Ischemic Stroke

Ischemic stroke is sudden neurological deficits due to focal cerebral ischemia with permanent stroke (z. B. positive results in diffusion-weighted MRI). Common causes include atherothrombotic (with decreasing frequency) occlusion of large arteries, cerebral embolism (embolic infarction); nichtthrombotischer closure of small, deep cortical arteries (lacunar infarcts) and proximal arterial stenosis with hypotension, which reduces cerebral blood flow in the edge zones (hemodynamic stroke) is diagnosed clinically, but CT and MRI are performed to exclude blood flow and to confirm the presence and extent of the insult. In certain patients can thrombolytic therapy, acute carried out, be useful. Depending on the cause of the stroke an endarterectomy or carotid stent, an antiplatelet medication or oral anticoagulants can reduce the risk of further insults. (Editor’s note: In Germany next Marcumar three other preparations for oral anticoagulation are available.)

Ischemic stroke is sudden neurological deficits due to focal cerebral ischemia with permanent stroke (z. B. positive results in diffusion-weighted MRI). Common causes include atherothrombotic (with decreasing frequency) occlusion of large arteries, cerebral embolism (embolic infarction); nichtthrombotischer closure of small, deep cortical arteries (lacunar infarcts) and proximal arterial stenosis with hypotension, which reduces cerebral blood flow in the edge zones (hemodynamic stroke) is diagnosed clinically, but CT and MRI are performed to exclude blood flow and to confirm the presence and extent of the insult. In certain patients can thrombolytic therapy, acute carried out, be useful. Depending on the cause of the stroke an endarterectomy or carotid stent, an antiplatelet medication or oral anticoagulants can reduce the risk of further insults. (Editor’s note: In Germany next Marcumar three other preparations for oral anticoagulation are available.) Etiology The following are the modifiable risk factors that contribute most to an increased risk of ischemic stroke: hypertension cigarette smoking dyslipidemia Diabetes Abdominal obesity alcohol shortage of physical activity high-risk diet (z. B. high in saturated fats, trans fats, and calories) psychosocial stress (eg., depression) heart disease (especially diseases that predispose to embolisms, such as acute myocardial infarction, infective endocarditis, and atrial fibrillation ) drugs (eg. as cocaine, amphetamines) Hypercoagulable vasculitis include the immutable risk factors: previous stroke Seniority stroke Family history Male sex Ischemia is most often caused by thrombi or emboli. Even on the basis of clinical criteria as lakunär classified infarctions (morphology, size and location) often contain small thrombi or emboli. A thrombosis atherothrombotic closure of the great arteries (atherosclerotic artery thrombus in a superimposed) is the most common cause of ischemic stroke. Atheroma, particularly ulcerated, predispose to thrombus formation. Atheroma may occur in any major cerebral artery and are often used in areas with turbulent flow, v. a. the area in front of the carotid bifurcation. A partial or complete thrombotic occlusion occurs mostly in the main stem of the middle cerebral artery and its branches, but is also common in the large arteries of the base of the brain, in deep perforating arteries and in small cortical branches. The basilar artery and the segment of the internal carotid artery between the cavernous sinus and supraclinoideus the processus are often sealed. Among the rarer causes of thrombosis include vascular inflammation as a result of disorders such as acute or chronic meningitis, vasculitis or syphilis; Dissection of the intracranial arteries or aorta; Hypercoagulability (. For example, antiphospholipid syndrome, hyperhomocysteinemia); Diseases with increased blood viscosity (e.g., polycythemia vera, thrombocytosis, hemoglobinopathies, disorders of plasma cells.); rare diseases (eg. B. fibromuscular Dsyplasie, Moyamoya, M. Binswanger). Mature oral contraceptives increase the risk of thrombosis. In children, sickle cell anemia is a common cause of ischemic Schlaganfall.Embolie emboli can settle in the cerebral arteries everywhere. Emboli can result from cardiac thrombi, in particular under the following conditions: atrial fibrillation Rheumatic Herzerkranungen (usually mitral stenosis) Z. n myocardial infarction vegetations on the heart valve in bacterial or marantic diagrammatic endocarditis heart valve prostheses Other sources are blood clots that form after open heart surgery, and atheromas. in neck arteries or the aortic arch. Rarely is an embolus from fat (after fracture of long bones), air (in DCS) or venous thrombi ovale from the right to the left side of the heart through a patent foramen with shunt access (paradoxical emboli). Emboli can spontaneously or after an invasive cardiovascular tear manipulation (z. B. Catheter). Rarely thrombosis of the subclavian artery has an embolic stroke in the vertebral artery or its branches to Folge.Lakunäre infarctions An ischemic stroke can be caused by lacunar infarcts. These small infarcts (? 1.5 cm) from the can nichtatherothrombotischen obstruction smaller penetrating arteries arise supply the deep cortical structures; the usual cause is a lipohyalinosis (degeneration of the media of small arteries and replacement by lipids and collagen). Whether emboli cause lacunar infarcts is controversial. Lacunar infarcts occur particularly in elderly patients with diabetes mellitus or poorly controlled Bluthochdruck.Andere causes Any factor that increases the systemic perfusion impaired (eg. As carbon monoxide toxicity, severe anemia or hypoxia, polycythemia, hypotension) the risk of all types of ischemic stroke. A stroke can occur along the boundaries between the areas of the arteries (watersheds). In such places, the blood supply is usually low, especially if the patients have hypotension and / or when important cerebral arteries are stenotic. Less common are ischemic stroke, the result of vasospasm (eg., During a migraine attack, after subarachnoid hemorrhage, after use of sympathomimetic drugs such as cocaine or amphetamine), or a sinus thrombosis (eg., During intracranial infection, post-operatively, peripartal, secondary to Hyperkoagulationsstörung ). Pathophysiology Inadequate blood flow