Mar 05, 2018
Stroke is a very serious and dangerous disease, accompanied by a lesion of the vessel, and then of the central nervous system. The word " stroke " is formed from the Latin insulto - "jumping, jumping" and means "attack, stroke, impact."And by definition WHO: Stroke is a rapidly developing focal or global impairment of brain function that lasts more than 24 hours or leads to death, with the exclusion of another genesis of the disease.
Stroke is understood as a clinical syndrome characterized by sudden symptoms of loss of local cerebral and sometimes cerebral functions( confirmed or not by computer tomography data) lasting more than 24 hours leading to death without any obvious cause other than vascular pathology. The causes that lead to a disruption in the delivery of blood can be such as rupture of a blood vessel when blood is poured into the brain tissue. The rupture is due to sudden fluctuations in blood pressure and a pathologically altered vascular wall. There is a violation of adequate blood flow, which leads to a deterioration in the supply of nerve cells, and this is very dangerous, since the brain constantly needs a lot of glucose and oxygen. How to treat this ailment with folk remedies, look here.
There are two types of strokes:
There are three main nosological forms - ischemic( thrombotic, non-embolic, embolic) stroke, cerebral hemorrhage, subarachnoid hemorrhage. In addition, subarachnoid-parenchymal, parenchymal-subarachnoid hemorrhages and "mixed" strokes may occur.
With hemorrhagic stroke, the blood leaves the bursting vessel under high pressure, pushes the brain tissue, forming a hematoma( blood tumor), and impregnates the brain region.
This discontinuity is due to sharp fluctuations in arterial pressure in the pathologically altered vessel wall by an atherosclerotic process - in 50% of cases.10% of cases occur on the pathologically altered vessel wall with a tumor, the use of drugs that promote blood flow and 20% of cases for all other causes of hemorrhagic stroke.
Cracks appear on the inner wall of the vessel. Through them, the walls of the vessel are saturated with blood.
After this, the process of necrosis develops in the wall of the vessel - the destruction of the walls inside the vessel.
Science has proven that such changes in blood vessels occur with a sharp increase in blood pressure - hypertensive crisis. While this process is going on inside the vessel, there is no external pathology.
But when the vessel bursts, the blood gets into the substance of the brain, destroying its tissue, a hemorrhage or hematoma is formed. They account for 85% of intracerebral hemorrhages. With hypertension, carotid arteries are most affected by severe changes.
The artery is destroyed by atheromatous plaques.
The heaviest - hemorrhages in the brain stem, where the vital centers are located, this leads to instant death. And the symptoms of hemorrhages in the brain also depend on their localization, as will be discussed in the stroke clinic. Read also a detailed and understandable article on symptoms, diagnosis, treatment and recovery after a hemorrhagic stroke. Learn how to ensure successful rehabilitation, keep working capacity, not to allow a second stroke.
Hemorrhagic stroke often develops at the age of 45-60 years, mainly with the same frequency in men and women. Appears suddenly, in the daytime, usually after a sharp excitement or overwork. Sometimes the stroke is preceded by flushes of blood to the face, headache, vision of objects in red, vomiting, frustration, increased breathing, a decrease in heart rate or, on the contrary, heartbeat. Sometimes the pupil dilates on the side of the lesion, the divergence of the eyeballs, the divergence of the eyeballs aside( paresis of the eye, lowering the angle of the mouth and chewing the cheeks on the side of the paralysis( symptom of the sail). On the side opposite to the outbreak, a symptom of hemiplegia is frequently found - the foot is turned outward,the hand falls like a whip, often a pulsation of blood vessels on the neck, breathing is hoarse with difficulty in inhaling or exhaling. The skin is cold, the pulse is intense, the arterial pressure is in most cases increased, swallowing disorder, zaderka incontinence or involuntary urination. When hemorrhage in the brainstem vital functions are violated and may occur sudden death.
For hemorrhage in the cerebellum characterized by dizziness with a sense of rotation of objects, sharp pain in the neck and neck, vomiting, narrowing of the pupils, speech is broken, the tension of the occipital muscles.
Acute form of stroke is characterized by the development within a few minutes of deep coma. Death occurs quickly, within a few hours, the same pattern is observed with extensive hemorrhage in the large hemisphere, brain bridge or cerebellum with a breakthrough of blood into the ventricles of the brain and defeat of the vital centers of the medulla oblongata.
Subacute form is characterized by a slow progression of symptoms or acute onset followed by short-term improvement and a new deterioration. In elderly and elderly people, hemorrhages proceed less violently than in young people, often manifesting with general cerebral symptoms. If there is a disturbance of the cerebral circulation, the disorder of recognition of objects may be felt, the hearing is preserved, but the patient does not recognize familiar voices, is poorly oriented in space, sees, but does not recognize objects from past experience. This occurs when the various parts of the cerebral cortex are affected.
The clinic for affecting the temporal lobe is characterized by speech disorder, auditory, taste hallucinations, dizziness, vestibular disorders.
Hemorrhage in the frontal lobe is characterized by a violation of the letter, convulsive seizures with a turn of the head and eyes in the opposite direction.
When you touch the palm of the hand, the grasping reflex appears, there is a mental disturbance, a tendency to flat jokes, a depressive state, walking is disturbed. The patient frantically grabs the bed, the wall and other objects, afraid to fall.
Most of the ischemic strokes( 60%) occur due to atherosclerosis. An important role in their development is played by the pathology of the extracranial parts of the carotid and vertebral arteries.
The most common artery compression is localized in the area of their division - the cervical spine. Because these areas are more often traumatized from the back wall of the spinal canal due to degenerative or inflammatory changes in the intervertebral joints. It is also possible to squeeze the vessel due to an anomaly in the development of the cervical spine.
• Complete closure of the vessel may occur due to clotting of the blood vessel with a thrombus, or with a thrombus rupture - embolism, or when closing with an atherosclerotic plaque.
Thrombi usually form in the area of a cholesteric plaque. Material for embolism can be blood clots from the heart and fragments of blood clots from disposed plaques in the arch of the aorta and carotid arteries. Ischemia of the brain can develop and without blockage of the vessel - with its narrowing( stenosis) or with an inflection. At the same time, fluctuations in blood pressure, deterioration of cardiac activity, blood loss, etc. are of great importance.by the type of cerebrovascular insufficiency. Ischemic strokes are different in size and location. Dimensions of strokes depend on the level of vascular lesions. Read more about the instructions on symptoms, diagnosis, treatment and recovery after an ischemic stroke. It is written in clear language. Learn how to ensure successful rehabilitation, keep the patient's high quality of life, prevent a second stroke.
Ischemic stroke( cerebral infarction) is observed most often, in middle-aged and elderly people, sometimes it is possible at a young age;in men it is noted somewhat more often than in women. The development of ischemic stroke is often preceded by short-term cerebral circulatory disorders, which are manifested by unstable lesions of the limbs, speech disorders, etc. Usually they are a consequence of a deficiency in the blood supply to the brain in the area in which the infarction later develops. In some patients the frequency of recurrent and ischemic attacks occurs immediately before the development of a cerebral infarction. With thrombosis( clotting of a blood vessel with a thrombus) of cerebral vessels, precursors of ischemic stroke are often present - dizziness, short-term consciousness disorder( half-unconscious condition), darkening in the eyes. Ischemic stroke can develop at any time of the day. Most often it occurs in the morning or at night. Sometimes the relationship of the initial manifestations of a stroke with the previous increased physical exertion, the influence of an emotional factor, the use of alcohol, the taking of a hot bath, a blood loss, or some disease, in particular, an infectious one, is established.
Often ischemic stroke develops after myocardial infarction. Characteristic is a gradual increase in focal neurological symptoms - for several hours, sometimes 2-3 days, less often for a longer time.
Acute development of ischemic stroke can occur with thrombosis of part of the internal carotid artery or with acute blockage of a large intracerebral artery. Approximately in 1/6 of the observations, a cerebral infarction( stroke) develops slowly - for several weeks or even months. Pathological symptoms are determined by the localization of a cerebral infarction( stroke), the affected vessel and the conditions of the circumferential circulation. For the plugging of the extracranial portion of the internal carotid artery, a period of visual impairment per eye is observed in combination with short-term paralysis and a sensitivity disorder in the opposite half of the body. Further persistent visual impairment develops, with optic nerve atrophy on the side of occlusion of the artery and paralysis on the opposite side;when there is a blockage of the left carotid artery, speech disorder often occurs, epileptiform seizures, a symptom of plugging of vertebral and basilar arteries outside the skull, in the cervical spine area is manifested by systemic dizziness, staggering during walking, twitching of eyeballs( nystagmus), ear noise, hearing loss and impairedeyes on both eyes. Sometimes coma develop, paralysis of the limbs, muscle tone decreases.
With cerebral infarctions in the vertebrobasilar region, the brainstem is most often affected - this is a very dangerous zone.
In case of ischemic brain damage, cholesterol increase, increased blood clotting, increased prothrombin, changes in encephalogram, rheovasogram, computed tomography are observed in the blood of patients. The ultrasonic Doppler method provides information on the state of blood circulation.
Mortality with hemorrhagic stroke is high, varies between 60-90%.Most patients die in the first two days, most of them in the first day. Mortality in ischemic stroke is observed within 20% of cases. With repeated ischemic strokes, progressive mental disorders develop.
Ischemic stroke is the most frequent form of acute disorders of cerebral circulation. They account for about 80% of the total number of strokes.
The concept of "ischemic stroke" reflects only the fact of the development of the disease, caused by a decrease in blood flow in a certain area of the brain and characterized by the formation of a limited infarction. A cerebral infarction is a zone of necrosis formed due to gross, persistent disturbances in the metabolism of neuronal and glial structures resulting from insufficient blood supply due to stenosis( occlusion) of the main arteries of the brain head or arteries leading to a perfusion pressure deficit or because of thrombosis orembolism of the arteries of the brain. Thus, all medical measures are aimed at arresting or compensating for pathological changes in the brain caused by a developed infarction.
Modern methods of instrumental studies( computer and nuclear magnetic resonance imaging, proton emission tomography, transcranial dopplerography, duplex scanning, subtraction angiography) allow us to classify acute cerebral ischemia in accordance with four principles:
1) In view of the duration of the neurological deficit, there are:
2) Classification, characterizing the degree of severity of patients. It provides:
3) The classification based on the localization of the cerebral infarction is based on the compliance of the topical characteristics of focal neurological symptoms with certain arterial basins: middle, anterior, posterior cerebral arteries;the main artery and their distal branches.
4) Pathogenetic classification includes:
Etiopathogenesis of cerebral infarction is most justified considering the concept of heterogeneity of ischemic stroke.
NV Vereshchagin characterized the role of pathology of the main arteries of the head, various heart lesions, violations of central and cerebral hemodynamics in the etiopathogenesis of ischemic stroke. The importance of changes in intracerebral arteries of small caliber, underlying the lacunar infarctions, has been proved significant in arterial hypertension. In addition, the role of changes in the rheological and coagulation properties of blood, changes in the thrombotic endothelial link, and the biomechanics of blood flow as the etiopathogenetic causes of cerebral infarction has been determined.
EI Gusev thoroughly described pathobiochemical changes in the brain structures leading to the formation of a cerebral infarction and defined measures for their correction.
Adaptation of the pathokinesis concept to the definition of the mechanisms of the development of cerebral infarction makes it possible to specify the conditions predisposing to its occurrence and the immediate causes of ischemic stroke.
Among the conditions predisposing to the development of cerebral infarction, it is legitimate to single out local and systemic factors.
The most frequent local factors are atherosclerotic lesions of the main arteries of the brain's head and arteries-stenosis( occlusion), as well as localized thrombus formation;various heart lesions as a source of cardioembolic cerebral infarcts;degenerative dystrophic changes in the cervical spine causing extracranial compression of the vertebral arteries. Relatively rare local factors include cranio-vertebral anomalies, fibromuscular dysplasia, pathological tortuosity of the main arteries of the head, dilated arteriopathy, arteritis.
Systemic factors include violations of central and cerebral hemodynamics, coagulopathy, erythrocytosis and polycythemia, oppression of gas transport properties of blood.
Local and system factors are in interconnection and interdependence, often inaccessible to recognition and evaluation.
Atherosclerosis .As the progression of atherosclerosis due to the accumulation of cholesterol there is a thickening of the intima-media complex, atheromatous plaques are gradually forming in the main and cerebral arteries. Morphological structure of plaques is different. Soft, loosened plaques are an embologenic substrate, and dense plaques contribute to the stenosis( occlusion) of arterial trunks, severely restricting blood flow.
The presence of one or multiple( echeloned) stenoses causes a number of negative effects. The dynamic properties of blood - volume and viscosity - deteriorate substantially. Sharply limited level of cerebral blood flow - its reduction to 60% is critical for the development of cerebral infarction.
Only multiple( echeloned) stenoses of extra- and intracranial arteries have independent significance in the pathogenesis of ischemic stroke. In other cases, acute cerebral ischemia occur when the cerebral blood flow is decompensated due to abrupt disturbances of the central hemodynamics.
Experimental and clinical instrumental studies have shown that hypertension stimulates and aggravates atherosclerotic lesions of the arterial system.
In addition, stenosis( occlusion) creates serious prerequisites for thrombosis.
Thrombosis. The main stages of thrombus formation are: endothelial damage to intima due to atheromatosis;slowing and turbulence of blood flow in the stenosis region;collision, aggregation, "sticking" of blood cells on the damaged endothelial site;reduction of oxygen capacity of red blood cells;coagulation of fibrin and inhibition of local fibrinolysis.
Depending on the specific ratios of the degree of intensity of the thrombus formation process, on the one hand, and the level of activity of the anti-clotting system of blood, on the other hand, either the thrombus forms or its lysis occurs, partial or sometimes complete. However, when the severity of atherosclerosis is severe, intima chemoreceptors lose the ability to perceive the effect of procoagulants( thromboplastin, thrombin), and there is no reflex activation of the anticoagulant system, or it is insignificant and does not prevent the further formation of a thrombus.
Heart lesions are an extremely frequent source of cardiocerebral, hemodynamic and lacunar cerebral infarcts.
This position is convincingly confirmed by the results of computed tomography, transcranial dopplerography, duplex scanning, ECG, transthoracic and esophagus Echo-KG, holter monitoring.
Cardiogenic pathology with the highest embolic potential in cardioembolic and lacunar infarctions, according to Suslin's data, includes atherosclerotic lesions of the aorta, aortic and mitral valves, left ventricular hypertrophy of the heart, intracardiac thrombi, various forms of cardiac arrhythmias, ischemic changesST wave on the ECG.In hemodynamic infarcts( cerebrovascular insufficiency), the embologenic potential is highest with a decrease in cardiac output due to a violation of the contractile function of the myocardium, with weakness of the sinus node and arterial hypotension in combination with stenosing lesions of the main arteries of the head. In 60% of patients there are combinations of these forms of cardiac pathology.
In addition to these heart injuries, the source of cardioembolism may include heart valve and rheumatic myocardiopathy, cardiac rhythm disturbances in hyperthyroidism, parietal thrombi in myocardial infarction, bacterial and non-bacterial endocarditis, cardiac muscle damage in AIDS, paradoxical embolisms with oval hole defects, andEmboli, formed after operations of coronary artery bypass grafting and transluminal angioplasty.
A specific feature of cardioemboli due to characterized heart lesions is the tendency to recur, and in some cases to simultaneous embolization of various cerebral arteries.
Clinical manifestations of cardiocerebral emboli are determined by a number of factors: the size of the embolus and the diameter of the occluded vessel, sometimes by subsequent thrombosis of the proximal part of the affected artery, the intensity of reflex thrombolysis, and the intensity of the "inclusion" of the collateral circulation. Thus, cardiocerebral emboli can manifest PNMC, a small stroke or a severe, massive stroke.
Changes in the cervical spine in the form of severe deforming spondylosis can play a significant role in the development of ischemic strokes in the vertebral-basilar basin. The mechanism of their development is the compression of the vertebral arteries either in the bone tunnel located in the transverse processes of the VI-II cervical vertebrae, or on the short atlanto-ocillital segment of the vertebral artery. Compression or permanent fixation of the vertebral artery can also occur with congenital craniocerebral anomalies - Klippel-Feil and Arnold-Chiari syndromes, with Kimmerle anomaly. The Klippel-Feil syndrome is a synostosis of the cervical vertebrae, sometimes combined with the occultization of the atlas and the splitting of the arches of these vertebrae. Arnold-Chiari Syndrome is a combination of malformations of the cerebellar amygdala with platybasia and / or coarctation of the large occipital foramen. Kummerle anomaly - the formation of the bone ring( bridge) on the posterior arch of the atlas in the area of the location of the vertebral artery.
Other rare local factors are fibromuscular dysplasia and tortuosity of the main arteries of the head, dilated arteriopathy, arteritis.
Fibromuscular dysplasia - congenital anomalies of the walls of the internal carotid, middle cerebral and vertebral arteries and their terminal branches in the form of multiple annular narrowing of the lumen, and sometimes small aneurysms. In the affected areas gradually formed bends or tortuosity, varying degrees of stenosis. As a result, conditions are created for local slowing and disturbance of laminar blood flow and, consequently, prerequisites for parietal thrombus formation and subsequent embolization of the arterial system of the brain.
