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INTRODUCTION

Cerebrovascular diseases include some of the most common and devastating disorders: ischemic stroke and hemorrhagic stroke. Stroke is the second leading cause of death worldwide, with 6.2 million dying from stroke in 2015, an increase of 830,000 since the year 2000. In 2016, the lifetime global risk of stroke from age 25 years onward was 25%, an increase of 8.9% from 1990. Nearly 7 million Americans age 20 or older report having had a stroke, and the prevalence is estimated to rise by 3.4 million adults in the next decade, representing 4% of the entire adult population. Conversely, case-specific disability-adjusted life-years due to stroke are falling, likely due to better prevention and treatment, but overall disease burden will continue to climb as the population ages, and stroke is likely to remain the second most common disabling condition in individuals aged 50 or older worldwide.

A stroke, or cerebrovascular accident, is defined as an abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. Thus, the definition of stroke is clinical, and laboratory studies including brain imaging are used to support the diagnosis. The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain and its vasculature. Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds. Neurologic symptoms are manifest within seconds because neurons lack glycogen, so energy failure is rapid. If the cessation of flow lasts for more than a few minutes, infarction or death of brain tissue results. When blood flow is quickly restored, brain tissue can recover fully and the patient’s symptoms are only transient: this is called a transient ischemic attack (TIA). The definition of TIA requires that all neurologic signs and symptoms resolve within 24 h without evidence of brain infarction on brain imaging. Stroke has occurred if the neurologic signs and symptoms last for >24 h or brain infarction is demonstrated. A generalized reduction in cerebral blood flow due to systemic hypotension (e.g., cardiac arrhythmia, myocardial infarction, or hemorrhagic shock) usually produces syncope (Chap. 21). If low cerebral blood flow persists for a longer duration, then infarction in the border zones between the major cerebral artery distributions may develop. In more severe instances, global hypoxia-ischemia causes widespread brain injury; the constellation of cognitive sequelae that ensues is called hypoxic-ischemic encephalopathy (Chap. 307). Focal ischemia or infarction, conversely, is usually caused by thrombosis of the cerebral vessels themselves or by emboli from a proximal arterial source or the heart (Chap. 427). Intracranial hemorrhage is caused by bleeding directly into or around the brain; it produces neurologic symptoms by producing a mass effect on neural structures, from the toxic effects of blood itself, or by increasing intracranial pressure (Chap. 428).

APPROACH TO THE PATIENT WITH CEREBROVASCULAR DISEASE

Rapid evaluation is essential for use of acute treatments such ...

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