Neuroimaging in the hyperacute period
In acute ischemia, every minute counts. During the first hours of the disease, standard X-ray computed tomography (CT) often fails to show the infarct core. Its primary task at this stage is to rule out intracerebral hemorrhage.
Multimodal magnetic resonance imaging is used for early verification of the diagnosis and determination of indications for thrombolysis:
- Diffusion-weighted MRI (DWI): instantly detects cytotoxic edema (the area of irreversible ischemia) as a hyperintense signal zone.
- Perfusion-weighted MRI (PWI): shows the perfusion deficit zone (the area of impaired blood flow that can still be salvaged).
- MR angiography: allows visualization of the site of arterial occlusion.
MRI is also the gold standard for detecting small (lacunar) infarctions in the posterior cranial fossa structures (e.g., in the medulla oblongata), as CT in this area produces numerous bone artifacts.
Comprehensive clinical examination
Determining the etiology of cerebral infarction requires a broad diagnostic workup. First and foremost, cardioembolic causes and pathology of the main head arteries are excluded.
- Cardiac evaluation: electrocardiography (ECG) is strictly indicated for all patients to detect arrhythmias and myocardial ischemia. If intracardiac thrombi, valvular disease, or endocarditis is suspected, transthoracic or transesophageal echocardiography is prescribed.
- Vascular imaging: color duplex scanning and angiography (CT or contrast X-ray) detect stenoses. A frequent finding is an atherosclerotic plaque in the area of the internal carotid artery (a. carotis interna).
- Laboratory tests: complete blood count with platelet count (to rule out erythremia, thrombocythemia), blood chemistry with mandatory lipid profile assessment, coagulogram, and infection screening (HIV, syphilis).
Principles of basic and specific therapy
Patients are hospitalized in specialized neurological units. Treatment is divided into two global areas: life support and restoration of blood flow.
Basic therapy does not depend on the stroke type. It includes respiratory management (up to mechanical ventilation), blood pressure control, and prevention of complications (deep vein thrombosis, pneumonia, pressure ulcers). For extensive cerebral edema, a 20% mannitol intravenous solution, hyperventilation mode, and in critical situations, decompressive craniectomy are used.
Specific therapy aims at vessel recanalization and prevention of recurrences:
- Thrombolysis: administration of tissue plasminogen activator (alteplase) at a dose of 0.9 mg/kg. The first 10% of the dose is given as a bolus, and the remaining 90% as an infusion over one hour. Strictly limited to the 4.5-hour window.
- Antithrombotic therapy: for the cardioembolic subtype, anticoagulants are used (heparin followed by warfarin or novel oral anticoagulants). For the non-cardioembolic subtype, antiplatelet agents are used (aspirin 150–300 mg/day).
Transient ischemic attack (TIA)
TIA is a condition in which neurological deficits are transient (typically lasting from a few minutes to hours, but no more than 24 hours) and are not accompanied by the formation of an infarction on MRI.
A specific sign of TIA in the carotid territory is transient monocular vision loss (amaurosis fugax). Despite complete clinical recovery, TIA is a formidable warning sign. About 30–40% of such patients suffer a true stroke within 5 years, with a fifth of them experiencing it within the first month.
Features of spinal cord ischemia
In addition to the brain, the spinal cord is also susceptible to ischemic injury. Its blood supply is provided by segmental vessels. The artery of Adamkiewicz (a. radicularis magna), which nourishes the lower thoracic and lumbosacral segments, plays a crucial role.
Interestingly, spinal ischemia can occur not only due to arterial occlusion, but also as a result of venous congestion. For instance, in the presence of an arteriovenous malformation, blood shunting occurs, leading to a rapid pressure increase in Batson's venous plexus and secondary damage to the spinal cord parenchyma.
Briefly: answers to topical questions
What clinical symptoms are characteristic of an infarction in the middle cerebral artery territory?
Clinical symptoms of an infarction in the middle cerebral artery territory depend on the level of occlusion and the side of the lesion. Occlusion of the main trunk or branches results in:
- Motor impairments — contralateral hemiplegia or hemiparesis (predominantly brachiofacial, with an emphasis on the arm and face), central-type paresis of the facial and tongue muscles, and cortical gaze palsy.
- Sensory impairments — contralateral hemianesthesia or hemihypesthesia.
- Visual disturbances — contralateral homonymous or upper quadrantanopia.
- Higher cerebral function disorders — involvement of the dominant hemisphere leads to total, motor, and/or sensory aphasia, acalculia, agraphia, motor apraxia; involvement of the non-dominant hemisphere leads to anosognosia, body scheme disorder, and constructive apraxia.
What pathogenetic subtypes of ischemic stroke are distinguished according to the TOAST classification?
According to the TOAST classification, ischemic strokes are differentiated into four main etiologic categories. The following pathogenetic subtypes are distinguished:
- Large vessel thromboembolic (large vessel thromboembolic) — involvement of major arteries.
- Cardioembolic (cardioembolic) — stroke caused by cardiac embolism.
- Small vessel (small vessel) — small vessel disease leading to lacunar infarctions.
- 'Other' etiologies ('other' aetiologies) — strokes with other or undetermined causes.
What antiplatelet agents, other than acetylsalicylic acid, are used for the secondary prevention of non-cardioembolic stroke?
For secondary prevention of non-cardioembolic stroke, other antiplatelet agents are used in addition to acetylsalicylic acid. These include:
- Clopidogrel — prescribed at a dosage of 75 mg/day.
- Dipyridamole + Acetylsalicylic acid (Aggrenox) — a combination drug containing extended-release dipyridamole (200 mg) and aspirin (25 mg), used twice daily.
What brain structures are the typical location of lacunar infarctions?
The typical location of lacunar infarctions includes deep brain structures supplied by small perforating arteries. The main lesion zones include:
- White matter of the hemispheres — periventricular and deep white matter (including the frontal and parietal lobes).
- Subcortical ganglia — basal ganglia.
- Internal capsule — a frequent site of involvement in various lacunar syndromes.
- Thalamus (optic thalamus).
- Brainstem — predominantly the ventral part of the pons.
- Cerebellum — involved less frequently.
Remember the key examination in the first hour: CT to rule out Blood (hemorrhage), MRI to find Targets for treatment (edema and perfusion deficit zone).
Class and exam questions
Why might a standard CT scan show nothing in the first few hours after symptom onset?
The formation of a visible infarction zone (decreased tissue density on CT) takes time. In the hyperacute period, standard CT is performed primarily to rule out hemorrhagic stroke, for which the treatment strategy is radically different.
What is perfusion MRI (PWI) used for?
This mode reveals the perfusion deficit zone—an area of the brain where blood flow is reduced, but cells are still alive. Combined with diffusion-weighted MRI, this helps determine whether thrombolysis is indicated.
How to prevent deep vein thrombosis in a paralyzed patient?
Elastic bandaging of the legs or compression stockings, passive gymnastics, elevated leg position, and prophylactic administration of low-dose heparin (5000 IU twice daily subcutaneously) are used.
What else to study on this topic
- Clinical manifestations of infarctions in the carotid and vertebrobasilar territories
- Mechanical thrombectomy: indications and technique
- Neurological deficit severity rating scales (NIHSS)
- Topography and embryogenesis of spinal cord blood supply
- Early rehabilitation protocols for patients with focal CNS lesions
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