NEUROLOGY AND NEUROSURGERY - YU. V. ALEKSEEENKO - 2014

ACUTE CEREBROVASCULAR ACCIDENTS

Acute cerebrovascular accidents (ACVAs) rank third among causes of mortality worldwide, following cardiovascular diseases and Cancer. The incidence of ACVAs in European countries ranges from 100 to 200 first-time events per 100,000 population per year. In Europe and the Americas, ischemic strokes account for 70-85% of ACVAs, intracerebral hemorrhages for 20-25%, and subarachnoid hemorrhages for 5% of cases. Thirty-day mortality following an ACVA depends on The Nature of the cerebrovascular event and is 8-15% for ischemic strokes, 42-46% for subarachnoid hemorrhages, and 48-82% for intracerebral hemorrhages. In developed economies, stroke is the leading cause of permanent disability. Notably, only 20% of stroke survivors return to work without significant functional limitations. While 60% of patients experience incomplete recovery of neurological Functions, 20% require permanent assistance and care in daily life. The financial burden of ACVAs is immense, consuming over 5% of healthcare resources in economically developed nations. Indirect economic costs are difficult to calculate precisely, yet they far exceed direct losses.

Classification of acute cerebrovascular accidents. Etiology. Pathogenesis. Terminology

Acute cerebrovascular accidents are pathological conditions characterized by sudden-onset disorders of Central Nervous system (CNS) function resulting from Brain tissue Damage caused by impaired cerebral Blood supply. ACVAs may be diffuse or localized, with brain tissue damage restricted to the vascular territory of a specific Arterial System. Depending on the duration of neurological deficits, ACVAs are classified into transient ischemic attacks (lasting less than 24 hours) and persistent cerebrovascular disorders—strokes (where clinical manifestations persist for more than 24 hours).

Inadequate delivery of oxygen and energy substrates to the brain via the cerebral Circulation can lead to ischemic stroke. Hemorrhagic stroke represents a form of CNS injury caused by the extravasation of blood beyond the cerebral vascular bed (intracranial Hemorrhage). Another major variant of ACVA is acute hypertensive encephalopathy, which occurs when cerebral blood flow autoregulation fails due to a sharp and substantial rise in systemic blood pressure. Modern classification systems also recognize minor stroke, defined as a stroke with reversible neurological deficits that resolve completely within 3 weeks.

Stroke is most commonly a predictable, albeit distant, complication of widespread (latent or overt), chronic progressive diseases predominantly affecting The Cardiovascular system, triggered by critical failures in cerebral blood flow autoregulation and the depletion of systemic and local (cerebral) compensatory mechanisms. The most common causes of ACVA include atherosclerotic cerebrovascular disease, arterial Hypertension, Diabetes Mellitus, or a combination thereof. THE SPECTRUM OF potential etiologies encompasses numerous recognized and relatively rare conditions:

   ▪ atherosclerotic lesions of extra- and intracranial vessels;

   ▪ arterial hypertension and symptomatic hypertension;

   ▪ diabetes mellitus;

   ▪ congenital Anomalies of the cardiovascular system (hypoplasia and pathological tortuosity of extracranial and cerebral Arteries, intracranial arterial and arteriovenous aneurysms, coarctation of the aorta, valvular Heart disease, etc.);

   ▪ cardiovascular diseases (atrial fibrillation and other Cardiac Arrhythmias, myocardial infarction, cardiomyopathies, etc.);

   ▪ blood disorders (polycythemia, leukemias, coagulopathies, etc.);

Arterial hypertension is well-established as a leading cause of ACVA. A 7.5 mmHg increase in diastolic blood pressure is associated with a doubling of stroke risk. Meanwhile, atherosclerosis of precerebral and cerebral vessels is the primary cause of luminal narrowing, reduced blood flow, and thrombotic or embolic complications. Approximately 20% of ischemic strokes result from cardiogenic embolism.

Additionally, the list of potential etiologic factors includes various toxic and dysmetabolic states, vasculitis, internal carotid and vertebral artery dissection, prosthetic heart Valves, infectious and oncological diseases, immune disorders, trauma, and other visceral pathologies.

The pathogenetic mechanisms of ACVA vary depending on the underlying pathology. Most ischemic brain injuries are caused by partial or complete occlusion of cerebral vessels and a critical reduction in cerebral perfusion. Non-thrombotic (hemodynamic) ischemic stroke can develop due to reduced blood flow resulting from the narrowing of extra- or intracranial arteries caused by atherosclerosis and atheromatous plaque formation, vessel wall inflammation, or congenital anomalies. Under such conditions, ischemic brain injury occurs when collateral circulation reserves are exhausted, systemic blood pressure becomes unstable, and cerebral autoregulation fails (e.g., severe hypotension, hemorrhage, hypovolemia). Thrombotic ischemic stroke develops when a cerebral or extracranial vessel lumen is narrowed or occluded by a thrombus, typically occurring in areas of sluggish flow and turbulence, such as arterial bifurcations or sites of atherosclerotic plaques. Embolic ischemic stroke arises from artery-to-artery embolism (due to ulcerated carotid or aortic arch plaques) or cardiogenic embolism (associated with valvular heart disease or arrhythmias). In many cases, ischemic brain injury occurs in watershed zones between major cerebral arteries or, less frequently, via "steal" phenomena, where reduced perfusion in one brain region results from blood being diverted to another vascular bed. It should be emphasized that any given etiology of ischemic stroke may involve multiple overlapping mechanisms. Conversely, the same mechanism of ischemic brain injury can be observed across different underlying pathologies.

Hemorrhagic stroke (more precisely, various types of non-traumatic intracranial hemorrhage) develops as a complication of arterial hypertension, the rupture of congenital arterial aneurysms, or compromised integrity of cerebral vessels due to structural wall changes (including atherosclerosis) and increased vascular permeability combined with coagulation disorders. Lipohyalinosis, fibrinoid necrosis in small penetrating cerebral arteries, and microaneurysm formation are considered key prerequisites for intracranial hemorrhage in hypertensive patients. While elevated blood pressure appears to be the logical direct trigger for vessel rupture and the onset of a cerebrovascular catastrophe, it does not account for all aspects of this process. At least half of all hemorrhagic strokes in hypertensive patients occur against a backdrop of relatively stable hemodynamics.

Intracranial hemorrhages include Subarachnoid Hemorrhage, where blood extravasating from cerebral vessels mixes with CEREBROSPINAL FLUID and spreads relatively evenly throughout the subarachnoid space. Intracerebral (parenchymal) hemorrhage involves blood infiltration and destruction of specific brain tissue areas adjacent to the bleeding source. Intraventricular Hemorrhage is another distinct anatomical variant. Occasionally, an intracerebral hematoma forms when blood breaches a damaged vessel, dissects into the brain parenchyma, and creates a localized, compact mass of clots and liquid blood. Additionally, hematomas may occasionally occupy epidural or subdural spaces. The vast majority of epidural and subdural hematomas are of traumatic origin. It is also common for a single patient to present with a combination of multiple topographical variants of intracranial hemorrhage.

A comprehensive understanding of the intricate interplay between causes, pathogenic mechanisms, and clinical presentations underpins the Modern concept of stroke heterogeneity. Ischemic strokes constitute the vast majority of ACVAs (approximately 80%). While cerebrovascular atherosclerosis most frequently leads to cerebral ischemia, it can occasionally result in intracranial hemorrhage. Similarly, arterial hypertension can precipitate both ischemic and hemorrhagic strokes, with an approximate ratio of 3:1, contrary to the traditional view that hypertensive patients are overwhelmingly predisposed to hemorrhagic events.

One must also acknowledge The Role of various contributing, or so-called precipitating, factors in the onset of ACVA. While not true primary causes, these factors frequently precede the cerebrovascular event and act as triggers that set the entire pathogenetic cascade in motion. These include physical and mental exhaustion, negative emotions, psycho-emotional stress, alcohol consumption, barometric pressure fluctuations, and other meteorological factors.

The mechanisms of CNS injury in ACVA are divided into Primary and secondary effects. Primary mechanisms involve structural damage to brain tissue resulting from hemorrhage or ischemic necrosis at the exact moment of the vascular event. Secondary mechanisms encompass subsequent metabolic, microcirculatory, and electrolyte disturbances, coagulation abnormalities, and other pathological processes that exacerbate brain edema (localized or generalized) and elevate intracranial pressure. Ultimately, this can lead to decreased cerebral perfusion, brain herniation, and patient death due to resulting Brainstem compression affecting Respiration and cardiac function. The clinical manifestations, severity, and prognosis of both ischemic and hemorrhagic strokes are primarily determined by the volume and Location OF THE primary brain lesion, as well as the status of cerebral perfusion (cerebral blood flow volume).

