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BRIEF COMMUNICATION Low superoxide dismutase activity in schizophrenic patients with tardive dyskinesia

Published online by Cambridge University Press:  01 September 1997

K. YAMADA
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
S. KANBA
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
S. ANAMIZU
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
K. OHNISHI
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
I. ASHIKARI
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
G. YAGI
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
M. ASAI
Affiliation:
From the Department of Neuropsychiatry, School of Medicine, Keio University, Tokyo, Japan
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Abstract

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Background. Tardive dyskinesia (TD) is a therapy-resistant adverse effect of neuroleptics. Although the exact pathophysiology of TD is unknown, oxygen radicals have been speculated to play a role in TD based on several lines of evidence. Superoxide dismutase (SOD) is a key enzyme which scavenges oxygen radicals. The authors investigated the association between erythrocyte SOD activity and TD.

Methods. Erythrocyte SOD activities were measured, blinded as to the presence or absence of TD, in 30 patients with schizophrenia who had been on typical neuroleptics for more than 10 years. TD severity was independently assessed, using the abnormal involuntary movement scale (AIMS), by two raters.

Results. There was a significant decrease in erythrocyte SOD activity in the definite TD group (N=10) as compared with the no TD (N=8) and questionable TD (N=12) groups. Erythrocyte Cu,Zn-SOD activities correlated with AIMS scores.

Conclusions. Patients with TD had low SOD activities as compared to those without TD. As a causal link between SOD activity and TD was not established in this study, larger prospective studies are warranted to determine whether patients with low SOD activity are susceptible to neuroleptic-induced TD.

Type
Brief Report
Copyright
1997 Cambridge University Press