Ischemic stroke, transient ischemic attack (TIA), cerebral ischemia

Pathophysiology of ischemic stroke

How formed and developed cerebral stroke? Typically, in the pathological process involved in stroke, one or more vessels of the brain. This may be carotid or vertebral artery and extending beyond them intracranial branches supplying arterial blood of different brain regions, depending on their passage therein. This pathological process can be observed:

• damage the brain directly to the vessel - in atherosclerosis, lipogialinoze, inflammation, amyloidosis, delamination (traumatic or spontaneous), congenital malformation, or aneurysm
• pathological process starts at a distance from the brain - embolism in the vessel in the cranial cavity of the heart or extracranial circulation pools, as well as reducing pressure or increased blood viscosity, resulting in insufficient blood flow through a vessel of the brain

During a certain time vascular lesions of the brain in a patient may not manifest clinically. This flow continues until no symptoms until it does not cause significant vasoconstriction and cerebral ischemia, or the vessel itself is not subjected to cerebral embolism, occlusion or rupture.

Stroke is defined as a neurological complication resulting from one of these pathologic processes cerebral vessels. Very narrow or close the lumen of the vessel of the brain and cause subsequent ischemia of brain tissue and the development of a heart attack (stroke) may:

• thrombus (clot)
• atheroma or embolism
• vessel rupture accompanied by intracerebral or subarachnoid hemorrhage

Other neurological symptoms occur secondary to vascular lesions:

• compression of cranial nerves aneurysm artery wall
• vascular headache (similar to migraine or artery hypertension)
• increased intracranial pressure (ICP), concomitant venous thrombosis

Vessels pass through our entire body, hence the variety of symptoms when the disease. Here are some of the most terrible in its consequences, destruction of the vascular bed person:

• stroke (cerebral infarction)
• myocardial infarction

A stroke occurs on the type of hemorrhagic and ischemic. Stroke is more common in hypertension, atherosclerosis of brain vessels and much less for other vascular diseases.

The pathogenesis of stroke is complex. This vascular disease of the brain are important:

• changes in vascular reactivity with a penchant for diagnostic reactions (vasoconstriction, angioparalysis, stasis, venous stasis)
• morphological changes in vessels (atheromatosis, arteriosclerosis, aneurysm)
• change in blood chemistry (increased clotting, increasing the viscosity eritrotsitemiya, thrombinemia)
• other hemodynamic factors (sharp fluctuations in blood pressure - increase or decrease, slowing blood flow)

Hemorrhagic stroke develops most often as a result of eritrodiapedeza as a result of neurogenic vasomotor impairments (spasm - paresis - stasis - increasing the permeability of vascular layer). Contributing factors include sharp fluctuations in blood pressure. Bleeding into the brain substance is more often observed in the inner bag and the basal ganglia, pons and cerebellum less.

Hemispheric and subcortical hemorrhage often accompanied by a breakthrough of blood in the ventricles side and 3, bleeding in the brain stem - a breakthrough in the 4 ventricle. In the center is formed hemorrhage red softening in the final stage - cyst glioznorubtsovye changes.

Ischemic stroke is caused by thrombosis, embolism, cerebral vascular spasm or prolonged blood stasis due angioparalysis. For the development of ischemic necrosis of the brain tissue it requires not a complete shutdown of blood flow and a decrease in its 40-50%. In 25% of cases of softening of the brain is the cause of thrombosis or narrowing of the extracranial major vessels (carotid and vertebral).

 

Ischemic stroke and cerebral metabolic impairment

For normal functioning of the brain must constantly receive the required amount of oxygenated blood, but even somewhat reduced arterial blood flow may be sufficient to prevent the onset of heart attack for an indefinite period.

