Prevention of neuronal cell death by anticonvulsants in experimental epilepsy (extended abstract).
In human temporal lobe epilepsy, neuronal cell damage is found in the hippocampus (1) as well as in the amygdaloid complex (2) and entorhinal cortex (3). Data from animal studies show that recurrent seizures selectively injure certain populations of neurons in the temporal lobe structures (4). Whether or not recurrent seizures cause neuronal damage in human epilepsy is still under investigation. A new challenge for anti-epilepsy medication is not only to suppress clinical seizures but also to prevent any neuronal damage caused by the seizures.
D000679:Amygdala / Q000187:drug effects / Q000473:pathology; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000473:pathology; D002220:Carbamazepine / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology; D006801:Humans; D007696:Kindling, Neurologic / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D013226:Status Epilepticus / Q000473:pathology*; D013702:Temporal Lobe / Q000187:drug effects / Q000473:pathology; D020888:Vigabatrin; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives* / Q000494:pharmacology
D000927:Anticonvulsants; D002220:Carbamazepine; D005680:gamma-Aminobutyric Acid; D020888:Vigabatrin