: brain CT (as indicated).
Recognition of a concussion is often a challenging task because it is based predominantly on subjective symptoms. In the diagnosis of concussion, it is especially important to assess the circumstances of the trauma and information from witnesses of the incident. A dual role can be played by traces of trauma on the head and factors such as alcohol intoxication, the psychological state of the victim, etc. Despite the absence of symptoms, CT data are crucial in confirming the diagnosis of mild TBI and diagnosing delayed intracranial structural lesions [9].
2.1 Complaints and Anamnesis
When taking an anamnesis in patients with suspected concussion, it is recommended to identify the mechanism of brain injury (non-contact acceleration/deceleration, contact impact-counterimpact, non-contact blast injury); the fact of consciousness impairment (absence of consciousness, confusion, moderate stupor) and its duration; the presence of post-traumatic amnesia and its duration. Impairment of consciousness may manifest immediately after the trauma or be delayed by several minutes [9].
LNC 5 LeC C
Comment: any patient with TBI must be examined as a patient with a trauma requiring surgical intervention. Thus, the primary assessment triad includes determining airway patency, respiratory and circulatory function, as well as the possibility of neck trauma.
Also, during anamnesis taking, it is necessary to assess the presence of concomitant non-traumatic factors and their possible impact on clinical manifestations (alcohol or other intoxication, psychological stress, pronounced musculoskeletal pain syndrome, cardiac, pulmonary diseases, syncopal, hypoglycemic states, history of epilepsy).
Such subjective symptoms as headache, nausea, dizziness, fatigue, irritability, forgetfulness can be used to confirm the diagnosis and plan objective diagnostic examinations, but should not serve as the sole basis for diagnosing concussion. Such symptoms can be observed in patients with injuries occurring without involvement of the cranium and brain, can be symptoms of concomitant conditions (neck strain, otoneurological disorders, chronic musculoskeletal pain, post-traumatic stress disorder, depression) and even be present in healthy individuals, for example, as manifestations of a stress response.
An important prognostic characteristic of the clinical course of concussion is the duration of post-traumatic (or anterograde) amnesia. Studies show that the outcome of mild TBI and the duration of temporary disability are determined to a greater extent by the duration of post-traumatic amnesia compared to the assessment of the level of consciousness using the GCS. In the case of post-traumatic amnesia of less than 24 hours, good recovery (according to the Glasgow Outcome Scale) is noted in 100% of patients [26].
2.2 Physical Examination
When examining the head in patients with suspected concussion, it is recommended to identify signs indicating the fact of sustained trauma (contusions, abrasions, wounds) and skull base fracture in case of brain contusion (ecchymoses in the mastoid process area, periorbital hematomas, discharge of fluid from the external auditory canals, nose, mouth) [9].
LNC 5 LeC C
2.2.1. Neurological examination
The patient is recommended to undergo a thorough neurological examination upon admission and dynamically, with assessment of status using the Glasgow Coma Scale (GCS) [5,6].
LNC 4 LeC C
It is recommended that all victims with suspected concussion undergo an appointment (examination, consultation) with a neurosurgeon or an appointment (examination, consultation) with a neurologist to establish a diagnosis [5,6].
LNC 5 LeC C
Comment: neurological status may reveal fine-amplitude nystagmus (40%), mild anisoreflexia of tendon and skin reflexes (20%), static ataxia (20%), dynamic ataxia (10%), increased tendon reflexes (20%), mild meningeal signs (10%), disappearing in 90% of patients within the first 4-5 days [5]. Skull bone damage is absent. The general condition of the victims usually improves significantly within the first, less often the second week after trauma, regardless of specific neurological symptoms.
2.3 Laboratory Diagnostics
Not required.
There are data in the literature on preliminary studies determining brain tissue damage proteins in serum in mild TBI (see Appendix B, p. 36).
2.4 Instrumental Diagnostics
Victims with concussion are recommended to undergo brain CT in the presence of risk factors. It is recommended to identify risk factors and determine mild TBI categories according to which brain CT is performed [14,15,18,25,27].