Dilatator arteriopathy, which develops with widespread lesions of the main arteries of the head, leads to loss of elasticity of the walls of the arterial trunks, as well as to the formation of pathological kinks and tortuosities. Because of the slowing and disturbance of laminar blood flow, thrombi are formed, which can later be a substrate for embolization of the brain vessels.
Arteritis that can contribute to the development of an ischemic stroke includes Takayasu's disease( "pulse-free disease"), Moya-Moya's disease( arteritis in the Willis circle), and infectious granulomatoic arteritis-the manifestation of AIDS, tuberculosis, syphilis, malaria and other diseases.
To this category of factors predisposing to the development of ischemic stroke include violations of central and cerebral hemodynamics, angiospasm with migraine, coagulopathy, erythrocytosis, suppression of gas transport properties of blood.
Violations of central hemodynamics. One of the leading systemic factors is the cardiac hypodynamic syndrome. It is characterized by clinical signs( circulatory insufficiency, hemodynamically significant disorders of the heart rhythm) and functional indices - decrease in the minute volume of blood( IOC) and shock volume of the blood( CRS).Cardiac hypodynamic syndrome is a consequence of various causes - arterial hypertension, myocardial hypokinesia of various etiologies, ISC reduction due to valve lesions or cardiac arrhythmias, transient myocardial contractility in angina pectoris and hypertensive crises. The IOC index is the most informative, integral indicator that characterizes the effectiveness of the heart irrespective of the above reasons, which can exert no influence on it. IOC is determined by means of Echo-CG.
The IOC indicator, indicative of compensation or decompensation of cerebral circulation, is of decisive importance. According to EA Shirokov, in people over 60 years the IOC value below 3 liters indicates a clear threat of development of ischemic stroke. This value is determined taking into account the fact that in the presence of atherosclerotic stenoses and occlusions of the main arteries of the head, the hemodynamic reserve of cerebral circulation - that is, the ability of the intracranial arteries to expand - is depleted or minimal.
In patients with severe atherosclerotic changes in the arterial system, IHD, heart failure and other pathological processes that reduce the effective work of the heart, often there is a hypokinetic variant of hemodynamics with low blood pressure and a sharp decrease in blood flow in the arterial system of the brain, especially in the vertebrobasilar basin. With an average blood pressure within 60 mm Hg. Art.and lower there comes a "breakdown" of autoregulation of cerebral circulation, and a decrease in the level of cerebral blood flow is the cause of thrombus formation - first in the distal( arterioles, capillaries), and then in the proximal parts of the vascular bed. In patients with a lost or extremely limited ability of blood vessels to constriction and vasodilation, "night" strokes often develop, since at this time of day the blood pressure level is the lowest.
The development of stroke in cardiac hypodynamic syndrome and arterial hypotension should be regarded as an ischemic stroke, the basis of which is cerebrovascular insufficiency( hemodynamic stroke).
Arterial hypertension accelerates the development of atherosclerotic lesions of the main arteries of the head and arterial system of the brain. The sudden sudden rise in blood pressure may be the immediate cause of the development of ischemic stroke as a factor that "mobilizes" the near-wall thrombi and their drift into the arterial system of the brain. In addition, sudden sudden increases in blood pressure in certain cases lead to the development of an ischemic stroke due to the angiospasm of small branches of the intracerebral arteries.
In the development of ischemic stroke in atherosclerosis and arterial hypertension, an important role is played by the increase in hydrodynamic resistance of blood, caused by the insufficiency or decrease in the activity of the endogenous factor responsible for the hydrodynamic characteristics of the blood flow. This new mechanism of autoregulation of cerebral blood flow was characterized by IV Gannushkina( 1984-1997).
Heart rhythm disturbance is one of the most important, frequent factors contributing to the introduction of arterio-arterial and embolus cavities in the brain cavities into the cerebral arteries. The most unfavorable in this respect is ventricular fibrillation, which occurs with extensive myocardial infarction, constant or intermittent atrial fibrillation and atrial fibrillation, as well as syndrome of sinus node involvement with alternating tachy- and bradysystole. The risk of embolization - often repeated - is highest in arrhythmias in combination with severe arterial hypertension.
Angiospasm with migraine. Severe, prolonged migraine attacks with sharp angiospasm lead to a local decrease, a slowdown in cerebral blood flow and the accumulation of a large number of procoagulants. Subsequent vasodilatation creates even more prerequisites for local parietal thrombosis, sometimes reaching a degree that, as the migraine attacks recur in the affected area of the middle and small arteries, stenoses gradually form, further contributing to the development of infarctions.
Other system factors - coagulopathy, erythrocytosis and polycythemia, oppression of gas transport properties of blood.
Coagulopathies, characterized by a sharp procoagulant activity, in patients with arterial hypotension or chronic heart failure, contribute to the formation of parietal thrombi in pre-capillaries and cerebral arteries of small caliber.
The syndrome of disseminated intravascular coagulation( ICD) is a special form of coagulopathy. It is expressed by a sharp hypercoagulation( primarily due to the inhibition of fibrinolysis and formation of fibrin masses), which blocks microcirculation. It is possible to form not only thrombotic masses, but hemorrhages. The cause of the ICE syndrome is cerebral trauma, various infectious processes( mainly caused by gram-negative pathogens), as well as AIDS and other pathological processes.
Erythrocytosis( an increase in the number of erythrocytes more than 5.5-6.0 x 104 and polycythaemia( an increase in the number of platelets more than 400 x 103 or the number of leukocytes more than 20 x 103) as independent forms of diseases of the blood system can - most often against the background of sudden changes in central hemodynamics -cause thrombosis of the arterial system of the brain with the subsequent formation of an infarction. Them often, thrombotic lesions of this genesis - that is, "overloading" the vascular bed with blood elements - are of a focal character, and may also have
The oppression of gas transport properties of blood occurs in hemoglobinopathies and anemia of various etiology - hypochromic, hypoplastic and caused by various chronic diseases. Easually occurring hemic hypoxia as the cause of ischemic stroke is the result of a violation of the gas transport function of erythrocytes, which occurs when carbon monoxide poisoningcarbon monoxide). Hemoglobin contained in erythrocytes binds firmly to CO, forming a carboxyhemoglobin, and is suppliede oxygen becomes impossible in brain structure. Hemical hypoxia can also occur with poisoning with aniline contained in some household chemicals. In these cases, acute cerebral ischemia develop due to the transformation of hemoglobin into met-hemoglobin.
The conditions considered in the previous section, predisposing to the development of ischemic stroke, are up to a certain point pathological processes that do not manifest acute cerebral ischemia. The immediate causes of ischemic stroke should be considered as factors that realize pre-existing conditions in a manifestation of brain damage with irreversible morphological changes.
The immediate causes of the development of ischemic stroke depend in each case on the significance, severity and interdependence of conditions predisposing to the onset of acute cerebral ischemia.
The causes directly provoking the onset of ischemic stroke are:
The use of positron emission tomography, magnetic resonance imaging and single photon emission computed tomography( SPECT) has made it possible to quantify the volumetric blood flow in cerebral vessels, as well as the severity and dynamics of damage to various brain structures.
It is established that metabolic changes in response to the development of acute focal cerebral ischemia develop in a regular sequence. With a decrease in cerebral blood flow below 0.55 ml( g / min), a primary reaction is detected, characterized by inhibition of protein synthesis in neurons. Reduction of cerebral blood flow below 0.35 ml( g / min) stimulates anaerobic glycolysis, and a decrease below 0.20 ml( g / min) leads to an excessive release of stimulating neurotransmitters and a pronounced disturbance in energy metabolism. With a decrease in cerebral blood flow below 0.10 ml( g / min), anoxic depolarization of cell membranes occurs.
These data are of great practical importance, since the "core"( central zone) of the infarct is formed 6-8 min after the development of acute focal ischemia, and for several hours the "core" of the infarction is surrounded by the zone of "ischemic penumbra" or penumbra.
Penumbra is a region of dynamic metabolic changes in which the cerebral blood flow is reduced to 0.20-40 ml( g / min).Under these conditions, only functional changes take place in neuronal structures, but the energy exchange is still relatively preserved and no sharp microvascular, including microrheological, disturbances are observed.
The duration of the Penumbra determines the time limits of the "therapeutic window" - the period during which the therapeutic measures are most promising and limit the volume of the infarction. Most of the infarction is formed 3-6 hours after the appearance of the first clinical symptoms of ischemic stroke, and the final formation is completed in 48-56 hours.
With extensive infarctions accompanied by perifocal edema, this period may be shorter.
Based on the above data, active therapy of ischemic stroke - primarily neuroprotective drugs and thrombolytics - should begin within the first three hours of the disease.
Ischemia, caused by a decrease in cerebral blood flow, causes a pathobiochemical cascade or "ischemic cascade."Acute deficit of macroergens( phosphocreatine, adenosine phosphate - ATP) leads to inhibition of aerobic utilization of glucose and activation of anaerobic glycolysis. Under these conditions, the main amount of glucose is transformed into lactic acid;progressing laktatsidoz, leading to vasodilation and hyperperfusion in the ischemia zone, which further exacerbates the disturbance of metabolism. Lactacidosis in combination with hypoxia disorganizes the function of the enzyme system that controls the transport of ions - there are gross changes in the respiratory chain of mitochondrial functions and the extinction of the electrical potential of cell membranes, that is, their depolarization and change in their permeability. This pathological process entails a passive outflow of potassium ions from neurons and an intense influx of calcium, sodium and chlorine ions in them, as well as intracellular accumulation of free fatty acids and water. In a complex, this leads to swelling of the dendrites and lysis of the cellular elements of the neurons - protein and lipid complexes of amino acids. In addition, the deflection of membrane structures intensifies lipid peroxidation and the accumulation of fatty acids - processes whose intensity largely determines the rate and prevalence of metabolic shifts leading to the formation of a heart attack.
The increased release of excitatory mediators, glutamate and aspartate, the inadequacy of their re-uptake by astroglia and utilization, the overexcitation of glutamate receptors and, as a result, the disclosure of calcium channels controlled by them, is very important in the extracellular space. An increase in the intracellular calcium content stimulates further pathobiochemical reactions leading to necrotic neuronal death and apoptosis. On this basis, the concept of glutamate "excitoxicity"( from excite - excite) is formulated, which plays an important role in the formation of cerebral infarction. As a result of the study of the level of antibodies to glutamate receptors, the dependence of the severity of stroke on the degree of release of glutamate and aspartate was established. Simultaneously it was proved that the death of neurons is caused not only by the accumulation of neurotoxic substances, but also by the deficiency of substances possessing neurotrophic action.
In the acute stage of ischemic stroke, the enzymatic activity of the body is disrupted. One of its manifestations is the formation in the neurons of free radicals that damage the endothelium of the vessels.
Depending on the degree of ischemia, the arachidonic acid cycle is activated with secondary accumulation of its products( prostaglandins, thromboxane, leukotrienes).These biologically active substances have a negative effect on vascular tone and the system of aggregation of blood elements, promote intensive aggregation of platelets and erythrocytes, as well as increase of blood viscosity, hematocrit, fibrinogen content.
In addition to gross local changes directly in the ischemic zone, pathological processes occur in the system of humoral and hormonal systems. The most important is reactive hyperglycemia, which is practically not doped with the corresponding drugs. Such changes contribute to the intensive glycosylation of hemoglobin, which entails a decrease in the gas transport properties of blood, which, with a deficiency in glucose and oxygen neurons, deepens lactic acidosis and generalized disorganization of metabolism.
Cerebral ischemia may also be accompanied by an increase in adrenaline and other catecholamine-vasopressor levels. However, their vasoconstrictor effect in conditions of severe passive vasodilation( vasoparalysis), caused primarily by a sharp lactic acidosis, may be minimal or absent altogether.
An important role during ischemic stroke is given to changes in the system of prostanoids, including prostaglandins, thromboxanes and prostacyclins. Multidirectional increase in the content of various prostanoids in the blood and CSF is accompanied by a change in the reactivity of the arteries in the ischemia zone and the procoagulant effect. The most pronounced shifts in the quantitative spectrum of prostanoids occur with thrombotic stroke, which affects the severity of the course, the incidence of complications and adverse outcomes.
A pathogenetically grounded sequence of stages of the "ischemic cascade", taking into account the cause-effect relations, was formulated in 1997 by EI Gusev, VI Skvortsova, N. S. Chekneva, E. Yu. Zhuravleva, E. V. Yakovleva. The following stages of the "ischemic cascade" are distinguished:
The outcome of the "ischemic cascade" is the formation of a heart attack in the brain. In this process, two mechanisms play a role: necrotic cell death and apoptosis( genetically programmed death).
The practical significance of the stepwise analysis of the "ischemic cascade" is emphasized;since each of the stages is a target for therapeutic effects. The greatest clinical effect is achieved with the appointment of therapy in the early stages. At the first stage, the most promising are measures aimed at improving the perfusion of brain tissue, at the 2-8th stage - neuroprotective or cytoprotective therapy. The most justified combination of both areas of intensive care.
The level of perfusion of the brain determines the extent of disorders of cellular metabolism: the blood flow in the ischemic zone can be different in severity and duration. Hypoperfusion in the ischemic zone first and most sharply occurs in the nucleus of the infarction;it is less pronounced in the penumbra zone. The death of neurons in the nucleus of the infarct and the possible reversibility of functions in the penumbra zone depend on the degree of hypoperfusion. The duration of the hypoperfusion stage is very variable;on average, it is considered equal to 12-18 hours.
The most unfavorable phenomenon is the "non-renewal of blood flow"( no reflow phenomenon) - the result of extremely low perfusion pressure and abrupt disturbances of microcirculation. With it, the death of neurons occurs both in the nucleus of the infarction and in the penumbra.
In the future, as a rule, reperfusion occurs - restoration of blood flow in the ischemic zone. Its level and rapidity of manifestation depend on a number of factors. The main ones are the degree of decrease in the caliber of the affected vessels and microcirculation disorders in them, the probability and volume of spontaneous lysis of thrombi and the intensity of the resumption of blood flow. With reperfusion, as a rule, there is hyperkininogenesis, characterized by vasodilation and impaired permeability of the blood-brain barrier. In conditions of reperfusion, the risk of hemorrhagic infarction increases. In addition, hyperperfusion creates conditions for the formation of cerebral edema, even more disorganization of cellular metabolism and as a result of neuronal death.
Brain edema is the result of rapid progressive changes in metabolism that spread in the conditions of angioparesis to the perifocal zone of the infarction. The moment that triggers the development of edema is the penetration of water into the neuron from the extracellular space, caused by a violation of membrane permeability.
The resulting swelling of the cells causes intracellular edema. With prolonged ischemia, extracellular( vasogenic) edema is attached to it due to a gradual damage to the blood-brain barrier and the accumulation of under-oxidized products in the affected area that are formed under conditions of anaerobic glycolysis. Vaginal edema develops mainly in white matter. With extensive heart attacks, gross disorganization of cerebral blood flow, edema spreads over vast areas. Thus, by increasing the mass of the damaged hemisphere( and in some cases the opposite) and, accordingly, the compression of the vessels, the level of perfusion of the brain is further reduced. Edema promotes the development of dislocation and subsequent wedging of brain structures. The dislocation of the hemispheres leads to their induction into the clump of the cerebellar nest and the development of the secondary stem syndrome, the gradual appearance, after the formation of the infarct in the hemisphere, of the symptoms of the lesion of the trunk and the medulla oblongata. Dislocation of the subtentorial structures occurs in the large occipital foramen. Dislocation syndromes are the most frequent direct cause of death of patients with cerebral infarction.
The clinical characteristics and consequences of ischemic stroke depend on the magnitude and location of the infarction. The latter are due to a complex of largely interdependent, but also mutually compensating factors. Such mechanisms are the development of acute cerebral ischemia( thrombosis, embolism, cerebrovascular insufficiency), a specific lesion zone, individual anatomical features of the structure of the arterial system of the brain, the potential for inclusion of collateral circulation, the degree of disorganization of autoregulation, which largely determines the level of perfusion pressure in the affected vascular pool.
It is almost impossible to predict the extent to which the presence of anastomoses and the level of collateral circulation are reflected in the clinical picture;very heterogeneous variants are possible. Thus, for example, severe stenoses of the internal carotid artery( more than 80%), but with the full functioning of the Willis circle, can be asymptomatic. Embolism of the distal segment of the posterior cerebral artery in a zone with a relatively poorly developed network of anastomoses can cause the formation of sufficiently extensive infarcts with a persistent neurologic deficit.
Individual features of anastomoses in a number of cases cause different variants of redistribution of blood flow within the entire cerebral vascular system, including perverse vascular reactions - steal syndrome.
Local stealing syndromes in close proximity to the source of ischemia can be manifested in two ways. The first - "direct stealing", described by N. Lassen, is a direct shortage of blood flow due to stenosis of the leading artery or a fall in it of perfusion pressure along the mechanism of autoregulation failure. The second option - "perverted robbery syndrome" or the Robin-Hood syndrome( a fabulous robber who robbed the rich and distributed wealth to the poor) - redistribution of blood from zones with a safe blood flow to the ischemic zone.
