MEG Studies of P50 Suppression in Schizophrenia

描述（由申请人提供）：在听觉配对刺激范式中，精神分裂症受试者的S1和S2振幅差异小于正常人。一系列报道表明，这种效应是由于患者的S1振幅较小，而不是S2振幅较大。这些发现与精神分裂症中听觉信息处理的其他研究报告一致，可能揭示了一种模式，其中包含了与这种疾病相关的神经病理的重要线索。本研究将利用143通道脑磁图和密集阵列脑电图研究听觉诱发反应（AERs）的认知和感觉相关性，以评估这种可能性。我们将使用稳态刺激和听觉怪异和范式来帮助澄清(1)在精神分裂症的听觉加工过程中，皮层神经元反应率和相关的信息整合能力的限制；(2)单纯听觉刺激的群体加工能否在精神分裂症患者中以“可控”的速度通过神经元活动的引导而正常化（这将有助于理解精神分裂症患者背景脑状态与听觉加工之间的关系），以及(3)精神分裂症患者的听觉加工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。(4)继发于左听皮层功能障碍的半球间交流是否是精神分裂症患者听觉识别异常的原因之一。分析将依赖于当前的分布式源重建、源和传感器空间的光谱相干性测量、光谱功率测量和使用现实头部模型的偶极子建模。据推测，精神分裂症患者随着时间的推移整合信息的能力有限，其次是神经元反应率的上限较低，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听觉信息处理系统的采样率较低，他们难以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，左听觉皮层的功能障碍阻碍了正常的半球间交流，从而干扰了在古怪型范式中产生正常识别型反应的能力。

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.