LNC 4 LeC C
Comment 1. Risk factors for mild TBI (according to the Canadian Closed Head Injury Rule - CHIP)
Comment 2: Classification revised and supplemented by the EFNS in 2012 [26].
Table 1. Categories of mild TBI for determining indications for brain CT.
Classification of mild TBI | GCS upon admission | Risk factors | Indications for immediate referral for CT |
|---|---|---|---|
Mild TBI | 13-15 | ||
Category 1 | 15 | None or 1 additional | none |
Category 2 | 15 | ≥ 1 major or ≥ 2 additional | yes |
Category 3 | 13-14 | yes | |
Decrease in GCS by 1 point | |||
If brain CT is impossible to perform, it is recommended to perform skull radiography in anteroposterior and lateral projections or tangential skull radiography to exclude skull fracture, and, if available in the medical institution, echoencephalography to exclude displacement of midline structures [5,9].
LNC 5 LeC C
2.5 Other Procedures
Patients with concussion, in the presence of complaints or for objective diagnosis, are recommended an examination by an ophthalmologist, otolaryngologist, and psychiatrist [3,5,9,10,20,25].
Level of Evidence (LoE) 4, Grade of Recommendation (GoR) C
Comment
Various functional studies (electroencephalography, ophthalmoscopy, duplex scanning of intracranial segments of brachiocephalic arteries, etc.) can indirectly contribute to the objectification of concussion in the acute period [28,35]. In cases of an asymptomatic disease course, to confirm the diagnosis of concussion, it is possible to perform a dynamic otoneurological examination (preferably using electrogustometry, audiometry, electronystagmography), which reveals symptoms of vestibular analyzer irritation in the absence of deficit signs [36,37,38,39].
Since the semiotics of concussion is very mild and can be observed due to a wide variety of pre-traumatic causes, the dynamics of signs acquire exceptional importance for diagnosis. Their usual disappearance within 3–5 days helps to confirm the diagnosis of concussion.
As an additional method to objectify the diagnosis of concussion, ophthalmoscopy can be performed on days 1–3, which may reveal fundus changes in 90% of patients in the form of retinal artery spasm (40%), venous congestion (20%), or arteriospasm against the background of venous congestion (30%) [5,29,30].
Psychiatric diagnosis is necessary to determine, when possible, the ratio of symptoms caused by: a) organic brain damage and b) psychogenic causes (in particular, determined by experiences of the trauma fact, the circumstances of its occurrence, and the need to adapt to its consequences).
3. Treatment, including drug and non-drug therapies, diet therapy, and pain management
3.1. Conservative management
For patients with concussion, bed rest with the elimination of all external stimulation (light, sound, sensory, etc.) throughout the entire observation period is not recommended, as it does not lead to improved recovery [24].
LNC 5 LeC C
Comment. The fact of hospitalization of patients with concussion under the age of 35 without a burdened premorbid history does not have any significant impact on the course and outcomes of this form of TBI. Previously, rest was recommended in the first 24–48 hours after concussion to alleviate clinical symptoms and reduce the metabolic demand of the brain. Due to a lack of supporting data, strict rest consisting of isolation and complete avoidance of stimuli until acute symptoms resolve is no longer recommended. A number of studies have found that this approach can lead to an increased symptom burden, a prolonged recovery period, and an increased risk of developing persistent symptoms compared to relative rest [5,12,45,46,47]. Once a diagnosis of concussion is established (ruling out brain contusion or compression), outpatient treatment of patients is permissible. The patient and their relatives must be warned that if the patient's condition worsens, an urgent repeat medical examination is necessary.
After the initial period of rest, a gradual return of the patient to normal daily activity is necessary.
Activities associated with the risks of repeated brain injury are not recommended until complete clinical recovery, which is characterized by complete regression of symptoms, normalization of physical examination data, and a return to normal daily activities. This is necessary to exclude the risk of developing Second Impact Syndrome, which in some cases manifests as a highly lethal condition—sudden diffuse brain edema [9].
It is recommended that patients with concussion avoid activities requiring attention and concentration, in particular refraining from screen use during the first 48 hours after concussion, as this accelerates the regression of concussion symptoms from 8 to 3.5 days [48].
