title: Petit mal epilepsy: a review and integration of recent information.
abstract: Petit mal (absence) epilepsy remains one of the most enigmatic of neurological disorders, and there is no widely accepted theory of its etiology. This review covers some of the current issues concerned with the disorder, including treatment and prognosis, neurochemical research, behavioral and psychophysiological effects of wave-spiked discharges, and EEG studies of seizure control. With respect to treatment, although effective drug therapy (valproic acid, ethosuximide) exists for the "pure" form of absence epilepsy, other forms, in which there is an admixture of grand mal seizures, are less amenable to pharmacotherapy. Moreover, the frequency of fatal hepatic toxicity following valproic acid therapy has been estimated at 1 in 20,000. With respect to prognosis, follow-up studies indicate that many patients do not outgrow the disorder but continue to suffer absence seizures well into adulthood. In recent years, there has been considerable research on the neurochemical basis of absence epilepsy. Current theories, including those that implicate gamma-aminobutyric acid, catecholamines, and "endogenous" epileptogens, are summarized; and requirements for an experimentally induced animal model of absence epilepsy are discussed. The majority of behavioral studies of the disorder have concerned the effects of petit mal-type discharges on sensory and cognitive processes. Some of these studies are reviewed; and recent work bearing on these issues, involving event-related brain potentials, is presented. Our review concludes with a discussion of research aimed at the development of electrophysiologically based approaches to the reduction of seizure frequency in patients with absence epilepsy.
mesh_terms: D000293:Adolescent; D000328:Adult; D000927:Anticonvulsants / Q000627:therapeutic use; D001569:Benzodiazepines / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D003071:Cognition; D003704:Dementia / Q000378:metabolism; D004569:Electroencephalography; D004594:Electrophysiology; D004832:Epilepsy, Absence / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D005071:Evoked Potentials; D006801:Humans; D009048:Motor Skills; D009638:Norepinephrine / Q000378:metabolism; D011379:Prognosis; D012677:Sensation; D012978:Sodium Oxybate / Q000378:metabolism; D014635:Valproic Acid / Q000009:adverse effects / Q000627:therapeutic use; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000927:Anticonvulsants; D001569:Benzodiazepines; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid; D012978:Sodium Oxybate; D009638:Norepinephrine