Functional Brain Mapping Laboratory, Department of Fundamental Neuroscience, University Medical School, University of Geneva, Geneva, Switzerland.
Functional Brain Mapping Laboratory, Department of Fundamental Neuroscience, University Medical School, University of Geneva, Geneva, Switzerland; EEG Brain Mapping Core, Center for Biomedical Imaging (CIBM) of Lausanne and Geneva, Lausanne, Switzerland.
Neuroimage Clin. 2017 Dec 21;17:976-986. doi: 10.1016/j.nicl.2017.12.028. eCollection 2018.
Carriers of the rare 22q11.2 microdeletion present with a high percentage of positive and negative symptoms and a high genetic risk for schizophrenia. Visual processing impairments have been characterized in schizophrenia, but less so in 22q11.2 Deletion Syndrome (DS). Here, we focus on visual processing using high-density EEG and source imaging in 22q11.2DS participants (N = 25) and healthy controls (N = 26) with an illusory contour discrimination task. Significant differences between groups emerged at early and late stages of visual processing. In 22q11.2DS, we first observed reduced amplitudes over occipital channels and reduced source activations within dorsal and ventral visual stream areas during the P1 (100-125 ms) and within ventral visual cortex during the N1 (150-170 ms) visual evoked components. During a later window implicated in visual completion (240-285 ms), we observed an increase in global amplitudes in 22q11.2DS. The increased surface amplitudes for illusory contours at this window were inversely correlated with positive subscales of prodromal symptoms in 22q11.2DS. The reduced activity of ventral and dorsal visual areas during early stages points to an impairment in visual processing seen both in schizophrenia and 22q11.2DS. During intervals related to perceptual closure, the inverse correlation of high amplitudes with positive symptoms suggests that participants with 22q11.2DS who show an increased brain response to illusory contours during the relevant window for contour processing have less psychotic symptoms and might thus be at a reduced prodromal risk for schizophrenia.
携带罕见的 22q11.2 微缺失的患者表现出较高比例的阳性和阴性症状,并且具有较高的精神分裂症遗传风险。在精神分裂症中已经描述了视觉处理障碍,但在 22q11.2 缺失综合征(DS)中则描述较少。在这里,我们使用高密度 EEG 和源成像在 22q11.2DS 参与者(N=25)和健康对照者(N=26)中进行视觉处理,使用错觉轮廓辨别任务进行研究。在视觉处理的早期和晚期阶段,两组之间出现了显著差异。在 22q11.2DS 中,我们首先观察到在 P1(100-125ms)期间,枕部通道的振幅降低,并且在背侧和腹侧视觉流区的源激活减少,在 N1(150-170ms)视觉诱发成分期间在腹侧视觉皮层内。在涉及视觉完成的较晚窗口(240-285ms)中,我们观察到 22q11.2DS 中全局振幅增加。该窗口中错觉轮廓的表面振幅增加与 22q11.2DS 中的前驱症状阳性量表呈负相关。在早期阶段,腹侧和背侧视觉区域的活动减少表明,在精神分裂症和 22q11.2DS 中都存在视觉处理障碍。在与感知闭合有关的间隔期间,高振幅与阳性症状的逆相关表明,在与轮廓处理相关的相关窗口中,对错觉轮廓表现出增加的大脑反应的 22q11.2DS 参与者具有较少的精神病症状,因此可能具有降低的精神分裂症前驱风险。