LeD 2 LoR C
It is not recommended to prescribe antiepileptic drugs (anticonvulsants) for prophylactic purposes to patients with concussion [23,26,31].
Level of Evidence (LE) 2, Grade of Recommendation (GR) C
3.1.1. Treatment of headache as a consequence of TBI
It is recommended that patients with concussion primarily receive non-pharmacological treatment for headache: sleep normalization, regular meals, adequate hydration, avoidance of stress factors, and moderate physical activity [9,40].
LNC 5 LeC C
To treat tension-type headache in patients with concussion, the following are recommended: analgesics (except opioids). If ineffective, the prescription of combined analgesics is recommended [41].
LNC 5 LeC C
The use of benzodiazepine derivatives for the treatment of sleep disorders in patients with concussion is not recommended [24,32,42].
LNC 5 LeC C
It is recommended to prescribe melatonin at a dose of 2 mg per day to patients with concussion presenting with sleep disorders [32].
Level of Evidence (LE) 2, Grade of Recommendation (GR) C
Comment. It is also possible to use melatonin at a dose of 3 mg [49].
3.1.2. Other therapy
In cases of soft tissue injury of the head, it is advisable to be guided by the Clinical Guidelines "Open Wound of the Head" when prescribing therapy [33].
Surgical treatment
In cases of soft tissue head injury in patients with concussion, when determining indications for surgical treatment, it is advisable to be guided by the Clinical Guidelines "Open Wound of the Head" [33].
4. Medical Rehabilitation and Sanatorium-Resort Treatment
Not required.
The need for rehabilitation arises only in cases of a complicated course of trauma and in the presence of comorbid pathology that exacerbates the manifestations of organic brain damage.
5. Prevention and Dispensary Observation
The prognosis for concussion is usually favorable: subjective and objective symptoms disappear relatively quickly, and the patient's functional capabilities are fully restored [5,13,18].
The frequency of clinically significant long-term (at one year post-trauma) consequences of mild TBI in premorbidly healthy individuals is observed in approximately 10–15% of cases [5].
It is recommended that patients with concussion undergo dynamic follow-up by a neurologist with an assessment of general condition as well as neurological and mental status at 1, 3, and 6 months post-concussion [5].
LNC 4 LeC C
6. Organization of Medical Care
It is advisable to transport a patient with concussion to the nearest multidisciplinary hospital capable of round-the-clock admission and treatment of patients with traumatic brain injury, equipped with a CT scanner, and having a neurosurgical, traumatological, or neurological department.
Outpatient treatment under the supervision of a neurologist is indicated for patients with concussion, provided that a brain CT scan has been performed or there are no indications for CT.
Hospitalization in a neurosurgical department is indicated for patients with concussion and bruised head wounds with blood loss and pronounced general cerebral symptoms. In the absence of a neurosurgical department, hospitalization in a traumatological or neurological department is indicated.
Discharge criterion: clinical improvement.
7. Additional Information
Not provided.
Criteria for Evaluating the Quality of Medical Care
No. | Quality criteria | Level of data reliability | Level of recommendation certainty |
|---|---|---|---|
1. | An admission evaluation (examination, consultation) by a neurosurgeon and/or an admission evaluation (examination, consultation) by a neurologist with an assessment of neurological status was performed upon admission. | 5 | C |
2. | Assessment of condition using the Glasgow Coma Scale was performed | 5 | C |
3. | Brain CT was performed in the presence of risk factors | 5 | C |
4. | In the absence of CT in the hospital, skull radiography in anteroposterior and lateral projections, or tangential skull radiography, and—if available in the medical institution—echoencephalography was performed |
References
Show references
Akimov G.A. et al. Features of the course of consequences of mild traumatic brain injuries in young individuals // Voenno-med. zhurn. - 1993. - Iss. 1. - P. 31-39.
Voskresenskaya O.N., Tereshchenko S.V., Sholomov I.I. Objective characteristics of the acute period of concussion. Zhurn. Neyrokhirurgiya, No. 4, 2003. - P. 31-35
Zaitsev O.S. Psychiatric aspects of traumatic brain injury and its consequences. - M.: MEDpress-inform, 2021. - 104 p.