Common embryo syndromes are most often expressed by a significant redistribution of blood from cortical anastomoses within the branches of one basin or by blood flow from the arteries of the carotid basin system to the arteries of the vertebral-basilar basin.
With the rapid formation of massive stenosis in the main arteries of the head or in the proximal part of the cerebral artery, in the conditions of a sudden disruption of autoregulation, but well-functioning anastomoses, there may be a decrease in blood flow in the arterial system of the opposite hemisphere. With a sharp suppression of cerebral blood flow as a result of interhemispheric diastase, can be filed by SB Sergievsky. EM Burtseva( 1992), to form "mirror" strokes.
Phenomena of stealing are sometimes the result of a sharply perverted, retrograde blood flow;with hemodynamic disorders observed in the distal areas. Sometimes there is a "subclavian stealing".
The inconsistency in the level of occurrence of embryonic syndrome, their intensity and prevalence in each specific case depends on the individual variability of the anatomical structure of the arterial system of the brain, all possible combinations of localization and the degree of expression of stenotic and occlusive changes in the vessels, hemodynamic level and functional consistency( or inconsistency) of the mechanism of autoregulation of the brainblood circulation.
The development of steal syndrome often contributes to the emergence of diagnostic difficulties due to the possible multifacetedness of neurological symptoms, and in some cases due to their "migration".
The exact characterization of the level, extent of steal syndrome and changes in the direction of blood flow can be determined as a result of TKUZDG.
The nature of hemodynamic and metabolic changes arising from ischemic stroke allows us to outline the main, most promising areas of intensive care:
In the near future, obviously, new drugs will also find use that specifically correct the negative effects of lactic acidosis and glutamate.
According to the American Medical Association( 1992), in 30% of cases the cause of heart attack is arterio-arterial thromboembolism from the extracranial arteries;in 20-25% of cases - intracardiac thrombi;in 15-20% of cases, lacunar infarcts occur, most often due to lesions of small arteries of the brain due to hypertension. In 30% of the cases, the causes of myocardial infarction remain unspecified.
Prodromal symptoms sometimes developing in weeks or even months before the stroke are nonspecific. Headache, dizziness, a feeling of "darkening" before the eyes are most often observed in cases of stroke in patients with a sharp increase in blood pressure. A serious precursor of an ischemic stroke are transient disorders of the cerebral circulation, especially frequent and increasingly prolonged. However, in their topical characteristics, they do not necessarily correspond to the basin in which the infarct is formed. To precursors are also single or repeated episodes of global amnesia - a sudden disorientation in the surrounding world, a memory of previous events. Attacks of global amnesia last from several hours to days.
Ischemic stroke can occur in a dream. According to W. Barnaby( 1990), 40% of thrombotic strokes and 17% of embolic ones develop in sleep. The rate of development of symptoms is a convincing sign that distinguishes embolic forms of stroke from thrombotic and due to cerebrovascular insufficiency. A sudden onset with loss of consciousness and the simultaneous appearance of distinct neurological symptoms is almost pathognomonic for emboli - mostly large arterial trunks. Embolisms more often than other forms of ischemic stroke develop with arrhythmia. Gradual increase in symptoms or their "flickering" during hours or sometimes 1-2 days is characteristic for two other clinical variants of ischemic stroke - thrombotic and hemodynamic( cerebrovascular insufficiency).With them, the prevalence of focal symptoms over cerebral palsy is characteristic. The topical characteristic of the neurological deficit corresponds to the lesions of certain vascular pools. Epileptic seizures in the acute stage of ischemic stroke are observed in 3-5% of cases and are predominantly generalized in nature.
The time during which the progression of symptoms is observed, and then their gradual regression, with all three variants of ischemic stroke is extremely variable. It depends on etiopathogenetic factors( embolism, thrombosis, cerebrovascular insufficiency), the caliber of the affected vessel and the volume of the ischemic area of the brain, the possibilities and rate of inclusion of the collateral circulation, the state of central hemodynamics, and the likelihood of complications.
This position is confirmed by two polar variants of the rate of development of ischemic stroke - from very rapid or sudden in embolisms to pseudotumorous, characterized by a rise in focal symptoms for weeks or even months. This variant is observed with slowly progressing stenoses of the main arteries of the head or large cerebral arteries.
The definitions of the term "acute stage of stroke" formulated at different times by WHO experts should be clarified. In 1969, WHO proposed to consider the "acute stage" the first 21 days after the disease. This provision is still used in many publications relating to the outcomes and prognosis of all forms of stroke. In 1977, WHO experts recommended that the acute stage be considered the first 48 hours after the onset of the disease. EI Gusev et al.(1997a) distinguish the most acute period - the first 3-5 days from the time of stroke, the acute period - up to 21 days, the early recovery period - 6 months and the late recovery period - up to two years after the disease.
However, from our point of view, it is justifiable to consider the acute stage a period of time during which the general cerebrovascular and / or focal symptoms increase and emergency intensive therapy and constant monitoring of the patient's condition are necessary. The sub-stage is the period of stabilization of the condition, when there is no immediate threat to the life of the patient.
In addition to ascertaining stages of stroke, it is advisable from the practical point of view to distinguish three variants of the current - progredient, recombinant and recurrent.
The prograde type is characterized by a steady suppression of vital functions, deepening of consciousness disorders, an increase in the severity of the neurological deficit, the early development of complications. The progestogenetic course occurs most often with thrombosis of the main artery, extensive hemispheric infarctions accompanied by rapidly developing cerebral edema and impaired liquor circulation, with early complications( pneumonia, purulent tracheobronchitis).This variant is more often observed in patients of senile age after repeated strokes - especially in cases of late hospitalization.
The re-gradient type of flow occurs predominantly with an incomplete, brief inhibition of consciousness or with the development of a neurological deficit without loss of consciousness. At the initial stage of the disturbance of vital functions are absent or amenable to rapid correction. Symptoms of fallout are relatively undefined. Recurrent flow, as a rule, occurs with limited infarctions caused by embolization or thrombosis of the terminal branches of the anterior, middle or posterior cerebral arteries, as well as with small ischemic foci in the brainstem. In part, the regressing course is associated with the often occurring spontaneous recanalization of thrombosed arteries.
The recurrent type of flow is characterized by an improvement in the condition that occurs when the symptoms recur after the onset of the stroke. Relapses can occur at different times and are due to many causes - repeated arterio-arterial or cardiac embryo, resumption of thrombosis, the development of a "combined" stroke, somatic complications - pneumonia, purulent tracheobronchitis, decompensation of cardiovascular insufficiency. Sometimes relapse occurs because of insufficiently intensive, adequate therapy, the appointment of contraindicated drugs, primarily vasodilators.
In cases where the measures necessary in each specific case do not stop the causes of deterioration, the recurrent type of flow can be transformed into a prograde one.
"Mirror" stroke - or, more accurately, a "mirror" infarction - the appearance of focal symptoms corresponding to its topical characteristic of a hemispheric lesion, the opposite of the one that was affected since the onset of the disease. The neurologic deficit caused by a "mirror" heart attack is manifested at various times from the moment of formation of the primary, primary focus - from 9-16 h to 3-5 days of the disease.
Most often the centers of "mirror" ischemia are localized in areas of adjacent blood supply vascularized by the terminal cortical branches of the anterior, middle and posterior cerebral arteries. With ischemic foci in the blood supply zone, carried out by branches of the anterior and middle cerebral arteries, a "mirror" heart attack is manifested by the emergence of a characteristic posture "man in the barrel" - a pronounced paresis of both hands with a relatively preserved force in the lower extremities. In case of "mirror" infarctions in the zone of the border blood supply, carried out by the branches of the middle and posterior cerebral arteries, bilateral visual disturbances occur( up to blindness to both eyes), as well as severe violations of gnostic functions and praxis. In ischemic lesions in the basins of both anterior cerebral arteriesa kind of syndrome that includes often asymmetric paresis of predominantly distal parts of the lower limbs, speech disorders, mental changes in the form of disorientation or pseudo-gendereating habits, as well as a bilateral grasping reflex, more pronounced and earlier appearing on the side opposite to the development of the primary( primary) infarction. With lesions of the cerebellum, "mirror" infarcts are rare.
Clinical diagnosis is based on the results of dynamic monitoring of neurological status. Appearance of symptoms corresponding to its topical characteristic of the foci, symmetrically located in relation to the one that originated at the beginning, indicates the development of a "mirror" infarction. With a high degree of reliability, the diagnosis is confirmed by CT or MRI.The zone of a "mirror" infarction is usually less than the primary( primary) area.
It has been proven by studies using proton emission tomography that the basis for a "mirror" infarction is the marked changes in cerebral blood flow symmetrical with respect to the primary( main) focus and the disorganization of cellular metabolism associated with them. However, the causes leading to the formation of a "mirror" stroke, to date, remain unclear. It is assumed that the "mirror" strokes arise due to the special individual features of the collateral circulation. In the disorganization of interhemispheric connections contributing to the formation of "mirror" infarctions, a certain role is played by neuropeptides, which have a specific effect on the side of the occurrence of motor disorders. When a "mirror" infarct occurs, therapy should be intensified.
Various terms are used to denote this variant of a stroke - "hemorrhagic infarction", "heart attack with a hemorrhagic component", "hemorrhage into a heart attack".Diagnosis based on clinical data is extremely difficult. More often hemorrhagic infarction develops on 2-4 days from the moment of disease and mainly at cardioembolic strokes. The only methods of reliable diagnosis are CT and MRI.Based on the results of these neuroendrogenological methods of investigation and autopsy, hemorrhagic transformation of infarcts is revealed in the first few hours, according to the data of individual authors, in 58-70% of cases.
The determining role in the development of hemorrhagic transformation is played by the rapid formation of extensive infarctions in conditions of recanalization of occluded arteries with high arterial pressure or embolus migration, the spread of thrombus to the distal sections of the vascular bed without recanalization of the damaged vessel. Hemorrhagic transformation with non-thrombotic softening( the mechanism of cerebrovascular insufficiency) can occur with sharply limited blood flow, with angioparosis and angiostasis. An indispensable condition contributing to hemorrhagic transformation of necrotic tissue is the increased permeability of the walls of small cerebral arteries, which determines the process of diapedesis. Essential is the release in the infarction zone of excessive concentrations of catecholamines and prostaglandins, severe disturbances of microcirculation, deterioration of the rheological properties of blood and the accumulation of products of impaired cellular metabolism.
The risk of hemorrhagic transformation depends on the volume of the infarction - if this volume exceeds 50 ml, the risk of hemorrhage into the necrosis zone is increased 5 times, and for large infarcts, characterized by computed tomography as a "mass effect" - 20 times.
About 50% of foci of hemorrhagic transformation are petechial and localized mainly in the cortex. About 25% are small hematomas more often in the basal ganglia. Larger foci of hemorrhage are detected in 17% of cases with extensive infarcts and in 7% of the hemorrhagic transformation zone on computer tomograms are similar to the pattern found in cerebral hemorrhages( summary data published by Shevchenko Yu. L. et al., 1997)
According to the morphological characteristic, the clinicalHemorrhagic infarctions of a small volume do not increase the course of the disease - "mute hemorrhagic transformation", occurring in 10-15% of patients with ischemic strokeIn patients with extensive infarctions, depending on the rate of their formation, it is common to distinguish two types of clinical course: subacute and acute Subacute type is observed mainly with low blood pressure. In the beginning, clinical symptoms resemble the most frequent variant of ischemicstroke with gradual development, predominance of focal symptoms over cerebral infarction. However, usually on the 2-5th day the condition quickly, jerks impaired - the severity of the neurological deficit increases. When symptoms appear that indicate the expansion of the zone of primary ischemia that has arisen, there may be an unclear oppression of consciousness. Skin symptoms and the appearance of a blood admixture to the CSF are uncharacteristic. The acute type of hemorrhagic infarction, according to the type of development, characterization and severity of the symptomatology, is more reminiscent of a hemorrhagic stroke. Suddenly or very quickly, a combination of sharply expressed cerebral, focal, and then envelope symptoms is revealed. There is hyperthermia and changes in the blood formula( leukocytosis, shift of the leukocyte formula to the left).In some cases, an insignificant admixture of blood is found in the cerebrospinal fluid. In acute type of hemorrhagic infarction, death most often occurs as a result of edema and dislocation of brain structures or extracerebral complications.
Thus, modern ideas about hemorrhagic transformation of cerebral infarction allow us to clarify the tactics of treatment with anticoagulants and to secure this type of therapy. Anticoagulants can be administered at the earliest possible time after the onset of a stroke, after a CT scan or an MRI to exclude hemorrhages. Given the most frequent timing of the emergence of signs of hemorrhagic infiltration of infarction( 2-4 days), in cases of worsening of the patients during these periods, a repeated CT or MRI study can be found that can detect the formation of a hemorrhagic infarction. Anticoagulants in such cases are immediately canceled.
This term designates the simultaneous occurrence of ischemic changes in one area of the brain and hemorrhages - in another. Sometimes such strokes are called "complicated".
According to the results of pathoanatomical studies, combined strokes are found in 3-23% of deaths due to acute disorders of cerebral circulation. The most common reasons for the development of a combined stroke are: marked angiospasm observed with subarachnoid hemorrhages and leading to the formation of "delayed" infarctions in the basin of the damaged artery;secondary trunk syndrome - small hemorrhages in the trunk and medulla oblongata, arising from extensive hemispheric infarctions with perifocal edema and leading to an "upper" wedge( protrusion of the medial part of the temporal lobe into the incision of the cerebellar nerve);rapid formation of major heart attacks( most often with embolic occlusion of the internal carotid or middle cerebral artery against a background of high blood pressure), often leading to the development of hemorrhagic foci in the affected, and often in the opposite hemisphere.
The only methods of diagnosis are computer or magnetic resonance imaging.
This term denotes the conditions under which a picture of acute disturbance of cerebral circulation develops, and in autopsy there is no macroscopic morphological change in the brain that can explain the clinical manifestations. In the vast majority of cases, the pseudo-stroke proceeds similarly to ischemic;rarely it resembles a cerebral hemorrhage.
Causes of pseudo stroke are pneumonia, acute or chronic cardiac or pulmonary heart failure, pancreatitis, myocardial infarction, severe alcohol intoxication, septic conditions, autointoxication in severe burns and cancer, diabetes, gastrointestinal bleeding, anemia, peritonitis.
The prerequisites for pseudo-stroke development are the morphofunctional inferiority of certain parts of the cerebral vascular system due to atherosclerotic lesions, previously suffered strokes, traumatic, inflammatory brain lesions. These prerequisites are realized in the acute
pattern of cerebral circulation disorders due to the usually onset of decompensation of central and / or cerebral hemodynamics, rapid suppression of hemostasis and gas transport properties of blood that cause hypoxia.
In the vast majority of cases, pseudo-is diagnosed in persons over 65 years of age.
An erroneous pseudo-stroke finding occurs in 3.6-6.3% of patients who were diagnosed with a stroke during their lifetime.
The reasons for the erroneous diagnosis are the prevalence of neurological symptoms over manifestations of somatic pathology, atypical course of chronic lesions of the cardiovascular system, pulmonary, hepatic, renal pathology. In addition, the cause of diagnostic errors in the overwhelming majority of cases is the severe severity of the condition of the patients at the time of hospitalization and the absence of reliable anamnestic data, as well as the difficulties of a detailed physical examination - 40-60% of this category of patients dies within the first three days of hospitalization.
Currently, the diagnosis of the true nature of the disease is much easier - the results of computer and magnetic-nuclear tomography can determine whether there are sufficiently extensive pathological foci that confirm the presence of acute impairment of cerebral circulation or the available symptoms are due to a severely flowing somatic pathology.
Hemorrhage in the brain( intracerebral hematoma) is a clinical form of acute impairment of cerebral circulation, caused by rupture of the intracerebral vessel and penetration of blood into the parenchyma. It should differentiate from subarachnoid hemorrhage, subdural hematoma and hemorrhagic infarction.
Causes of hemorrhage in the brain can be trauma, sudden sharp increases in blood pressure, secondary hemorrhages in the trunk and medulla oblongata( secondary stem-medullary syndrome with dislocation and wedging of massive supratentorial infarcts accompanied by brain edema), as well as arteritis, coagulopathy and brain tumors. These pathological processes lead to hemorrhage in the presence of pre-existing changes in the arterial system of the brain. In the overwhelming majority of cases, this is the arterial hypertension-specific hyalinosis of the arteries of small caliber and arterioles, in which multiple microaneurysms are formed, and sometimes local necrosis of intima. Hemorrhages also occur in areas where malformations are localized - microangiomas, microangiopathies, telangiectasias, cavernomas.