In ischemic stroke, a zone of the "ischemic penumbra" (an area of potentially reversible ischemic injury) surrounds the necrotic core. Although Cell death within this zone ultimately enlarges the infarct, these Cells remain viable for some time despite reduced perfusion. Neuronal function in the penumbra can be restored if cerebral blood flow is promptly reestablished and neuroprotective agents are administered. The duration of the so-called "therapeutic window," during which these changes remain reversible with appropriate Treatment, is difficult to determine precisely (likely spanning hours or days) and exhibits high inter-individual Variability, partly due to the asynchronous development of heterogeneous pathogenetic mechanisms across different brain regions.

Brain edema develops within minutes of focal ischemia and progresses over several days (initially cytotoxic, followed by vasogenic). It peaks around days 2-4 and, in favorable cases, gradually resolves over 1-2 weeks. The severity of brain edema directly correlates with infarct size. Notably, large ischemic lesions frequently undergo hemorrhagic transformation, which is typically associated with a poorer prognosis. In cases of favorable recovery, the necrotic brain tissue is gradually replaced by a gliomesodermal scar or a cyst.

In hemorrhagic stroke, delayed cerebral vasospasm warrants special attention among secondary injury mechanisms. It develops several days after the initial event and leads to paradoxical secondary ischemic brain injury. This process is triggered by Hemoglobin breakdown products from erythrocytes degraded within the cerebrospinal fluid.

The onset of an ACVA is typically characterized by the sudden appearance and rapid progression of generalized and focal neurological deficits, often accompanied by systemic disturbances. General cerebral manifestations include Various Forms of cephalalgia, altered consciousness, seizures, and related symptoms of elevated intracranial pressure and meningeal irritation. Focal neurological deficits are defined by the BOUNDARIES OF THE specific ischemic territory and vary widely. The most common manifestations include motor deficits (hemiparesis), sensory disturbances (hemihypesthesia), speech disorders (aphasia), visual field defects (hemianopia), gaze abnormalities (diplopia), coordination deficits (ataxia), and brainstem signs (bulbar syndrome: dysarthria, dysphagia, dysphonia), among others.

Stroke, like Other forms of acute central nervous system injury, may be accompanied by a complex of nonspecific systemic abnormalities that typically resolve spontaneously within a few days. Most commonly, these include a moderate increase in blood pressure, blood glucose levels, ERYTHROCYTE SEDIMENTATION RATE (ESR), and peripheral blood leukocyte count. Naturally, such deviations—disregarding other factors—cannot be regarded as conclusive signs of arterial hypertension, diabetes mellitus, or an infectious disease. Naturally, The rate of development and The ratio of generalized, focal, and specific clinical manifestations depend on the underlying mechanisms and the type of acute cerebrovascular accident (ACVA).

With a favorable clinical course, a regression of generalized and focal neurological deficits is typically observed. This process may occur entirely within the acute phase of the stroke. As it slows down, the recovery process can continue for several months or even years. One year post-ACVA, the condition is referred to as the consequences of a prior stroke. The periodization of cerebrovascular disorders is presented in the table.

Class="center">Table. Periodization of Acute Cerebrovascular Accidents

Transient Cerebrovascular Disorders

The defining criterion for transient cerebrovascular disorders is the reversibility of the resulting neurological deficits within 24 hours; however, the timeframe for these conditions is rather conventional. It must be emphasized that determining the transient nature of an ACVA is always performed retrospectively, only after the identified deficits have resolved. Two forms of transient cerebrovascular disorders are distinguished: transient ischemic attacks (TIAs) and hypertensive crises.

The causes of TIAs may include any of the cardiovascular diseases mentioned in the list of ACVA etiologic factors. Against the backdrop of systemic hemodynamic instability and insufficient regional compensatory mechanisms of cerebral blood flow, these conditions can lead to a temporary decrease in cerebral perfusion and The Development of ischemic brain injury in critical supply zones. Specific mechanisms may include artery-to-artery microembolism, reduced blood flow due to stenosis of cerebral and major vessels, the "steal" phenomenon combined with a drop in blood pressure, etc. Unlike reversible clinical manifestations, localized ischemic brain injury may be persistent and irreversible, and in some cases, it is detected using neuroimaging techniques (CT, MRI). Thus, recurrent TIA episodes, sometimes running a subclinical course, lead to the accumulation of small cysts and atrophic Changes in the brain tissue. This explains the patterns underlying The formation of qualitatively different pathological states—chronic or progressive cerebrovascular disorders (dyscirculatory encephalopathy) with persistent neurological deficits.

Clinical manifestations of TIAs most frequently last for several seconds or minutes, and their nature depends on the localization of the circulatory disorder. During a TIA in the Internal Carotid Artery system, sensory disturbances (paresthesias, hypoesthesia) in one-half of the face and Tongue, the arm, or the entire contralateral half of the body are most commonly observed. Sensory deficits are often accompanied by weakness in the arm or leg, and speech disturbances (aphasia). Partial or secondary generalized epileptic seizures may also occur. Sometimes, sudden blindness or Vision loss in one eye combined with hemiparesis in the contralateral limbs is possible.

TIAs in the vertebrobasilar system are characterized by attacks of systemic vertigo, Hearing impairment, hemianopia, double vision (diplopia), bulbar symptoms (dysarthria, dysphatia, dysphonia), ataxia, and alternating syndromes. Episodes of sudden muscular hypotonia leading to a fall and brief immobility without loss of consciousness (drop attack) may develop, provoked by turning or hyperextending the HEAD. In Unterharnscheidt syndrome, these disorders are accompanied by a loss of consciousness. TIAs can also present with transient memory impairment for current events while memory for the distant past remains intact.

During hypertensive crises, characterized by a sharp rise in blood pressure, generalized symptoms predominate—diffuse headache, nausea, vomiting, and autonomic disturbances (hyperhidrosis, tachycardia, Skin flushing, chills). Alterations in consciousness and emotional state, such as drowsiness, stupor, anxiety, and agitation, may also occur.

The challenge in recognizing TIAs is that their duration is most commonly just a few seconds or minutes. A detailed medical history frequently helps clarify the true nature and Water/144.html">Origin of the symptoms of transient cerebrovascular disorders. In most cases, the Diagnosis of a TIA is retrospective, meaning it is established only after the symptoms of the condition have disappeared. The recurrence of TIA episodes indicates an increased risk of stroke and necessitates an investigation to determine the exact etiology and specific mechanisms of the cerebrovascular disorders. Approximately 30–40% of patients who have suffered a TIA may develop a stroke within the next 5 years. A TIA occurring against the Background of cardiac pathology (especially cardiac arrhythmias) indicates not only a significant probability of stroke but also a risk of myocardial infarction and other life-threatening conditions. Under such circumstances, color-coded duplex sonography (CCDS), MR angiography, and in some cases, traditional or digital cerebral angiography, as well as coagulation studies, are required. If syncopal episodes are present, an EEG and a thorough cardiac workup are indicated. The onset of TIAs calls for systemic, pathogenetically substantiated Prevention of ACVAs.

Ischemic Stroke

The Clinical presentation of ischemic stroke (IS) is characterized by the dominance of focal brain injury signs within the acute cerebrovascular event. The sudden onset of a stroke occurs more frequently with embolisms. In thrombotic stroke, a fluctuation of neurological symptoms and a gradual development of neurological deficits may take place. In some patients, the picture of neurological disorders is discovered in the morning upon waking. Severe alterations in consciousness, intense headache, and vomiting can be observed in infarctions of the brainstem, Cerebellum, and extensive hemispheric infarctions.

During the first few days following an ischemic stroke, 70–80% of patients experience elevated blood pressure, which subsequently returns to baseline levels gradually. Strokes in the carotid territory occur 5–6 times more frequently than in the vertebrobasilar territory. Approximately 20% of patients with ischemic stroke in the carotid system exhibit a progressive clinical course, meaning a gradual worsening of neurological deficits over several hours or days. In lesions of the vertebrobasilar system, this pattern of stroke development is observed in 40% of patients.

Circulatory Disorders in the internal carotid artery system manifest as contralateral hemiparesis, hemihypoesthesia, and hemianopia. When the dominant hemisphere (more frequently the left) is affected, aphasia, alexia, agraphia, and apraxia also occur. Damage to the nondominant hemisphere is typically accompanied by anosognosia and body scheme disorders. Involvement of the paracentral lobules in the ischemic zone may result in pelvic organ dysfunction. Mood changes and other signs of frontal lobe dysfunction are sometimes observed, along with vision loss on the ipsilateral side of the ischemia.