Kasumova S.Yu. Pathological anatomy of traumatic brain injury // Clinical Guidelines for Traumatic Brain Injury. - M.: Antidor, 1998. - Vol. 1. - P. 169-225.
Likhterman L.B., Kravchuk A.D., Filatova M.M. Concussion: treatment tactics and outcomes. // Annals of Clinical and Experimental Neurology. - 2008. - Vol. 2. - No. 1. - P. 12-21.
Grote S. et al. Diagnostic value of the Glasgow Coma Scale for traumatic brain injury in 18,002 patients with severe multiple injuries // Journal of neurotrauma. - 2011. - Vol. 28. - No. 4. - P. 527-534
Likhterman L.B., Potapov A.A. Classification of traumatic brain injury // "Clinical Guidelines for Traumatic Brain Injury". - M.: Antidor, 1998. - Vol. 1. - P. 47-123.
Nepomnyashchiy V.P., Likhterman L.B., Yartsev V.V., Akshulakov S.K. Epidemiology of traumatic brain injury // Clinical Guidelines for Traumatic Brain Injury (ed. by A.N. Konovalov, L.B. Likhterman, A.A. Potapov). - M.: "Antidor", 1998. - Vol. 1. - P. 129-147.
Surgery of severe traumatic brain injury. Under the general editorship of V.V. Krylov, A.E. Talypov, O.V. Levchenko. M., ABV-press, 2019. 859 p.
Greenberg M.S.:Nandbook of Neurosurgery. Third Edition. Greenberg Graphics,Inc. Lakeland, Florida, USA, p.526,1994.
Kraus J.F. Neurotrauma. Chapter 2. Epidemiology of brain ingury. Ed. R. Narayan et al.- McGraw Hill – USA. – 1996. – P. 13-30.
de Kruijk J.R., Leffers P., et al. / Effectiveness of bed rest after mild traumatic brain injury: a randomized trial of no versus six days of bed rest. // J Neurol Neurosurg Psychiatry. 2002 Aug; 73 (2). – P.167-72.
Letarte Peter B. / What is the Outcome of Patients with mild, Moderate or Severe traumatic Braim Injury // Neurotrauma. Evidence – Based Answers to Common Questions. – Alex B. Valadka Brian T. Andreus. – “Thieme” New York Stuttgart. – P. 235-242.
Sherman C. Stein, Mark G. Burnett / When Are Computed Tomography Scans and Skull X- Rays Indicated for Patients with Minor Head Injury? // Neurotrauma. Evidence – Based Answers to Common Questions. – Alex B. Valadka Brian T. Andreus. – “Thieme” New York Stuttgart. – P.19-24.
Stein S.C., Ross S.E.: The value of computed tomographic scans in patients with low-risk head injury. Neurosurgery 26: 638-640,1990.
Genarelli T.A. Cerebral concussion and diffuse brain injuries // In: Copper P. Head Injury. – Baltimore, 1993. – P.137-158.
Genarelli T.A., Ommaya A.K., Thibault L.E. Comparison of linear and rotational acceleration in experimental cerebral concussion. In 15th Stapp Car Crash Conference Proceedings. – New York: SAE, 1971 . – P. 797-803.
Gomez PA, Lobato RD, Ortega JM, De La Cruz J (1996). Mild head injury: differences in prognosis among patients with a Glasgow Coma Scale score of 13–15 and analysis of factors associated with abnormal CTfindings. Br J Neurosurg 10:453–460.
Haydel M.J., Preston C.A., Mills T.J. et al. (2000). Indications for computed tomography in patients with minor head injury [see comments]. N Engl J Med 343:100–105.
Krauss JK, Tränkle R, Kopp KH. Post-traumatic movement disorders in survivors of severe head injury. Neurology. 1996 Dec;47(6):1488-92.
Mott TF1, McConnon ML, Rieger BP. Subacute to chronic mild traumatic brain injury. Am Fam Physician. 2012 Dec 1;86(11):1045-51.
