the spread and recurrence of isolated seizures [10,11]. Failure occurs because excitation is excessive and/or inhibition is ineffective. Multiple mechanisms probably are involved. Glutamate is the major amino acid excitatory neurotransmitter in the brain. Its role in the pathogenesis of SE was suggested by an outbreak of illness caused by eating mussels contaminated with domoic acid, an analogue of glutamate [12]. Some affected individuals had prolonged seizures thought to be caused by excessive activation of excitatory amino acid receptors. Other excitatory neurotransmitters that contribute to SE include aspartate and acetylcholine [11]. Gammaaminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain, and antagonists to its effects or alternations in its metabolism in the substantia nigra may contribute to SE [13]. In a rat model, for example, the rate of GABA synthesis in the substantia nigra declined significantly during induced SE [14]. Other inhibitory mechanisms include the calcium iondependent potassium ion current and blockage of Nmethyld aspartate (NMDA) channels by magnesium. Neuronal loss — Though the outcome of SE generally is favorable in the absence of an underlying neurologic condition, minor amounts of neuronal loss are thought to occur with every episode, particularly if prolonged. (See 'Outcome' below.) Over time, this loss may accumulate and lead to significant impairment. Disturbance of the NMDA channels appears to be an important mechanism of neuronal injury in SE [11]. When neurons are depolarized, calcium enters the cell through NMDA channels and causes injury or death. Other possible contributing factors include hypoxia, excessive release of excitatory amino acids and calcium, increases of various proteins, including those that promote apoptosis (programmed cell death), alterations in receptor populations, and, in the temporal lobe, sprouting of dentate granule cells [15,16]. Abnormalities on magnetic resonance imaging (MRI) and release of the neuronspecific enolase are markers of neuronal damage.
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