Childhood Strokes

Childhood StrokesChildhood Strokes Description, Causes and Risk Factors: Childhood strokes, though perceived to be relatively rare, have an incidence approximately equal to pediatric brain tumors. Epidemiological studies have revealed an annual incidence of 2.5-2.7 pediatric strokes per 100,000 children. The common underlying risk factors for childhood strokes include hypertension, diabetes mellitus, atherosclerosis, cardiac arrhythmias and valvular abnormalities. In childhood, however, the potential etiologies are many and the diagnostic challenge can be formidable. Congenital cyanotic heart disease is the most frequent cause of childhood strokes. The incidence of stroke in pediatric cardiac patients is 4%, and 75% of the stokes occur within the first two years of life. Potential mechanisms of childhood strokes include: hyperviscosity and diminished oxygenation of blood, paradoxical emboli from right-to-left shunting, and emboli from vegetations secondary to valvular disease. Other abnormal structural defects predisposing to emboli include: atrial myxoma, cardiac rhabdomyoma, cardiomyopathies, bacterial endocarditis, rheumatic heart disease, and prosthetic valves. Cardiac arrhythmias, particularly atrial fibrillation, as in adults, predispose to emboli. In one third of thrombotic carotid artery occlusion, a preceding infection is noted, often in the pharynx or cervical area. Pharyngitis, cervical adenitis, tonsillitis, sinusitis, and retropharyngeal abscess have all been reported to be precursors of internal carotid artery thrombosis. The mechanism is likely to be local inflammation of the arterial wall. Cat-scratch fever, varicella, mycoplasma, and viral encephalitis have also been associated with cerebrovascular disease. A variety of hematological causes will lead to arterial ischemic disease in children, though venous occlusion and hemorrhagic events may also occur in the same disease processes. Hyperviscosity syndromes (polycythemia, hyper-leukocytosis, and thrombocytosis) can lead to arterial occlusion. Hemoglobinopathies, the prototype of which is sickle cell disease, are often complicated by stroke. The incidence of stroke in sickle cell disease is between 5% and 10%, with the median age of the first stroke being seven years of age. Recurrence without treatment occurs in up to 90% of patients, most within three years. There has been a recent recognition of the importance of hypercoagulable states. These may be genetically acquired, associated with autoimmune and other systemic disorders, or found independent of an underlying disease. Antithrombin III, protein C, and protein S are naturally occurring anticoagulants whose deficiencies are inherited as an autosomal recessive trait. These and various other mutations and deficiencies involving the coagulation cascade have been described in childhood stroke and continue to be an area of active research. Several inborn errors of metabolism are associated with cerebral infarction. Homocystinuria, due to defect of methionine metabolism, may present as a thrombotic syndrome. High levels of homocystine lead to endothelial damage and increased platelet aggregation. Young adults heterozygous for homocystinuria are also felt to be at increased risk. Stroke-like episodes in a nonvascular distribution are seen in mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). This recently described disorder is due to a mutation of mitochondrial DNA and may require muscle biopsy to confirm. Disorders of lipid metabolism continue to generate interest. Though hypercholesterolemia is emerging as a risk factor for adult cerebrovascular disease, its role in children is less certain. Progeria, familial hypoalphalipo-proteinemia, Tangier disease and several familial forms of hypercholesterolemia are conditions associated with stroke in children and young adults. Autoimmune disorders may lead to cerebrovascular disease through a vasculitis or by inducing a hypercoagulable state. A hypercoagulable state is created by antiphospholipid antibodies, which includes the lupus anticoagulant and the anti-cardiolipin antibody. In systemic lupus erythematosus, neurologic involvement is seen in over 50% of patients. Polyarteritis nodosa, Wegener's granulomatosis, Henoch-Sch

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