Lesions of the middle cerebral artery branches may cause central paresis of the facial, lingual, and hand Muscles, or contralateral hemiparesis and hemihypoesthesia, sensory aphasia (when the dominant hemisphere is affected), hemianopia, anosognosia, and body scheme disorders (when the nondominant hemisphere is affected).

A stroke in the anterior cerebral artery territory manifests as hemiparesis with predominance in the proximal arm and distal leg, or monoparesis of the contralateral leg. Mild sensory disturbances in the paretic limbs, urinary retention, or incontinence may occur. Occasionally, aphasic disorders, impoverished spontaneous speech, and psychiatric symptoms (reduced motivation, agitation, or disinhibition) are observed.

Circulatory disorders in the vertebrobasilar system present with a wide range of clinical manifestations. Typical features include systemic vertigo, ataxia, oculomotor disorders (diplopia, strabismus, nystagmus), homonymous hemianopia, and other visual disturbances. Bulbar symptoms (dysarthria, dysphatia, dysphonia) and bilateral motor deficits may develop. Lesions at various levels of the brainstem result in alternating syndromes featuring cranial nerve palsies on the side of the lesion and long-tract sensory and motor deficits on the contralateral side. Depression of consciousness and psychiatric impairments are possible. Occlusion of the vertebral or posterior inferior cerebellar artery leads to infarction of the Medulla Oblongata and the inferior portion of the cerebellar hemisphere. It manifests as Wallenberg–Syndrome (Wallenberg-Zakharchenko syndrome), the full constellation of which includes vertigo, nausea, vomiting, impaired pain and Temperature Sensation on the ipsilateral face, cerebellar ataxia, Horner's syndrome, dysphatia, dysphonia, and dysarthria, as well as contralateral pain and temperature hypoesthesia of the limbs and trunk. Cerebellar infarction presents with vertigo and ataxia. Alterations in consciousness and contralateral homonymous hemianopia may also occur.

Occlusion of the Basilar artery is accompanied by oculomotor disorders, tetraplegia, altered consciousness, and vital function impairment, which in most cases leads to a fatal outcome. When Branches of the basilar artery are affected, consciousness usually remains intact, and alternating syndromes are detected (e.g., peripheral Facial Nerve palsy on the ipsilateral side and hemiplegia on the contralateral side).

Lacunar stroke accounts for 15–30% of all ischemic stroke cases. These are small ischemic lesions that form in the White matter OF the cerebral hemispheres (periventricular region, Basal Ganglia, thalamus), brainstem, and cerebellum. Their development is attributed to damage to small penetrating branches of the middle cerebral artery, posterior cerebral artery, and basilar artery resulting from age-related changes, arterial hypertension, and diabetes mellitus. Poor collateral circulation in the territory of the penetrating arteries, when they are damaged, leads to the formation of a small ischemic zone that eventually transforms into a tiny cyst (lacuna), which gave this type of ACVA its terminological name.

Most frequently, a lacunar stroke develops suddenly, without impairment of consciousness, psychiatric functions, or epileptic seizures. The most common variant of lacunar stroke is a "pure motor stroke." It is characterized by unilateral isolated motor deficits—central paresis of the arm, leg, face, or tongue. The ischemic lesion is localized in the posterior limb of the internal capsule, the basis pontis, the corona radiata, the cerebral peduncle, or The basis of the medulla oblongata.

In a "sensory-motor stroke," a combination of unilateral motor and sensory deficits is noted. The ischemic lesion in such cases is located in the posterior limb of the internal capsule, the corona radiata, the genu or anterior limb of the internal capsule, or the thalamus. A "pure sensory stroke," when the ischemic lesion is localized in the thalamus, is characterized by sensory disturbances (most commonly pain and temperature) on the contralateral side.

With a limited ischemic lesion of the basis pontis and the anterior limb of the internal capsule, "dysarthria–clumsy hand syndrome" may develop. This presents as mild weakness and clumsiness in the hand, and unilateral central facial Muscle paresis. Central hemiparesis and limb ataxia—"ataxic hemiparesis"—develops with an ischemic lesion in the posterior limb of the internal capsule, the basis pontis, or the corona radiata. Lacunar strokes may be asymptomatic and discovered incidentally during CT or MRI examinations.

The prognosis for ischemic strokes depends on the localization and volume of the ischemic brain injury, the severity of brain edema, as well as the presence of comorbid conditions and complications (Pneumonia, pressure ulcers, urosepsis, etc.). In the acute phase of the disease (first 30 days), approximately 15–25% of patients die. In lacunar strokes, only 2% of affected individuals die during the same timeframe. Recovery of neurological functions occurs most intensively during the first 3 months post-stroke. By the end of the first year, about 60–70% of ischemic stroke patients are alive, and at five and ten years, approximately 50% and 25%, respectively. Recurrent ACVAs following an ischemic stroke may occur in 30% of patients within the subsequent 5 years. However, heart disease remains the most frequent cause of death in stroke survivors.

Hemorrhagic Strokes

Quite often, hemorrhagic stroke occurs as a complication of arterial hypertension, which involves lipohyalinosis and fibrinoid degeneration of small arterial vessels, along with the formation of microaneurysms. The hemorrhage results from the rupture of a modified vessel or microaneurysm, leading to hemorrhagic imbibition of the brain tissue. In arterial hypertension, bleeding most frequently occurs within the basin of the perforating cerebral arteries—specifically in the region of the basal ganglia (approximately 50%), thalamus (15%), cerebral white matter (15%), Pons (10%), and cerebellum (10%). Blood breakthrough into the subarachnoid space or the ventricular system is quite common and significantly worsens the clinical course and prognosis of the disease.

Additionally, the rupture of an arteriovenous aneurysm sometimes serves as the cause of hemorrhage. In older age, Cerebral Hemorrhage may develop as a consequence of cerebral amyloid angiopathy. Other, rarer causes of brain hemorrhages include systemic disorders of cerebral vessels, cerebral atherosclerosis, anticoagulant therapy, and hemorrhagic syndromes of other origins. Intracranial hemorrhages may manifest as a brain tumor or metastatic lesion, and can also be triggered by alcohol intoxication or substance abuse.

As noted earlier, non-traumatic intracranial hemorrhages can be intracerebral, involving hemorrhagic imbibition of brain tissue or the formation of a hematoma—a localized and well-defined accumulation of blood within the cerebral parenchyma. Furthermore, intracranial hemorrhages may be subarachnoid or intraventricular. Epidural and subdural hematomas are overwhelmingly traumatic in origin, though in some cases they develop against the background of arterial hypertension or due to other causes.

The zone of hemorrhage undergoes destruction of Nervous Tissue and compression of surrounding brain structures by the escaped blood. This leads to cerebral vasospasm, microcirculatory disturbances, and ischemic disorders. Consequently, brain edema and intracranial pressure progressively increase. The displacement of brain structures can result in the compression of the brainstem, which is frequently the cause of a fatal outcome. Under a favorable course of events, the extravasated blood may form a fibrin clot, transform into a liquid mass, and gradually undergo resorption. Over time, a cyst forms at the site of the hemorrhage.

Hemorrhagic stroke typically develops suddenly, during the daytime, usually during a period of active physical exertion. However, it can also occur during rest or even Sleep. Intracranial hemorrhages are characterized by a combination of general cerebral and focal neurological deficits, with general cerebral symptoms frequently predominating over focal ones. Patients experience intense headache, nausea, and vomiting, and exhibit meningeal syndrome. Various states of impaired consciousness may be observed—ranging from obtundation, stupor, or psychomotor agitation to deep coma—along with disruptions in respiratory rhythm. The onset of hemorrhage may be accompanied by epileptic syndrome. Among focal neurological deficits, hemiparesis and hemianesthesia, speech disorders, oculomotor impairments, coordination disorders, as well as bulbar and alternating syndromes are most commonly present. The nature of focal neurological disorders depends on the localization of the hemorrhage.

Pronounced autonomic disorders and systemic reactions are present from the very beginning of the disease. Characteristic features include elevated blood pressure, tachycardia, facial flushing, fever, elevated ESR, leukocytosis, and an increased concentration of glucose in the peripheral blood.

Hemorrhagic stroke is typically characterized by prominent general cerebral symptoms and, overall, a more severe clinical course. At the same time, CT and MRI examinations of patients with acute cerebrovascular accidents reveal that small-scale hemorrhages can present similarly to ischemic strokes, manifesting solely with focal neurological symptoms or even remaining asymptomatic. An unfavorable outcome within the first 30 days of the disease may occur in 40-60% of patients. Recurrent intracerebral hemorrhage develops in only 4% of cases, though the risk of recurrent bleeding is somewhat higher in cases of ruptured arteriovenous malformations.