Massive hemorrhages of various etiologies are characterized by ambiguous localization. Hemorrhages due to arterial hypertension and localized at the border of gray and white matter - lobar hematomas, are of limited nature and occur relatively rarely. On the basis of clinical data, they are difficult to differentiate from heart attacks;the results of CT and MRI studies are of decisive importance in such cases. In 80% of cases, hemorrhages due to hypertension are caused by rupture of the lenticulostrial arteries and their branches, leading to destruction of the basal ganglia, inner and outer capsules, and also the visual cusp. Often they are accompanied by a breakthrough of blood in the lateral ventricles, and sometimes in the subarachnoid space. Hypertonic hemorrhages in the cerebellum are caused by rupture of the cerebellar arteries and are often accompanied by a breakthrough of blood in the IV ventricle or in the subarachnoid space. Quickly forming hematoma severely restricts the subtentorial space and leads to gross violations of liquor circulation. Hemorrhages in the trunk or medulla oblongata quickly lead to death.
Hemorrhages due to a breach of integrity by microangiomas, as a rule, develop as a diapedesis. Hemorrhagic foci are localized in the same zones as hypertensive hemorrhages, but the degree of damage to the brain structures is less pronounced.
If the patients do not die, the hemorrhagic focus undergoes successive changes. Initially, the poured blood forms a fibrin clot, which then turns into a liquid mass, which gradually undergoes resorption. Subsequently, the hemorrhage zone is preformed into a cyst surrounded by a fibro-cystic membrane.
Clinical manifestations of hemorrhages in the brain are determined by the volume of blood flow, localization of intracerebral hematoma and the rate of its formation. Neurological symptoms are caused by three main factors:
Prodromal symptoms are almost absent. Only occasionally there are nonspecific manifestations - headache, a sense of anxiety or unmotivated anxiety, dizziness, noise in the ears. Seizure fits in the anamnesis are to a certain extent characteristic only for breaks in intracerebral angiomas.
Pathognomonic for hemorrhages is an acute sudden onset with a severe headache. Following it, usually at the same time there are depression of consciousness, vomiting, rough symptoms of loss. Soon shell symptoms are attached. However, with a deep coma, they are usually absent. Quite often hemispheric hemorrhages are accompanied by convulsive seizures.
There are three variants of the course of hemorrhages - acute, subacute, chronic.
Acute option - the clinical picture of hemorrhage in the form of deep coma and the symptoms of wedging develops within seconds or a few minutes. Death comes in a few hours or days. This type of development takes place in 70-80% of the patients being hospitalized. In fact, it takes place more often, because with the acute development of hemorrhages, many patients die before hospitalization.
Subacute type also characterized by an acute onset, but then the clinical manifestations stabilize for some time, and there are no symptoms that indicate the development of wedging. Some regress of depression of consciousness and focal symptoms can be observed. However, due to the formation of cerebral edema 2-3 days later, and sometimes later, the symptoms of increased intracranial pressure appear again - an increase in the severity of focal and shell symptoms, the appearance of signs of wedging. Often the cause of worsening condition are repeated hemorrhages.
The chronic type of hemorrhage development is rare - mainly in cases when they develop as a diapedesis. It is difficult to differentiate from pseudotumorous syndromes, which cause a sharp increase in intracranial pressure. As a rule, the true nature of the disease can be clarified by careful analysis of anamnestic information. Diseases manifested psevdotumoroznym syndrome, manifest paroxysmal headaches and dizziness, slow progression of focal symptoms. The results of CT-examination and MRI are of decisive diagnostic value.
Depending on etiology and localization, hematomas differ in clinical differences, which to some extent affect therapeutic tactics.
Hemorrhages in the area of the striatum( fence) almost always develop in patients with severe arterial hypertension and mainly during the day. Often they occur with a sharp physical strain or stress. Occasionally they may be preceded by prodromal phenomena in the form of blurred, transient paresis, short-term episodes of depression, headache, or dizziness.
Symptoms develop, as a rule, suddenly and reach maximum severity within a few seconds. Patients immediately fall, and coma sets in. Because the hematoma is localized in the immediate vicinity of the inner capsule, paralysis or pronounced flaccid paresis immediately appears on the side opposite to the developed hematoma;Pathological symptoms are found. Characteristic are the deviation of the view towards the affected hemisphere, as well as various forms of breathing disorders, hyperthermia, vomiting, bradycardia. Blood pressure is often increased. As the volume of the hematoma increases and rapid development of perifocal edema, intracranial pressure increases, early symptoms of upper and then lower wedge are revealed.
With the breakthrough of massive hematomas of this localization in the lateral ventricle, an even sharper deterioration of the state suddenly occurs. Deep coma develops, tendon reflexes fade away, stop pathological symptoms are not caused. Violation of stem functions manifests itself by abrupt changes in breathing, bradycardia, followed by tachycardia and rough changes in the heart rhythm, as well as hyperthermia and hyperglycemia. When phenomena of increasing respiratory depression and hemodynamics quickly die.
With an early drainage of the ventricular system, no lethal outcome occurs, but the patients still have a gross neurological deficit.
Hemorrhages in the visual cusp are often accompanied by a breakthrough of blood in the third ventricle. The clinical picture is similar to that described above with breakthroughs in the lateral ventricle. Hemorrhages of small volume are manifested by thalamic syndrome. It is characterized by contralateral homonymous hemianopsia, contralateral hemiparesis, hemianesthesia and "thalamic arm" - flexion in wrist and metacarpophalangeal joints with simultaneous extension in interphalangeal joints. Sometimes choreoathetotic hyperkinesis occurs on the side of the lesion. Thalamic pain, as a rule, appears after some time after a hemorrhage.
Hemorrhages in the variola bridge occur usually in patients with severe arterial hypertension. Symptoms and outcomes depend on the localization of hematomas. Extensive hemorrhages with a breakthrough in the IV ventricle or spreading rostral to the visual hillock or caudal to the medulla oblongata very quickly end in death. Minor hemorrhages cause a rapid depression of consciousness and the appearance of symptoms of the defeat of the Varoliev Bridge. Hemorrhages in the Varoliev Bridge are not usually limited to a one-sided lesion, and therefore, in most cases, bilateral lesions of the cranial nerves and tetraparesis occur.
Hemorrhages in the area of the Varolieva bridge and the midbrain may be a manifestation of a secondary stem syndrome that occurs with the upper inclinations - dislocation and caudal displacement of supratentorial structures due to massive hemispheric infarctions and hemorrhages accompanied by edema.
Hemorrhages in gray matter and the border zone differ from hemorrhages in the striatum and the visual cicatrice by two circumstances. The first - unlike the latter, they arise mainly not on the soil of arterial hypertension, but due to arterial dysplasias( microangiopathies, microangiomas), coagulopathies and unspecified causes. Secondly, they flow more easily and in some cases are available for surgical treatment.
The clinical picture is caused by the localization of hematomas and their volume. Lobar hematomas extend to a restricted area of one of the hemisphere's lobes. Parenchymal-subarachnoid hemorrhage usually occurs with superficially located microaneurysms or angiomas.
Both of these forms manifest less pronounced forms of oppression of consciousness and less severe neurological deficit in comparison with hemorrhages in the region of the striatum and the visual hillock. However, with hemorrhages in the white and especially in gray matter, focal and generalized seizures occur much more frequently.
With hematomas in the temporal and parietal lobes, contralateral hemiparesis( hemiplegia) with low muscle tone predominates and oppression or increased tendon reflexes, pathological stop symptoms. When the dominant hemisphere is affected, aphasic disorders of various forms and degrees of severity are revealed. Hematomas in the occipital lobe are characterized by homonymous contralateral hemianopsia. The lesions of the pyramidal system are expressed, as a rule, mainly only by an increase in the tendon reflexes. Hematomas in the frontal lobe of the dominant hemisphere are manifested by motor aphasia and also not pronounced pyramidal symptoms. As consciousness is clarified, violations of mental functions are found.
Massive hemorrhages, accompanied by extensive edema, lead to the dislocation of the hemispheres and subsequent upper vklineniyu. With hemorrhages in the temporal lobe, it is asymmetric and primarily manifests itself by compression of the root of the oculomotor nerve on the side of the lesion.
Hemorrhages in the cerebellum develop, as a rule, in patients with severe arterial hypertension. The course and outcome depend on the size of the hematoma. Massive hematomas break into the subarachnoid space or the ventricular system. Quickly develop coma, severe respiratory depression and hemodynamics;a lethal outcome occurs within the next 24 hours. This type of flow is observed in 20% of hemorrhages in the cerebellum. In most cases, the disease is less catastrophic. First, there is a sharp headache, mainly in the occipital region, dizziness, repeated vomiting. Then, stiff neck and ataxia are identified. Often there is a forced pose of the head - tilt back or to the side. Later on, depression of consciousness quickly comes and a characteristic triad of symptoms is revealed: miosis, periodic breathing and evasion of the eye, opposite to the focus of the lesion. Increasing intracranial pressure in the subtenorial space and with such subacute flow leads to the development of a lower wedge with a lethal outcome. In some cases, cerebral hemorrhage has a chronic course. The initial stage is characterized by a lower severity of cerebral symptoms;Symptoms of cerebellar involvement are more clearly revealed.
Breakthrough of blood into the ventricular system occurs with extensive hematomas( more than 30 cm3 in volume) localized in deep brain structures near the midline. According to NV Lebedeva( 1978), hemispheric hematomas are complicated by a breakthrough in the ventricles of the brain in 48-85% of cases. The breakthrough of the blood of superficially located hematomas into the subarachnoid space occurs much less frequently, and the combination of a breakthrough of blood into the gastric system and the subarachnoid space - in isolated cases. The clinical picture in all such situations is characterized by extreme severity of the condition of the patients. In most cases, the forecast is unfavorable. Exact diagnosis is possible only by CT and MRI.
Massive hemorrhages, especially localized in the immediate vicinity of the liquor-conducting system, often early in the period from the moment of the disease are complicated by acute occlusive hydrocephalus. Hemorrhages in the visual hillock and basal nuclei block the liquor communications at the level of the third ventricle and lateral ventricle on the same side. A sharp violation of the circulation of the CSF promotes the dislocation of the hemispheric structures and the development of the upper wedge. Hemorrhages of subtenental localization lead to the compression of the Sylvian aqueduct or to filling with blood of the III and IV ventricles with a subsequent increase in their volume and the rapid formation of acute occlusive hydrocephalus leading to lower incidence.
Subarachnoid hemorrhage is a syndrome caused by the penetration of blood into the subarachnoid space. Features of the clinical picture are associated with the diversity of etiopathogenetic factors that cause the disease. In 43% of cases, subarachnoid hemorrhages develop up to the age of 50 years.
The most common causes of non-traumatic subarachnoid hemorrhage are ruptures of arterial or arteriovenous aneurysms( 70-80% and 5-10%, respectively).The frequency of infectious-toxic, paraneoblastic, fungal vascular lesions located in the subarachnoid space, arteritis of various etiologies, blood system diseases( hemorrhagic diathesis, thrombocytopenia, hemophilia, some forms of leukemia, coagulopathy), thrombosis of cerebral veins and sinuses is a total of 5-10%.In 10-12% of cases, the cause of the disease can not be established.
Pre-existing lesions of arteries located in the subarachnoid space include congenital anomalies of their development( microangiopathy, angiodysplasia, arterial and arteriovenous malformations).These pathological changes can occur latent or sometimes manifest as nonspecific symptoms of brain damage. Gradual progression of violations of the morphological structure of arteries located in the subarachnoid space is greatly facilitated by arterial hypertension( development of hyalinosis) and changes characteristic of atherosclerosis [Samoylov VI, 1990].
Factors directly provoking the development of subarachnoid hemorrhage include:
In some cases, the specific factor that triggered the occurrence of subarachnoid hemorrhage remains unclear.
Causal and temporal association of these factors with the development of subarachnoid hemorrhage is not always revealed. Initially, there may be an abrupt wall of the shell artery, resulting gradually to a complete disruption of the integrity of the vessel or the formation of aneurysms, subsequently torn, most often due to a sharp rise in blood pressure.
Data on the incidence of aneurysm ruptures are presented by angiography: anterior connective and general anterior arteries in 40-50% of cases, internal carotid and posterior connective artery - 15-20%, middle cerebral artery - 15-20%, main and posteriorthe cerebral artery - 3-5%, other localization - 4-9%.
The bulk of the discharged blood accumulates mainly in the subarachnoid space in the basal tank area.
Differences in etiopathogenesis determine the non-uniformity of development and course of subarachnoid hemorrhage. First of all, it concerns the rate of the onset of symptoms of the disease. For subarachnoid hemorrhages due to rupture of aneurysms and a breakthrough into the subarachnoid space of hemispheric hemorrhages, the sharpest onset is characteristic. In other cases - with infectious-toxic, fungal, paraneboletic lesions of the shell arteries, blood diseases, severe insolation - subarachnoid hemorrhages develop, as a rule, in the diapedesis type. Accordingly, the disease is less acute and less severe.
The amount of blood flowing into the subarachnoid space and its distribution in it is significant in the development and course of subarachnoid hemorrhages.
From the practical point of view the most informative should be considered the syndromological classification proposed by BM Nikiforov( 1972).He identified 4 clinical syndromes:
It is right to distinguish four main factors characterizing the damaging effect of subarachnoid hemorrhages on the brain, the meninges and the arterial system of the brain. These are:
Penetration of blood into the subarachnoid space - especially due to rupture of aneurysms - is a gross adverse effect on the hypothalamic-diencephalic structures of the brain. In most cases, it has a reflex character, but massive subarachnoid hemorrhages in the base of the brain can cause morphological changes in the diencephalic stem structures - perivascular hemorrhages or thromboses accompanied by perifocal edema. In any case, sharp irrigation of the hypothalamus and neighboring stem structures( including the limbic-reticular complex) entails depression of consciousness and disorganization of homeostasis. The latter is expressed by the release into the blood of excess concentrations of neurotransmitters and hormones, high concentrations of prostaglandins, decay products of erythrocytes, which alter the functional state of the cardiovascular system in a reflex and humoral way, and also promote the development of cerebral angiospasm. At the same time, the symptoms appear due to the disregulation of the functions of the diencephalo-stem structures, such as increased blood pressure, tachycardia, respiratory disorders, hyperglycemia, hyperthermia, etc.
The most important factor that exerts an extremely sharp damaging effect on the brain is arterial angiospasm, most often observed after aneurysmal subarachnoid hemorrhage. As a rule, it develops distal to the damaged area of arteries, but often extends to the entire vascular pool, and often to neighboring ones.
Angiospasm of different degrees of severity occurs at different stages of the disease, according to different authors, in 12-85% of patients with subarachnoid hemorrhage. The mild and short angiospasm characteristic of ruptures of small aneurysms may not manifest as a worsening of the general condition and focal symptomatology. Expressed and prolonged angiospasm leads to a sharp increase in vascular resistance and, accordingly, to ischemic zone distal to the affected area of the artery, and quite often wide enough vascular areas. Under these conditions, conditions are created for the formation of "delayed" cerebral infarcts, that is, formed after a certain period of time after the development of subarachnoid hemorrhage( more often - 4-12th day).
The timing of the onset of angiospasm may be different - 2-3 days, 7-10 days, 14-21th day from the moment of the disease. The most dangerous in this regard, the gap, are 5-13th day.
These data substantiate very important in practical terms provisions. The first is the greatest promise of early( within the first 72 hours) operations with the goal of eliminating the causes of aneurysmal hemorrhage, conducted before the emergence of persistent angiospasm. The second provision concerns immediate indications for the appointment of calcium channel blockers immediately after the development of the disease.
A significant role in the course of subarachnoid hemorrhage is caused by severe disorders of liquor circulation, which follow the developing subarachnoid hemorrhage. The blood that enters the cerebrospinal fluid extends through the subarachnoid space. When ruptures of aneurysms in the convectional region of the subarachnoid space, the blood forms flat accumulations at the site of the rupture, accumulates in the basal cisterns on the base and spreads through the cerebrospinal fluid system in the caudal direction up to the terminal cistern of the spinal cord. Massive hemorrhages from the aneurysms in the region of the Willis circle are often accompanied by the penetration of blood accumulated in the basal cisterns into the IV ventricle, and then through the cerebral water pipe to the 3rd ventricle and through the interventricular opening into the lateral ventricles. Blood also penetrates the subarachnoid space of the spinal cord.
The most catastrophic consequences of the accumulation of massive blood clots on the basis of the brain are tamponade IV of the ventricle or dissociation of cerebral and spinal liquor spaces with the subsequent development of acute occlusive hydrocephalus.
The use of TKUZDG and experimental reproduction of subarachnoid hemorrhage allowed to answer in a somewhat schematic form the question of how long bleeding lasts in the subarachnoid space and what contributes to its cessation. Summarized by J. Zentner, J. Schramm( 1992), published data indicate that the breakthrough of blood into the subarachnoid space very quickly causes an extremely sharp but short-term increase in intracranial pressure to the level of diastolic or even average blood pressure. The exact mechanism that realizes a rapid increase in intracranial pressure has not yet been clarified, but it is precisely this that leads to the cessation or slowing of the flow of blood into the subarachnoid space. As the increase in intracranial pressure lasts a minute, the further course of the arising pathological process can be twofold. The first option - during the time of a sharp increase in intracranial pressure due to concomitant angiospasm and rapid thrombus formation of the damaged area of the artery, the hemorrhage stops after a short time( minutes).The second option - during the time of a sharp increase in intracranial pressure, hemorrhage is not suspended, but a very different time in each specific case continues until a dense fibrin clot forms in the area of rupture or diapedesis.
