Ischemic stroke continues to have a major impact on the public health of our nation. Ranking among the leading causes of death, stroke is far more disabling than fatal and results in enormous costs measured in both health-care dollars and lost productivity. Once considered untreatable, ischemic stroke has become subject to intensive scrutiny in recent years. Considerable research has led to a better delineation of risk factors, as well as an expanded understanding of pathophysiologic subtypes. Innovative acute therapies are being applied in a manner analogous to the treatment of acute myocardial infarction that emerged more than a decade ago. There are still many unanswered questions regarding the most effective therapies to prevent first or recurrent stroke, however recent clinical trials have helped clarify the best options for stroke prevention in a variety of settings.
Definitions of TIA and Stroke
Ischemic stroke is characterized by the abrupt or ictal onset of neurologic dysfunction due to inadequate perfusion of the brain. By conventional clinical definitions, if the neurological symptoms continue for more than 24 hours, a person is diagnosed with ischemic stroke. Otherwise, a focal neurological deficit lasting less than 24 hours is defined as a transient ischemic attack (TIA). However, with the advent of more sensitive brain imaging, acute cerebral infarcts have been identified even when symptoms last less than 24 hours. The most recent definition of ischemic stroke for clinical trials has required either symptoms lasting more than 24 hours or imaging an acute, clinically-relevant infarct among those with rapidly vanishing symptoms. When the diagnosis of stroke is made, the duration and severity of the clinical syndrome helps classify it as minor or major ischemic stroke.
Definition of the Infarct Subtype
There are multiple mechanisms which may lead to brain ischemia. Hemodynamic infarction originates when there is an impediment to normal perfusion usually caused by a severe arterial stenosis or occlusion due to atherosclerosis and coexisting thrombosis. Embolism occurs When a particle of thrombus originating from a more proximal source (arterial or cardiac) travels through the vascular system and leads to a distal occlusion. Small vessel disease occurs when lipohyalinosis or local atherosclerotic disease leads to an occlusion of a small penetrating artery. Less frequent conditions which lead to reductions in cerebral perfusion and result in infarction are: arterial dissection, primary or secondary vasculitis, hypercoagulable states, vasospasm, systemic hypotension, hyperviscosity, moyamoya disease, fibromuscular dysplasia, extrinsic compression of the major arteries by tumor and occlusion of the veins that drain the brain. The relative frequency of each major subtype of infarction varies from study to study. The proportion with cardioembolic or lacunar infarcts is approximately 15% to 30% each, atherosclerotic infarcts occur in 15% to 40%, and less common causes account for about 5%. Infarcts of indeterminate cause comprise as many as 40% of strokes in some series.
The infarct subtype categories are far from ideal with many examples of controversies regarding classification, reliability and validity. The distribution of infarct subtypes depends upon the sample from which cases are drawn (hospital or population-based), the geographic region of the study, the demographic and risk factor profile of the cohort, the timing and sophistication of the work-up and the design of investigator-driven diagnostic algorithms. Part of the difficulty regarding classification of ischemic stroke stems from the inability to discriminate between infarct subtypes on clinical grounds alone. Some clinical characteristics are helpful in distinguishing subtypes, such as fractional arm weakness (shoulder different from the hand), hypertension, diabetes, and male gender which are more frequently found in the atherosclerotic category. Besides a greater frequency of cardiac disease, patients with cardioembolic infarction more often present with reduced consciousness and have an abrupt onset. However, clinical features at stroke onset are not reliable enough to lead to a definite determination of infarct subtype without confirmatory laboratory data.
Brain imaging with head computerized tomography (CT) or magnetic resonance imaging (MRI) will clearly separate hemorrhage from infarction and small, deep infarcts from larger, cortical or deep infarcts. Differentiating the underlying mechanism of the brain infarct is rarely possible based solely on the infarct topography. Non-invasive duplex Doppler and transcranial Doppler helps identify those with large artery carotid, vertebral or intracranial stenosis or occlusion. However, the relevance of findings such as a 40-60% carotid stenosis is still questionable. Corroborating evidence regarding the status of the cerebral vasculature is obtained from magnetic resonance angiography and conventional cerebral angiography. Electrocardiography and transthoracic echocardiography identify potential cardioembolic sources such as atrial fibrillation, valvular disease, anterior wall myocardial infarction, and intracardiac thrombus. The etiologic significance of other findings such as mitral valve prolapse, mitral annular calcification and patent foramen ovale need to be decided based upon the presenting clinical syndrome. Newer technologies such as transesophageal echocardiography and hematologic testing have helped classify some patients who might have been classified as cryptogenic in the past. The final decision regarding the infarct subtype requires considering the presenting clinical syndrome in conjunction with the pertinent positive and negative findings from brain, vascular and cardiac imaging studies.
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