Povlishock J.T. An Overview of barin injury models. / In Raj K. Narayan, James E. Wilberger, jr., John T. Povlishock Neurotrauma. – USA, 1996 – Chapter 97. – P. 1325-1336.
Schierhout G., Roberts I. (1998). Prophylactic antiepileptic agents after head injury: a systematic review. J Neurol Neurosurg Psychiatry 64:108–112.
Silverberg Noah D, William J Panenka, Pierre-Paul Lizotte, Mark T Bayley, Derry Dance, Linda C Li Promoting early treatment for mild traumatic brain injury in primary care with a guideline implementation tool: a pilot cluster randomised trial. BMJ Open. 2020; 10(10): e035527. Published online 2020 Oct 20. doi: 10.1136/bmjopen-2019-035527
Smits M, Dippel DW, de Haan GG, et al. Minor head injury: guidelines for the use of CT. A multicenter vali- dation study. Radiology 2007; 245: 831–838.
Vos P.E. et al (2012). Mild traumatic brain injury. European Journal of Neurology 2012, 19: 191–198.
Useche J.N., Bermudez S. Conventional computed tomography and magnetic resonance in brain concussion // Neuroimaging Clinics. - 2018. - Vol. 28. - No. 1. - P. 15-29.
McCrea M. et al. Acute effects and recovery after sport-related concussion: a neurocognitive and quantitative brain electrical activity study //The Journal of head trauma rehabilitation. – 2010. – Vol. 25. – No. 4. – P. 283-292.
Daikhes N.A. et al. Structure of auditory system injuries in the acute period of traumatic brain injury //Meditsinskaya pomoshch. – 2006. – No. 6. – P. 28-31.
Likhterman L.B. Cerebral concussion //Neurosurgery. – 2002. – No. 2. – P. 4-8.
Bazarian J. J. et al. Recommendations for the emergency department prevention of sport- related concussion //Annals of emergency medicine. – 2020. – Vol. 75. – No. 4. – P. 471-482.
Grima N. A. et al. Efficacy of melatonin for sleep disturbance following traumatic brain injury: a randomised controlled trial //BMC medicine. – 2018. – Vol. 16. – No. 1. – P. 1-10.
Clinical Guidelines. Open head wound, 2022.
Grote S. et al. Diagnostic value of the Glasgow Coma Scale for traumatic brain injury in 18,002 patients with severe multiple injuries //Journal of neurotrauma. – 2011. – Vol. 28. – №. 4. – P. 527-534.
Mizrahi E. M., Kellaway P. Cerebral concussion in children: assessment of injury by electroencephalography //Pediatrics. – 1984. – Vol. 73. – No. 4. – P. 419-425.
Kong T. H. et al. Clinical features of fracture versus concussion of the temporal bone after head trauma //Journal of audiology & otology. – 2019. – Vol. 23. – No. 2. – P. 96.
Vander Werff K. R., Rieger B. Impaired auditory processing and neural representation of speech in noise among symptomatic post-concussion adults //Brain injury. – 2019. – Vol. 33. – No. 10. – P. 1320-1331.
Isakov A.Y. Audiometry in assessing the severity of combined brain and ENT organ injuries in the acute period of traumatic disease //Medicine of Kyrgyzstan. – 2010. – No. 7. – P. 28-30.
Kisilevski V. et al. Results of otovestibular tests in mild head injuries //International Tinnitus Journal. – 2001. – Vol. 7. – No. 2. – P. 118-121.
Lew H. L. et al. Characteristics and treatment of headache after traumatic brain injury: a focused review //American journal of physical medicine & rehabilitation. – 2006. – Vol. 85. – No. 7. – P. 619-627.
Lucas S. Headache management in concussion and mild traumatic brain injury //PM&R. – 2011. – Vol. 3. – P. S406-S412.
Flanagan, S. R., Greenwald, B., & Wieber, S. (2007). Pharmacological Treatment of Insomnia for Individuals With Brain Injury. The Journal of Head Trauma Rehabilitation, 22(1), 67–70
Wäljas M, Iverson GL, Lange RT, Hakulinen U, Dastidar P, Huhtala H, et al. A prospective biopsychosocial study of the persistent post-concussion symptoms following mild traumatic brain injury. J Neurotrauma. 2015;32(8):534–47.