10 seconds after cardiac arrest, loss of consciousness occurs. In animal experiments, the complete cessation of blood flow for 3 minutes causes irreversible cerebral infarction. While the reduction in blood flow and leads to cerebral ischemia, it remains viable for a long time before the development of heart attacks or restore blood flow to normal. For example, patients who underwent embolization in the vessels of the brain or spasm after subarachnoid hemorrhage, often fully or partially recover. This suggests that the function of certain areas of the brain after ischemia for several hours or even days, can be restored. This led to the formation of ideas about the surrounding ischemic infarct area (the penumbra, a halo) of the brain.

The extent of possible brain function recovery after ischemia is not clear. But we know that once the cells have undergone brain infarction (stroke), cell membrane integrity is lost neurons disrupted blood-brain barrier (BBB), high-energy phosphate metabolism terminated in mitochondria.

 

Ischemic stroke and neural tissues pathological changes

Initially, the infarct area of the brain looks pale. Within a few hours or days, mainly in the gray matter of the brain may develop with congestion hyperemia, expansion of blood vessels and small petechiae (hemorrhagic infarction).

The reason for hemorrhagic infarction (stroke) is unclear, but it is generally considered as a consequence of embolism blocking major arterial vessel, such as the trunk of the middle cerebral artery or one of its major branches. Within a few hours embolus travels dissolves (lysis) and split, making it possible to restore arterial blood circulation in the area of ​​cerebral infarction. Recirculation of blood can cause hemorrhagic infarction and apparently enhances the formation of edema after a breach of the blood brain barrier. On the other hand, the primary intracerebral hemorrhage destroys brain tissue in the region of hemorrhage and compressing the surrounding tissue.

If the patient developed ischemic stroke or intracerebral hemorrhage occurred or been observed transient episodes of cerebral ischemia, the indication for adequate treatment is an accurate diagnosis. It is based on determining the nature and localization of brain lesions, vascular pathological processes causing existing neurological symptoms in a patient, and anatomical details of any intact tract of collateral blood flow in the ischemic area.

The anatomical restoration of brain tissue occurs only in the formation of scar tissue in fibroglioznoy site infarction or hemorrhage. Thus, therapeutic measures may have only preventive effect. They should be aimed at the protection of both normal and ischemia-prone part of the brain from primary and recurrent pathological processes, as well as from the consequences of stroke, including compression of intracranial hemorrhage or cerebral edema. This preventive treatment of stroke brain has three objectives:

• the prevention of stroke due to the reduction of risk factors
• prevent a first or recurrent stroke by removing the underlying destruction - for example, during surgery to remove atherosclerotic plaque from the lumen of the carotid artery (carotid endarterectomy)
• prevention of secondary brain damage due to maintain adequate blood flow (perfusion) in the edge portions of the ischemic areas and reducing the edema of the brain tissue

Except for the elimination of risk factors, all aspects of the treatment of stroke is quite contradictory. Convincing evidence of the effectiveness of therapeutic approaches often does not happen. Thus, the modern treatment of stroke is essentially empirical and based on the knowledge of the doctor's degree of risk related to various diagnostic and therapeutic methods.

Strokes are classified according to their putative pathophysiological mechanisms. In each case, a stroke may be defined as the clinical manifestations and principles of diagnosis and treatment. In the diagnosis of stroke or transient ischemic attack (TIA), primarily evaluate the initial clinical manifestations and their dynamics, ie. E. To decide whether "a stroke or transient ischemic attack syndrome (TIA)?".

Currently, the improvement of clinical diagnostics and radiation methods of investigation allow to clarify the nature and location of stroke, as well as explore the accompanying vascular lesions with a high frequency and accuracy, which makes treatment more targeted, feasible and necessary. These include:

• MR angiography (magnetic resonance angiography) of the brain
• CT, spiral CT-angiography of the neck vessels and brain with intravascular contrast

 

Ischemic stroke syndromes

Features of the onset of stroke, along with a specific objective and subjective neurological symptoms suggests the localization of brain damage and its cause. In most cases, the sudden appearance of an acute focal neurological symptoms suggesting a possible stroke, especially if these impairments correspond to a specific vascular beds. So, hemiparesis and aphasia are associated with damage to the basin of the middle cerebral artery of the dominant hemisphere, and the sudden loss of visual fields - posterior cerebral artery; the development of "clean" hemiparesis suggests a small "lacunar" Stroke center in the internal capsule, or base of the brain corresponding to the pool of small penetrating branches, respectively, of the middle cerebral artery or principal.

