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INTRODUCTION

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Stroke is one of the most common primary neurologic disorders in hospitalized patients. Stroke care maybe divided into (a) an immediate phase of stroke recognition to define ischemic or hemorrhagic stroke, with possible urgent therapeutic intervention in the emergency department, intensive care unit, or other hospital areas; and (b) an acute management phase with subsequent initiation of secondary stroke prevention therapies.

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Stroke is defined as abrupt neurologic dysfunction due to disturbances in the brain supply of blood, oxygen, and glucose. Stroke occurs because of either ischemia or hemorrhage, resulting in damage manifested by persistent clinical deficits, or accompanied by characteristic abnormalities on brain imaging. In acute ischemic stroke (AIS), not all brain tissue is salvageable. The ischemic penumbra is the part of the brain tissue that is oligemic, but not infarcted, and can potentially recover without damage at the lowest threshold of cerebral blood flow (CBF).1,2 When disturbances are self-limited, correlating with transient focal neurological deficits, and not accompanied by neuroimaging changes, the cerebrovascular event is called a transient ischemic attack (TIA).

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On average, every 40 seconds someone in the United States has a stroke, and someone dies of stroke approximately every 4 minutes.3 About 87% of all strokes are ischemic strokes (IS), 10% are intracerebral hemorrhage (ICH), and 3% are subarachnoid hemorrhage (SAH). In the last decade, the relative rate of stroke deaths fell by 35.8%.3 Significant improvements in stroke outcomes have occurred concurrently with improved risk factor control. Despite gradual declines in overall stroke mortality, stroke remains a leading cause of death and disability. The aphorism “Time is Brain” highlights the degree to which brain tissue depends on an uninterrupted blood supply. Saver quantified the urgency of stroke treatment and calculated that the typical stroke patient loses 1.9 million neurons each minute following stroke onset: “Compared with the normal rate of neuronal loss in brain aging, the ischemic brain ages 3.6 years each hour without treatment”.4 By comparison, someone who suffers a myocardial infarction (MI) can lose 10% of myocardial tissue and still run a marathon but losing much less than 10% of certain brain tissue segments can result in devastating disability.4

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A mechanistic approach is helpful in evaluating stroke patients and is the basis for the organization of this chapter. The main division is between ischemic (IS) and hemorrhagic stroke (HS). Determination of ischemic subtype is made after the immediate evaluation, and eligibility for thrombolysis does not depend on IS subtype. There are several IS classifications, but the TOAST classification is the most useful, with a mechanistic scheme consisting of five major categories: (1) large-vessel atherothromboembolic stroke; (2) cardioembolic stroke; (3) small-vessel stroke; (4) stroke of other determined etiology; and (5) stroke of undetermined etiology.5 The strength of the modified TOAST scheme is that it incorporates newer imaging modalities in the definition of IS subtypes.6 This mechanistic approach provides a framework ...

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