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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