Abstract:

The present study was undertaken to clarify the role of 丫-aminobutyric acid(GABA) in the pathophysiology of tardive dyskinesia. GABA concentrations in CSF were m easured in 14 schizophrenic patients without tardive dyskinesia, 15 schizophrenic patients with tardive dyskinesia and 18 neurologic patients without psychotic symptoms. In addition, GABA concentrations in CSF and clinical improvement of tardive dyskinesia w ere checked for dyskinetic schizophrenics after 8 weeks of treatm ent with sodium valproate, the GABAergic drug. Results were as follows: 1 ) A significant reduction in CSF GABA levels was observed in dyskinetic schizophrenics compared with the neurologic patients. 2) CSF GABA levels in schizophrenic patients without tardive dyskinesia were not significantly differnet from those in neurologic patients, although the data suggested a decrease in CSF GABA levels in schizophrenic patients. 3) A significant decrease in dyskinetic symptoms occurred with the administration of sodium valproate, associated with increase in CSF levels of GABA. The results of this study can be taken as a strong suggestion that GABA system is involved in the pathophysiology of tardive dyskinesia.