In developed countries, vascular brain disease statistics are the third leading cause of death after cardiovascular diseases and cancer. In addition, adults of all nervous diseases, vascular lesions of the brain are more likely to lead to disability. The prevalence of vascular brain lesions on statistics is about 800 per 100 000 population. About 5% of those aged over 65 years ever been a stroke of the brain.
Ischemic stroke causes
How formed and developed ischemic stroke (cerebral infarction)? Typically, in the pathological process of stroke involved one or more vessels of the brain. It may be drowsy or vertebral arteries and waste away from their intracranial branches, which supply a variety of arterial blood brain regions depending on their passage in it. In this pathological process can be observed:
- lesion of the vessel of the brain directly - with atherosclerosis, lipogialinoze, inflammation, amyloidosis, exfoliating (traumatic or spontaneous), congenital malformation or aneurysm
- pathological process begins at a distance from the brain - embolism in a vessel in the skull cavity of the heart or extracranial circulation pools, as well as reducing pressure or increasing the viscosity of the blood, leading to failure of blood flow through the vessel of the brain
For some time the vessel of the brain lesion in a patient may not manifest clinically. Such a course without symptoms lasts as long as it does not cause significant narrowing of the vessel and ischemia of the brain while he or vessel of the brain do not undergo embolization, occlusion or rupture.
Stroke is defined as a neurological complication that occurs as a result of one of these pathological processes of cerebral vessels. Sharply restrict or close the lumen of the brain and cause subsequent ischemia of brain tissue and the development of infarction (stroke) can be caused by:
- atheroma or embolus
- rupture of the vessel is accompanied by intracerebral or subarachnoid hemorrhage
Other neurological symptoms occur secondary to vascular lesion:
- compression of the cranial nerves, aortic artery wall
- vascular headache (like migraine or arteritis, hypertension)
- increased intracranial pressure (ICP), concomitant venous thrombosis
Prevalence of stroke mechanisms according to age group:
Prevalence in younger age group (18-44 yr), %
Prevalence in older age group (>65 yr), %
|Large-vessel atherosclerotic disease
Cerebral metabolism and ischemic stroke (cerebral infarction)
For normal functioning of the brain must continuously receive the required number of oxygen-rich blood, but even more reduced arterial blood flow may be sufficient to prevent the onset of infarction for an indefinite period.
10 seconds after cardiac arrest occurs loss of consciousness. In animal experiments, the complete cessation of blood flow within 3 minutes causes irreversible brain infarction. While the reduction in blood flow leads to ischemia of the brain, it remains viable for a long time before developing heart attacks or restore blood flow to normal. For example, patients who underwent embolization of cerebral vessels or spasm after subarachnoid hemorrhage, often fully or partially recover. This suggests that the function of individual areas of the brain after ischemia for several hours or even days, can be restored. This led to the formation of ideas about the environmental focus of myocardial ischemic areas (penumbra, halo) of the brain.
Degree possible to restore brain function after ischemia is not clear. But we know that once brain cells were subjected to a heart attack (stroke), loss of integrity of cell membranes of neurons, disrupted blood-brain barrier (BBB), high-energy phosphate metabolism ceases in the mitochondria.
Pathological changes in brain tissues after ischemic stroke
Initially, cerebral infarction area looks pale. Within a few hours or days, mainly in the gray matter of the brain may develop stagnation with hyperemia, dilation of blood vessels and small punctate (petechial) hemorrhages (hemorrhagic infarction).
The cause hemorrhagic infarction is unclear, but is generally regarded as the 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 moves, dissolved (lysis) and splits, which makes 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 blood-brain barrier breach. On the other hand, primary intracerebral hemorrhage destroys brain tissue in the area of hemorrhage and compresses the surrounding tissue.
If the patient developed an ischemic stroke or intracerebral hemorrhage has occurred, or were observed transient episodes of cerebral ischemia, the indication for adequate treatment is accurate diagnosis. It is based on determining the nature and localization of focal brain lesions, vascular disease process, which determines the existing neurologic symptoms in the patient and the anatomical details of any ways of intact collateral blood flow in the ischemic area.
Anatomic reconstruction of brain tissue occurs only due to the formation of scar tissue in fibroglioznoy place infarction or hemorrhage. Thus therapeutic measures may have a preventive value. They should be directed to the protection of both normal and affected ischemic region of the brain from the primary and recurrent pathological processes, as well as the effects of the stroke, including compression of brain edema or intracranial hemorrhage. This is a preventive treatment of brain stroke has three goals:
- stroke prevention by reducing risk factors;
- prevention of first or recurrent stroke by removing the underlying lesion - for example, during surgery to remove atherosclerotic plaque from the lumen of the carotid artery (carotid endarterectomy );
- prevention of secondary brain injury by maintaining adequate blood flow (perfusion) in the marginal areas of ischemic areas and reduce swelling of brain tissue.
Except for the elimination of risk factors, all aspects of stroke treatment are rather contradictory. Convincing evidence of the effectiveness of treatment approaches often are not. Thus, the modern treatment of stroke is largely empirical and based on the knowledge the doctor about the risks that accompany the various diagnostic and therapeutic methods.
