Glutamatergic dysfunction in catatonia? Successful treatment of three acute akinetic catatonic patients with the NMDA antagonist amantadine.
Therapeutic efficiacy of the NMDA antagonist amantadine is reported in three acute neuroleptic free akinetic catatonic patients. Intravenous infusion of amantadine led to the resolution of catatonic symptoms and considerable reductions of scores in various motor scales (Simpson Angus scale for extrapyramidal side effects (SEPS), the abnormal involuntary movement scale (AIMS), Rogers catatonia and schizophrenia scales). The therapeutic effect of amantadine showed a characteristic temporal pattern with most pronounced effects four to six hours after administration and recurrence of catatonic symptoms by 24 hours later, at least partially. Such a temporal pattern of therapeutic efficacy and decreasing efficacy occurred in all three patients on all days. The results suggest the central importance of glutamatergic dysfunction in catatonic syndrome.
Northoff
G
G
Department of Psychiatry, University of Frankfurt, Germany.
Eckert
J
J
Fritze
J
J
D000328:Adult; D000547:Amantadine / Q000627:therapeutic use*; D002389:Catatonia / Q000188:drug therapy* / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors*
D018698:Glutamic Acid; D016202:N-Methylaspartate; D000547:Amantadine