Neural damage in the lenticular nucleus linked with tardive dyskinesia in schizophrenia: a preliminary study using proton magnetic resonance spectroscopy

被引:17
作者
Ando, K
Takei, N
Matsumoto, H
Iyo, M
Isoda, H
Mori, N
机构
[1] Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan
[2] Inst Psychiat, London, England
[3] Chiba Univ, Sch Med, Dept Psychiat & Neurol, Chiba 280, Japan
[4] Hamamatsu Univ Sch Med, Dept Radiol, Hamamatsu, Shizuoka 43131, Japan
关键词
magnetic resonance spectroscopy; tardive dyskinesia; schizophrenia; basal ganglia system; choline;
D O I
10.1016/S0920-9964(01)00290-0
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
We investigated, using proton magnetic resonance spectroscopy (H-1-MRS), whether the tardive dyskinesia (TD) often seen in schizophrenic patients is associated with cellular abnormalities in the basal ganglia system. The subjects in (his study included schizophrenic patients with TD (TD group. n = 7), schizophrenic patients without TD (non-TD group, n = 7), and healthy volunteers (N group, n= 7). We examined the H-1-MRS peaks of N-acetylaspartate (NAA), choline (Cho), and creatine (Cr) in the regions of the left and right lenticular nucleus. In the left lenticular nucleus, the Cho/Cr ratio was significantly greater in the TD and non-TD groups than in the N group (Mann-Whitney U test; p < 0.007 and p < 0.006, respectively). Further, a significant linear trend was observed in the means of the ratio across the three groups (p < 0.005) the TD group was the highest, the N group the lowest, and the non-TD group intermediate. No significant difference in the NAA/cr ratio was found among groups. These results indicate that neural abnormalities in the basal ganglia may be linked with the neuroleptic medications and the process of the fundamental illness per se, and that more excessive damage to this neural substrate may lead to development of TD. However, as this is a preliminary study, further studies with a large number of subjects are required to verify our findings. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:273 / 279
页数:7
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