Cerebrovascular Diseases PDF

Cerebrovascular diseases  Cerebrovascular diseases are brain disorders caused by pathologic processes involving blood vessels. the three main pathogenic mechanisms are: (1) thrombotic occlusion (2) embolic occlusion (3) vascular rupture. Cont. …. Stroke is the clinical design...

Cerebrovascular diseases  Cerebrovascular diseases are brain disorders caused by pathologic processes involving blood vessels. the three main pathogenic mechanisms are: (1) thrombotic occlusion (2) embolic occlusion (3) vascular rupture. Cont. …. Stroke is the clinical designation applied to all of these conditions when symptoms begin acutely. Hypoxia, Ischemia, and Infarction  cerebral blood flow normally remains stable over a wide range of blood pressure and intracranial pressure because of autoregulation of vascular resistance. Cont. …. the brain may be deprived of oxygen by two general mechanisms: 1. functional hypoxia, caused by a low partial pressure of oxygen (e.g., high altitude), impaired oxygen- carrying capacity e.g., severe anemia. 2. ischemia, either transient or permanent, due to tissue hypoperfusion.  Global Cerebral Ischemia widespread ischemic-hypoxic injury can occur in the setting of severe systemic hypotension, usually when systolic pressures fall below 50 mm Hg, as in cardiac arrest and shock. the clinical outcome varies with the severity and duration of the insult. when the insult is mild, there may be only a transient postischemic confusional state, with eventual complete recovery. Cont. …. in severe global cerebral ischemia, widespread neuronal death occurs irrespective of regional vulnerability, patients who survive often remain severely impaired neurologically and in a persistent vegetative state. Morphology in the setting of global ischemia, the brain is swollen, with wide gyri and narrowed sulci. Early changes, occurring 12 to 24 hours after the insult, include acute neuronal cell change (red neurons). Subacute changes, occurring at 24 hours to 2 weeks, include necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis Cont. …. Repair, seen after 2 weeks, is characterized by removal of necrotic tissue and gliosis  A B A. Acute hypoxic-ischemic injury in the cerebral cortex. The cell bodies are shrunken and eosinophilic (“red neurons”), and the nuclei are pyknotic. B. Collection of microglial cells forming a poorly defined nodule, a common finding in viral infections. Focal Cerebral Ischemia cerebral arterial occlusion leads first to focal ischemia and then to infarction in the distribution of the compromised vessel. the size, location, and shape of the infarct and the extent of tissue damage that results may be modified by collateral blood flow. Cont….. Embolic infarctions more common than infarctions due to thrombosis, cardiac mural thrombi are a frequent source of emboli; myocardial dysfunction, valvular disease, and atrial fibrillation are important predisposing factors. Cont….. Thrombotic occlusions causing cerebral infarctions usually are superimposed on atherosclerotic plaques. common sites are the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery, it can cause small infarcts of only a few millimeters in diameter, so-called “lacunar infarcts” Cont….. Infarcts can be divided into two broad groups:  nonhemorrhagic infarcts result from acute vascular occlusions and may evolve into hemorrhagic infarcts when there is reperfusion of ischemic tissue, either through collaterals or after dissolution of emboli. Morphology hemorrhagic infarcts usually manifest as multiple, sometimes confluent, petechial hemorrhages Cont….. the macroscopic appearance of a nonhemorrhagic infarct evolves over time.  in the first 6 hours, the tissue is unchanged in appearance  by 48 hours, the tissue becomes pale, soft, and swollen. Cont. …  from days 2 to 10, the injured brain turns gelatinous and friable, and the boundary between normal and abnormal tissue becomes more distinct as edema resolves in the adjacent viable tissue.  from day 10 to week 3, the tissue liquefies, eventually leaving a fluid-filled cavity, which gradually expands as dead tissue is resorbed Cont….. Microscopically the tissue reaction follows a characteristic sequence, after the first 12 hours, ischemic neuronal change (red neurons) and cytotoxic and vasogenic edema appear.  Intracranial Hemorrhage hemorrhages within the brain are caused by: (1) hypertension and other diseases leading to vascular wall injury (2) structural lesions such as arteriovenous and cavernous malformations (3) tumors. Subarachnoid hemorrhages most commonly are the result of ruptured aneurysms  Primary Brain Parenchymal Hemorrhage spontaneous (nontraumatic) intraparenchymal hemorrhages are most common in mid to late adult life, with a peak incidence at about 60 years of age. most are due to the rupture of a small intraparenchymal vessel. Hypertension is the leading underlying cause, and brain hemorrhage accounts for roughly 15% of deaths among individuals with chronic hypertension. Cont….. hypertensive intraparenchymal hemorrhages typically occur in the basal ganglia, thalamus, pons, and cerebellum, with the location and the size of the bleed determining its clinical manifestations. if the individual survives the acute event, gradual resolution of the hematoma ensues, sometimes with considerable clinical improvement. Morphology on microscopic examination, early lesions consist of clotted blood surrounded by edematous brain tissue.  Subarachnoid Hemorrhage and Saccular Aneurysms the most frequent cause of clinically significant nontraumatic subarachnoid hemorrhage is rupture of a saccular (berry) aneurysm. hemorrhage into the subarachnoid space also may result from vascular malformation, trauma, rupture of an intracerebral hemorrhage into the ventricular system, coagulopathies, and tumors. Cont….. about 90% of saccular aneurysms occur in the anterior circulation near major arterial branch points multiple aneurysms exist in 20% to 30% of cases. healing and the attendant meningeal fibrosis and scarring sometimes obstruct CSF flow or disrupt CSF resorption, leading to hydrocephalus.  Vascular Malformations Vascular malformations of the brain are classified into four principal types based on the nature of the abnormal vessels: arteriovenous malformations (AVMs), cavernous malformations, capillary telangiectasias, and venous angiomas. Cont….. AVMs, the most common of these, affect males : females (2:1)and most commonly manifest between 10 and 30 years of age with seizures, an intracerebral hemorrhage, or a subarachnoid hemorrhage. The risk for bleeding makes AVM the most dangerous type of vascular malformation. Thanks for attention Thanks for attention Thanks for attention Any Questions?