Symptoms of ischemic stroke

Symptoms of ischemic stroke are varied and depend on the location and volume of the brain lesion. The most common location of the brain infarction is the carotid (80-85%), less often - the vertebrobasilar basin (15-20%).

Infarctions in the middle cerebral artery supply basin

A feature of the blood supply basin of the middle cerebral artery is the presence of a pronounced collateral circulation system. With occlusion of the proximal part of the middle cerebral artery (segment M1), subcortical infarction may occur, while the cortical area of the blood supply remains unaffected with sufficient blood flow through the meningeal anastomoses. In the absence of these collaterals, extensive infarction in the area of the blood supply of the middle cerebral artery may develop.

In case of infarction in the area of blood supply of superficial branches of the middle cerebral artery, deviation of the head and eyeballs towards the affected hemisphere may occur acutely; in case of damage to the dominant hemisphere, total aphasia and ipsilateral ideomotor apraxia may develop. In case of damage to the subdominant hemisphere, contralateral disregard of space, anosognosia, aprosody, and dysarthria develop.

Infarctions of the brain in the region of the upper branches of the middle cerebral artery are clinically manifested by contralateral hemiparesis (mainly of the upper limbs and face) and contralateral hemianesthesia with the same predominant localization in the absence of visual field defects. With extensive lesions, concomitant abduction of the eyeballs and fixation of gaze toward the affected hemisphere may occur. With lesions of the dominant hemisphere, Broca's motor aphasia develops. Oral apraxia and ideomotor apraxia of the ipsilateral limb are also common. Infarctions of the subdominant hemisphere lead to the development of spatial unilateral neglect and emotional disorders. With occlusion of the lower branches of the middle cerebral artery, motor disorders, sensory agraphia, and astereognosis may develop. Visual field defects are often detected: contralateral homonymous hemianopsia or (more often) superior quadrant hemianopsia. Dominant hemisphere lesions lead to the development of Wernicke's aphasia with impaired speech comprehension and retelling, paraphasic semantic errors. Infarction in the subdominant hemisphere leads to the development of contralateral neglect with sensory dominance, anosognosia.

Infarction in the striatocapsular artery supply basin is characterized by severe hemiparesis (or hemiparesis and hemihypesthesia) or hemiplegia with or without dysarthria. Depending on the size and location of the lesion, paresis predominantly affects the face and upper limb or the entire contralateral half of the body. With extensive striatocapsular infarction, typical manifestations of occlusion of the middle cerebral artery or its pial branches (e.g., aphasia, neglect, and homonymous lateral hemianopsia) may develop.

Lacunar infarction is characterized by development in the area of blood supply of one of the single perforating arteries (single striatocapsular arteries). Development of lacunar syndromes is possible, in particular isolated hemiparesis, hemihypesthesia, ataxic hemiparesis or hemiparesis in combination with hemihypesthesia. The presence of any, even transient signs of deficit of higher cortical functions (aphasia, agnosia, hemianopsia, etc.) allows reliable differentiation of striatocapsular and lacunar infarctions.

Infarctions in the anterior cerebral artery supply basin

Infarctions in the anterior cerebral artery blood supply basin occur 20 times less frequently than infarctions in the middle cerebral artery blood supply area. The most common clinical manifestation is motor disturbances; with occlusion of the cortical branches, in most cases, motor deficit develops in the foot and the entire lower limb and less pronounced paresis of the upper limb with extensive damage to the face and tongue. Sensory disturbances are usually mild and sometimes completely absent. Urinary incontinence is also possible.

Infarctions in the posterior cerebral artery supply basin

With occlusion of the posterior cerebral artery, infarctions of the occipital and mediobasal parts of the temporal lobe develop. The most common symptoms are visual field defects (contralateral homonymous hemianopsia). Photopsies and visual hallucinations may also be present, especially when the subdominant hemisphere is affected. Occlusion of the proximal segment of the posterior cerebral artery (P1) can lead to the development of infarctions of the brainstem and thalamus, due to the fact that these areas are supplied by some of the branches of the posterior cerebral artery (thalamosubthalamic, thalamogeniculate, and posterior choroidal arteries).

Infarctions in the vertebrobasilar blood supply basin

Occlusion of a single perforating branch of the basilar artery results in localized brainstem infarction, particularly in the pons and midbrain. Brainstem infarctions are accompanied by cranial nerve symptoms on the ipsilateral side and motor or sensory disturbances on the opposite side of the body (so-called alternating brainstem syndromes). Occlusion of the vertebral artery or its main penetrating branches originating from the distal parts may result in lateral medullary syndrome (Wallenberg syndrome). The blood supply to the lateral medullary region is also variable and may be provided by small branches of the posterior inferior cerebellar, anterior inferior cerebellar, and basilar arteries.

Classification of ischemic stroke

Ischemic stroke is a clinical syndrome of acute vascular damage to the brain, it can be the outcome of various diseases of the cardiovascular system. Depending on the pathogenetic mechanism of development of acute focal cerebral ischemia, several pathogenetic variants of ischemic stroke are distinguished. The most widely used classification is TOAST (Trial of Org 10172 in Acute Stroke Treatment), it distinguishes the following variants of ischemic stroke:

• atherothrombotic - due to atherosclerosis of large arteries, which leads to their stenosis or occlusion; when an atherosclerotic plaque or thrombus fragments, arterioarterial embolism develops, which is also included in this type of stroke;
• cardioembolic - the most common causes of embolic infarction are arrhythmia (atrial flutter and fibrillation), valvular heart disease (mitral), myocardial infarction, especially those less than 3 months old;
• lacunar - due to occlusion of small-caliber arteries, their damage is usually associated with the presence of arterial hypertension or diabetes mellitus;
• ischemic, associated with other, rarer causes: non-atherosclerotic vasculopathy, blood hypercoagulation, hematological diseases, hemodynamic mechanism of development of focal cerebral ischemia, dissection of the arterial wall;
• ischemic of unknown origin. This includes strokes with an unknown cause or with two or more possible causes, when it is impossible to make a final diagnosis.

Based on the severity of the lesion, a minor stroke is distinguished as a special variant, the neurological symptoms associated with it regress within the first 21 days of the disease.

In the acute period of stroke, according to clinical criteria, mild, moderate and severe ischemic stroke are distinguished.

Depending on the dynamics of neurological disorders, a distinction is made between a developing stroke (“stroke in progress” - with increasing severity of neurological symptoms) and a completed stroke (with stabilization or reverse development of neurological disorders).

There are various approaches to the periodization of ischemic stroke. Taking into account epidemiological indicators and modern ideas about the applicability of thrombolytic drugs in ischemic stroke, the following periods of ischemic stroke can be distinguished:

• the acute period is the first 3 days, of which the first 3 hours are defined as the therapeutic window (the possibility of using thrombolytic drugs for systemic administration); if symptoms regress in the first 24 hours, a transient ischemic attack is diagnosed;
• acute period - up to 28 days. Previously, this period was defined as up to 21 days; accordingly, as a criterion for diagnosing a minor stroke, regression of symptoms up to the 21st day of the disease is still maintained;
• early recovery period - up to 6 months;
• late recovery period - up to 2 years;
• period of residual effects - after 2 years.

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