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精神分裂症与视觉后向掩蔽:目标增强的普遍缺陷。

Schizophrenia and visual backward masking: a general deficit of target enhancement.

机构信息

Laboratory of Psychophysics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne Lausanne, Switzerland.

出版信息

Front Psychol. 2013 May 14;4:254. doi: 10.3389/fpsyg.2013.00254. eCollection 2013.

Abstract

The obvious symptoms of schizophrenia are of cognitive and psychopathological nature. However, schizophrenia affects also visual processing which becomes particularly evident when stimuli are presented for short durations and are followed by a masking stimulus. Visual deficits are of great interest because they might be related to the genetic variations underlying the disease (endophenotype concept). Visual masking deficits are usually attributed to specific dysfunctions of the visual system such as a hypo- or hyper-active magnocellular system. Here, we propose that visual deficits are a manifestation of a general deficit related to the enhancement of weak neural signals as occurring in all other sorts of information processing. We summarize previous findings with the shine-through masking paradigm where a shortly presented vernier target is followed by a masking grating. The mask deteriorates visual processing of schizophrenic patients by almost an order of magnitude compared to healthy controls. We propose that these deficits are caused by dysfunctions of attention and the cholinergic system leading to weak neural activity corresponding to the vernier. High density electrophysiological recordings (EEG) show that indeed neural activity is strongly reduced in schizophrenic patients which we attribute to the lack of vernier enhancement. When only the masking grating is presented, EEG responses are roughly comparable between patients and control. Our hypothesis is supported by findings relating visual masking to genetic deviants of the nicotinic α7 receptor (CHRNA7).

摘要

精神分裂症的明显症状具有认知和精神病理学性质。然而,精神分裂症也会影响视觉处理,当刺激呈现的持续时间很短,并且随后有遮蔽刺激时,这种影响就变得尤为明显。视觉缺陷非常有趣,因为它们可能与疾病的遗传变异有关(内表型概念)。视觉遮蔽缺陷通常归因于视觉系统的特定功能障碍,例如大细胞系统的低活动或高活动。在这里,我们提出视觉缺陷是与增强弱神经信号有关的一般缺陷的表现,这种情况发生在所有其他类型的信息处理中。我们总结了以前使用闪光掩蔽范式的发现,其中一个短暂呈现的游标目标随后是一个掩蔽光栅。与健康对照组相比,掩蔽光栅使精神分裂症患者的视觉处理恶化了近一个数量级。我们提出这些缺陷是由注意力和胆碱能系统的功能障碍引起的,导致与游标对应的弱神经活动。高密度的电生理记录(EEG)显示,精神分裂症患者的神经活动确实大大减少,我们将其归因于游标增强的缺失。当仅呈现掩蔽光栅时,患者和对照组的 EEG 反应大致相当。我们的假设得到了与烟碱型乙酰胆碱受体α7 亚基(CHRNA7)的遗传变异相关的视觉掩蔽发现的支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d612/3653113/72b91bccc95d/fpsyg-04-00254-g0001.jpg

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