• A double-blind, placebo-controlled trial of γ-vinyl γ-aminobutyric acid (GVG) and 4,5,6,7-tetrahydroisoxazolo-(5,4-c) pyridine-3-ol (THIP) was carried out in drug-free schizophrenic patients with tardive dyskinesia. A significant decrease in dyskinetic symptoms occurred with the administration of GVG, associated with a twofold increase in cerebrospinal fluid levels of GABA; THIP produced a more moderate, yet consistent decrease in the involuntary movements. A pathophysiologic role for γ-aminobutyric acid (GABA)-mediated neuronal transmission in tardive dyskinesia was explored by analyzing cerebrospinal fluid GABA concentrations in drugfree schizophrenic patients with and without tardive dyskinesia. A significant reduction in cerebrospinal fluid levels of GABA was observed in the dyskinetic schizophrenics compared with the nondyskinetic controls. These data compliment a growing body of experimental evidence suggesting a critical role for GABA-ergic neurons in the pathophysiology of tardive dyskinesia.
Thaker GK, Tamminga CA, Alphs LD, Lafferman J, Ferraro TN, Hare TA. Brain γ-Aminobutyric Acid Abnormality in Tardive Dyskinesia: Reduction in Cerebrospinal Fluid GABA Levels and Therapeutic Response to GABA Agonist Treatment. Arch Gen Psychiatry. 1987;44(6):522–529. doi:10.1001/archpsyc.1987.01800180032006
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