At the beginning of disease symptoms are moderate to severe, are fluctuating in nature, they gradually flatten or increase. It is the dynamics of neurological symptoms gives an indication of thrombotic, embolic or hemorrhagic lesions. But, for example, a sudden deep coma can occur both in the main artery embolism, and in subarachnoid hemorrhage or bleeding at the base of the bridge in hypertension. To clarify the nature of the lesion, leading to coma, to be considered during the inspection detectable neurological symptoms and its dynamics. However, to establish the exact details of the dynamics of the early stages of the disease is difficult. The patient is often unable to recall them without any prompting.

Sometimes the patient is determined by the location of the lesion, such as, for example, in cases of anosognosia defeats non-dominant hemisphere. Most important medical history information, manage to find out from the patient's family members.

Thus, the diagnosis of stroke symptoms is based on clinical symptoms and a characteristic set of subjective and objective symptoms.

In hemorrhagic stroke localization and size of hemorrhage, as well as their type (subarachnoid or intracerebral) determine the characteristic symptoms of a stroke. Meanwhile, hospital ischemic stroke depends not only on the nature of the pathological process, the size of the source, localization of vascular lesions, but also on the capacity of collateral circulation. Often the value of collateral blood flow is sufficient to prevent a heart attack or a significant reduction in its size, which affects the development of the symptoms of a stroke.

Collateral blood flow may be sufficient to complete occlusion of large arterial trunk was not accompanied by neurological symptoms and visible damage of the brain parenchyma. In other cases, occlusion of large arteries may lead to a softening of the brain tissue around the pool of blood supply. There are many variants of infarct, which differ in size, shape, stage of development, that is determined by the possibilities of collateral blood supply. Collateral blood flow is dependent on the anatomy of blood vessels, speed of occlusion, indices of systemic blood pressure. These factors, as well as possible, and others, such as impairments of viscosity, polycythemia, a pathology of red blood cells, occasionally may act negatively and lead to ischemia in pools of blood supply to partially overlapped arteries.

Collateral blood flow not only affects the deep penetrating vessels coming from the trunk of the middle cerebral artery (artery lenticular nucleus and the striatum), distal vertebral artery, the main artery and arterial circle of Willis. They supply blood to the deep white and gray matter of the brain stem, thalamus, basal ganglia, and the radiant crown. Blockage of one of these small penetrating vessels like atherothrombotic nature, and at lipogialinoze and embolism leads to the development of small "lacunar" heart attacks.

The terms "in the development of a stroke" (also called progressive stroke) and "the completed stroke" should be mentioned specifically. If neurological deficit is growing or fluctuating nature of that mark in the course of patient care, says the development of stroke; if the further increase of symptoms occurs, talk about the completed stroke.

The progressive course of a stroke explained by several mechanisms, including increasing narrowing artery thrombus development of brain edema, occlusive thrombus spread branches collateral blood supply to the site of brain ischemia, as well as systemic factors, such as hypotension. Although in some cases these factors can play a role, it is more likely that fluctuating neurological deficit is the result of multiple distribution, migration, lysis and dispersion caused by emboli or repeated embolism arterio-arterial nature or variations of collateral blood flow through the circle of Willis, anastomoses zones adjacent blood supply and orbital or cervical-vertebral collaterals.

The assumption that certain forms of vascular lesions of the brain occurs, not only for different symptoms of a stroke, but also when combined with risk factors. Development aterotrombotichkogo stroke can often think that the patient holds asymptomatic or clinically manifest vascular disease affecting the coronary and peripheral vessels. On the other hand, heavy atherothrombotic vascular disease of any location gives grounds to consider the atherothrombotic process as the cause of ischemic stroke.