Strokes are classified according to their putative pathophysiological mechanisms. In each case, a stroke can be defined as the clinical manifestations and principles of diagnosis and treatment. In the diagnosis of stroke or transient ischemic attack (TIA) primarily assess the initial clinical manifestations and their dynamics, ie, to decide whether "stroke syndrome or transient ischemic attack (TIA)?".
At present, the improvement of clinical diagnosis, and radiation research methods can clarify the nature and location of stroke, as well as explore their concomitant vascular lesions with a high frequency and accuracy, which makes treatment more focused, feasible and necessary. These include:
- MR angiography (magnetic resonance angiography), cerebrovascular
- CT of the neck vessels and brain (CT-angiography) with intravascular contrast
Ischemic stroke neurological symptoms
Features of stroke onset, along with the specific objective and subjective neurological symptoms suggest localization of brain injury and its cause. In most cases, the sudden appearance of an acute focal neurological symptoms indicate a possible stroke, especially if these impairments match the specific vascular bed. So, hemiparesis and aphasia associated with damage to the pool of middle cerebral artery of the dominant hemisphere, and the sudden loss of visual field - the posterior cerebral artery, the development of "clean" hemiparesis suggesting a small "lacunar" stroke lesion in the internal capsule or the base of the brain corresponding to the pool of small penetrating branches, respectively, of the middle cerebral or basilar artery.
At the beginning of the disease symptoms are moderately or severely, have fluctuating nature, they gradually flatten or increase. It is the dynamics of neurological symptoms gives an indication of thrombotic, embolic or hemorrhagic nature of the lesion. But, for example, a sudden deep coma may occur as embolism of the basilar artery, and in subarachnoid hemorrhage or hemorrhage into the base of the pons in hypertension.
To determine the nature of defeat, leading to coma, it is necessary to take into account detectable when viewed from neurologic symptoms and its dynamics. However, to establish exactly the details of the dynamics in the early stages of the disease is difficult. The patient is often unable to recall them without help, and sometimes the patient's condition is determined by the localization of lesions, such as in anosognosia in the non-dominant hemisphere lesions cases. Often, important medical history information can not figure out a sick family member.
Thus, the diagnosis of stroke symptoms based on clinical symptoms and a characteristic set of subjective and objective symptoms.
Haemorrhagic stroke localization and size of hemorrhage as well as their type (subarachnoid or intracerebral) determine the characteristic symptoms of stroke. Meanwhile, hospital ischemic stroke depends not only on the nature of the pathological process, the size of the hearth, the localization of vascular lesions, but also on the capacity of collateral circulation. Often the value of collateral blood flow sufficient to prevent a heart attack or a significant reduction in its size, which affects the development of stroke symptoms.
Collateral blood flow may be sufficient to complete occlusion of a major arterial trunk was not accompanied by neurological symptoms and visible lesions of the brain parenchyma. In other cases, the occlusion of large arteries can lead to softening of the brain tissue around the pool of blood supply. There are a variety of myocardial lesions, which differ in size, shape, stage of development, as determined by the possibilities of collateral circulation. Collateral blood flow depends on the anatomy of the vessels, the rate of occlusion, systemic blood pressure parameters. These factors, as well as, perhaps, others, such as impairment of the viscosity, polycythemia, the pathology of red blood cells, occasionally can act adversely and lead to ischemia in pools of blood supply is partially occluded arteries.
Collateral blood flow not only affects the deep penetrating vessels coming from the trunk of the middle cerebral artery (artery of lenticular nucleus and the striatum), distal vertebral arteries, 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 as atherothrombotic nature, and at lipogialinoze embolism and lead to the development of small "lacunar" infarcts.
The terms "stroke in development" (also known as progressive stroke), and "completed stroke" must be mentioned separately. If neurologic deficit is growing or fluctuating nature of that mark in the process of monitoring the patient, talking about the development of stroke, but if the symptoms continued growth does not, talk about a completed stroke. The progressive course of stroke explained by several mechanisms, including increasing arteriostenosis thrombus, the development of cerebral edema, thrombus propagation with occlusion of the branches of the collateral blood supply to the site of cerebral ischemia, as well as systemic factors, such as hypotension.
Although in some cases, these factors may play a role, is more likely that fluctuating neurological deficit is the result of multiple proliferation, migration, dispersal and lysis of emboli or arterial embolism caused by repeated blood - character or variations of collateral blood flow through Willis' artery, anastomosis of adjacent zones of blood supply and orbital, or cervical vertebral - collaterals.
The assumption that certain forms of cerebral vascular lesions occur not only when the various symptoms of stroke, but also when combined with risk factors. Development aterotrombotichkogo stroke often suggests that the patient is asymptomatic or symptomatic vascular disease in coronary and peripheral vascular disease. On the other hand, serious atherothrombotic vascular lesion localization provides any grounds for considering the atherothrombotic process as a cause of ischemic stroke. If the patient is diagnosed with atrial fibrillation, valvular heart disease, myocardial infarction, or bacterial endocarditis, which are the source of emboli, their presence indicates the nature of embolic stroke.
