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Aggravation of Generalized Epilepsies
Author(s) -
Berkovic Samuel F.
Publication year - 1998
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1998.tb05115.x
Subject(s) - carbamazepine , epilepsy , medicine , sodium channel , neuroscience , generalized epilepsy , blockade , anesthesia , partial seizures , psychology , psychiatry , sodium , receptor , chemistry , organic chemistry
Summary: Generalized epilepsies are treatable with a number of antiepileptic drugs (AEDs) that are effective in different seizure types and epilepsy syndromes. The mechanisms of action of these AEDs are incompletely understood but include inhibition of low‐threshold calcium currents and of voltage‐gated sodium channels and facilitation of GABA A receptor currents. The mechanisms of aggravation are also unknown but could include elevation of brain GABA, blockade of voltage‐gated sodium channels, and idiosyncratic toxicity reactions. Anecdotal reports suggest that aggravation of generalized epilepsy can occur with virtually all AEDs. The best‐documented examples are aggravation of absences by carbamazepine and aggravation of symptomatic generalized epilepsies by vigaba‐trin. Therefore, the physician must be constantly aware of the problem of aggravation of seizures by AEDs. With careful diagnosis of the epileptic syndrome and an awareness of the problem, aggravation of seizures can be minimized.