Abstract

Subclinical seizure activity has gained attention from an increased understanding of the potential harmful effects of clinical seizure activity. Investigations in the most extreme case of seizure activity—status epilepticus—demonstrate that prolonged seizure activity can cause neuronal death.1 Animal experiments of convulsive status epilepticus and some models of nonconvulsive status epilepticus show that prolonged seizure activity causes immediate necrotic cell death and delayed apoptotic cell death, primarily from activation of NMDA-mediated glutamatergic excitotoxic pathways. It is reasonable to consider that briefer periods of seizure activity cause cell death and this is true in some animal models of limbic seizures. However, there are few data demonstrating that discrete seizures cause cell death in humans so caution should be exercised in directly extrapolating this to subclinical seizures. The utility of prolonged EEG monitoring in the intensive care unit has been investigated for various conditions. A decrease in …

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