Anterior cingulate abnormality as a neural correlate of mismatch negativity in schizophrenia

Anterior cingulate abnormality as a neural correlate of mismatch negativity in schizophrenia
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前扣带回异常与精神分裂症失配负性的神经相关性

DOI:
10.1159/000355296
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发表时间:
2013
期刊:
Neuropsychobioloy
影响因子:
--
通讯作者:
Aoki S
Aoki S
中科院分区:
--
文献类型:
--
作者:
Hayakawa Y;Kirino E;Shimoji K;Kamagata K;Hori M;Ito K;Kunimatsu A;Abe O;Ohtomo K;Aoki S

文献摘要

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脑边缘回路,尤其是前扣带回,与精神分裂症的病理生理和认知变化有关。先前的弥散张量成像研究表明,精神分裂症患者前扣带(AC)的完整性异常。然而,AC束完整性异常与精神分裂症病理生理的关系尚未得到充分的研究。方法采用基于束的空间统计方法,对9例精神分裂症患者和9例对照组的脑白质分数各向异性(FA)进行体素组比较。然后,我们通过使用特定的通道测量来测量AC中的FA。同时对所有受试者的失配负性(MMN)潜伏期和振幅进行评估。结果在精神分裂症患者中,基于神经束的空间统计显示,与对照组相比,包括双侧AC在内的广泛白质区域FA减少。通道特异性测量证实了双侧AC区域FA的特异性减少。AC中FA的减少与患者组MMN潜伏期延长相关。结论我们对精神分裂症患者AC结构和电生理变化的研究表明,边缘-皮层结构网络的破坏可能是精神分裂症患者MMN变化的神经基础的一部分。
BackgroundLimbic circuitry, especially the anterior cingulate gyrus, has been implicated in the pathophysiology and cognitive changes of schizophrenia. Previous diffusion tensor imaging studies have demonstrated that the integrity of the anterior cingulum (AC) is abnormal in schizophrenia. However, the relationship between the abnormal AC tract integrity and the pathophysiology of schizophrenia has not been fully studied.MethodsWe performed a voxelwise group comparison of white matter fractional anisotropy (FA) by using tract-based spatial statistics in 9 patients with schizophrenia and 9 matched controls. We then measured FA specifically in the AC by using a tract-specific measurement. The latency and amplitude of the mismatch negativity (MMN) were also evaluated in all subjects.ResultsIn patients with schizophrenia, tract-based spatial statistics showed a reduction in FA in broad white matter areas, including the bilateral AC, compared with controls. Tract-specific measurements confirmed the specific reduction of FA in the region of the bilateral AC. The decreased FA in the AC was correlated with prolonged MMN latency in the patient group.ConclusionOur study of AC structure and electrophysiological changes in schizophrenia suggest that the disruption of limbic-cortical structural networks may be part of the neural basis underlying the changes in MMN in schizophrenia.