Spontaneous (non-traumatic) subarachnoid hemorrhage occurs in the majority of cases (70–85%) As a result of the rupture of an arterial aneurysm. Arteriovenous aneurysms are a significantly less frequent cause. In many cases of non-aneurysmal subarachnoid hemorrhages, the underlying cause cannot be established. Arterial aneurysms are most commonly localized at the Base of the brain in the anterior PARTS OF THE circle of Willis, predominantly at vessel branching points. Apparently, arterial aneurysms represent a congenital defect of the cerebral Vascular System. Sometimes they are incidental findings during autopsy and angiographic examinations (up to 5% of cases); thus, in many instances, they follow an asymptomatic course and do not lead to cerebral vascular disorders. Aneurysmal rupture usually occurs in the region of its fundus or lateral wall, where the muscular layer is absent and the aneurysm wall is thinned. The size of the aneurysm may gradually increase with age. Factors contributing to aneurysm rupture are considered to include arterial hypertension, smoking, and alcohol abuse.

During a subarachnoid hemorrhage, a proportion of erythrocytes in the cerebrospinal fluid are destroyed due to an osmolar gradient. The resulting hemoglobin degradation products and A number of other factors trigger secondary cerebral vasospasm. This typically appears 3–5 days after the hemorrhage, peaks within 5–14 days, and gradually regresses over 2–4 weeks. In half of the cases, vasospasm causes delayed ischemic neurological deficit in the clinical picture of the disease. Subarachnoid hemorrhage is accompanied by the active clearance of red Blood Cells from the cerebrospinal fluid, leading to the development of obstructive or mixed Hydrocephalus. Two weeks after the onset of hemorrhage, only xanthochromic discoloration of the cerebrospinal fluid remains. In the immediate days and weeks following the aneurysmal rupture, There is a risk of rebleeding, which proves fatal in more than half of the cases.

Subarachnoid hemorrhage usually has a sudden onset. In the majority of cases, its initial symptom is an intense headache, which patients frequently describe as being "struck in the head" or feeling a "spread of heat in the head." Concurrently, patients experience nausea, vomiting, pain in the lower back and spine along THE Vertebral Column, photophobia, and generalized hyperesthesia. Various levels of impaired consciousness (obtundation, stupor, and coma) are detected in 50–60% of patients, while some develop psychomotor agitation and epileptic seizures. Within the first hours of the disease, nuchal rigidity and other meningeal signs (Kernig's and Brudzinski's signs) appear. Focal neurological symptoms are initially usually minor—most commonly anisoreflexia and oculomotor disorders. As cerebral vasospasm intensifies during the second week of the disease, additional symptoms of secondary ischemic brain damage (such as hemiparesis and speech disturbances) may emerge. Body temperature rises during the first day of the illness. Most patients also experience an elevation in blood pressure, which typically returns to baseline levels within a few days. Subarachnoid hemorrhage is occasionally complicated by myocardial ischemia and cardiac arrhythmias.

Recurrent subarachnoid hemorrhage is accompanied by the return of severe headache, depressed consciousness, and The Emergence of new focal neurological deficits. Its probability within the first month of the disease is approximately 30%.

To determine the optimal management strategy for patients with subarachnoid hemorrhage, the Hunt and Hess scale has been proposed, which provides 5 grades of patient severity:

I - asymptomatic or mild headache and slight meningeal signs;

II - moderate to severe headache; pronounced meningeal signs; cranial nerve (oculomotor) palsy;

III - depression of consciousness to obtundation; moderately severe neurological deficit;

IV - stupor; severe neurological deficit (hemiparesis or hemiplegia); pronounced signs of autonomic dysregulation;

V - comatose state.

Mortality from subarachnoid hemorrhage is quite high, reaching approximately 40% within the first 30 days. Roughly 15% of patients with aneurysmal subarachnoid hemorrhages die immediately after the onset of the disease, even before reaching medical facilities.

Acute Hypertensive Encephalopathy

Acute hypertensive encephalopathy is a complication of arterial hypertension and certain other symptomatic hypertensive states, occurring with a significant rise in blood pressure (diastolic blood pressure exceeding 120 mmHg). This pathological condition arises from The breakdown of cerebral blood flow autoregulation, whereby a sharp increase in systemic blood pressure disrupts vascular tone regulation and leads to passive dilation of the cerebral arteries. Under such circumstances, excessive cerebral perfusion develops, accompanied by brain edema, elevated intracranial pressure, and—as a consequence of this chain of events—the threat of slowed and critically reduced volumetric cerebral blood flow.

The clinical picture of acute hypertensive encephalopathy develops over several hours against the background of a marked increase in blood pressure, manifesting as diffuse headache, nausea, and vomiting. Patients typically develop psychomotor agitation, followed by a gradual depression of consciousness. Some patients experience epileptic seizures. Examination reveals meningeal signs, whereas distinct focal neurological deficits are generally absent. CT or MRI scans detect signs of cerebral edema. Ophthalmoscopy reveals papilledema, arteriolar spasm, and retinal hemorrhage. The main therapeutic goals for this pathological condition are the normalization of blood pressure and the management of cerebral edema.

Diagnosis of Acute Cerebrovascular Accidents and Patient examination protocol

The diagnostic protocol for acute cerebrovascular accidents (ACVA) is aimed at simultaneously addressing several objectives:

   1. determining the volume and localization of the brain lesion;

   2. differentiating between ischemic and hemorrhagic brain injury;

   3. Determination of the pathogenetic variant of acute cerebrovascular accident and underlying etiology;

   4. exclusion of other causes of neurological deficit (tumor, trauma);

   5. recognition of complications;

   6. clarification of significant comorbid conditions.

The diagnosis of acute cerebrovascular accident (CVA) is most often based on the sudden onset of focal neurological symptoms typical of damage to one of the cerebral vascular systems and/or severe general cerebral symptoms (impaired consciousness, meningeal syndrome). The assumption of CVA is supported by a history of known causative conditions (arterial hypertension, atherosclerotic cerebral vascular disease, heart disease, diabetes mellitus, etc.), a patient age over 50 years, and a history of heavy smoking and alcohol abuse.

The most informative instrumental imaging method for detecting CVA is X-ray CT. When examining the brain, it can reveal a decrease in brain tissue density in the ischemic zone as early as the first hours after stroke onset, and even signs of thrombosis in certain intracranial vessels. Later on, a zone of cerebral edema, ventricular system distortion, signs of hemorrhagic transformation, and shift disorders may be detected. MRI is also a highly informative diagnostic method for cerebrovascular lesions. Importantly, X-ray CT and MRI reliably differentiate between ischemic brain damage and intracranial hemorrhages. In addition, these Methods help identify conditions that may be accompanied by neurological deficits and mimic the presentation of CVA (brain tumor, traumatic brain injury, demyelinating diseases).

In the absence of CT or MRI, cerebrospinal fluid examination via lumbar puncture is recommended to rule out intracranial hemorrhage. In ischemic stroke, the cerebrospinal fluid is usually unchanged. Echoencephaloscopy can be used to detect shifts in median brain structures, which is typically absent in the hyperacute period of ischemic stroke and more commonly observed in intracranial hemorrhages or other space-occupying brain lesions.

Non-invasive ultrasound methods—such as carotid duplex scanning and transcranial Doppler sonography of cerebral arteries—are used to clarify the cause and pathogenetic features of ischemic stroke. They allow for the detection of developmental anomalies, arterial stenosis and occlusion, precise localization and Structure of atherosclerotic plaques, and the characteristics of collateral Blood Circulation. Cerebral intravenous or intra-arterial digital subtraction angiography is the most effective method for identifying cerebral vascular pathology. These methods help detect tortuous vessels, occlusions, stenotic areas, atherosclerotic plaques, aneurysms, and other abnormalities. However, cerebral angiography is an invasive method and can be considered a minor surgical Procedure. Therefore, angiography is reserved for cases where Surgical treatment is anticipated or in young patients with an undetermined cause of the disease. Magnetic Resonance angiography has become increasingly widespread in recent times. The optimal and safest approach is to compare the results of ultrasound and Magnetic resonance imaging of the cerebral vasculature.

It should be emphasized that previously, the only way to determine the localization of ischemic or hemorrhagic brain damage was through the analysis of focal neurological deficits, which frequently led to contradictory or erroneous Conclusions. This was inevitable because, for example, ischemic stroke most often develops in watershed areas against the background of established compensatory mechanisms and individual features of brain vascularization. Nowadays, this task is accomplished by correlating neurological symptoms, CT changes in the brain tissue, and the state of cerebral vessels determined via cerebral angiography or MR angiography.