If the patient diagnosed with atrial fibrillation, valvular heart disease, myocardial infarction, or bacterial endocarditis, are a source of emboli, their presence indicates the character of the embolic stroke. Severe hypertension invariably accompany lipogialinoz small vessels, lacunar stroke and atherothrombotic lesion carotid bifurcation, the trunk of the middle cerebral artery, vascular vertebrobasilar system.

Hypertension also predisposes to the appearance of deep intracerebral hemorrhage. According to some authors, holding Antihypertensive therapy is the most important factor in reducing the incidence of stroke. Smoking and familial lipemia, although less frequently than hypertension, combined with an increased risk of atherosclerosis and, in particular, ischemic brain disease.

The clinical picture of stroke is divided into four periods, the recovery period (10-15 days to several months and even up to 1-2 years) rezudialny characterized by the presence of persistent sequelae. Differential diagnosis of hemorrhagic and ischemic stroke is often difficult. Errors in determining the nature of the stroke from 10 to 27%.

 

The symptoms of transient ischemia (TIA)

Clinical manifestations and temporal profile of a transient ischemic attack (TIA) provides insights into the nature and location of its underlying pathophysiology of arterial. The term "transient ischemic attack" (TIA) generally refers to any sudden arisen focal deficit regressed completely in less than 24 hours. This definition is too broad, as it includes a lot of syndromes, and some of them are not necessarily caused by ischemia such as focal syndrome epilepsy or migraine, accompanied by neurological symptoms. In addition, symptoms of ischemia persists longer than one hour, may indicate that a certain portion of the brain tissue underwent heart attack.

Specific symptoms of transient ischemic attack (TIA) indicate involvement in the pathological process of the area that supply blood to certain arteries:

• carotid artery
• middle cerebral artery
• vertebral-basilar system
• small penetrating arteries (lacunar transient ischemic attack (TIA))

Duration, and frequency of stereotyped repetitive episodes indicate their pathophysiological mechanisms. For example, repeated (5-10 times a day), short (15 minutes or less), the same type of attacks of weakness in the hands or the entire hand with accompanying speech disorders with or without cause to think about narrowing or occlusion of the proximal arterial insufficiency of collateral blood supply, leading to transient focal ischemia ("low-flow") cortex contralateral hemisphere of the brain. On the other hand, the speech disorder only attack and weakness in the hands or a hand (the latter may be absent) of 12 hours can be observed in cerebral ischemia caused by emboli with the possible formation of infarct in the left frontal lobe.

Transient short episode of pure pyramidal hemiparesis involving the muscles of the face, arms, legs and feet are not accompanied by speech impairments (dysphasia), or ignoring half of the body, evidence of transient ischemia in the internal capsule, for example in the pool of blood supply to one of the small penetrating arteries coming out of the barrel middle cerebral artery (artery lenticular nucleus and the striatum). When acute stroke in the basin of the arteries occurs lesion, the size of which is less than 1 cm - lacuna. Such a impairment can be described as "lacunar transient ischemic attack" (TIA).

Transient ischemic attack (TIA) in the vertebral-basilar system, if they are the result of the proximal basilar or bilateral distal vertebral artery stenosis is usually manifested in the form of short-term bouts of dizziness, double vision, and dysarthria. Repeatability and brevity of these attacks allows to think more about the transient decrease in cerebral blood flow than an embolism.

In general, transient ischemic attack (TIA) are caused by two main factors: focal reduction of blood supply and embolism. The mechanism of transient ischemic attack (TIA) embolic origin is obvious, in this case for the purpose of treatment is necessary to establish a source of embolism. To a lesser degree of knowledge of the mechanisms of transient ischemic attack (TIA) due to a decrease in local cerebral blood supply. Probably, arterial stenosis or occlusion of a critical degree cause a decrease in blood flow to a particular area of ​​a normal brain.