The subsequent sharp increase in the intracranial volume due to the blood flowing into the cavity of the skull and, consequently, the rapid increase in intracranial pressure is not compensated for by a sufficient level of resorption of the cerebrospinal fluid mixed with the blood into the venous system. Following the increase in intracranial pressure sharply increases resorption resistance - 9-10 times with the most massive subarachnoid hemorrhages and 5-6 times with less severe forms of the disease. The increase in resistance to resorption is due to the blockade of erythrocytes, fibrin and other components of the blood of the zones of "absorption of cerebrospinal fluid" - granulations of the arachnoid, arachnoidal villi and other ways of outflow of liquor "into the venous system.
A sharp decrease in cerebid resorption associated with the accumulation of blood decay products in it sharply increases the prerequisites for angiospasm development distal to the artery rupture zone.
Disorganization of liquor circulation is also facilitated by the gradual formation of the fibroblastic process in the areas of accumulation of blood elements( histiocyte lymphocyte reaction).The formation of adhesions in the soft dura mater further complicates the movement of the cerebrospinal fluid. Large accumulations of blood in the area of the base of the skull can cause such a reactive change not only in the soft dura mater, but also in the ventricular system with the involvement of vascular plexuses.
The increase in fibrinolytic activity of CSF occurs as a reflex humoral reaction to the formation of a fibrin clot at the site of the artery rupture. This phenomenon can cause lysis of the resulting clot and lead to repeated subarachnoid hemorrhages in the area that has already arisen.
In later periods, spikes of the membranes with the underlying cerebral substance can be formed involving the vessels and cranial nerves, i.e. morphological changes similar to aseptic leptomeningeitis. In the area of soft-tissue adhesions with arteries located in them, repeated breaks often occur at the site of the former rupture, that is, relapses of subarachnoid hemorrhages. Their cause is primarily the lysis of insufficiently formed blood clots at the site of aneurysm rupture under conditions of sharp reflex activation of the fibrinolytic activity of the cerebrospinal fluid. Relapses of subarachnoid hemorrhages are promoted by sharp increases in blood pressure, especially when the adhesion process in the mild cerebral membrane is insufficient.
The concept of risk factors arose on the basis of a unique scientific experiment that was conducted for more than forty years in the small American city of Framingham. Scientists observed the health of tens of thousands of people. To date, this and other studies have established more than 280 risk factors, one way or another leading to a stroke( including atherosclerosis, hypertension).However, only some of them deserve serious consideration.
This, for example:
- age( over 40 years);
- male gender;
- smoking is one of the biggest shame of mankind( after drug addiction), because smoking is a disgusting man-made disease. A person voluntarily and even voluptuously undergoes chronic generalized poisoning. As a result, he gradually develops up to several dozen diseases, of which at least ten are extremely dangerous, including stroke of the brain. It is dangerous both active and passive smoking. The average life expectancy of a smoking person is less than that of a non-smoker, for 12 years. Currently, there is a fierce struggle between lawmakers of different countries to prevent, or at least limit, smoking. Especially active and successful in this respect are the United States and some European countries. Through the promotion of healthy lifestyles and the prestige of smoking in the United States, smoking has been reduced in the population from 65 to 15%.They were able to impose on the tobacco companies the largest in the history of mankind's fine - 500 billion dollars, which must be paid within 25 years to compensate for the damage caused to them by the health of American citizens.
Tobacco is dangerous because when smoking is released a large amount of nicotine, hydrogen sulfide, carbon monoxide and carbon dioxide and other harmful substances. The main malicious factor of tobacco is nicotine. Its high content promotes the production of norepinephrine in the body, the excess of which affects the brain. Smokers have a 15-20% increase in blood clotting time, platelet clotting is increasing, which leads to the formation of thrombi.
In people who smoke, the incidence of atherosclerosis increased 21 times that of non-smokers.
To combat smoking used a variety of methods, special conversations with smokers, hypnotics and acupuncture, drug therapy, etc.
The effect of all methods is relatively modest - a persistent smoking cessation within two years was observed by no more than 20% of the drinkers. Our own observations show that a stroke patient reduces smoking, feeling the horror associated with the situation. The saying of Professor Forgelson is known: "Half of the patients quit smoking after the first stroke, and the rest - after the second."Unfortunately, we have to add: if they survive.
Nevertheless, many of these patients who have twice or thrice risked their lives, do not stop smoking! Despite the fact that smokers lose one day of their lives in a week, 20% of vascular diseases develop due to tobacco abuse. Tobacco, according to experts, causes more damage to blood vessels than increased cholesterol in the blood.
To alleviate these symptoms, it should be remembered that the thirst for smoking lasts 2-4 minutes and eventually wanes. Take something by mouth - drink water or juice. Eat fruit or brush your teeth. Take care of your hands. Play with a coin or pencil, do house cleaning, clean up the workplace, wash the machine. Breathe deeply - this will help overcome the desire to smoke. Drink more fluids, get distracted by anything, stroll along the street or inside the building.
Recently it has become, as it were, "fashionable" to discuss its weight and ways of reducing it anywhere, just not in the doctor's office! In general, this is understandable. In the country, the "boom" of losing weight, the corresponding conversations and advertising of various means, nevertheless the effect is somehow not very noticeable. Now in the world a huge number of obese people - more than 1 billion. According to the World Health Organization, one-fifth of the world's population suffers from obesity. In developed countries, half the population has an overweight body. Even in China, the number of fat residents has increased to 15%.And what about us? In Russia, only women with an overweight of about 45%!
The main reason for increasing body weight is the discrepancy between energy received from food and its consumption. Simply put, a modern person eats a lot, usually a high-calorie food, but the level of physical activity is getting lower and lower.
Excessive body weight is a risk factor. In obese people, the circulatory system functions with an additional load. This helps increase cholesterol, triglycerides of uric acid, reduce the level of good cholesterol. In 1986, scientists made an outstanding discovery. They proved that on the surface of the liver cells there are special receptors that recognize and embrace "bad cholesterol".After they absorb "bad cholesterol", he undergoes splitting in the liver. The number of receptors on the liver cells is constantly changing. When the amount of cholesterol in the blood does not exceed normal values, their amount decreases. When a lot of cholesterol is injected into the body or when its synthesis from connected animal fats increases, newer and newer receptors immediately begin to form in healthy people, which destroy excess cholesterol. In obese patients, the ability to form receptors decreases - from moderate to severe. In such cases, the mechanism of encompassing the molecules of cholesterol in the blood constantly remains elevated and even high and very high. In such cases, the development of atherosclerosis, and then a stroke, is increasing. However, overweight is only part of the problem.
For health it is more important, in which part of the body are deposited eaten buns. I'll have to look at myself in the mirror. If the shape of your body looks like a pear, it's not so scary.
But if fat is mainly deposited on the stomach by the type of "apple", then you have a significantly increased risk of atherosclerosis, diabetes, hypertension, and therefore stroke. It goes without saying that the weight should be watched. For self-monitoring, it is important to determine not so much your own weight as the body mass index( weight / height, where the weight is measured in kilograms, the growth in meters).This indicator should be between 25 and 30. It is also useful to know the relationship between the circumference of the waist and hips. In men, it should not exceed 0.95, and in women it should be 0.8.According to the conclusion of the World Health Organization, men need to be concerned about health at the waist circumference more than 94 cm, - women - more than 80 cm and take more active actions with the circumference of the abdomen more than 102 cm( men) and more than 88 cm( women).
With pronounced obesity, the skin folds in the abdominal region, the backs look like dangling skin areas with subcutaneous tissue of great thickness. Expressed changes are observed on the part of all organs and blood vessels, damage to the brain vessels. Often they are combined with hypertension and hypercholesterolemia.
Therefore, in order to reduce weight, it is necessary to limit the calorie content of food and enhance physical activity. Caloric content of diets for obese patients should be approximately the same as in Table.
Daily set of products for a diet of obese patients
Variants of calorie-reduced diets for obese patients
Treatment of starvation in obese patients is impractical. Treatment with their medications that reduce appetite is dangerous. Psychotherapy is more effective. With a flexible, confident, optimistic, offensive tactic of a doctor-psychotherapist, the patient will believe the doctor, and this will give a good effect.
Physiotherapy exercises should be combined with all methods of weight loss. The therapeutic effect of physical exercises is based on a significant increase in energy costs, normalizing all types of metabolism, increasing blood lipid lowering and increasing the patient's ability to work.
The problem of maintaining a normal weight is closely related to overcoming hypodynamia in the entire population, especially in middle-aged people and in the elderly.
Stress is understood as a condition arising from the action of extreme or pathological stimuli on the body and the presentation of any requirements to it. It can have three stages of development: the stage of anxiety, in which the initial forces of the organism are mobilized;stage of increased resilience;stage of exhaustion, which is observed when exposed to a strong stimulus or with prolonged exposure to a weak stimulus, and also with functional weakness of the adaptive mechanisms of the organism.
A stress reaction can occur under the influence of trauma, the effects of various pathological stimuli, as well as emotional stress( emotional stress).The origin and nature of stress is determined by the susceptibility of the organism, which in turn depends on the hereditary properties of the organism, the earlier transferred effects, on age and other factors.
The occurrence of stress can be caused by emotional arousal, circulatory disorders, increased adrenaline, one of the most important trigger mechanisms of stress response. Stress affects all body systems: nervous, vascular, metabolism, inhibits the activity of the cerebral cortex.
Social factors can provoke hypertension and stroke. In our country, the number of stresses and depressions has increased. And this mostly affected people of a young age. The connection of vascular diseases with stress is well illustrated by the example of South Korea: in the representatives of the poorest population of this country, the most affected by the war, pathoanatomical dissections showed pronounced vascular lesions, although rice and cabbage are their main food products, and they rarely consume meat, milk and butter. Undoubtedly, for the development of manifestations of atherosclerosis, stroke, especially cerebral vascular lesions, stressful situations related to occupational conditions are important.
This is most pronounced in people of intellectual work, in urban dwellers in comparison with the rural population. In recent years, the picture has changed somewhat, as the townspeople began to pay more attention to their health, practicing physical education, observing proper nutrition, reading literature about the prevention of diseases. There were many drugs that prevent depression, removing anxiety( coaxil, stimuloton, afobazol and many others) that strengthen the nervous system. In addition, multivitamins and microelements are used.
The prevalence of hypodynamia in modern conditions is increasing due to the processes of urbanization, the widespread introduction of means of movement, automation and mechanization of labor into everyday human activity. The reduction in the share of manual non-mechanized labor is accompanied by a relative increase in the number of professions associated with the performance of operator functions, as well as with the use of intellectual labor in the life of modern society. Improving living conditions, increasing the role of modern means of communication( computer, telephone, television) objectively contribute to the spread of more passive forms of leisure, as the social and intellectual needs of the population are increasingly satisfied in a relatively less mobile way of life.
In this regard, the problem of hypodynamia grows into a social problem, the successful solution of which depends on the joint efforts of physicians, psychologists, sociologists, as well as representatives of public and sports organizations.
Hypodinamy leads to a decrease in energy metabolism and the need for food, the development of detrended vessels, including the brain, and promotes the development of atherosclerosis, stroke.
Therapeutic and preventive measures for hypodynamia are diverse.
The main value among them belongs to physical training. The nature of the training varies depending on the specific conditions for the onset of hypodynamia( hygienic gymnastics, industrial gymnastics, health and exercise therapy).
Some non-specific measures also have a positive preventive effect - hardening, ultraviolet irradiation, inhalation of gas mixtures, oxygen poor, breathing exercises, etc. In the diet should include fruits, vegetables, potassium salts, calcium, phosphates and vitamins, the loss of which increases with hypodynamia.
If smoking is more or less clear: it simply needs to be deleted from our lives, then it is unlikely to be done with alcohol. We have repeatedly observed in our country prohibitions on the use of alcohol. This option of state bans in Russia and appeals to observe moderation do not work.
In modern recommendations, it is safe to take a daily intake of up to 30 ml( 15 ml for women) of pure alcohol. A man can drink 70-75 ml of drinks with a fortress of 40 °, or 280 ml of wine with a strength of 12 °, or 700 ml of beer with a strength of 5 ° per day. Excessive intake of alcohol can lead to a stroke, a heart attack. .
If you take medication, then the consequences can not be positive.
In alcohol abusers, the likelihood of developing a stroke increases by a factor of 1.7 compared with few or none at all.
Heredity - inherent in all organisms property to ensure in a number of generations the continuity of the same signs and features of their development. It is determined by the material factors called genes. They contain all the hereditary information. The carrier of gene information is DNA.DNA is a complex molecular intracellular system that ensures the storage and sale of information. Material carriers of heredity contain information for the development of not only normal, but also pathological signs.
During development, the genotype constantly interacts with the environment. Under its influence, hereditary changes change. Consider, for example, hypercholesterolemia. This disease often manifests itself under the constant influence of adverse or harmful environmental factors( physical or mental fatigue, violation of diet, etc.).It can be attributed to a group of diseases with hereditary predisposition. This group includes hypertension, obesity, and many others.
Family hypercholesterolemia belongs to the most common hereditary disorders of lipid metabolism. The basis is the mutation of the gene. In some patients, the clinical signs of atherosclerosis appear at an early age, while in others, in the 4-5th decade of life.
When looking at the patient, attention is drawn to the tuberculate and tendinous xanthomas, which are localized in the region of the feet, eyelids, brushes, elbows and knee joints.
The diagnosis is made on the basis of the detected xanthoma, high blood cholesterol, a family history, a genetic anamnesis. Family hypercholesterolemia is referred to as primary. Secondary hypercholesterolemia arises as a result of a dietary error with excessive consumption of split fats, obesity, excessive alcohol consumption, diabetes mellitus, etc. The risk of developing vascular diseases in this group of people is very high. Therefore, lipid-lowering treatment is prescribed. The drugs of choice are statins.
First of all, the reasons that contribute to the occurrence of a stroke include the following:
1. Atherosclerosis of cerebral vessels. A person is born with clean elastic vessels. Over time, fatty substances( lipids) are deposited in the vascular wall in the form of strips of yellow color.
Gradually these strips under the influence of many factors, turn into plaques-atheromas. They are the main cause of the disease, called "atherosclerosis."Vessels lose their elasticity, become brittle, their lumen decreases.
The insidiousness of atherosclerosis lies in the fact that it develops gradually, asymptomatically, imperceptibly undermines the circulatory system and how a bolt from the blue can collapse on a person, having struck it with a stroke.
In the 20th century, due to new living conditions associated with rapid scientific and technological progress, modern civilization, the course of atherosclerosis took a malignant character, the pace of its progression increased dramatically, the disease began to develop at a younger age. It is established that at present 20% of men aged 30-34 years are diagnosed with atheromatous plaques of the IV-V class( ie the most complicated and dangerous for life).A hundred years ago, women practically did not suffer a stroke. Now this disease has become common and for them not only during menopause, but also before its onset. Previously, this disease was the lot of intellectuals, townspeople. Now vascular diseases are more and more affected by physical labor and rural residents. What is the reason for such a change in the composition of the victims of atherosclerosis?
To the degree of their education. It's no secret that more highly educated people read more, including literature on health issues. They are better informed about the increase in the number of vascular diseases in society, about their causes and methods of prevention.
Therefore, such people show great concern for their health. People of physical labor are usually far from such issues, in their understanding of health - it is something self-fulfilling, eternal, does not need care. The causes of malignant course of atherosclerosis and related diseases are the conditions of modern life and hereditary-family predisposition.
High blood cholesterol is the main cause of atherosclerosis. In the norm of cholesterol in the blood is 5.2 mmol / l;
insignificant hypercholesterolemia - 6,5-6,7 mmol / l;moderate - 6,7-7,8 mmol / l;Heavy -> 7.8 mmol / l. In the development of atherosclerosis of cerebral vessels and other organs, various cholesterol and other substances of fat character, synthesized in the body itself, participate.
In addition, the high content of cholesterol in the blood is promoted by the rich in them and so-called fatty acids food. Fatty acids are found in large quantities in dairy products, in fat of any animals. The only exception is fish oil, rich in saturated fatty acids with anti-atherosclerotic properties.
All vegetable oils also act as an antiatherosclerotic.
Cholesterol( lipid) or fat performs important biochemical functions in the human body. He is free and bound. Free is necessary for the formation of hormones and bile acids, it is a part of the nervous tissue and all the cellular membranes of the human body;bound cholesterol( cholesterol compounds with bile acids) predominates in the cells of the adrenal cortex, in plasma, in atherosclerotic plaques. Triglycerides( esters of bile acids and alcohol) are a part of lipoproteins. Fatty acids are synthesized in the body from the products of the decomposition of carbohydrates and come with food. Fatty acids are involved in lipid metabolism.
Lipoproteins are lipid-protein formations, consisting of proteins of cholesterol, triglycerides, etc. High and low density lipoproteins are of the greatest importance in vascular pathology.
