Because there is biochemical evidence of decreased GABAergic function in Parkinson's disease, sodium valproate, an inhibitor of GA BA 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.
|Original language||English (US)|
|Number of pages||7|
|Journal||Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques|
|State||Published - Aug 1979|
ASJC Scopus subject areas
- Clinical Neurology