ECGs should be recorded for all patients with CVA, as this allows for the detection of rhythm disturbances, myocardial ischemia, and other abnormalities. These can either be the cause of the CVA or concomitant pathological conditions resulting from sympathoadrenal myocardial activation (cardiocerebral and cerebricardiac syndromes). When valvular disease, cardiomyopathy, aneurysm, or ventricular tumor is suspected, echocardiography is indicated. Transthoracic echocardiography is essential in cases of ischemic stroke of undetermined origin in patients under 45 years of age. Chest radiography helps detect lung diseases (pneumonia, tumor, tuberculosis) and evaluate the size of The Heart and aorta. The examination plan also includes:

   • Complete blood count (including platelet count),

   • Blood chemistry panel determining glucose, urea, creatinine, bilirubin, AST, ALT, Cholesterol, triglycerides, high- and low-density Lipoproteins;

   • Determination of potassium, sodium, chlorides, and plasma osmolality;

   • Blood gas analysis and acid-base balance parameters;

   • Coagulogram including fibrinogen, fibrinolytic activity, Thrombin time, prothrombin, blood clotting time, antithrombin III, and hematocrit;

   • Erythrocyte aggregation capacity and blood viscosity;

   • Urinalysis;

   • Determination of blood type and Rh factor;

   • HIV blood test;

   • HBs antigen blood test;

   • Wassermann reaction.

Management of Patients with Acute Cerebrovascular Accidents

Experience shows that the most effective management of patients with CVA can be provided in specialized stroke units. Basic and specific (differentiated) therapy is administered. In some cases, initial therapeutic measures in patients with CVA should aim to restore airway patency (airway clearance, preventing tongue fall-back, etc.), manage epileptic syndrome, heart failure, or cardiac arrhythmias.

Blood Pressure Control

Elevated blood pressure during the first 24 hours of a CVA is observed in the majority of patients. Given the disruption of cerebral autoregulation mechanisms and increased intracranial pressure, this phenomenon can be regarded as a systemic compensatory reaction. It aims to maintain adequate perfusion in the zone of critical blood supply impairment by overcoming the resistance of stenosed vessels and recruiting collateral circulation. Under such circumstances, antihypertensive drugs administered in the first few hours after ischemic stroke onset may cause an undesirable drop in mean arterial pressure and a dangerous reduction in cerebral perfusion within the ischemic brain lesion. At the same time, blood pressure must be reduced in cases of intracranial hemorrhage and certain cardiac disorders. Accordingly, in arterial hypotension, fluid administration is necessary, along with dopamine 0.5% 10-15 ml intravenously per hour until pressure stabilization, norepinephrine, dextrans, or 100-150 ml of type-specific fresh frozen plasma twice on the first day of the disease.

It is generally considered that in ischemic stroke, blood pressure within the limits of SBP <220 mm Hg and DBP <120 mm Hg does not require intervention. For patients with a history of hypertension, the optimal blood pressure level in the hyperacute phase of acute cerebrovascular accident (CVA) can be considered 180/100-105 mm Hg. In other cases, it is advisable to maintain a moderate elevation in blood pressure at 160-180/90-100 mm Hg. Rapid reduction of blood pressure must be avoided! When administering antihypertensive therapy, 24-hour ambulatory blood pressure monitoring is of critical importance.

In many patients with ischemic stroke, blood pressure normalizes spontaneously within the subsequent 3-4 days. If this does not occur, the administration of antihypertensive medications is recommended for gradual blood pressure reduction, since after 7-10 days the risk of adverse effects from such therapy decreases substantially. The table below presents some general recommendations for blood pressure control in the hyperacute phase of ischemic stroke, though they are not exhaustive. The Selection of drugs also remains a challenging task, as it is associated with numerous limitations and unpredictable effects, and is not yet flawlessly substantiated from the standpoint of evidence-based medicine.

Blood pressure control in ischemic stroke (within the first 24-48 hours)

At the same time, there are several well-founded indications for urgent antihypertensive therapy during the first hours after the onset of CVA symptoms:

   ▪ acute myocardial ischemia (although a sudden drop in blood pressure is likewise undesirable for patients with myocardial infarction);

   ▪ heart failure;

   ▪ ACUTE RENAL FAILURE;

   ▪ acute hypertensive encephalopathy;

   ▪ intracranial hemorrhage (following CT confirmation).

Management of cerebral edema and increased intracranial pressure

As is known, cytotoxic brain edema and elevated intracranial pressure develop within the first 24-48 hours of an ischemic stroke and are accompanied by progressive depression of consciousness and focal neurological deficits. Under such circumstances, a neutral and slightly elevated head position at an angle of 30° is recommended. Fluid administration is restricted to 1 L/m² of the patient's body surface area per day. It is necessary to monitor plasma osmolality, which should not exceed 295 mosmol/kg. Osmotherapy is performed by intravenous administration of 20% mannitol at 25-30 g every 3-6 hours (for no more than 2 days). Osmotherapy is effective for a duration not exceeding 48-72 hours. When brain edema develops against the background of hemorrhagic stroke, 20% mannitol is prescribed at 0.25-0.5 g/kg every 4 hours, but for no more than 5 days. Additional administration of 10% oral glycerol solution and furosemide 20-80 mg every 4-12 hours is possible. A certain reduction in intracranial pressure can be achieved by maintaining a regimen of moderate hyperventilation, as well as by prescribing sedatives and muscle relaxants. In massive infarctions within the middle cerebral artery territory and in the absence of a response to therapeutic measures, decompressive hemicraniectomy may be considered.

Blood glucose management

Systematic monitoring of blood glucose levels is essential. When an acute cerebrovascular event develops against the background of diabetes mellitus, glucose METABOLISM becomes destabilized, and hyperglycemia in the acute stroke period significantly worsens the prognosis. Hypoglycemia also worsens CVA outcomes and can mimic the clinical picture of a stroke (including the development of focal neurological signs). During an acute cerebrovascular event, the uncontrolled administration of large amounts of glucose must be avoided (no more than 40 g per day). Correction of hyperglycemia (> 10 mmol/L) is carried out via Insulin titration. Hypoglycemia (<2.8 mmol/L) is compensated by the administration of 10% glucose.

Body temperature control

It is well established that elevated body temperature contributes to the enlargement of the ischemic brain lesion zone and exerts a negative impact on CVA outcomes. When body temperature rises above 37.5 °C, the administration of antipyretics (such as paracetamol 500 mg), NSAIDs, antihistamines, and external cooling is recommended. In the event of a bacterial infection, early administration of Antibiotics is mandatory.

Oxygenation

Continuous monitoring of blood oxygen saturation allows for the timely detection of signs of respiratory failure caused by hypoventilation, airway obstruction, or aspiration. Ensuring adequate oxygenation helps prevent the exacerbation of Metabolic Disorders within the ischemic penumbra zone. The administration of 2-4 L O₂/min via a nasal cannula is recommended.

Fluid and electrolyte balance management

Careful monitoring of fluid intake and output is necessary to prevent a reduction in plasma volume, an increase in hematocrit, and a deterioration of blood rheological properties. Under conditions of elevated intracranial pressure, it is generally recommended to maintain a slightly negative balance (approximately a 300-500 mL negative balance daily). Uncontrolled fluid administration can lead to pulmonary edema, cardiac decompensation, and the progression of cerebral edema.

Treatment and prevention of epileptic seizures

Seizure disorders are observed in 4-6% of patients with ischemic stroke. Seizures most commonly occur in cases of ischemia within the carotid system during the first 48 hours. Primarily partial or secondary generalized seizures are observed. Under such circumstances, the administration of diazepam 10-20 mg IV is recommended. If ineffective, 20% sodium oxybutyrate is administered intravenously, and nitrous oxide with oxygen is used. If necessary, anti-epileptic drugs, such as carbamazepine, are subsequently prescribed for prophylactic purposes.

Neuroprotective, metabolic therapy, and vasoactive agents

There is a large and fairly heterogeneous group of drugs whose MECHANISM OF ACTION aims to correct neurotransmitter and neurometabolic processes in order to prevent or minimize brain tissue damage under conditions of ischemic or toxic central nervous system injury, as well as to stimulate recovery processes. They possess diverse sites of action and mechanisms, and can be classified into various pharmacological groups, which is reflected in modern pharmacotherapeutic terminology and classification systems for these medications. Most commonly, Discussion centers on

neuroprotective and reparative therapy, utilizing antioxidants and antihypoxants, nootropics, neurotrophic agents, neuromodulators, and stimulators of neuroplastic processes (emoxypine, actovegin, cytoflavin, cerebrolysin, cerebromedin, semax, cortexin, gliatilin, piracetam, phenotropil, Glycine, citicoline, and others).

