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纹状体异常与非临床精神病中的自发性运动障碍。

Striatal abnormalities and spontaneous dyskinesias in non-clinical psychosis.

机构信息

University of Colorado Boulder, Department of Psychology and Neuroscience, United States; University of Colorado Boulder, Center for Neuroscience, United States.

出版信息

Schizophr Res. 2013 Dec;151(1-3):141-7. doi: 10.1016/j.schres.2013.10.003. Epub 2013 Oct 22.

Abstract

BACKGROUND

Accumulating evidence suggests that individuals experiencing non-clinical psychosis (NCP) represent a critical group for improving understanding of etiological factors underlying the broader psychosis continuum. Although a wealth of evidence supports widespread neural dysfunction in formal psychosis, there has been little empirical evidence to inform our understanding of putative vulnerability markers or brain structure in NCP. In this study, we examined the neural correlates of spontaneous movement abnormalities, a biomarker previously detected in NCP that is linked to abnormalities in the striatal dopamine.

METHODS

We screened a total of 1285 adolescents/young adults, and those scoring in the upper 15th percentile on a NCP scale were invited to participate; 20 of those invited agreed and these individuals were matched with healthy controls. Participants were administered a structural scan, clinical interviews, and an instrumental motor assessment.

RESULTS

The NCP group showed elevated force variability and smaller putamen (but not caudate), and there was a significant relationship between motor dysfunction and striatal abnormalities for the sample. Elevated force variability was associated with both higher positive and negative symptoms, and there was a strong trend (p=.06) to suggest that smaller left putamen volumes were associated with elevated positive symptoms.

CONCLUSIONS

The results are among the first to suggest an association between neural structure and a risk marker in NCP. Findings indicate that vulnerabilities seen in schizophrenia also characterize the lower end of the psychosis spectrum.

摘要

背景

越来越多的证据表明,经历非临床精神病(NCP)的个体代表了一个关键群体,可以帮助我们更好地理解精神病谱广泛存在的病因因素。尽管有大量证据支持正式精神病中广泛的神经功能障碍,但几乎没有实证证据可以帮助我们了解 NCP 中的潜在脆弱性标志物或大脑结构。在这项研究中,我们研究了自发性运动异常的神经相关性,这是 NCP 中之前检测到的生物标志物,与纹状体多巴胺异常有关。

方法

我们共筛选了 1285 名青少年/年轻人,邀请那些在 NCP 量表上得分在前 15%的人参加;邀请了 20 人,他们同意参加,这些人被与健康对照组相匹配。参与者接受了结构扫描、临床访谈和仪器运动评估。

结果

NCP 组表现出较高的力变异性和较小的纹状体(但不是尾状核),并且样本中运动功能障碍与纹状体异常之间存在显著关系。较高的力变异性与较高的阳性和阴性症状都有关,并且存在强烈的趋势(p=.06)表明,左侧纹状体体积较小与阳性症状升高有关。

结论

这些结果是首次表明 NCP 中的神经结构与风险标志物之间存在关联的研究之一。研究结果表明,精神分裂症中出现的脆弱性也表现为精神病谱的低端。

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