Nelson LD, Temkin NR, Dikmen S, Barber J, Giacino JT, Yuh E, et al. Recovery after mild traumatic brain injury in patients presenting to US Level I Trauma Centers: a transforming research and clinical knowledge in traumatic brain injury (TRACK-TBI) study [published correction appears in JAMA Neurol. 2019 Dec 1;76(12):1520.
Silverberg ND, Iaccarino MA, Panenka WJ, Iverson GL, McCulloch KL, Dams-O’Connor K, et al. Management of concussion and mild traumatic brain Injury: a synthesis of Practice guidelines. Arch Phys Med Rehabil. 2020;101(2):382–93.
De Luigi AJ, Bell KR, Bramhall JP, Choe M, Dec K, Finnoff JT, et al. Consensus statement: an evidence-based review of exercise, rehabilitation, rest, and return to activity protocols for the treatment of concussion and mild traumatic brain injury. PM R. 2023;15(12):1605–42.
Leddy JJ, Burma JS, Toomey CM, Hayden A, Davis GA, Babl FE, et al. Rest and exercise early after sport-related concussion: a systematic review and meta-analysis. Br J Sports Med. 2023;57(12):762–70.
Macnow T, Curran T, Tolliday C, Martin K, McCarthy M, Ayturk D, et al. Effect of screen time on Recovery from Concussion. JAMA Pediatr. 2021;175(11):1–8.
Kulikova I.S., Vinogradov O.I., Kuznetsov A.N. Correction of sleep disorders in patients with mild traumatic brain injury in the early recovery period. S.S. Korsakov Journal of Neurology and Psychiatry. 2014;114(5):75-77.
Appendix A1. Working Group Composition
1) Potapov A.A., MD, neurosurgeon, Academician of the RAS, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
2) Krylov V.V., MD, neurosurgeon, Academician of the RAS, Head of the Department of Neurosurgery and Neuroresuscitation, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Moscow;
3) Kravchuk A.D., MD, neurosurgeon, Professor, Head of the Department of Neurotraumatology, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
4) Likhterman L.B., MD, neurologist, Professor, Chief Researcher, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
5) Goryaynov S.A., PhD, neurosurgeon, Senior Researcher, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
6) Alexandrova E.V., PhD, neurologist, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
7) Eolchiyan S.A., MD, neurosurgeon, Senior Researcher, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
8) Zaitsev O.S., MD, Professor, Chief Researcher, psychiatrist, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
9) Zakharova N.E., MD, neuroradiologist, Professor of the RAS, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
10) Latyshev Ya.A., PhD, neurosurgeon, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
11) Okhlopkov V.A., PhD, Associate Professor, neurosurgeon, Senior Researcher, National Medical Research Center of Neurosurgery named after Academician N.N. Burdenko, Moscow;
12) Grin A.A., MD, neurosurgeon, Head of the Neurosurgery Department, N.V. Sklifosovsky Research Institute of Emergency Medicine, Moscow;
13) Talypov A.E., MD, neurosurgeon, Leading Researcher of the Neurosurgery Department, N.V. Sklifosovsky Research Institute of Emergency Medicine, Professor of the Department of Fundamental Neurosurgery, Institute of Professional Education, N.I. Pirogov Russian National Research Medical University, Moscow;
14) Prirodov A.V., MD, neurosurgeon, Leading Researcher of the Neurosurgery Department, N.V. Sklifosovsky Research Institute of Emergency Medicine, Professor of the Department of Fundamental Neurosurgery, Institute of Professional Education, N.I. Pirogov Russian National Research Medical University, Moscow;
15) Shelyakin S.Yu., PhD, neurosurgeon, Head of the Department of Emergency Neurosurgery, Clinical Hospital of Emergency Medical Care (Smolensk).
Conflict of interest: none.
Appendix A2. Methodology for Developing Clinical Guidelines
In these clinical guidelines, all data are ranked by level of reliability (evidence) depending on the quantity and quality of studies on the issue.