Low-density lipoproteins consist mainly of cholesterol and protein esters. Normally, the blood of low-density cholesterol should be less than 2.2 mmol / l. Anything higher than this value is a pathology and is subject to correction with diet and special medicines. The higher the index, the more intensive the treatment should be.
Low-density lipoproteins are used to settle on the inner wall of the artery and form plaques - fat-protein complexes. These are the so-called "bad" cholesterol.
Counterweight to "bad" cholesterol is conventionally the so-called "good" cholesterol.
High density lipoproteins.
These are anti-atherogenic lipoproteins that reverse cholesterol transport from the vascular wall to the liver, from which it is excreted as bile acids. Normally, high-density cholesterol is 0.9-1.9 mmol / l. Good cholesterol is produced in the body under the influence of systematic moderate moderately intense physical training. Very intensive training and / or exercise, on the contrary, suppress the synthesis of this useful cholesterol in the body. Clinical laboratories already determine the level of cholesterol in the blood, therefore, patients should correctly understand the results of their history. The culture of health and normal cholesterol prevails in the USA.Americans avoid buying and eating foods that contain cholesterol and animal fats, from which it can be produced in the body. Even on bottles of mineral water and other beverages they have written "does not contain cholesterol."
Should we be surprised at this state of things that we have the highest mortality in the world of atherosclerosis and its complications? Of course, it is absolutely necessary for us to come as soon as possible to this meticulous follow-up of medical recommendations, so that our unfortunate and carefree society will be freed from the incredible spread of atherosclerosis, leading to such a serious complication as a stroke.
The following target levels of total cholesterol have been established:
The following ingredient in blood lipids( fats) is triglycerides( norm 0.5-2.1 mm / L).Even at normal levels of all kinds of cholesterol, but high levels of triglycerides of blood, it is possible to develop atherosclerosis, and hence, stroke and other vascular diseases. Their content in the blood increases with alcohol abuse, with diabetes, obesity, addiction to fatty foods, etc.
Still, the significance of hypertriglyceridemia( high triglyceride levels in the blood) in the development of atherosclerosis and its complications is lower than the significance of a high level of "bad" cholesterol or a low level of "good" cholesterol.
Doctors also use the term combined hyperlipidemia when the patient has a high level of two "bad fats" - low-density cholesterol and triglycerides.
When high( high) cholesterol and( or) triglyceride levels are combined with insufficient concentration of "good" cholesterol( HDV) in the blood, they speak of dyslipidemia( multidirectional but harmful changes in lipid levels of blood fats).The predictions for combined hyperlipidemia are serious, the treatment of patients is difficult, but if it is possible to achieve normalization of the pathological levels of different blood lipids, the success expressed in real prevention of the predicted complications overcomes these difficulties.
Treatment for atherosclerosis is a very difficult task, the solution of which can only be done by a qualified specialist provided that the patient fully understands and closely follows the patient's medical recommendations over a long period of time. Along with the diet must be taken statins( pravastatin, lovastatin, simvastatin, atorvastatin, fluvastatin, etc.).The main effect of statins is that they prevent the formation of "bad" cholesterol in the liver.
Arterial hypertension is especially dangerous in that it greatly increases the risk of cerebral circulation( stroke).
In the causes of hypertension and atherosclerosis, there are many common mechanisms of development, including endothelial dysfunction. Endothelium of arteries is the most superficial layer of their internal wall. It consists of a thin film - all in one cage. In the presence of risk factors, endothelium isolates the biological substances acting negatively on the arteries. This is accompanied by an increase in blood pressure.
The combination of these two diseases increases the risk of stroke fivefold. Hypertension has a different origin. But irrespective of its nature, at all people with high arterial blood pressure the development of atherosclerosis accelerates, its severity increases. The higher the blood pressure and the longer it lasts, the stronger atherosclerosis and the more frequent complications develop.
There are a variety of medications that make it possible to select individualized treatment for each patient. But, as observations of various clinicians show, there are big problems in the treatment of patients with hypertension, depending on the patients themselves.
The first half of patients suffering from hypertension simply do not know about their illness, and therefore, of course, are not treated. The second half of the patients are those who know about their illness, but are not treated at all. Further more interesting.
Of patients with hypertension and taking drugs, only half are effectively treated. The fact is that most patients simply do not pay attention to their hypertension, although they know about its existence, and those who have been prescribed treatment are literally "wise" with drugs at their discretion - refuse treatment, start and soon stoptreatment or significantly reduce the dose of drugs;many in the order of "experiments" arrange breaks in treatment, "to see - what will happen."The reasons for such an irresponsible and insecure freelancer lie in our low discipline, misconceptions about our own illnesses, distrust towards doctors, treatment, in an incredibly naive empty hope of a miracle. And in fact, is it not so? Let's consider the arguments of our patients to justify their wrong actions( according to the frequency of their occurrence in the stories of the patients):
It should be noted in the strongest terms that all the above arguments( and many not mentioned here for the sake of brevity) are absolutely untenable, and the actions of patients on their owncessation and change of treatment can be dangerous( for example, sudden withdrawal of beta-blockers leads to an unexpectedly high rise in blood pressure and a strong increase in the work of the heart due to so-calledemogo "cancel phenomenon").Apparently, there are numerous objective and subjective reasons for the incorrect behavior of patients with respect to treatment. The main of them is the low culture of attitudes toward one's health, the lack of convincing and adequately perceived by the interested person( i.e., the patient, his relatives) information about goals, objectives, basic mechanisms of action and the final results of treatment. The latter largely depends on the understanding between the doctor and the patient. The axiomatic authority of medical recommendations in the eyes of the patient in the old days was: "Even poison is taken from the doctor's hands."Modern doctors lost credibility, but if it was absolute, the patient's patient explanation of all the sides of the action of the prescribed treatment( including the procedure for stopping or changing the dose) is an elementary task of the doctor. If this does not happen, then there is a clear lack of work in the doctor.
There is another axiom concerning the patient: "You doubt - always consult your doctor".This means that in doubtful cases it is recommended to overcome your limitations and directly ask the doctor to clarify all of the above issues. Of course, such trusting relationships are possible with a well-established health care system, where the patient and the doctor act as partners in the common cause. Unfortunately, the existing healthcare system in the country is far from this model. Therefore, a patient with hypertension should know the following rules and act in accordance with them.
Hypertension, even without atherosclerosis, is an independent and quite common disease:
Correct and long-term( several years) treatment of the initial stage of hypertension in 30% of patients can lead to complete cure of the disease;
In studies of recent decades, a close relationship between cardiac( cardiac) and cerebrovascular( cerebral) pathology has been demonstrated: coronary heart disease, myocardial infarction, postinfarction cardiosclerosis, unstable and stable angina and cardiac rhythm disturbance, cardiac remodeling. Underestimation of cardiac pathology in a patient with stroke can cause a recurrent stroke. Atrial fibrillation is the main cause of thromboembolic strokes. The risk of recurrent stroke in patients with atrial fibrillation is high and is about 12% per year.
Therefore, all this category of patients should be under special control of therapists and neurologists. Current evidence suggests that all patients with atrial fibrillation, regardless of whether their sinus rhythm is restored or they continue to receive medications that reduce the heart rate, need to receive indirect anticoagulants, taking into account the same risk of developing recurrent thromboembolic complications.
Upon admission to the treatment department, patients are examined. Their goal is to assess the general condition of the patient and determine whether there is a violation of cerebral circulation, what is his nature( hemorrhagic or ischemic).This is done by a laboratory method: the analysis of blood and cerebrospinal fluid;instrumental methods of investigation - computed tomography( CT), magnetic resonance imaging( MRI) and ultrasound doppler.
Computed tomography. This method catches X-rays with special sensors that have high sensitivity and the ability to capture the slightest nuances of X-ray absorption by various structures of the human body. Further information is computer processed and displayed as an image on the screen.
In 1979, the inventors of this method Allan Cormac and Godfried Hounsfield were awarded the Nobel Prize in Physiology or Medicine.
Magnetic resonance imaging( MRI) was also awarded the Nobel Prize in Medicine. This discovery was a breakthrough in medicine, diagnosis and treatment. At present, 60 million diagnostic tests are performed every year in the world using the MRI method. The method is based on the ability of the nuclei of hydrogen atoms, which is in all organs and tissues of the body, to generate an electromagnetic response after exposure to them by a magnetic field and radio waves. This response in the form of energy radiation is perceived by special sensors and converted into digital values with subsequent output of the image to the screen of tomographs. Each method is good in its own way, has its positive and negative sides.
Ultrasound dopplerography( ultrasound) is the visualization of ultrasound waves reflected by various internal structures of the body and absorbed by them. Such a study is completely harmless.
Dopplerography is a kind of ultrasound that allows you to see the lumen of the vessel, assess the degree of its narrowing and the state of the blood flow. The essence of the effect lies in the fact that when a body is struck against a moving body, the wave( sound or light) changes its characteristics. These changes are captured by the sensors and displayed on the screen.
Instrumental methods include:
A specific feature of strokes is the rapid deterioration of patients, the early occurrence of violations of vital functions and severe extracerebral complications. This determines the need for the earliest possible diagnosis, emergency care and continuity of diagnostic and treatment activities at the prehospital stage and in hospitals.
The solution of these problems is ensured by the functioning of the system of stage care for patients with stroke.
The overwhelming majority of stroke cases on the prehospital stage are non-specialized care - by the doctors of the emergency ambulance brigades. For emergency recognition of the main forms of acutely developing brain lesions, including stroke, a diagnostic algorithm is used that helps to recognize the nature of the disease in the most complex clinical situations( Table 13).In cases where there is no anamnestic information, the patient is unconscious at the site of first aid, using the simplest diagnostic techniques allows doctors of the emergency and emergency emergency brigades to recognize the cause of acute brain damage in 72-79% of cases. Strokes( without specifying the type) are correctly diagnosed in 87-91% of cases. Thus, profile hospitalization is provided in accordance with the nature of acute brain lesions.
Algorithm for diagnosing emergency conditions in patients with depressed consciousness( sopor, coma) depending on the results of neurological examination and body temperature
All the diseased in the street and in public places( institutions, shops, street transport, baths) are urgently transported by line brigadesemergency or emergency care in the nearest hospitals.
Doctors of the line brigades of ambulance and emergency help who are at home at home, and in some cases district therapists or neurologists of polyclinics provide non-specialized assistance before transportation to the hospital. From the doctors of the above categories there is no need to specify the type of stroke( ischemic - hemorrhagic).Sufficient is the statement of "acute disturbance of cerebral circulation".Therefore, they only carry out emergency therapy. The directions and amount of emergency medical interventions depend in each case on the degree of severity of the condition of the patients and the severity of specific syndromes. It should be emphasized that all the recommended therapeutic methods are provided in the Standards of emergency medical care at the prehospital stage.
The appointment of activities relating to non-specialized care and pre-staging of patients should be considered justified, since they are usually carried out in the very first hours after the onset of the stroke, that is, within the "therapeutic window" of six hours. Thus, prerequisites are created for more effective therapy in hospitals.
The best option is to carry out emergency therapy followed by hospitalization.
However, if the doctor who provides first aid does not have enough specialist emergency care or there are no necessary conditions at the place of care( for example, the unsanitary condition of the room where the patient is located excluding the possibility of intravenous infusion), emergency hospitalization is indicated.
Contraindications to transportation from home are atonic coma( 5-4 points on the scale of Glasgow);Uncontrollable at the site of first aid acute abnormalities of breathing, pulmonary edema, epileptic status and severe arterial hypotension.
Specialized care at the prehospital stage is provided by neurological( neuroreanimation) ambulance teams operating in large cities. Diagnostic tasks, solved by doctors of neurological teams, are characterized in tab.
Diagnostic problems solved by physicians of neurological teams with the help of instrumental laboratory methods
.the data allow to differentiate the stroke from other acute brain injuries on the basis of a minimum of laboratory and instrumental data with an accuracy of 87-92% and to determine the profile of emergency hospitalization.
The volume of emergency care provided by neurological ambulance teams is described in section 13.2.
Profile hospitalization. To doctors who provide first aid for a stroke, it is very important to make the right choice of the hospitalization profile for patients with acute cerebrovascular disorders.
The profile of hospitalization is determined by the severity of the condition of the patients. Indications for the profile hospitalization of stroke patients are summarized in Table.
Indications for the profile hospitalization of patients with stroke
It should be taken into account that the results of the pre-hospital examination, because of the absence of anamnestic information and / or extreme severity of the patients' condition, in some cases do not differentiate the stroke from other urgent conditions due to brain damage -severe closed craniocerebral trauma, encephalitis, meningoencephalitis, severe endogenous or exogenous intoxications.
In such situations, patients are hospitalized in multidisciplinary hospitals, which have the capacity to clarify the diagnosis.
When patients are admitted to the hospital, stage-by-stage diagnostics are carried out, providing:
The phased diagnostic principle determines the therapeutic tactics, in particular the use of emergency neurosurgical interventions where necessary.
1st stage. Anamnestic data and symptomatology, diagnosed as a result of somatoneurological examination, confirming the diagnosis of a stroke and its type( ischemic or hemorrhagic).
2nd stage. Clarification of the nature of the stroke is based on a comprehensive analysis of anamnestic data, information on the pace of stroke, the nature and severity of neurological symptoms, as well as on the results of modern diagnostic instrumental methods.
Anamnestic data and somatoneurological symptoms that clarify the nature of the stroke
Legend: "+" - rare, moderately pronounced symptom;"++" is a pronounced symptom.
An algorithm recommended by the American Association of Neurologists can help to clearly plan diagnostic and therapeutic activities.
Clinical symptoms, the results of echoencephaloscopy and at various periods of CSF research in ischemic and hemorrhagic stroke since the onset of
A specific feature of strokes is the rapid variability of clinical symptoms. Since the first aid is sick at various times from the moment of the disease, the nature and severity of the symptoms are largely different. In order to clarify the type of stroke in the early periods( the first 6 hours) and later( the second day) in Table.generalized clinical symptoms and results of the study of cerebrospinal fluid in the specified time periods.
Currently, a number of technical non-invasive methods of neuroimaging are used to determine the morphological changes in the main arteries of the head and intracranial arteries, changes in cerebral hemodynamics, changes in brain substance and cerebrospinal fluid, and the state of energy metabolism in any region of the brain.
In accordance with physical and technical principles, X-ray methods( craniography, cerebral angiography, computed tomography), radiological methods( radioisotope methods, including single-photon emission computed tomography, positron emission tomography), magnetic resonance imaging( magnetic resonance imagingand magnetic resonance angiography), ultrasonic methods( ultrasound dopplerography for the examination of the condition of the main arteries of the head, ultrasonic echoesgraphy, transcranial Doppler ultrasound, duplex scanning, transcranial sonography with color Doppler scan in real time).The detailed characteristics of these methods obtained as a result of their application in specific clinical situations and in various forms of involvement of the vascular system and brain structures are described in detail by NV Vereshchagin, VV Borisenko, AG Vlasenko( 1993), and A. VBy Holin( 1994).
Craniography, computed tomography( CT), magnetic resonance imaging( MRI), magnetic resonance angiography, transcranial dopplerography( cerebral Dopplerography), angiography are used to diagnose and differential diagnosis of strokes from these methods in everyday practice. In addition, echoencephaloscopy and EEG are used.
The defining task is possibly an earlier differentiation of ischemic from hemorrhagic stroke. It is these data that determine the purpose of differentiated therapy.
Craniography is necessary to exclude damage to the skull bones due to injuries resulting from a fall due to rapid loss of consciousness in the acute development of a stroke. In addition craniography is shown to exclude damage to the bones of the skull due to "light" craniocerebral trauma, accompanied by a "light gap" before the appearance of neurological symptoms. Such clinical situations often resemble the development of ischemic stroke. It should be emphasized that neither CT nor MRI makes it possible to reveal with full certainty the damage to the skull bones.
Computed tomography has principal advantages over the results of somatoneurological examination. According to VA Karlov, based on a very large array of clinical and anatomical observations, the number of erroneous clinical diagnoses in the acute stage of hemorrhagic stroke differed from the erroneous diagnoses by CT results by 8.5 times - 17% and 2%, respectively. With ischemic stroke, similar indicators differed by 2 times - respectively 15% and 8%.Differences in the nature of the disease( extensive posttraumatic edema, brain tumor) in cases when the hemorrhagic stroke was clinically diagnosed differed, in comparison with the CT results, by 3%, 12% and 4%, respectively. Similar differences in cases when ischemic stroke was clinically diagnosed, and CT results recorded a different type of disease were 1.7 times different, 10% and 6%, respectively.
According to J. Toole( 1995), CT allows to differentiate ischemic stroke from hemorrhagic in 95%, and MRI - in 91-92% of cases. All intracerebral hematomas with a volume greater than 1 cm3 and almost 95% of subarachnoid hemorrhages by CT and MRI can be diagnosed in 95% of cases.
The timing of identifying areas of hemorrhagic or ischemic brain damage is paramount. However, despite a large number of studies, there is no single point of view on this issue. It is suggested that ischemic foci can be detected in the first 6 hours after the onset of neurologic symptoms, and sometimes even only 1-2 days or 2-3 days.