Severe arterial hypertension invariably accompany lipogialinoz small vessels, lacunar stroke and atherothrombotic carotid bifurcation lesion, trunk of the middle cerebral artery, the vertebrobasilar vascular system. Hypertension also predisposes to the appearance of deep intracerebral hemorrhage. According to some authors, an antigipertenzionnoy therapy is an important factor in reducing the incidence of stroke. Smoking and family lipemia, although less common than hypertension, combined with an increased risk of atherosclerosis and, in particular with ischemic brain disease.
Transient ischemic attack (TIA) neurological symptoms
Clinical manifestations and temporal profile of transient ischemic attack (TIA) allow us to assess the nature and location of the underlying pathophysiology of the arterial. The term "transient ischemic attack" (TIA) usually refer to any sudden focal deficit, completely regressed in less than 24 h. This definition is too broad because it includes so many syndromes, some of which are not necessarily caused by ischemia, such as syndrome of the focal epilepsy or migraine, accompanied by neurological symptoms. In addition, symptoms of ischemia, persisting longer than one hour may indicate that a certain area of brain tissue underwent a heart attack.
Specific symptoms of transient ischemic attack (TIA) indicate involvement in the pathological process of supplying blood specific artery:
- carotid artery
- middle cerebral artery
- vertebral-basilar system (vertebrates and basilar artery)
- small penetrating artery (lacunar transient ischemic attack)
Duration, and frequency of stereotyped repetitive episodes indicate their pathophysiological mechanisms. For example, repeated (up to 5-10 times a day), short (15 min or less) the same type of attacks of weakness in the wrist or the whole hand with underlying speech or no cause to think about narrowing or occlusion of the proximal artery insufficiency of collateral blood supply, leading to transient focal ischemia ("low bloodflow") of the cortex of the contralateral cerebral hemisphere. On the other hand, the only fit speech disorders and weakness in the wrist or hand (the latter may be absent) of 12 h can be observed in cerebral ischemia caused by embolism, with the possible formation of the infarct in the left frontal lobe.
Transient short episode of pure pyramidal hemiparesis involving facial muscles, arms, legs and feet, not accompanied by a speech disorder (dysphasia), or ignoring half of the body, shows a transient ischemia in the internal capsule, for example in a pool of blood supply of one of the small penetrating arteries originating from the trunk middle cerebral artery (artery of lenticular nucleus and the striatum). In acute disorders of cerebral circulation in the basin of the arterial lesion occurs, no larger than 1 cm - lacuna. Such a impairment may be designated as "lacunar transient ischemic attack".
Transient ischemic attack (TIA) in the vertebral-basilar system, if they are the result of narrowing (stenosis), the underlying plot or bilateral upper- primary (distal) part of the vertebral arteries, usually manifested in the form of short bouts of dizziness, diplopia and dysarthria. Repeatability and brevity of these episodes can think more about the transient reduction of cerebral blood flow than of embolism.
In general, transient ischemic attack (TIA) are due to two main factors: focal reduction in perfusion and embolism. The mechanism of transient ischemic attack (TIA) embolic origin is obvious, while 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 the decrease in local cerebral blood flow. Probably the arterial stenosis or occlusion of the critical degree of causing a reduction in blood flow to certain areas of the normal brain. Plays an important role insufficiency of collateral blood flow to the ischemic area, but due to the transient nature of the ischemia is also necessary to take into account factors such as blood viscosity, elasticity of the vascular layer and other yet unknown factors. These forms of transient ischemic attack is best regarded as a true TIA, ie, episodes neembolicheskogo genesis.
Unlike stroke, cerebral manifestations of transient ischemic attack (TIA) completely regressed, but they serve as a warning about the possibility of subsequent stroke. Therefore, the pathophysiological mechanisms of stroke and transient ischemic attack (TIA) must be considered together. In fact, the doctor can not help the patient with transient ischemic attack (TIA), not knowing what caused it.
Transient ischemic attack (TIA), such as stroke, is a syndrome, which requires setting a more specific diagnosis.
Cerebrovascular diseases differential diagnosis with other neurological disorders
The diagnosis of vascular lesions of the brain is based solely on the recognition of symptoms of stroke. On the other hand, the diagnosis of stroke is always in doubt. There are three criteria to identify stroke:
- pace of development of the clinical syndrome
- signs of focal brain lesions
- clinical condition
Time profile of stroke is usually described by means of precise characteristics of prodromal phenomena and dynamics of the onset of 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 is expedient to increase the observation time for a few days or weeks, as the most frequent cause of diagnostic errors are insufficient data on the development of stroke.
Several neurological disorders reminiscent of their clinical course of vascular lesions of the brain. In the absence of some details of the history of the disease in a patient, difficulties arise in the diagnosis of subdural hematoma, brain tumor, brain abscess, and senile dementia.