There is an extensive body of experimental evidence confirming the efficacy of most of the aforementioned drugs under conditions of modeled ischemic brain injury. There are also numerous publications indicating positive results from The Use of neuroprotective agents in the acute and, particularly, recovery periods of stroke. Nevertheless, multicenter randomized clinical trials have yet to yield clear and reliable confirmation of the effectiveness of many agents when evaluated against primary endpoints (such as mortality, severity of neurological deficit, limitation of functional independence, etc.). In some cases, improvement is achieved primarily in subjective disorders, reflecting a positive therapeutic impact on patients' quality of life. However, given the difficulties in verifying such symptoms and impairments, this positive dynamic generally remains somewhat questionable and warrants further research and validation.

From a practical standpoint, neuroprotective therapy—unlike in experimental settings—remains predominantly empirical. This is due to the complexity and individual Features of the pathological processes occurring during acute cerebrovascular accidents (stroke), as well as the lack of readily available clinical, biochemical, or instrumental indicators that can justify the selection of the most effective agent and an adequate therapeutic window for a specific patient. In most cases, such therapy is pathogenetically sound; however, given the heterogeneity of stroke mechanisms, routine or template application frequently falls short of expectations.

In both the acute and recovery periods of stroke, various groups of vasoactive agents (e.g., theophylline, etc.) are utilized. It is generally believed that they have a negligible impact on stroke outcomes; nevertheless, there are specific indications for their use.

Nutrition, Nursing Care, and Regimen

Comatose patients require adequate nutrition, management of pelvic organ functions, and meticulous care of the skin, eyes, and Oral Cavity. During the first few days, nutrition is provided via intravenous nutrient solutions. Subsequently, enteral feeding is established via a nasogastric tube. The duration of bed rest is determined by the patient's clinical status, the time required for neurological stabilization, and the condition of major somatic functions. If neurological disorders are stable and the patient's condition is satisfactory, bed rest may be limited to 3–5 days; under other circumstances, it may last up to 2 weeks. Among rehabilitative measures, physical therapy and speech therapy are of paramount importance. Early mobilization is essential not only for the full recovery of motor functions but also for the prevention of deep vein thrombosis in the extremities. Later on, social and domestic rehabilitation is initiated. In certain cases, the rehabilitation program must be coordinated with a cardiologist.

Prevention of Complications

Pneumonia is one of the most frequent complications in the early period of acute cerebrovascular accidents, accounting for 15–25% of unfavorable outcomes. Pneumonia in stroke patients can be either aspiration- or hypostatic-induced. According to some data, aspiration may occur in up to 25% of patients with hemispheric ischemic strokes and can reach 70% in patients with bilateral or brainstem lesions. Consequently, during the initial examination of stroke patients, ruling out dysphagia is recommended through the assessment of voice quality, the pharyngeal reflex, voluntary coughing, and a specific small-volume water swallow test (5 ml). Early mobilization and breathing exercises are recommended to prevent pneumonia. If pneumonia develops, antibiotics are prescribed (though not for prophylactic purposes).

Urinary Tract infections are a frequent complication of acute cerebrovascular accidents and simultaneously a cause of hyperthermia. Urinary retention is quite common in the hyperacute phase of a stroke. In most cases, hospital-acquired urinary tract infections are associated with Urinary Bladder catheterization.

Pulmonary Embolism is responsible for approximately 25% of unfavorable outcomes in patients with ischemic stroke. In the absence of preventive measures, deep vein thrombosis can occur in 60–70% of patients with hemiplegia. Prevention of this complication is achieved by administering low doses of heparin—7,500–10,000 IU subcutaneously every 12 hours. The use of compression stockings is also recommended. It should be borne in mind that 70–80% of patients with pulmonary embolism present with characteristic symptoms of this complication, namely dyspnea and chest pain. Daily physical examination of the stroke patient's legs is necessary to detect signs of deep vein thrombosis.

Approximately 40–70% of patients with acute cerebrovascular accidents have concurrent coronary artery disease. Myocardial infarction and cardiac arrhythmias account for up to 15% of deaths in ischemic stroke.

Pressure ulcers are a widespread problem in immobilized individuals. To prevent pressure ulcer formation, turning patients every 2–3 hours is recommended. Between 24 and 48 hours after the stabilization of neurological deficits in ischemic stroke, initiating passive exercises is recommended, repeated 3–4 times daily with a gradual expansion of the physical therapy regimen.

Differentiated Therapy for Ischemic Stroke

The most appropriate method for correcting ischemic brain lesions is the restoration of perfusion within the affected area of brain tissue. However, the possibilities for reperfusion are extremely limited. It is most effective and safest within the first 3–6 hours. Restoring perfusion even a few minutes after the onset of ischemia does not guarantee the complete recovery of normal circulation. In the first few minutes after blood flow is restored, hyperemia develops in the affected brain tissue, followed by post-ischemic hypoperfusion. The longer the duration of ischemia, the higher the risk of reperfusion injury to the brain tissue and hemorrhagic transformation within the ischemic zone. For thrombotic or embolic occlusion of medium and large arteries, thrombolysis is the most effective approach.

Thrombolytic therapy is performed using recombinant tissue plasminogen activator (rt-tPA — alteplase) at a dose of 0.9 mg/kg intravenously (10% of the dose administered as a bolus, and the remainder infused slowly over one hour) within 3 hours of the onset of initial ischemic stroke symptoms. Contraindications to thrombolytic therapy include hemorrhagic diathesis/syndromes, signs of hemorrhagic transformation of the ischemic stroke, severe arterial hypertension, and a large area of ischemic brain injury. Prior to thrombolytic therapy, a CT scan is mandatory for all patients. The wider application of thrombolytic therapy is hindered by delayed hospital admission to specialized centers. Even under optimal patient selection criteria, thrombolytic therapy can be administered to approximately 5–10% of ischemic stroke patients. Thrombolysis is not indicated for hemodynamic-type ischemic strokes. The use of streptokinase in ischemic stroke patients carries an unacceptable risk of hemorrhagic complications, making its use in such cases clinically unjustified.

Heparin therapy in ischemic stroke is associated with a notably high rate of hemorrhagic complications and, consequently, is not currently recommended for widespread use. Nevertheless, there are certain clinical indications where the use of heparin (predominantly for prophylactic purposes) can be considered justified or even necessary.

Early administration of acetylsalicylic acid (100–300 mg daily) within the first 48 hours of an ischemic stroke reliably reduces the incidence of early mortality and recurrent strokes.

Differentiated Therapy for Hemorrhagic Strokes

Unlike bleeding in other anatomical locations, prolonged bleeding into the cranial cavity (lasting more than a few seconds or minutes) is generally not observed in patients who survive until hospital admission. Vasospasm, the activation of local hemostatic mechanisms, and elevated intracranial pressure under such circumstances lead to vascular thrombosis and the rapid cessation of bleeding. Therefore, the primary goals in intracranial hemorrhages are the prevention of recurrent bleeding, the mitigation of vasospasm and subsequent ischemia, and the prevention of life-threatening hydrocephalus.

Consequently, in cases of subarachnoid hemorrhage, strict bed rest is recommended for at least 3–4 weeks. When an arterial aneurysm is detected, surgical intervention—namely aneurysm clipping—is evaluated. In some cases, this surgery can be performed early (within 24–48 hours) following a subarachnoid hemorrhage. Such a strategy helps minimize the risk of rebleeding and reduces the likelihood of vasospasm and cerebral ischemia. However, in the presence of severe impaired consciousness and other serious neurological deficits, surgery should be deferred due to the high probability of an adverse outcome. More frequently, such Procedures are performed several weeks after conservative treatment and patient stabilization. If obstructive hydrocephalus develops, ventricular system shunting is performed. When arteriovenous malformations are identified, surgical treatment is typically carried out 1–2 weeks after the initial hemorrhage.

Antifibrinolytic therapy reduces the likelihood of recurrent bleeding. The most effective approach is the intravenous administration of aminocaproic acid at 30–36 g per day. However, the use of such agents significantly increases the risk of ischemic brain injury, thromboembolic complications, and the progression of hydrocephalus. Currently, the prevailing view is that antifibrinolytic therapy should be used solely in cases of recurrent bleeding.

To prevent vasospasm, nimodipine (Nimotop) is administered intravenously as an infusion or orally. To maintain hypervolemia and hemodilution, at least 3 liters of fluid (isotonic sodium chloride solution) per day and 250 ml of a 5% albumin solution 4–6 times daily are administered.

Lowering blood pressure in subarachnoid hemorrhage reduces the risk of recurrent cerebrovascular events, but it increases the probability of secondary ischemia. Presumably, lowering blood pressure in such scenarios is necessary only when it is markedly elevated.

