Epilepsia
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The role of gamma-aminobutyric acid (GABA) transmission in the control of convulsive epileptic seizures is considered from the perspective of the actions of drugs that augment GABA transmission in the brain. In particular, the effects of a directly acting GABAA receptor agonist, muscimol, is compared with the effects of a GABA-elevating agent, gamma-vinyl GABA (GVG, vigabatrin), in animal models of convulsive seizures. Evidence indicates that there are certain regions of the brain where enhanced GABA transmission is anticonvulsant; in other regions, blockade of GABA transmission exerts anticonvulsant actions. ⋯ The direct stimulation of postsynaptic GABA receptors (by direct receptor agonists) bypasses normal mechanisms of synaptic transmission and can evoke abnormal neurological symptoms, whereas the enhancement of presynaptic availability of GABA avoids these complications. GVG acts to boost presynaptic GABA stores, which can then be utilized physiologically; this may account for the relatively low incidence of CNS-related side effects with anticonvulsant doses of GVG. It is suggested that greater attention be focused on ways of enhancing endogenous GABA availability in future drug development for the control of seizure disorders.
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Thirteen patients with "epileptic amnesic syndrome" (EAS) presented with adult-senile onset of a severe memory complaint that started before or at the same time as seizures. All were diagnosed as temporal lobe epilepsy (TLE). The seizures were stereotyped, with only short loss of contact and oral automatisms, and because they were not obvious or disturbing, they remained underdiagnosed for a long time. ⋯ Neuropsychological investigation ruled out global mental deterioration, showing only selective memory impairment in a few long-term tasks and dissociation between formal findings and the relevant memory complaint. These cases have uniform anamnestic, clinical, and neuropsychological characteristics and represent a particular clinical expression of TLE, namely EAS. We suggest that an epileptic origin be entertained in patients presenting repeated amnesic attacks resembling TGA or who complain of persistent memory disturbance, after more common etiologies have been excluded.