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精神分裂症患者大脑整体信号改变。

Altered global brain signal in schizophrenia.

机构信息

Department of Psychiatry andInterdepartmental Neuroscience Program, Yale University, New Haven, CT 06511;Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven, CT 06519;

Center for Neural Science, New York University, New York, NY 06510;

出版信息

Proc Natl Acad Sci U S A. 2014 May 20;111(20):7438-43. doi: 10.1073/pnas.1405289111. Epub 2014 May 5.

DOI:10.1073/pnas.1405289111
PMID:24799682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4034208/
Abstract

Neuropsychiatric conditions like schizophrenia display a complex neurobiology, which has long been associated with distributed brain dysfunction. However, no investigation has tested whether schizophrenia shows alterations in global brain signal (GS), a signal derived from functional MRI and often discarded as a meaningless baseline in many studies. To evaluate GS alterations associated with schizophrenia, we studied two large chronic patient samples (n = 90, n = 71), comparing them to healthy subjects (n = 220) and patients diagnosed with bipolar disorder (n = 73). We identified and replicated increased cortical power and variance in schizophrenia, an effect predictive of symptoms yet obscured by GS removal. Voxel-wise signal variance was also increased in schizophrenia, independent of GS effects. Both findings were absent in bipolar patients, confirming diagnostic specificity. Biologically informed computational modeling of shared and nonshared signal propagation through the brain suggests that these findings may be explained by altered net strength of overall brain connectivity in schizophrenia.

摘要

神经精神疾病,如精神分裂症,表现出复杂的神经生物学特征,长期以来一直与分布性脑功能障碍相关。然而,尚无研究检验精神分裂症是否存在全局脑信号(GS)的改变,GS 是一种源自功能磁共振成像的信号,在许多研究中常被视为无意义的基线而被丢弃。为了评估与精神分裂症相关的 GS 改变,我们研究了两个大型慢性患者样本(n = 90,n = 71),并将其与健康受试者(n = 220)和被诊断为双相情感障碍的患者(n = 73)进行了比较。我们发现并复制了精神分裂症患者皮质功率和方差的增加,这一效应可预测症状,但被 GS 去除所掩盖。GS 效应独立于 GS 效应,精神分裂症患者的体素信号方差也增加。这些发现均不存在于双相情感障碍患者中,证实了诊断特异性。通过对大脑中共享和非共享信号传播的生物启发计算模型进行分析,这些发现可能可以通过精神分裂症患者整体脑连接强度的改变来解释。

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