Some clarity in this discussion question was made by studies in which the dependence of the timing of detection of pathological foci on their volume is specially analyzed. By CT of hemorrhage more than 2-3 mm in diameter are detected in the first hours from the moment of their appearance, and foci of a smaller volume - by the end of 1 day or on the 2nd day. As the period increases from the moment of hemorrhagia to their periphery, zones of reduced density are revealed, caused by necrosis of the brain areas adjacent to the hematoma, as well as by perifocal edema.
When using MRI, hemorrhagic foci are detected, usually before the ischemic ones, because the blood spilled into brain tissue and the rapidly accumulating products of erythrocyte decay in the perifocal zone are detected in the T-1 mode as zones of increased density. Such changes are formed much faster than the zones of reduced density, characteristic of ischemic brain lesions.
Areas of reduced density in CT without contrasting in large, rapidly-infarcting infarcts, especially with the development of the "mass effect" due to compression, displacement of the ventricular system or the rapid development of severe occlusive hydrocephalus are detectable - depending on the volume of infarction - for 1-3 days.
Perhaps the earliest detection of hemorrhagic and ischemic foci is facilitated by the use of magnetic resonance angiography. To contrast the arterial system of the brain, the drug magnevit, administered intravenously before the beginning of neuroendgenological research, is used.
The most important advantages of CT and MRI are the ability to exclude hemorrhage in the early stages of the disease, as well as diagnose hemorrhagic infarction - depending on its volume - in the period from 8 to 48 hours.
The advantage of MPT over CT is the ability to recognize ischemic foci in the structures of the brain stem, which can not be done by CT because of bone artefacts. MRI accurately identifies changes in the white matter of the hemispheres, unlike CT, which better records changes in the gray matter.
With subarachnoid hemorrhage, CT and MRI allow detecting the spread of blood in the subarachnoid space, but do not provide an opportunity to determine the exact localization of the source and etiology of subarachnoid hemorrhage. CT scan more often and earlier reveals subarachnoid hemorrhages than MRI.Concerning the importance of CT and MRI in terms of early diagnosis, there are different points of view. According to K. Siegel( 1988), by CT, subarachnoid hemorrhages are diagnosed during the first day in 95% of patients, and on the third day - in 74%;In the following days, the possibility of detecting a hemorrhage sharply decreases. The possibility of early detection of subarachnoid hemorrhages in 85-90% of cases is confirmed by WHO experts( Report. .., 1989).At the same time, according to other neuroradiologists and neurologists, both methods are effective for diagnosing subarachnoid hemorrhages in 75-80% of cases only in a relatively late time - starting from 2-3 days since the moment of the disease. CT and MRI are also informative in the formation of sufficiently massive clusters of blood in the region of the base of the brain or in large furrows and ridges of the convective surface. Subarachnoid hemorrhages of small volume( less than 2 mm in diameter) are difficult to diagnose.
Subarachnoid-parenchymal hemorrhages, as well as hemorrhages due to rupture of arteriovenous aneurysms, are detected much earlier. In addition, in these cases, it is sometimes possible to determine the localization of the source of hemorrhage.
At a later date, after subarachnoid hemorrhage, CT and MPT studies can determine ischemic foci due to acute angiospasm. In subarachnoid hemorrhages of paraneoblastic origin, intracranial tumors can be detected.
The results of CT and MRI should be evaluated in conjunction with clinical data. In cases where the latter with sufficient convincing evidence of subarachnoid hemorrhage, and the results of CT and MRI are negative, it is necessary to study the cerebrospinal fluid.
Transcranial dopplerography( cerebral Doppler) in the first hours after the disease does not allow to differentiate adequately ischemic stroke from hemorrhagic in cases when the latter is not accompanied by penetration of blood into the subarachnoid space. Intraventricular and intraluminal hemorrhages of specific patterns can not be detected, although in these cases the edema of the brain tissue develops faster than when the infarct is formed and is more pronounced.
This method is most reliable and informative for subarachnoid hemorrhages, which are accompanied by the outflow of blood near( around) large segments of the pial arteries of the brain( middle and anterior), in the region of the vessels of the base of the brain and in the basal cistern. In these cases, a syndrome of cerebral vasospasm develops, the pathogenesis of which is associated either with the vascular system or with compression of the arteries.
Diagnosis of cerebral vasospasm is based on the values of the linear velocity of blood flow and the Purcell index. Values are usually evaluated in the middle cerebral artery, as it is more similar in its anatomical location to the axis of the ultrasound beam and only true high flow rates can be recorded in it.
There is a close correlation between the degree of angiospasm and the absolute values of the linear velocity of blood flow. It is accepted to distinguish three degrees of the manifestation of cerebral angiospasm: mild degree( up to 120 cm / s);medium degree( up to 200 cm / s);Heavy degree( over 200 cm / s).
However, when measuring high speeds in order to avoid gross errors it is necessary to take into account the specifics of the work, the equipment used.
As the degree of spasm increases, the ratio of blood flow rates in the middle cerebral artery and internal carotid artery varies. Ratio - linear velocity of blood flow in the middle cerebral artery / linear velocity of blood flow in the internal carotid artery is normally 1.2-2.5.By the value of this index, one can judge about the severity of angiospasm in MCA: mild degree( 2,6-3,0);medium degree( 3,1 -6,0);a severe degree( 6.1 -6.9).
Vasospasm in the main artery can also be accompanied by acceleration of blood flow to 100-130 cm / s. However, the correspondence between angiographically confirmed narrowing of the lumen and an increase in the linear velocity of the blood flow is less than in the location of the middle cerebral artery. According to different authors, high values of the flow rate along the main artery are found in 30-50% of observations.
More stable is the increase in resistance index Purselo - 0,6-0,99.
These data are extremely important for detecting angiospasm and monitoring its dynamics, which in turn is necessary for the adequate implementation of therapy aimed at arresting angiospasm.
Transcranial dopplerography has features in the acute period of ischemic stroke( stroke "in motion"), during the reperfusion syndrome and with the formed postischemic focus. The acute disturbance of the blood flow of the ischemic character in the terminal arteries of the brain develops due to the sudden drop in perfusion pressure in the larger arterial trunk from which they form.
The reasons for this may be:
All these reasons have diagnostic Doppler criteria - in the form of patterns of stenosis or thrombosis, a decrease in the blood flow velocity in the large arteries of the affected basin to the "residual flow" or the absence of flow in them. With the consistency of anastomoses in adjacent arteries, compensatory hyperperfusion or hypoperfusion associated with the phenomenon of "stealing" can be observed. On some arteries( anterior cerebral artery, main artery, suprablock artery) in some cases it is possible to detect reverse( retrograde) blood flow. The combination of cerebral ischemia with edema of tissues makes it difficult to locate arteries;especially it is difficult in cerebral vasospasm.
The most important prognostic indicator is the range of cerebrovascular reactivity. In the acute period, it is close to zero, in some cases, the reactivity to the samples can be inverted( perverse).
Typically, 6-24 hours after the onset of the stroke, a period of reperfusion occurs in the affected vascular pool due to the inclusion of compensation mechanisms, partial or complete recanalization of thrombi( if this is possible), which is also accompanied by severe hemodynamic disorders, in particular, post-ischemic hyperperfusion syndrome("Luxurious perfusion"), which in half of the cases is accompanied by a significant( 1.5-2 times) increase in systolic blood flow with sharply reduced systole-diastoleeskim ratio, reduced peripheral resistance and lack of responses to functional assays. Hyperperfusion can be observed for several days, gradually decreasing with a favorable course of stroke.
At the end of reperfusion, a new blood flow is formed in the affected basin, often reorganized in direction, with a reduced linear velocity of blood flow corresponding to the volume of the blood supply area( this is associated with the asymmetry of the flows along the same arterial trunks in the postinsult period).In the future there is a gradual restoration of reactivity of cerebral vessels with a new range, altered parameters of peripheral resistance and tone.
Carrying out of transcranial Doppler ultrasound before the appointment of therapy allows to avoid erroneous use of vasodilators, to determine the time necessary for the infusion therapy to be performed, and to assess its adequacy.
From the diagnostic positions it is important that with thrombosis, stenosis, pronounced perifocal edema, an increase in intracranial hypertension, characteristic changes in the Doppler spectrum appear. The results of transcranial dopplerography make it possible to judge the inclusion of collateral blood flow, the emergence of the phenomenon of "stealing", "impoverished perfusion", hyperperfusion syndrome, brain death.
In recent years, there have been reports on the use of the most modern, modified techniques - color Doppler echo- tomography and duplex scanning. According to P. Salpierto et al.(1996), by color Doppler echo tomography it is possible to determine stenosis or occlusion of the main artery, as well as the process of its recanalization. A. Kenton et al.(1996) cited data indicating the possibility of using these modifications of Doppler ultrasound for early differential diagnosis of hemorrhagic and ischemic stroke. At the same time, T. Takada et al.(1996) indicate that the appearance of embolic signals during the above modifications of Doppler ultrasound does not allow differentiating arterio-arterial embolisms from cardiogenic ones.
The combined use of transcranial dopplerography and positron emission tomography was discussed in 1997 by J. Mayer et al. According to their observations, transcranial Dopplerography records only the presence and prevalence of angiospasm due to subarachnoid hemorrhage, and proton-emission tomography makes it possible to establish the degree of disorganization of the metabolism in the area of the brain affected by angiospasm.
Angiography is the most important method for diagnosing subarachnoid hemorrhage. It makes it possible to identify or exclude the presence of arterial and arteriovenous aneurysms, to establish their shape and localization, as well as to detect angiospasm, its prevalence and to evaluate features of cerebral blood flow. In addition, angiography makes it possible to diagnose simultaneous brain damage - subarachnoid-long-parenchymal hemorrhage. With arteriovenous aneurysms, the sources of their blood supply are revealed, which is important for choosing surgical tactics.
Various technical modifications of angiography are used - total angiography by Selinger, revealing the condition of all vascular pools;selective angiography, contrasting individual vascular pools;superselective angiography, contrasting arteries of small caliber;angiography in oblique, axial and semi-axial projections, specifying the localization of aneurysms and the sources of its blood supply;tomoangiography, characterizing the spatial relationships of aneurysms and surrounding vessels and brain structures;CT and MRI with the introduction of contrast agents;digital( or numerical) substraction angiography - computer processing of data on the state of the arterial bed after the introduction of a contrast agent in the left ventricle of the heart( by catheterization) or in the arterial system;substraction angiography, in which the best visibility of the vessels is achieved by "washing off" the image of the skull bone structures.
In connection with the improvement of technique and angiographic research, the frequency of aneurysm detection was 95% by the beginning of the 1990s. Negative results of angiography can be caused by a small diameter of aneurysms( less than 2 mm), concomitant angiospasm, rapid thrombosis of small aneurysms, inaccuracies in the technical performance of the study.
The results of angiography are the determining guide for resolving the issue of the surgical treatment of subarachnoid hemorrhages due to rupture of arterial aneurysms and arteriovenous malformations, as well as for the choice of surgical intervention methods. They identify urgent and relative indications for angiography.
Immediate indications are clinical situations in which surgical operations are most promising in order to eliminate the source of hemorrhage. Emergency angiography is indicated for patients whose severity corresponds to the first degree according to the classification of BA Samotokin and VA Khilko or I to III degrees according to the classification of Hunt and Hess( Table).
Classification of the degree of severity of the condition of patients that determine the therapeutic tactics of
Relative indications are heavier forms of subarachnoid hemorrhage - severity of patients, corresponding to grade II according to the classification of BA Samotoki and VA Khilko or III degree according to Hunt's classification andHess. Angiography with a more severe severity of the state is unjustified, since operations in such cases, as a rule, are very little promising or unsuccessful. The question of angiography can be treated as the condition improves.
Contraindications to angiography, according to the published data, are expressed clinical manifestations of atherosclerosis and arterial hypertension, however, these pathological processes, as shown above, are taken into account by both classifications of the severity of the patients' condition.
Serious contraindication is the individual intolerance of contrast agents, which can lead to severe allergic reactions, and sometimes to severe abnormalities of vital functions. In this regard, in all cases, before the angiography, a sample should be tested for sensitivity to contrast agents.
Complications of angiography have been observed in recent years in connection with the improvement of the technique of research and the accumulation of experience in 0.2-1.5% of cases. They are manifested by the appearance of focal symptoms of varying severity and duration, primarily because of the angiospasm that has arisen or increased as a result of the introduction of a contrast agent. There may be epileptic seizures. Extremely rare myocardial infarction, sudden cardiac arrest and respiratory depression.
In recent years, with sufficient conviction, it has been confirmed that the determining factor for the success or failure of surgical interventions is the condition of patients at the time of surgery. In this respect, the reports of K. Siegel( 1992) and J. Zentner, J. Schramm( 1992), which testify to the correlation of the degree of severity of the condition of patients and various terms from the moment of the disease, are very convincing. During the first 24 hours after the disease, the condition of patients corresponded to 1-11 degrees of severity according to Hunt and Hess classification in 52-41% of cases. The following day the number of this category of patients was significantly reduced;people with a heavier course of subarachnoid hemorrhages were highly prevalent.
Thus, it is proved that as early as possible surgical interventions to eliminate aneurysmal subarachnoid hemorrhage is most promising. Carrying out early angiography and the operation following aneurysmal hemorrhage immediately avoids the onset of severe angiospasm starting from 4-5 days and the possible recurrence of enveloped hemorrhages at a later date.
Recently, contrast magnetic resonance imaging has been used to diagnose subarachnoid hemorrhages. After intravenous administration of contrast agent( magenvit), the arterial system of the brain clearly contrasts and pathological changes in it are revealed.
For hemorrhage in the brain, angiography is indicated primarily in cases where hematomas that are available for surgical removal are diagnosed by preliminary CT or MRI examination. The question of the possibility and prospects of surgical interventions is most expedient to be solved taking into account the severity of the patients' condition, that is, being guided by the data summarized in Table. A specific type of surgery is determined by neurosurgeons.
In ischemic stroke, angiography is practically not used at present. In rare cases, when large hemispheric infarctions are surgically removed, the main diagnostic guidelines are CT and MRI.
In the earliest time since the development of ischemic stroke, the results of the study are negative. After 6-12 hours as the infarct is formed, additional signals can be detected. With the rapid formation of massive infarcts, distinct echoencephaloscopic signs of displacement of the median structures appear only on day 2-3 after the disease, and they are caused by the already formed perifocal edema.
With extensive supratentorial hematomas in the next few hours, in the overwhelming majority of cases, signs are revealed that indicate the displacement of the median structures in the direction opposite to the affected hemisphere. This phenomenon is directly due to the increase in the mass of the corresponding hemisphere due to the outflow of blood. The sharpest displacement of the M-echo occurs when hemorrhages in the paramedian structures. With hemorrhages with a break in the ventricles and their tamponade, additional signals are recorded that indicate the expansion of the third ventricle.
For the diagnosis of subarachnoid hemorrhage, this method is not very informative in cases where there is no penetration of blood into the parenchyma of the brain. However, with subarachnoid-parenchymal hemorrhages, especially massive, with echoencephaloscopy, additional signals are determined that allow one to judge with certainty about the side of localization of the vascular focus.
The main goal of the CSF study is to confirm the ischemic nature of the stroke by eliminating hemorrhage( intracerebral or subarachnoid) at the same time.
In the first hours after the development of ischemic stroke, the cerebrospinal fluid in most cases is not changed - it is colorless, transparent;the protein content and cytosis do not exceed normal values. In the following days, the protein content may increase. A particularly significant increase in the protein content is found, as a rule, on the 3-5th day with extensive infarcts localized near the liquor-conducting pathways. Cytosis in this case increases to a lesser extent( protein-cell dissociation).It should be borne in mind that according to different authors, in 8-14% of cases, colorless, transparent liquor is found in patients with limited( lobar) hematomas, not accompanied by the penetration of significant amounts of blood into the ventricular system and subarachnoid space. In such cases, the use of luminescent samples and the spectrophotometry of CSF is recommended. Their results indicate the absence of blood pigments in cerebrospinal fluid in ischemic stroke or the presence of different amounts of bilirubin, oxy- and methemoglobin in limited intracerebral hematomas.
Signs that distinguish the "waypoint" blood in case of an unsuccessfully performed lumbar puncture from the blood admixture to the cerebrospinal fluid are characterized by the presence of the same uniform color of the liquor in all portions, the detection of fresh or leached erythrocytes in the sediment, the combination of hemorrhages( subarachnoidal and intracerebral, communicating with the cerebrospinal spaces)the presence of erythrocytes with hyperalbuminosis. With the "road" nature of the blood, subsequent portions of CSF are less stained with blood than the first;there are no xanthochromia, erythrocytes and hyperalbuminosis.
The need for reanalysis of cerebrospinal fluid in ischemic stroke most often occurs in cases of worsening( increasing neurological deficit, the onset or deepening of depression) that occurs after a period of stabilization or regression of the symptoms that initially appeared. Detection of a blood admixture to the cerebrospinal fluid in such cases confirms hemorrhagic transformation of the cerebral infarction. In this case, the increased protein content and, less rarely, the appearance of erythrocytes and pleocytosis are more often detected.