The important role played by lack of collateral blood flow to the ischemic area, but due to the transient nature of ischemia is also necessary to take into account indicators such as blood viscosity, elasticity of the vascular layer and other as yet unknown factors. These forms of transient ischemic attack (TIA) is best considered as a true TIA, t. E. As episodes neembolicheskogo genesis.

Unlike brain stroke symptoms of transient ischemic attack (TIA) completely regressed, but they serve as a warning about the possibility of a subsequent stroke. Therefore, pathophysiological mechanisms of stroke and transient ischemic attack (TIA) must be considered together. In fact, the doctor is unable to help the patient during transient ischemic attack (TIA), not knowing what caused it.

Transient ischemic attack (TIA) as a stroke is a syndrome that requires setting a more specific diagnosis.

 

Ischemic stroke, transient ischemic attack (TIA) and cerebral ischemia diagnosis

Ischemic stroke, transient ischemic attack (TIA) and cerebral ischemia diagnosis includes:

• examination of the patient neurologist
• examination of the cervical spine biomechanics - muscle tone, range of motion, the position of the vertebrae at rest and movement (X-rays with functional tests)
• the study of the neck vessels and brain - UZDG, rheovasography (REG)
• MRI angiography of cerebral vessels
• CT, spiral CT of the neck vessels and brain (CT angiography)
• blood tests (biochemistry, complete blood count)
• ECG

Observing the dynamics of changes in the brain tissue after an ischemic stroke important during active thrombolytic therapy to dissolve the thrombus and for the control of possible parenchymal hemorrhages with thrombolytics treatment.

 

Cerebrovascular diseases differential diagnosis

The diagnosis of vascular lesions of the brain is based solely on the recognition of stroke syndrome. On the other hand, the diagnosis of stroke is always in doubt. There are three criteria for the identification of stroke:

• the rate of of development of the clinical syndrome
• signs of focal brain lesions
• clinical condition

Time profile of stroke is usually described by the precise characteristics of prodromal phenomena and dynamics of disease onset neurological disorders, considered in conjunction with the clinical condition at the time of the survey. If there is no information about the patient, to clarify the features of the disease it is advisable to increase the observation time for a few days or weeks, as the most common cause of diagnostic errors are insufficient data on the development of stroke.

Several neurological diseases reminiscent of their clinical course vascular brain lesions. In the absence of some details of the history of the disease there are difficulties in the diagnosis of subdural hematoma, brain tumor, brain abscess, and senile dementia.

This also applies to such pathology as chronic vertebrobasilar insufficiency (VBI) when disturbed blood flow in the vertebral arteries. They supply blood to the rear parts of the brain, the cerebellum and the brain stem. This leads to unsteadiness when walking, dizziness, lability intracranial pressure, the emergence of feelings of nausea and the urge to vomit, etc.

 

Ischemic stroke, transient ischemic attack (TIA) and cerebral ischemia treatment

After the doctor will set the exact diagnosis (ischemic stroke, transient ischemic attack (TIA), cerebral ischemia), depending on the severity of the disease the patient will be asked to conservative or surgical treatment of the disease.

Research has established the most favorable time period of treatment of ischemic stroke thrombolytic drugs. It was found that the first 4.5 hours after the formation of ischemic stroke are the most important for thrombolytic treatment. Spent thrombolytic treatment in this time period ballroom with ischemic stroke reduced further the risk of mortality, the level of neurological deficit (paresis and paralysis in the first 90 days after the stroke) and prevents the occurrence of severe complications such as parenchymatous hemorrhage.

Depending on the type of impairments of cerebral blood flow in the patient and can require the following treatment steps:

• drug therapy (vascular, nootropic drugs and fortifying)
• therapeutic massage
• physiotherapy
• medical gymnastics
• acupuncture
• surgical treatment