Seizures

Recent advances in neuroimaging have yielded additional information regarding the development of cerebral edema associated with seizures. Although cerebral edema is unlikely to be clinically manifest following most seizure activity, additional pathophy-siologic insight has been gleaned from recent reports of magnetic resonance imaging (MRI) in status epilepti-cus (Fig. 9). Prolonged seizure activity may lead to neuronal energy depletion with eventual failure of the Na + /K+ ATPase pump and concomitant development of cytotoxic or ischemic edema. Unlike ischemia produced by occlusion of a cerebral artery, a more heterogeneous cellular population is affected. The reactive hyperemic response driven by excessive metabolic demands increases the hydrostatic forces across a BBB already damaged by the vasogenic component of ischemic edema. The disruption of normal ionic

gradients, extracellular accumulation of excitotoxic factors, and lactic acidosis further exacerbate vaso-genic edema. Consequently, cessation of seizure activity usually results in the complete resolution of cerebral edema.

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