Treatment of Parkinson's disease with sodium valproate: clinical, pharmacological, and biochemical observations.
Because there is biochemical evidence of decreased GABAergic function in Parkinson's disease, sodium valproate, an inhibitor of GABA catabolism, was administered to eight Parkinsonian patients. Valproate treatment did not significantly alter any Parkinsonian feature, but tended to increase the dyskinesia in the "on-off" patients. The increased dyskinesias were not a result of altered peripheral metabolism of L-dopa. Despite obtaining high plasma levels of valproate, no consistent alteration of CSF GABA levels could be demonstrated. Thus, in these patients, an effect of valproate on GABA metabolism is unproven, and in turn, the role of GABA in Parkinsonism and dyskinesia uncertain.
D000368:Aged; D002230:Carbidopa / Q000008:administration & dosage; D002986:Clinical Trials as Topic; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000134:cerebrospinal fluid / Q000188:drug therapy*; D014635:Valproic Acid / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D005680:gamma-Aminobutyric Acid / Q000134:cerebrospinal fluid
D007980:Levodopa; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid; D002230:Carbidopa