In the early period after the development of ischemic stroke( 1-3 days) in CSF, an increase in the activity of enzymes( creatine phosphokinase, lactate hydrogenase, gamma-glutamyl-transpeptidase, aspartate aminotransferase, alkaline phosphatase) and lactate increase is determined. These changes indicate the development of brain hypoxia, and the degree of their severity indicates the volume of the formed infarction and, to some extent, the prognosis.
Special attention is paid to the question of the dangers associated with lumbar puncture. They occur with severe and extensive cerebral hemorrhages with a rapid development of perifocal edema, which often spreads directly to unaffected areas of the brain, accompanied by a worsening of liquor circulation and venous outflow, which increase the volume of intracranial contents. In these situations, conditions are created in which even minor interventions in the form of lumbar puncture often entail the dislocation of the brain structures and the subsequent development of the syndromes of the "upper" and "lower" wedges. The clinical criterion in such cases is the rapid development of coma.
With massive hemorrhages, the admixture of blood to the CSF is detected at the earliest stage of the disease. Its quantity is largely due to the localization of the hematoma with respect to the liquor-conducting pathways, that is, the presence or absence of breakthrough of the hematoma into the subarachnoid space or ventricular system.
With a limited, small amount of lobar hematomas localized at a distance from the liquor communications, the admixture of blood to the CSF may initially be absent and is detected in minimal amounts only 2-3 days after the development of the hemorrhage. If the patient's condition remains relatively satisfactory, differential diagnostic difficulties can arise, that is, suspicion of a mixed stroke or hemorrhagic infarction. The final clarity regarding the nature of the pathological process in such cases is made by the results of CT and MRI studies.
With subarachnoid hemorrhage, the admixture of blood in the liquor is crucial to confirm the diagnosis. Sometimes in the nearest future from the moment of the disease( 1-5 h) with lumbar puncture, the impurity of the blood is not yet detected. If in such cases the clinical picture is typical for subarachnoid hemorrhage, the puncture should be repeated after 4-6 hours. At any time, the above mentioned dangers of lumbar puncture should be taken into account. The amount of slowly withdrawn CSF should not exceed 3 ml.
Detection of a blood admixture to the cerebrospinal fluid makes it impossible to judge either the etiology of subarachnoid hemorrhage or the localization of the source.
Laboratory tests of CSF allow to determine approximately the amount of blood flowing into the cerebrospinal fluid, that is, the massiveness of hemorrhages, its prescription, and also to exclude the possibility of an admixture to the CSF of "official" blood because of an unsuccessful lumbar puncture.
The amount of blood flowing into the liquor is determined by the formula:
It's even easier to navigate the color of the liquor. So, in the pink liquor the number of erythrocytes is 20 - 50 x 109 / l and more.
The prescription of subarachnoid hemorrhage can be judged with a certain degree of accuracy by the number of erythrocytes and by the degree of xanthochromia( yellow staining).
For 2-3 days, 25-30% of erythrocytes are removed from the cerebrospinal fluid in the subdural space, 60-95% of the remaining erythrocytes on the 3-4th day. With subarachnoid hemorrhages of aneurysmatic etiology in unoperated patients, complete sanation of the CSF occurs a month or more later, with hemorrhages of another genesis - by 14-20 days.
Xanthohromia of CSF is caused by the decay in it of hemoglobin of erythrocytes. Its intensity increases by 2-4 days, and then gradually decreases [Makarov A. Yu., 1984).According to VI Samoilova( 1990), xanthochromia is eliminated in case of aneurysmal hemorrhage in unoperated patients by 12-18 days, and in hemorrhages of a different etiology - at earlier times.
The content of protein in CSF varies widely - from 0.6 to 24.6 g / l. It is the least significant for aneurysmal hemorrhage in elderly and senile patients;a higher protein content is found with subarachnoid hemorrhages of a different etiology. Pleocytosis is different - from 0.1 to 0.3x109 / L and largely correlates with the volume of blood flow. It is mainly due to the reaction of the meninges to the spilled blood. In the first days neutrophils predominate, and later - lymphocytes and macrophages.
The data given on the dynamics of changes in cerebrospinal fluid combined with the clinical characteristics of the patients' condition allow one to orientate in the degree of intensity and duration of therapeutic measures.
In conclusion, it should be emphasized that in the presence of CT and MRI in patients with ischemic stroke and cerebral hemorrhage in most cases, it is possible to avoid lumbar punctures.
This method is ineffective for diagnosing ischemic and hemorrhagic forms of stroke, as well as for differentiation from other focal brain lesions. With massive infarcts, extensive hemorrhages in the parenchyma of the brain and subarachnoid space, changes in the EEG can be detected, indicating their localization. In the early periods of the disease EEG may be unchanged or identify patterns that are not specific for stroke.
This method is used in angioneurology relatively recently. Trans-esophageal and, more rarely, transthoracic echocardiography is used. The purpose of these diagnostic methods is to identify sources of cardiogenic embolic cerebral infarcts and their differentiation from arterio-arterial infarcts. By echo electrocardiography it is possible to visualize intracardial thrombi, segments of dilated cardiomyopathy and ventricular aneurysms, loose fragments of affected mitral valves, a sharp prolapse of the mitral valve - that is, very frequent causes of embolization of the arterial system of the brain, leading to heart attacks( often repeated) and transient cerebral circulatory disorders. It is essential to determine the density and volume of possible sources of cardiogenic emboli.
There is a positive experience that firstly, the listed forms of heart lesions can be detected only by trans-esophageal and transthoracic echocardiography and, secondly, the undeniable etio-pathogenetic significance of these forms of cardiac pathology in the occurrence of cerebral infarcts. Thus, the mentioned heart lesions, associated with the risk of ischemic stroke and frequent repeated transient disorders of cerebral circulation, were detected in patients with acute cerebral ischemia in
5 times more often than in the control group without heart lesions, respectively in 21% and 4%.According to A. Cohen et al.(1996), the risk of cardiogenic embolisms with the listed forms of cardiac pathology is almost 2 times higher than in healthy individuals under the age of 45 - 22% and 12%, respectively.
The ability to differentiate with trans-esophageal and transthoracic echocardiography cardiogenic and arterio-arterial thrombi is now extremely important in connection with attempts to widely use thrombolytic drugs for emergency therapy of ischemic strokes( see section "Treatment of Ischemic Stroke with Thrombolytic Agents").
First, you do not need to panic and get lost. You need to focus on the person whose life depends on you, too. The main principles of stroke treatment are urgency, intensity, causal orientation. Of these, the time factor and intensity of therapy during the first 6 hours of the disease( during the "therapeutic window") determine the outcome of the stroke both in terms of survival rate and in minimizing the degree of brain function impairment, since all activities are directed to correction of the underlying vascular disease,repeated seizures, restoration of quantitative and qualitative indices of cerebral blood flow and normalization of impaired brain functions. From the relatives and surrounding sick people depends on his correct behavior at this time. First of all, you need to call an ambulance doctor who will give recommendations and help, and if necessary, he will hospitalize the patient in a hospital. Before this patient can not be moved, it is necessary to protect him from physical exertion, not to let him get up, move. If it needs to be moved to another, more convenient place, then only in a horizontal position.
All medical measures, which will be discussed in this chapter, are conducted in a hospital in the neurological department. If the patient is not transportable( a deep coma with gross disruption of vital functions), a hospital at home is organized. Emergency stroke treatment is aimed at eliminating the vital( vital) disorders occurring in the body and involves influencing the factors that contribute to the spread and deepening of the pathological process in the brain:
It is very important to carefully observe the patient throughout the stroke period, because in the transitionfrom the comatose state to the other, provided to himself, makes attempts to sit down, turn around, etc. These attempts can cost him his life.
Since the first days of illness, it is necessary to prevent the development of pressure sores.
Loin, sacrum, buttocks and legs should be cleaned daily with camphor or ordinary alcohol.
The patient is placed on a rubber circle. Bedding it must be kept in order( avoid folds of sheets, bread crumbs).It should always be dry and clean.
Bedsores occur in the nape of the neck, shoulder blades, elbows, sacrum, knees, heels and buttocks. Danger of decubitus is that necrosis can penetrate deep into the cartilage and bones. Such wounds, as a rule, become infected and can be a source of infection of the whole organism.
Most often they occur in incontinent urine, feces, with anemia( anemia), concomitant infectious complications, in thin patients.
Food should be full and easily digestible. Food should be enough and it should contain all the necessary nutrients. It is best to use special nutrient mixtures that are sold in a pharmacy without a prescription.
Stroke should be started as early as possible in order to prevent weight loss and mobilize the body to fight the disease.
So that your lips do not dry out and crack, they need to be moistened with hygienic lipstick or a special cream;
- to prevent itching, which can arise from taking medication or as a reaction to care products and washed laundry( powder, bleach), you can wipe the skin with a solution of drinking soda;
- should prevent joint stiffness in the paralyzed limb. With forced immobility and lack of movement, contractures( stiffness) arise. To this end, it is necessary to properly fold the limb, carry out passive curative gymnastics and combine it with a massage.
Currently, the concept of immediate hospitalization of patients with acute impairment of cerebral circulation is adopted. This is due to the fact that in the first hours, after taking the necessary therapeutic actions, you can significantly reduce the focus of brain damage.
First, with stroke, brain cells are damaged and cerebral edema develops. Edema promotes increased intracranial pressure. Due to this, a dislocation( displacement) of the brain develops and as a result, compression of the nervous tissue occurs. The most pronounced onset of edema on the second-fifth day, and it decreases from the second week after the onset of stroke.
In the place of damage to the brain tissue, necrosis is formed, followed by a cyst or scar. Depending on the area of the brain supplying blood to the artery, a different localization, the extent of the lesions and, accordingly, the clinical picture are determined. When a large artery is affected, which nourishes a large area of the brain, the disease develops catastrophically quickly, passing through all stages, beginning with the brain edema and ending with its dislocation and death. With minor disturbances, stroke can occur with subtle symptoms.
The most modern methods of investigation have made a significant correction in the understanding of local processes that arise in nerve cells in case of a lack of nutrition.
It turned out that with ischemic stroke between dead( necrotic) and living cells there is a zone of cells with insufficient circulation, in which the disturbances are functional, i.e. reversible. They can be brought back to life, if during the first 6 hours to restore blood supply, after this period they die. This transition zone is called ischemic penumbra.
In a hemorrhagic stroke, a similar pattern is observed - brain damage also develops gradually: approximately 26% of the hematomas build up within an hour after the onset of the stroke, and 12% within 12 hours.
Hence the conclusion that effective and urgent medical measures, carried out in the early period( during the so-called therapeutic window) of the disease, can significantly reduce the focus of brain damage and help avoid complications.
1) Treatment of hemorrhagic stroke. The main task in this stroke is to control blood pressure and stop bleeding in the brain. Reducing blood pressure helps reduce blood pressure on the walls of blood vessels and the bleeding quickly stops. Regulation of blood pressure is carried out by antihypertensive agents in tablets, capsules, and there are also those that are administered intravenously. Modern preparations: prestarium, enap, enam, enalapril, renitek and many others. Everything depends on the general condition of the patient, the level of blood pressure and its fluctuations. This is necessary if suddenly a small hemorrhage and bleeding can stop by itself, without surgery. Basic therapy includes lower body temperature, elevated head position, relief of pain and cramps.
A neurosurgical operation is performed in the case of a large hematoma, which compresses adjacent brain structures. With any hemorrhage in the brain, a serious complication is cerebral edema. One of the main methods of treating cerebral edema is the administration of osmotic diuretics.
2) Treatment of ischemic stroke is aimed at improving the blood supply to the brain. For this, first of all, the regulation of cardiac activity and arterial pressure, the increase in blood flow to the brain through expansion of cerebral vessels and reduction of spasm of blood vessels, improvement of peripheral circulation, normalization of blood coagulation, increased resistance to hypoxia of brain tissue and improved brain nutrition are carried out first.
For this purpose, the following are used:
- vasodilator preparations: euphyllin, nicotinic acid, papaverine, halidor;etc.
- to reduce blood coagulability and the activity of the blood coagulation system - blood dilution - intravenously inject polyglucin or reopolyglucin;anticoagulants are used: heparin, finylin, dicumarin, etc. In hypertensive crisis, it is advisable to reduce blood pressure slowly and smoothly for several hours. With increased life-threatening pressure, the pressure decreases rapidly within 15-30 minutes. For this purpose, the nematop is administered intravenously. Then the patient is transferred to tableted drugs that lower blood pressure.
Type of surgery is determined by the nature of the stroke. In hemorrhagic stroke surgical intervention is aimed at eliminating pathological factors that can lead to death of patients in those cases when hemorrhage did not cause incompatible with life brain damage. When an intra-cerebral hematoma occurs, the intervention is reduced to the removal of the blood that has spilled out.
Contraindications to surgical intervention are multiple vascular lesions, a combination of the underlying disease with severe heart and kidney damage, high blood pressure, elderly age, deep location of the hemorrhage focus.
Preferred timing of the operation is considered the end of the first or 2-3 weeks after a stroke.
Outcomes of surgical treatment of hemorrhagic stroke are better in younger people. The most favorable outcomes in patients operated in a coma.
With ischemic strokes, surgical treatment in the area of the softening focus and on the main vessels is possible.
The greatest number of operations was performed on the carotid, subclavian, middle cerebral arteries, on vertebrates, on the brachiocephalic trunk. In all these vessels, surgical interventions are performed in connection with their obstruction or stenosis( constriction), most often of atherosclerotic origin. Postoperative mortality decreased to 1.5-1.0% due to surgical treatment.
When a patient emerges from an acute period after a stroke, the main factor determining the prognosis is the restoration of impaired functions of the body and the implementation of measures to prevent repeated strokes.
The term "rehabilitation" comes from the Latin word "ge" - renewal and "habilitas" - ability, suitability. This is a set of measures aimed at restoring the lost health and ability to work of people with reduced physical or mental capabilities as a result of a stroke. This complex includes: physiotherapy, medical therapy, physiotherapy, massage, etc.
All patients who have received a stroke need rehabilitation, as this disease is the most massive and most disabling, which significantly affects the quality of life of tens of millions of people in the world.
In Russia, according to the Scientific Research Institute of Neurology of the Russian Academy of Medical Sciences, by the end of the acute period( 21 days), paralysis is observed in 81.2% of surviving patients, speech disorders - in 35.9%, dysarthria - in 13.4%.Totally dependent on the surrounding everyday life 25.5% of patients, in part - 57.5%.
In developed countries, rehabilitation is given great importance and does not regret spending money on it. In the US, these costs are $ 15-20 billion per year.
Under the influence of rehabilitation activities, the functions of the dead begin to be performed by other nerve cells, the brain is reorganized. Conducted medical measures lead to the improvement of the work of cells, whose activity was disturbed by the edema of the brain.
The principle of rehabilitation of stroke survivors lies in its early onset, complexity, perseverance, continuity, duration, maximum active participation of the patient. All this is possible only against the backdrop of the positive attitude and firm desire of the patient to carry out rehabilitation measures.
Obligatory participation in the process of rehabilitation of relatives and relatives. The tasks of rehabilitation are restoration of motor activity, elimination of speech disorders, removal of astheno-depressive syndrome.
With timely and complete rehabilitation, it is possible to achieve that up to 95% of patients do not need extraneous care.
Medication rehabilitation: treatment with drugs that improve cerebral blood flow with vasodilator effect: nicergoline( sermion);cavinton, cinnarizine, etc.;
In the treatment of patients after a stroke with paralysis, even in the early stages, therapeutic exercise and massage are used. This is necessary to improve blood supply and muscle trophism in the affected limbs, prevents the development of contractures, restores movement in the paralyzed limbs. From the first days begin to apply a special styling of paralyzed limbs. With hemiplegia and hemiparesis, which occur with ischemic stroke, treatment with the position begins with the 2-4th day of the disease;with hemorrhage to the brain - on the 6th-8th day( if the patient's condition allows this treatment).Laying on the back is carried out in a posture opposite to the Wernick-Mana posture( the hand and leg are paralyzed): the shoulder is withdrawn to the side at an angle of 90 degrees, the elbow and fingers are unbent, the hand is held by the long( the palm is fixed to it);the entire limb is fixed in this position with the help of sandbags. The paralyzed leg is bent at the knee joint at an angle of 15-20 degrees, a knurled roll of gauze and cotton wool is placed under the knee.
The stop is given the position of the back folding at an angle of 90 degrees and keeps it in this position with a wooden stand.
Stacking on the back periodically alternates with stacking on a healthy side;while the paralyzed limbs are bent in the elbow, hip, knee and ankle joints and held on the cushion. The patient's position on the back and healthy side is changed every 1 / 2-2 hours. Then they go to therapeutic gymnastics( LFK).
The appointment of patients with exercise therapy increases the patient's confidence in the favorable outcome of the disease, distracts from "care for the disease", helps to eliminate anxiety and improves the nervous and mental state. Physical exercises contribute to the emergence of positive emotions in patients.