Cerebrovascular Diseases (CVD) are the group of diseases of the brain based on acute and chronic disturbances of cerebral hemocirculation caused by different pathological changes of the cerebral blood vessels. Generally CVD is a result of cerebral forms of atherosclerosis and arterial hypertension. Besides that diabetic microangiopathy plays substantial role in disturbances of cerebral hemocirculation in CVD. Rarely CVD develop due to primary vasculites (Takajasu’s disease, Horton’s disease) or due to congenital vascular abnormalities (arterio-venous aneurisms, hypoplasia of cerebral arteries). Two principal forms of CVD are differentiated – acute and chronic ones.
Chronic forms of CVD develop due to gradually progressing atherosclerosis and arterial hypertension. Morphologically the process is characterized by atrophy of the cortex (mainly in cerebral atherosclerosis) or the white substance of the brain (mainly in arterial hypertension) with the secondary internal hydrocephalus. Clinically the process manifests itself in neurological and psychic symptoms (vascular encephalopathy). Patients with vascular encephalopathy represent themselves the group of high risk for acute forms of CVD.
Acute forms of CVD are represented by insults which can be of ischemic or hemorrhagic types. Ischemic insult manifests itself in hemodynamic necrosis of the cortex and white substance. Necrosis usually develops as a result of pronounced stenosis of arteries caused by atherosclerotic plaques or as a result of thromboembolism of cerebral arteries from the left chambers of the heart. Development of ischemic insult can be facilitated by acute and chronic heart failure due to ischemic heart disease or different valvular defects of the heart.
Zonation of ischemic insult
Ischemic insult has three zones: the central necrosis, adjacent zone of irreversible dystrophy (umbra, shade) and peripheral zone of reversible dystrophy (penumbra, hulf-shade). It is established that necrosis of the brain substance forms within 6 hours after ischemic stroke , so that to diminish the size of infarction in is absolutely necessary to deliver the patient to the hospital as early as possible, but not later than 6 hours (“therapeutic window”). Ischemic insult is characterized by slow onset, without painful syndrome and clinically manifests itself by flabby paresis and paralysis of the limbs or facial muscles.
Hemorrhagic insult represents itself hemorrhage in the form of hemorrhagic imbibitions of the brain substance or hematoma which usually develops in patients with cerebral form of arterial hypertension in condition of hypertensive stroke. Hemorrhagic insult occurs mostly in the basal nuclei of the brain and not rare is complicated by intraventricular bleeding which usually leads to death. Clinically hemorrhagic insult is characterized by sudden onset with severe headache and leads to the loss of consciousness within few minutes.
Ischemic and especially hemorrhagic insults are characterized by very high mortality (up to 60-70%) because of massive destruction of the brain substance with progressing oedema of the brain, or secondary pneumonias which usually develop in acute period of the process. If patients survive necrotic tissues and hematomas undergo resorption with cyst formation. Spacious damage of the brain in survived patients makes them invalids.