Visual sensory processing deficits in schizophrenia: is there anything to the magnocellular account?
Visual sensory processing deficits in schizophrenia: is there anything to the magnocellular account?
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DOI：
10.1016/j.schres.2012.05.022
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发表时间：
2012-08
影响因子：
4.5
通讯作者：
Foxe, John J.
中科院分区：
文献类型：
--
作者：
Lalor, Edmund C.;De Sanctis, Pierfilippo;Krakowski, Menahem I.;Foxe, John J.
视觉处理研究多次表明，与健康对照者相比，精神分裂症患者的视觉处理能力受损。脑电图 (EEG)，特别是视觉诱发电位 (VEP) 研究已经确定了这种损伤的早期标志，即患者及其临床上未受影响的一级亲属 VEP 的 P1 成分减少。许多行为和神经影像学研究表明，皮质下大细胞通路或皮质视觉背侧流的特定功能障碍与这种损伤有关。在这项研究中，使用 VESPA（视觉诱发扩频分析）方法获得了对棋盘刺激的对比调制的脑电图反应。这是在高对比度条件下进行的，为了使刺激偏向大细胞通路，在低对比度条件下进行。标准 VEP 也是使用高对比度图案反转棋盘获得的。使用高密度头皮电记录测量了 29 名符合 DSM-IV 精神分裂症标准的个体和 18 名对照受试者的反应。重复之前的研究，与对照组相比，患者 VEP 的 P1 成分大幅降低（Cohen’s d = 1.11），而 VESPA 对高对比度刺激的反应没有相应差异。此外，低对比度 VESPA 显示患者和对照组之间没有差异。此外，对于 VEP 或高对比度 VESPA 的 C1 组件，患者和对照之间没有发现差异。基于 VEP 和 VESPA 之间不同的采集方法，我们从对比度增益控制和皮质水平功能障碍的可能性方面讨论这些结果，当使用低对比度刺激偏向该通路时，沿着大细胞通路进入 V1 的初始传入活动保持完整。
Visual processing studies have repeatedly shown impairment in patients with schizophrenia compared to healthy controls. Electroencephalography (EEG) and, specifically, visual evoked potential (VEP) studies have identified an early marker of this impairment in the form of a decrement in the P1 component of the VEP in patients and their clinically unaffected first-degree relatives. Much behavioral and neuroimaging research has implicated specific dysfunction of either the subcortical magnocellular pathway or the cortical visual dorsal stream in this impairment. In this study, EEG responses were obtained to the contrast modulation of checkerboard stimuli using the VESPA (Visual Evoked Spread Spectrum Analysis) method. This was done for a high contrast condition and, in order to bias the stimuli towards the magnocellular pathway, a low contrast condition. Standard VEPs were also obtained using high contrast pattern reversing checkerboards. Responses were measured using high-density electrical scalp recordings in 29 individuals meeting DSM-IV criteria for schizophrenia and in 18 control subjects. Replicating previous research, a large (Cohen’s d = 1.11) reduction in the P1 component of the VEP was seen in patients when compared with controls with no corresponding difference in the VESPA response to high contrast stimuli. In addition, the low-contrast VESPA displayed no difference between patients and controls. Furthermore, no differences were seen between patients and controls for the C1 components of either the VEP or the high-contrast VESPA. Based on the differing acquisition methods between VEP and VESPA, we discuss these results in terms of contrast gain control and the possibility of dysfunction at the cortical level with initial afferent activity into V1 along the magnocellular pathway being intact when processing is biased towards that pathway using low contrast stimuli.
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