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INTRODUCTION

Sudden onset of a neurologic deficit from a vascular mechanism: ∼85% are ischemic; ∼15% are primary hemorrhages (subarachnoid [Chap. 20] and intraparenchymal). An ischemic deficit that resolves rapidly without radiologic evidence of an infarction is termed a transient ischemic attack (TIA); 24 h is a commonly used boundary between TIA and stroke, although most TIAs last between 5 and 15 min. Stroke is a leading cause of neurologic disability in adults; ∼150,000 deaths annually in the United States. Much can be done to limit morbidity and mortality through prevention and acute intervention.

PATHOPHYSIOLOGY

Ischemic stroke can be due to embolic occlusion of large cerebral vessels; source of emboli may be heart, aortic arch, or other arteries such as the internal carotids. Small, deep ischemic lesions are most often related to intrinsic small-vessel disease (lacunar strokes). Low-flow strokes are occasionally 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.

CLINICAL FEATURES

Ischemic Stroke

Abrupt and dramatic onset of focal neurologic symptoms is typical. 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 19-1). Transient monocular blindness (amaurosis fugax) is a particular form of TIA due to retinal ischemia; pts describe a shade descending over the visual field and the ipsilateral carotid artery is often implicated.

TABLE 19-1Anatomic Localization in Stroke

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