in a single cerebral artery can often be compensated for by an efficient Kollateralensystem, especially between carotid and vertebral arteries by anastomoses of the circle of Willis and to a lesser extent between the large arteries that supply the cerebral hemispheres. However, the blood flow in the collaterals may be obstructed by atherosclerosis and other acquired arterial lesions due to the normal variability in the circle of Willis and in the caliber of various collateral vessels, thereby increasing the likelihood that the blockage of a single artery leads to ischemia. Some neurons die when the perfusion> 5 min is <5% of normal, but the extent of damage depends on the severity of ischemia. In mild cases, the injury is progressing slowly, even if the perfusion is 40% of normal, 3-6 hours may pass completely lost to brain tissue. If severe ischemia (d. H decrease in perfusion.) However, about> 15-30 min persists, the affected tissue dies off completely (infarction). In hyperthermia damage occurs faster in hypothermia slower one. If indeed one is tissue ischemia, but no irreversible damage has not yet occurred, the rapid restoration of blood flow can reduce the amount of insults or undo it. Through intervention, it may, for. B. succeed the moderate ischemic areas (penumbra), often heavily ischemic areas surrounded (these areas exist because of the collateral flow) to save. Among the mechanisms of ischemic lesion include edema, microvascular thrombosis, programmed cell death (apoptosis) and infarction with cell death. Inflammatory mediators (eg., IL-1B, tumor necrosis factor-?) contribute to edema and microvascular thrombosis. A strong or extensive edema may increase intracranial pressure. Many factors can contribute to cell death; they comprise the emptying of the ATP memory, loss of ionic homeostasis (incl. intracellular calcium accumulation), an oxidative lipid cell membrane damage by free radicals (an iron-mediated process) excitatory neurotoxins (eg., glutamate) and intracellular acidosis by lactic acid accumulation. Symptoms and signs The symptoms depend on the affected part of the brain. The pattern of neurological failures can often on the affected artery include (see Table: Selected stroke syndromes), but the correlation is often inaccurate. The deficits can reach their maximum within minutes after the start, typically at an embolic stroke. Less commonly, the deficiencies develop slowly, usually about 24 to 48 hours (as a “progressive stroke”) is typically in atherothrombotic stroke. For most insults to a one-sided neurological disorder image (often beginning in one arm, then spread ipsilateral) developed without causing headaches, other pain or fever. The progression usually runs gradually, punctuated by periods of stability. A stroke is considered incomplete if after it is completed, a residual function in the affected area remains, which speaks for vital tissue on the verge of damage. Embolic insults frequently occur during the day; Headache may precede the neurological deficits. Thrombosis occurs preferentially at night and is therefore often only noticed when you wake up. Lacunar infarcts can cause one of the classic lacunar syndrome (z. B. purely motor hemiparesis, sensory purely hemianaesthesia, ataxic hemiparesis, dysarthria clumpsy-hand syndrome). Signs of cortical dysfunction (z. B. aphasia) are missing. Multiple lacunar infarcts can lead to multi-infarct dementia. An attack can often occur as a thrombotic stroke in the onset of symptoms in the form of an embolic. Seizures can also occur months to years later; subsequent seizures caused by scarring or hemosiderin deposition at the site of ischemia. Deterioration during the first 48-72 hours after onset of symptoms, particularly in increasing cognition is impaired, is often caused by cerebral edema as by an expansion of the infarct. If the infarct is not very large or extended, the function improves, usually within the first few days; a further improvement can still occur gradually up to one year. Diagnostic imaging and primary clinical evaluation cerebral glucose test at the bedside clarification of the cause When sudden neurological deficits that can be assigned to a specific arterial supply area, the diagnosis can be suspected. Ischemic stroke must be distinguished from other causes by similar focal deficits (eg. As hypoglycemia, post-ictal [Todd’sche] paralysis, hemorrhagic stroke, rarely migraine). Sometimes “stroke mimics” called. Headaches, coma or stupor and vomiting are more common in hemorrhagic insults. The clinical differentiation between the types of stroke is imprecise; However, some evidence on the basis of symptom progression, time of onset and the nature of the deficit can help. Although the diagnosis is clinical, neuroimaging and glucose test is required. First, a CT is performed to rule out intracerebral hemorrhage, but also subdural or epidural hematoma and rapidly growing, bleeding or suddenly symptomatic expectant tumors. The CT detection even by a large ischemic insult the front flow path can be very subtle during the first hours only; Hypodensity in the parenchyma, catch reduced demarcation of the basal ganglia and cortical sulci and the elapsed tape or hyperdense Media mark Within 6 to 12 hours of ischemia medium until large infarcts than hypodensities to become visible; small infarcts (z. B. lacunar infarcts) may be visible only with the MRI. A diffusion-weighted MRI (high sensitivity for early ischemia) can be performed immediately after the first CT imaging. Loss of cortical ribbon with permission of the publisher. From Geremia G., W. Greenlee In Atlas of Cerebrovascular Disease. Edited by P. B. Gorelick and M.A. Sloan. Philadelphia, Current Medicine, 1996. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/insular_ribbon_loss_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / manual / professional / images / insular_ribbon_loss_high_de.jpg lang = en & thn = 0 ‘, title:’? loss of cortical band ‘description:’ u003Ca id = “v38396794 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eDie CT scan shows a lapse of sylvian groove and the cortical band (straight arrows) at the site of infarction compared with the normal cortical band (curved arrows). u003c / p u003e u003c / div u003e ‘credits’ with permission of the publisher. From Geremia G.

Health Life Media Team

Leave a Reply