The management of intracerebral hemorrhages incorporates the core components of basic supportive therapy. In this context, lowering blood pressure to approximately 150/90 mmHg is advisable. In Cerebellar hemorrhage (exceeding 3 cm in diameter), early surgical intervention (prior to the onset of brainstem compression symptoms) can be life-saving. For intracerebral hemorrhages in other locations, the efficacy of surgical treatment remains a matter of debate. To save the patient's life, an attempt at surgical removal of a lateral hemispheric hematoma with a volume greater than 40 ml may be undertaken, utilizing stereotactic and endoscopic techniques.

Prevention of Acute Cerebrovascular Accidents

Secondary Prevention

1. Use of Antiplatelet Agents and Anticoagulants

Antiplatelet agents and anticoagulants effectively reduce the risk of recurrent ischemic stroke. Based on current research findings, the following recommendations can be made:

   ■ For stroke prevention, the combination of aspirin and dipyridamole is more effective than monotherapy with either agent alone.

   ■ If combination therapy is not feasible, low- to medium-dose aspirin (50-325 mg daily) should be prescribed as the first-line drug of choice for secondary stroke prevention.

   ■ Clopidogrel is more effective than acetylsalicylic acid in preventing atherothromboembolism. It can also be considered a first-line drug for patients with acetylsalicylic acid intolerance, those at high risk of recurrent stroke, and those who experience a recurrent stroke while on acetylsalicylic acid therapy.

   ■ Patients with confirmed cardioembolic stroke and a high risk of recurrence (atrial fibrillation, rheumatic heart disease, heart failure, cardiomyopathy, atrial septal defect, or patent foramen ovale with confirmed shunting) should receive anticoagulants. The target international normalized ratio (INR) should be maintained within 2.0-3.0 (INR, international normalized ratio, represents the ratio of the patient's plasma prothrombin time to that of normal or standard plasma, i.e., the reciprocal prothrombin index).

   ■ Patients with prosthetic heart valves require long-term anticoagulant therapy in all cases. The target international normalized ratio should be maintained within 3.0-4.0.

2. Angiosurgery

Carotid endarterectomy (CEA) following a stroke may be performed taking into account the following recommendations (applicable only to centers with a perioperative complication rate of less than 6%):

   ■ CEA is indicated for patients without severe neurological deficits following a recent stroke who have greater than 70% carotid stenosis. The procedure should be performed within 180 days of stroke onset.

   ■ CEA may be indicated for a subset of patients without severe neurological deficits and with 50% to 69% carotid stenosis. The subgroup most likely to benefit from CEA consists of men presenting with symptoms of a recent hemispheric stroke.

   ■ CEA is not recommended for patients with less than 50% stenosis.

Patients with contraindications to CEA and those with an arterial lesion inaccessible for surgery may undergo carotid percutaneous transluminal angioplasty and stenting. Additionally, carotid percutaneous transluminal angioplasty and stenting may be indicated for patients with restenosis following prior CEA.

Primary Prevention

1. Lifestyle Modification and Risk Factor Management

Primary prevention aims to reduce the risk of disease in clinically healthy individuals. Several lifestyle and physiological factors have been identified whose modification lowers the risk of stroke:

Arterial Hypertension. Arterial hypertension is the most common and most modifiable risk factor. Treating arterial hypertension reduces the risk of stroke. Blood pressure should be lowered to normal levels (<140/85 mm Hg) through lifestyle modifications and/or pharmacological treatment.

Diabetes Mellitus. Diabetes mellitus is an independent risk factor for ischemic stroke, although The Link Between tight glycemic control and reduced stroke risk has not yet been definitively proven. Nevertheless, such control is beneficial for preventing other comorbidities.

Hypercholesterolemia. A clear correlation has been established between total blood cholesterol levels and CORONARY HEART DISEASE, whereas this association is less pronounced for ischemic stroke. Nonetheless, statin therapy (simvastatin or pravastatin) reduces the risk of stroke in patients with coronary heart disease.

Smoking. Cigarette smoking is an independent risk factor for stroke (conferring up to a 6-fold increase in disease risk). In individuals who quit smoking, the risk of stroke drops by approximately 50%.

Alcohol Consumption. Moderate alcohol consumption (e.g., two glasses of wine per day) is associated with a reduced risk of stroke. Alcohol abuse increases the risk of both ischemic and hemorrhagic stroke.

Physical Activity. Regular and vigorous physical exertion appears to lower the risk of stroke. This protective effect may be mediated through positive impacts on body weight, blood pressure, blood cholesterol levels, and glucose tolerance.

2. Use of Antiplatelet Agents and Anticoagulants

Acetylsalicylic Acid. There is currently no proven scientific rationale for prescribing aspirin to asymptomatic individuals for the purpose of primary stroke prevention. However, the risk of myocardial infarction is reduced.

Coumarin Derivatives. Asymptomatic patients with atrial fibrillation, particularly those at high risk due to coexisting heart conditions (heart failure, valvular disease, etc.), should undergo primary prevention in accordance with the following recommendations:

   ■ Patients with atrial fibrillation and a high risk of stroke should receive long-term oral anticoagulant therapy. The international normalized ratio (INR) should be maintained at a target value of 2.5 (range 2.0–3.0). For patients older than 75 years, a lower target INR of 2.0 (range 1.6–2.5) should be maintained.

   ■ Patients with atrial fibrillation under the age of 65 with no underlying heart disease or with contraindications to anticoagulants should receive 300 mg of aspirin daily.

   ■ Patients with atrial fibrillation over the age of 65 and at low risk of stroke should be prescribed anticoagulants as first-line therapy.

3. Surgical Management of Asymptomatic Carotid Stenosis

The outcomes of carotid endarterectomy (CEA) in asymptomatic patients remain a subject of debate, and therefore the procedure is generally not recommended for this patient category. It is believed that CEA for asymptomatic carotid stenosis is beneficial only in patients with greater than 60% stenosis and low surgical risk (< 3%), provided their life expectancy is at least five years.

Clinical Cases

Case 1

A 68-year-old man suddenly lost consciousness during the day. He developed vomiting, deep noisy breathing, and motor restlessness. Examination reveals deviation of the head and eyes to the left, and smoothing of the right nasolabial fold. Muscle hypotonia is present in the right arm and leg. Tendon Reflexes are decreased on the right, and pathological plantar reflexes are elicited on the same side. He responds to painful stimuli by contracting the muscles of his left arm and leg. There is no response to pain on the right side. No meningeal signs are detected. Blood pressure is 175/100 mmHg,

pulse is 90 bpm. Atrial fibrillation with a heart rate of approximately 115 bpm. Respiration is noisy and rhythmic, 24 breaths per min. He has a known 5-year history of atrial fibrillation.

   • How can the patient's condition be classified?

   • List the criteria for assessing his condition.

   • Name the main neurological disorders.

   • Explain the pathogenesis of muscle hypotonia and depressed tendon reflexes.

   • Formulate the topical diagnosis.

   • What is the most likely mechanism of the cerebrovascular accident?

   • What type of cerebrovascular event (ischemic or hemorrhagic) can be suspected?

   • Formulate a preliminary clinical diagnosis.

   • Outline the main directions for Differential diagnosis.

   • Describe the plan for instrumental neurological examination.

   • Determine The Scope of emergency somatic evaluation.

   • Propose a regimen for baseline and targeted therapy, assuming intracranial hemorrhage has been ruled out.

   • Determine the prognosis of the disease.

   • Indicate the most frequent complications during the acute phase of the disease.

Case 2

A 68-year-old woman with a history of coronary artery disease and arterial hypertension experienced the acute onset of true vertigo, nausea, and vomiting in the morning. Following the administration of antianginal and antihypertensive medications, her condition improved. In the evening, she developed a feeling of heaviness in the head, swallowing difficulties, and hoarseness. Physical examination revealed mild lethargy. Horner's syndrome was observed on the right. Dysphasia, dysphonia, deviation of the uvula to the left, and right-sided facial hypoesthesia were noted, and the gag reflex was impaired. The tongue was midline, with no significant articulation impairment. The patient performed coordination tests unsteadily on the right. Anisoreflexia was present (S > D), along with pathological plantar signs on the left. Decreased strength in the left arm and left-sided hemihypoesthesia were documented. Meningeal signs were absent. Blood pressure was 190/100 mmHg, pulse 86 bpm, regular. It is known that over the past three years, she has had several episodes of vertigo, tinnitus, hoarseness, speech and swallowing difficulties lasting from several minutes to one and a half hours. These episodes occurred against the background of blood pressure fluctuations and cardiac discomfort, resolving spontaneously or after taking antihypertensive and vasoactive medications. With treatment over a span of one and a half weeks, swallowing, vocal resonance, as well as strength and sensation in the right arm recovered. Ataxia resolved entirely. Anisoreflexia persisted.

