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79 Stroke

Stroke refers to acute vascular events involving the brain or brainstem. Childhood stroke occurs at a rate approximating that of childhood brain tumors. It is among the top 10 causes of death in children and is a significant cause of morbidity among survivors. Pediatric stroke can be subdivided into perinatal stroke, occurring from 28 weeks of gestation to 1 month of age, and childhood stroke, occurring from 1 month to 18 years. Important subtypes of stroke include arterial ischemic stroke (AIS), watershed infarction, intracerebral hemorrhage (ICH), and cerebral sinus venous thrombosis (CSVT). AIS is usually defined as an acute neurologic deficit of any duration consistent with focal brain ischemia conforming to an arterial distribution. Transient ischemic attacks (TIAs) are defined as focal deficits in a vascular territory lasting less than 24 hours, with some authors including the caveat that there must be no magnetic resonance imaging (MRI) evidence of infarction (Figure 79-1).

Etiology and Pathogenesis

Estimates of the incidence of stroke in children range from two to 13 per 100,000 children per year. As opposed to adults in which ICH accounts for about 15% of stroke, ICH accounts for about half of pediatric stroke. The incidence of perinatal stroke is approximately one per 4000 live births, with 80% of these secondary to AIS. One-quarter of all strokes in children take place during the perinatal period. The incidence of cerebral venous sinus thrombosis is approximately 0.3 to 0.7 per 100,000 per year, with almost half of these occurring in the perinatal period. Strokes are more common in boys than in girls, with 55% to 60% of all childhood strokes occurring in boys. In the United States, strokes are more common among African American children, even when controlling for the presence of sickle cell disease (SCD).

Unlike adults, in whom hypertension, diabetes, and atherosclerosis predominate as risk factors for ischemic stroke, children presenting with AIS have much more varied etiologies. Approximately 50% of children presenting with stroke have an obvious underlying cause at the time of presentation, with arteriopathy, congenital heart disease, and sickle cell anemia representing some of the most common causes. In an additional 20% to 40%, an underlying cause can be found with further investigation. Somewhere between 10% and 30% are cryptogenic. Factors associated with pediatric AIS include inherited or acquired prothrombotic states, cardiac disease, arteriopathies or vasculopathies, trauma, and infections (Box 79-1). In older teenagers, traditional risk factors for adults, such as hypertension, diabetes, high cholesterol, and smoking, may also play a role. Cocaine or sympathomimetic medications are additional risk factors. Watershed strokes can be seen after cardiac arrest or other causes of shock, near drowning, and cardiac surgery.

Box 79-1 Etiologies of Pediatric Arterial Ischemic Stroke








CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; CNS, central nervous system; MELAS, mitochondrial encephalopathy with lactic acidosis and strokelike episodes.

ICH in children is also etiologically distinct from ICH in adults. Unlike adults, in whom hypertension and amyloid angiopathy are the most common causes, childhood ICH is most commonly caused by ruptured vascular malformations (e.g., arteriovenous malformations, cavernomas, and aneurysms), hematologic abnormalities, and brain tumors (Box 79-2 and Figure 79-2).

The major risk factors for CSVT include dehydration, head and neck infections, hypercoagulable states, malignancies, congenital heart disease, inflammatory bowel disease, oral contraceptives, and the use of certain chemotherapeutics.

AIS occurs when occlusion of an artery with a thrombus or embolus prevents blood flow to the region supplied by that artery. In watershed infarctions, global or near-global hypoperfusion preferentially damages areas on the border of two different vascular territories. The end result is a complex chain of events in cerebral neurons and support cells in which lack of oxygen and glucose leads to mitochondrial dysfunction, ion pump failure, calcium influx, and glutamate-induced neurotoxicity, eventually producing cell necrosis or apoptosis. The extent of ischemic damage to the region is determined by oxygen demand, collateral blood flow, and time to reperfusion. After an acute ischemic insult, there is a core area of infarction in which cells have sustained irreversible injury. This core is surrounded by an area with reversible ischemia known as the ischemic penumbra. If no further improvement of blood flow takes place or if additional insults occur, the tissue within the penumbra will eventually infarct over a period of hours to days, potentially causing additional neurologic impairment. In TIAs perfusion is restored before infarction can take place, and neuronal dysfunction induced by ischemia is reversed.

In ICH, blood extravasates into the brain parenchyma (intraparenchymal hemorrhage) into the ventricles (intraventricular hemorrhage), or into the subarachnoid space (subarachnoid hemorrhage). Intraparenchymal hemorrhage causes neuronal damage through a combination of mechanical damage and chemical irritation. Secondary ischemic stroke can occur as well because of mechanical deformation of cerebral vasculature by mass effect, vasospasm, and altered pressure dynamics leading to decreased cerebral perfusion pressure. Intraventricular hemorrhage can lead to hydrocephalus.

In CSVT, obstruction of venous blood by clot formation alters blood flow dynamics and overall venous drainage is decreased. Increased cerebral venous pressure causes resistance to cerebral perfusion and can cause venous infarction or hemorrhage. All contribute to increasing intracranial pressure (ICP).

Clinical Presentation

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