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Sudden onset of a neurologic deficit from a vascular mechanism: 85% are ischemic; 15% are primary hemorrhages [subarachnoid (Chap. 19) and intraparenchymal]. An ischemic deficit that resolves rapidly is termed a transient ischemic attack (TIA); 24 h is a commonly used boundary between TIA and stroke whether or not a new infarction has occurred, although most TIAs last between 5 and 15 min. Recently proposed new definitions classify all brain infarctions as strokes regardless of duration of symptoms. Stroke is the leading cause of neurologic disability in adults; 200,000 deaths annually in the United States. Much can be done to limit morbidity and mortality through prevention and acute intervention.


Ischemic stroke is most often due to embolic occlusion of large cerebral vessels; source of emboli may be heart, aortic arch, or other arterial lesions such as the carotid arteries. Small, deep ischemic lesions are most often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are seen with severe proximal stenosis and inadequate collaterals challenged by systemic hypotensive episodes. Hemorrhages most frequently result from rupture of aneurysms or small vessels within brain tissue. Variability in stroke recovery is influenced by collateral vessels, blood pressure, and the specific site and mechanism of vessel occlusion; if blood flow is restored prior to significant cell death, the pt may experience only transient symptoms, i.e., a TIA.


Ischemic Stroke

Abrupt and dramatic onset of focal neurologic symptoms is typical of ischemic stroke. Pts may not seek assistance on their own because they are rarely in pain and may lose appreciation that something is wrong (anosognosia). Symptoms reflect the vascular territory involved (Table 18-1). Transient monocular blindness (amaurosis fugax) is a particular form of TIA due to retinal ischemia; pts describe a shade descending over the visual field.


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