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Atherosclerotic Infarction
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Atherosclerotic plaque at a bifurcation or curve in one of the larger vessels leads to progressive stenosis with the final large artery occlusion due to thrombosis of the narrowed lumen. Arteriosclerotic plaques may develop at any point along the carotid artery and the vertebral-basilar system, either extracranial or intracranial. The most common sites are the bifurcation of the common carotid artery into the external and internal carotid arteries, the origins of the middle and anterior cerebral arteries, and the origins of the vertebral from the subclavian arteries. The site of infarction depends on the collateral flow, but is usually in the distal fields or border zones. Specifying the degree of stenosis that will lead to perfusion difficulty is dependent on multiple factors and is often not easily defined. Classification schemes have relied on stenoses greater than 70 to 80% as more predictive of impending hemodynamic compromise.
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Infarcts are also produced by emboli arising from the proximally-situated atheromatous lesions to otherwise healthy branches located more distal in the arterial tree. This mechanism of infarction has earned its own category, tandem arterial pathology. Embolic fragments may arise from extracranial arteries affected by stenosis or ulcer; stenosis of any major cerebral artery stem; the stump of the occluded internal carotid artery; and even from intracranial tail of the anterograde thrombus atop an occluded carotid. Making the diagnosis of an antherosclerotic infarction depends upon finding a stenosis or occlusion on carotid/vertebral Duplex Doppler, transcranial Doppler, magnetic resonance angiography, or even conventional cerebral angiography.

Cardiac Embolism

The most common sources of cardiac embolism include: atrial fibrillation, valvular heart disease (mitral stenosis, mitral regurgitation, rheumatic heart disease); intracardiac thrombus particularly along the left ventricular wall (mural thrombus) after anterior myocardial infarction or in the left atrial appendage in patients with atrial fibrillation; ventricular or septal aneurysm; and cardiomyopathies leading to stagnation of blood flow and an increased propensity for the formation of intracardiac thrombus.
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Embolism is inferred when the brain image demonstrates an infarction confined to the cerebral surface territory of a single branch, combinations of infarcts involving branches of different divisions of major cerebral arteries, or hemorrhagic infarction. The difficult problem in arriving at a diagnosis of embolism is the identification of the occluding particle and the source. Mural thrombi and platelet aggregates are remarkably evanescent, as has been inferred by findings on angiography. Embolic fragments are found in over 75% of cases angiogramed within 48 hours of onset of the stroke, and are then gone when angiogram is repeated later. Embolic obstruction of an arterial lumen is cleared most commonly by recanalization and fibrinolysis. The evanescent quality of emboli may explain the wide variation in the frequency with which this subtype is diagnosed in retrospective or prospective studies of stroke.
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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.
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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.
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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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Introduction
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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.
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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.
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In light of these studies, the ACIP and the American Academy of Pediatrics (AAP) formulated a series of recommendations for the routine use of varicella vaccine. Varicella vaccine may be given simultaneously with measles-mumps- rubella vaccine (MMR), but the vaccines should not be mixed in one syringe or administered in the same site. No data suggest any adverse interaction between varicella and other vaccines administered routinely to children. Postimmunization serologic testing is not recommended for young children or adolescents. For health care workers employed in areas with immunocompromised children, postimmunization serologic testing may be helpful in documenting seroconversion and simplifying management of exposures in high-risk areas.
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The vaccines are not licensed for use in immunocompromised children or adults, including those who have congenital immunodeficiency, blood dyscrasias, leukemia, lymphoma, symptomatic HIV infection, or those receiving immunosuppressive agents or corticosteroids (2 mg/kg per day or greater for longer than 1 month). No precautions need to be taken in immunized patients whose families contain immunocompromised members because transmission of vaccine virus has been documented infrequently, and the virus has been shown to retain its attenuated phenotype. However, if a rash develops in the vaccinee, contact with immunosuppressed patients should be avoided for the duration of the rash. Varicella vaccine may be given to patients who have acute lymphocytic leukemia after they have been in remission for 1 year and have a lymphocyte count greater than 700/mcL and a platelet count greater than 100,000/mcL within 24 hours of immunization. Patients who have undergone immunosuppressive therapies may be vaccinated after at least 3 months has passed and evidence of immune suppression is lacking. Patients receiving greater than 2 mg/kg of systemic cortico-steroid therapy must be off steroids for at least 1 month prior to receiving the vaccine. Inhaled or intranasal corticosteroids are not a contraindication to varicella vaccination.
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With routine administration of varicella vaccine to all young children and to those individuals not previously infected, there is reason to believe that chickenpox can be eliminated. Maxaman