   • Assess the patient's condition upon initial examination.

   • Specify the criteria for evaluating her condition.

   • List the primary neurological disorders.

   • Explain THE ORIGIN OF the right-sided cranial nerve involvement and the left-sided hemisyndrome.

   • Formulate a probable topical diagnosis.

   • Provide a topical and clinical evaluation of the neurological episodes described in the patient's history.

   • What is the most likely mechanism of the cerebrovascular accident?

   • What type of cerebrovascular event (ischemia or hemorrhage) can be suspected?

   • Formulate a preliminary clinical diagnosis.

   • Outline the instrumental neurological examination plan.

   • Determine the scope of emergency somatic examinations.

   • Define the directions for differential diagnosis.

   • WHAT IS A minor stroke?

   • Propose a plan for basic and targeted therapy, provided intracranial hemorrhage is ruled out.

   • Determine the prognosis of the disease.

   • List the most common complications during the acute phase of the disease.

Case 3

A 36-year-old man was admitted to the neurology department in a state of psychomotor agitation. He is disoriented and gives irrelevant Answers TO QUESTIONS. According to the history, he developed a severe headache at work, collapsed, and experienced nausea and vomiting. Neurological examination reveals nuchal rigidity, bilateral Kernig's signs, and pain upon ocular movement. Findings include left-sided ptosis, divergent strabismus of the left eye, and anisocoria (S> D). Tendon reflexes are brisk in the upper extremities, whereas knee and Achilles reflexes are depressed. Bilateral Babinski signs are present. Body temperature is 37.8°C. Blood pressure is 175/90

mmHg, pulse is 88 bpm. A complete blood count reveals leukocytosis at 10 • 10⁹/L.

   • How would you classify the patient's condition?

   • List the criteria for evaluating his condition.

   • Identify the primary neurological disorders.

   • Explain the origin of the focal neurological symptoms.

   • Formulate a topical diagnosis.

   • What type of cerebrovascular event (ischemia or hemorrhage) can be suspected?

   • What signs may indicate the hemorrhagic nature of a cerebrovascular accident?

   • Formulate a preliminary clinical diagnosis.

   • Specify the possible causes for the development of meningeal syndrome.

   • List the most common causes of intracranial hemorrhages.

   • Describe the protocol for instrumental neurological examination.

   • Determine the scope of emergency somatic examination.

   • Propose a regimen for basic and differentiated therapy if intracranial hemorrhage is confirmed.

   • Determine the prognosis of the disease.

   • List the most frequent complications of the acute phase of the disease.

Scenario 4

A 72-year-old woman is brought to the emergency department in a severe, unconscious state. According to witnesses, she lost consciousness and fell on the street about half an hour ago. A generalized tonic-clonic seizure was observed, accompanied by foaming at the Mouth and Urinary Incontinence. The patient is well-nourished. Her face is hyperemic. Breathing is noisy and deep. Pulse is 112 bpm, regular. Blood pressure is 240/120 mm Hg. Body temperature is 39°C. Consciousness is lost—coma. Moderate nuchal rigidity; Kernig's signs are absent. Mild anisocoria is observed: the right pupil is larger. The eyeballs are deviated to the right. The left cheek "sails" during respiration. Muscle tone is decreased on the left. Tendon reflexes S <D. She does not respond to painful stimuli. Babinski signs are present bilaterally. Periodic tonic tension of the left arm and leg occurs. Blood tests reveal a somewhat elevated glucose level.

   • Assess the patient's condition upon initial examination.

   • List the criteria for evaluating her condition.

   • Name the primary neurological disorders.

   • Explain the origin of the focal neurological symptoms.

   • Formulate a probable topical diagnosis.

   • Determine the probable cause of the cerebrovascular accident.

   • What type of cerebrovascular accident (ischemia, hemorrhage) can be suspected?

   • What signs indicate the hemorrhagic Nature of the cerebrovascular accident?

   • What signs are characteristic of intraventricular hemorrhages?

   • How can the elevated Blood Glucose Level be interpreted?

   • Formulate a preliminary clinical diagnosis.

   • Describe the protocol for instrumental neurological examination.

   • Determine the scope of emergency somatic examination.

   • Determine the main directions for differential diagnosis.

   • Propose a plan for basic and differentiated therapy.

   • Determine the prognosis of the disease.

   • List the most common complications of the acute phase of the disease.

Case 5

A 25-year-old man, while feeling entirely well and at work in the morning, suddenly experienced a sensation of being struck in the head. Following this, he lost consciousness and collapsed. Upon regaining consciousness, he complained of a severe headache, nausea, blurred vision, and vomiting. On examination, he was lethargic and difficult to engage. Left-sided ptosis was noted, along with restricted upward, downward, and inward Movements of the left Eyeball. Pupillary reflexes and the corneal reflex were absent on the left side. Anisocoria was present (S> D). Pronounced nuchal rigidity and bilateral Kernig's signs were observed. Tendon reflexes were slightly hyperactive on the right. BP 140/90 mmHg. Pulse 100. Blood tests revealed leukocytosis of 12 x 10⁹/L, ESR 13 mm/h. The cerebrospinal fluid was moderately blood-tinged.

   • List the main neurological disorders.

   • Determine the leading neurological symptom complex.

   • Explain the origin of the oculomotor disturbances.

   • Formulate the topical diagnosis.

   • Formulate a preliminary clinical diagnosis.

   • Outline the directions for differential diagnosis.

   • Outline the scheme for instrumental and somatic examination.

   • Formulate indications for cerebrospinal fluid analysis.

   • Formulate indications for cerebral angiography.

   • Indicate the most likely result of the angiographic examination.

   • Explain the MAIN MECHANISMS OF brain injury in intracranial hemorrhages.

   • Outline the patient management plan.

   • Describe the pharmacotherapy program.

   • Outline the options and principles of surgical treatment.

   • Determine the prognosis of the disease.

Case 6

A 32-year-old man complains of periodic frontal and temporal headaches and a pulsatile noise in the left side of his head. He reports infrequent attacks that begin with speech arrest, clonic twitching of the facial muscles and the right hand, and then, following loss of consciousness, generalize to the Muscles of the entire body. Four years ago, he was hospitalized for a month due to a subarachnoid hemorrhage that developed without apparent cause during routine moderate physical activity. Several weeks after discharge, seizure episodes and head noise appeared. Six months ago, he experienced a recurrence of a condition similar to the previous one, although the cerebrospinal fluid was not analyzed. He suffered from severe headaches, nausea and vomiting, pain upon eye movement, elevated blood pressure, and weakness in the right extremities. With treatment, his condition gradually improved. Examination reveals asymmetrical reflexes with D> S.

   • List the main neurological disorders.

   • Describe the leading neurological symptom complex.

   • Formulate the topical diagnosis.

   • Formulate a preliminary clinical diagnosis.

   • Outline the directions for differential diagnosis.

   • Describe the plan for instrumental and somatic examination.

   • State the indications for cerebral angiography.

   • Indicate the most probable results of the angiographic examination.

   • Explain the mechanisms of brain injury caused by arteriovenous malformations.

   • Specify the diagnostic criteria for subarachnoid hemorrhage.

   • Propose a patient management plan.

   • Outline the pharmacotherapy program.

   • Describe the options and principles of surgical treatment.

   • Determine the prognosis of the disease.

Case 7

A 28-year-old man fell from a height of 1.5 meters while renovating his home and hit his head. He did not lose consciousness, and his condition remained largely unchanged. Three days later, he woke up in the morning experiencing dizziness and a pulsating noise primarily in the right side of his head. Vision in his right eye deteriorated. Physical examination reveals right-sided exophthalmos. Hyperemia and edema of the eyelids and soft Tissues of the Orbit are noted. Limitation of mobility of the right eyeball is detected. Movements in the arms and legs are not restricted, and tendon reflexes are symmetrical. There are no meningeal signs.

   • List the main neurological disorders.

   • Explain the changes in the right orbital region.

   • Formulate a preliminary clinical diagnosis.

   • Outline the directions for differential diagnosis.

   • What additional diagnostic procedures help clarify the origin of these symptoms?

   • Outline the instrumental examination protocol.

   • State the indications for cerebral angiography.

   • Describe the likely findings of the angiographic examination.

   • Explain the mechanisms underlying the formation of carotid-cavernous fistulas.

   • Indicate the potential complications of this condition.

   • Outline the patient management plan.

   • Describe the pharmacotherapy program.

   • Outline the options and principles of surgical treatment.

   • Determine the prognosis of the disease.