MEG Studies of P50 Suppression in Schizophrenia

描述（由申请人提供）：在听觉配对刺激范例中，精神分裂症受试者的S1和S2振幅之间的差异小于正常人。一系列报告表明，这种效应是由患者中较小的S1振幅引起的，而不是较大的S2振幅。这些发现与其他关于精神分裂症听觉信息处理的研究报告一致，也许揭示了一种模式，其中包含有关这种疾病神经病理学相关性的重要线索。拟议的研究将通过使用143通道MEG和密集阵列EEG研究听觉诱发反应（AER）的认知和感觉相关性来评估这种可能性。我们将使用稳态刺激和听觉oddball和范式，以帮助澄清（1）皮层神经元反应率的限制和相关的能力，整合信息随着时间的推移在听觉处理精神分裂症，（2）精神分裂症患者对简单听觉刺激的群体加工是否可以通过以“可管理”的速率夹带神经元活动而正常化（这将对理解精神分裂症中背景脑状态和听觉处理之间的关系具有意义），以及（3）精神分裂症中的听觉处理异常是否主要与左半球功能障碍相关并且是幻听存在的预测因子，以及（4）继发于左侧听觉皮层功能障碍的大脑半球间通讯是否是精神分裂症患者听觉识别异常的原因。分析将依赖于当前的分布式源重建，在源和传感器空间的频谱相干性的措施，频谱功率的措施，和偶极子建模使用现实的头部模型。据推测，精神分裂症患者有一个有限的能力，随着时间的推移，整合信息继发于神经元反应率的低上限，这种影响主要是由于左听觉皮层功能障碍。事实上，精神分裂症患者的右侧听觉皮层功能正常。由于精神分裂症患者的听觉信息处理系统的低采样率，他们很难恢复最初的刺激信息，这种异常可能促进幻觉现象的发展。此外，左听觉皮层功能障碍阻碍了正常的半球间交流，这干扰了在oddball型范式期间测量的产生正常的兴奋型反应的能力。

DESCRIPTION (provided by applicant): During auditory paired-stimulus paradigms, schizophrenia subjects have smaller differences between S1 and S2 amplitudes than normal. A series of reports indicate this effect results from smaller S1 amplitudes, not larger S2 amplitudes, among patients. These findings are consistent with reports from other studies of auditory information processing in schizophrenia, perhaps revealing a pattern that contains important clues about the neuropathological correlates of this illness. The proposed research will evaluate this possibility by studying the cognitive and sensory correlates of auditory evoked responses (AERs) using 143-channel MEG and dense array EEG. We will use steady-state stimulation and auditory oddball and paradigms to help clarify (1) The limits on cortical neuronal response rates and the associated ability to integrate information over time during auditory processing in schizophrenia, (2) whether group processing of simple auditory stimuli can be normalized among schizophrenia patients by entrainment of neuronal activity at a 'manageable' rate (which will have implications for understanding the relationship between background brain states and auditory processing in schizophrenia), and (3) whether auditory processing abnormalities in schizophrenia is primarily associated with left hemisphere dysfunction and is a predictor of presence of auditory hallucinations, and (4) whether interhemispheric communication secondary to dysfunction of left auditory cortex is a cause of auditory recognition abnormalities among schizophrenia patients. Analyses will rely on current distributed source reconstructions, measures of spectral coherence in source and sensor space, measures of spectral power, and dipole modeling using realistic head models. It is hypothesized that schizophrenia patients have a limited ability to integrate information over time secondary to a low ceiling on neuronal response rates and that this effect is primarily due to left auditory cortex dysfunction. Indeed, right auditory cortex will be found to function normally among schizophrenia patients. Because of a low sampling rate on schizophrenia patients' auditory information processing systems, they have difficulty recovering the initial stimulus information, an abnormality that could facilitate the development of hallucinatory phenomena. In addition, dysfunction of left auditory cortex impedes proper inter-hemispheric communication, which interferes with the ability to generate normal recognition-type responses measured during oddball-type paradigms.