Scale for assessing levels of reliability of evidence (LRE) for diagnostic methods (diagnostic interventions)
LoE | Definition |
|---|---|
1. | Systematic reviews of studies with reference standard control or systematic reviews of randomized controlled trials with meta-analysis |
2. | Individual studies with reference standard control or individual randomized controlled trials and systematic reviews of studies of any design, except randomized controlled trials, with 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 |
Scale for assessing levels of reliability of evidence (LRE) for prevention, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, therapeutic, and rehabilitation interventions)
LoE | Definition |
|---|---|
1. | Systematic review of randomized controlled trials with meta-analysis |
2. | Individual randomized controlled trials and systematic reviews of studies of any design, except randomized controlled trials, with meta-analysis |
3. | Non-randomized comparative studies, including cohort studies |
4. | Non-comparative studies, case report or case series, case-control study |
5. | Only justification of the mechanism of action of the intervention (preclinical studies) or expert opinion is available |
Scale for assessing levels of recommendation grades (LRG) for prevention, diagnostic, treatment, and medical rehabilitation methods, including those based on natural therapeutic factors (preventive, diagnostic, therapeutic, and rehabilitation 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 adequate quality evidence (all considered efficacy criteria (outcomes) are unimportant, all studies are of low methodological quality, and their conclusions on the outcomes of interest are inconsistent) |
The methods used to formulate the recommendations were expert consensus. Cost analysis was not performed, and pharmacoeconomic publications were not analyzed.
Clinical guidelines are updated every 3 years.
Target audience for these clinical guidelines:
Neurosurgeons;
Medical students, residents, and postgraduate students.
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 medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.
Appendix A3. Reference Materials
These clinical guidelines were developed taking into account the following regulatory legal documents:
Order of the Ministry of Health of the Russian Federation No. 931n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to the Adult Population in the Profile 'Neurosurgery'."
Order of the Ministry of Health of the Russian Federation No. 388n dated June 20, 2013, "On approval of the procedure for the provision of emergency, including specialized emergency, medical care."
Resolution of the Government of the Russian Federation No. 554 dated July 24, 2000, "On approval of the Regulations on the State Sanitary and Epidemiological Service of the Russian Federation and the Regulations on State Sanitary and Epidemiological Standardization" (Collected Legislation of the Russian Federation, 2000, No. 31, Art. 3295; 2004, No. 8, Art. 663; No. 47, Art. 4666; 2005, No. 39, Art. 3953).
Appendix B. Physician Action Algorithms
Appendix C. Patient Information
Information is not available.
Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools
Appendix G1. Glasgow Coma Scale
Russian title: Glasgow Coma Scale (Teasdale G.M., Jennett B. 1974).
Original title (if any): Glasgow Coma Scale.
Source (official developer website, validation publication): Grote S. et al. Diagnostic value of the Glasgow Coma Scale for traumatic brain injury in 18,002 patients with severe multiple injuries //Journal of neurotrauma. – 2011. – Vol. 28. – No. 4. – P. 527-534.
Type: rating scale.
Purpose: assessment of the level of consciousness.
Content (template) and Key (interpretation):
Eye response (E)
Spontaneous – 4 points
To speech – 3 points
To pain – 2 points
No response – 1 point
Verbal response (V)
Oriented, answers questions quickly and correctly – 5 points
Disoriented, confused speech – 4 points
Word salad, answer does not make sense in relation to the question – 3 points
Inarticulate sounds in response to the question – 2 points
No speech – 1 point
Motor response (M)
Executes movements on command – 6 points
Purposeful movement in response to painful stimulus (pushing away) – 5 points
Withdrawal of the limb in response to painful stimulation – 4 points
Pathological flexion in response to painful stimulus (decortication) – 3 points
Pathological extension in response to painful stimulus (decerebration) – 2 points
No movement – 1 point
Interpretation of results
15 points — clear consciousness;
14–13 points — moderate obtundation;
12–10 points — deep obtundation;
9–8 points — stupor;
7–6 points — moderate coma;
4–5 points — deep coma;
3 points — tonic-free (atonic) coma.