Early-stage visual processing and cortical amplification deficits in schizophrenia
Early-stage visual processing and cortical amplification deficits in schizophrenia
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DOI：
10.1001/archpsyc.62.5.495
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发表时间：
2005-05-01
影响因子：
--
通讯作者：
Javitt, DC
中科院分区：
文献类型：
--
作者：
Butler, PD;Zemon, V;Javitt, DC
背景资料：精神分裂症患者在早期视觉处理中表现出缺陷，可能反映了大细胞视觉通路的功能障碍。大细胞系统正常运作的非线性放大模式介导的谷氨酸能（N-甲基-D-天冬氨酸）受体。调查精神分裂症的大细胞功能障碍，因此允许潜在的病因hypothesis. Objective. To评估精神分裂症的大细胞功能障碍，相对于已知的神经化学和神经解剖学底物，并检查视觉通路功能障碍的电生理和行为措施之间的关系，并与更高的认知缺陷的关系。在州立精神病住院医院和县精神病门诊机构进行的组间研究。33例符合DSM-IV诊断标准的精神分裂症或情感性精神障碍患者和21例年龄相仿的非精神科志愿者组成对照组。主要观察指标：（1）大细胞和小细胞诱发电位，采用非线性（Michaelis-Menten）和线性对比度增益方法;（2）行为对比敏感度测量;（3）白色物质完整性;（4）视觉和非视觉神经心理学测量，（5）临床症状和社区功能测量。结果：患者产生的诱发电位在大细胞偏向刺激时显著降低，但在小细胞偏向刺激时不显著降低（P = 0.001）。Michaelis-Menten分析表明大细胞系统的对比度增益降低（P = .001）。患者对大细胞偏向刺激的对比敏感度降低（P <0.001）。诱发电位缺陷与视辐射中白色物质完整性降低显著相关（P <0.03）。诱发电位缺陷预测对比敏感度受损（P = .002），对比敏感度受损又与复杂视觉处理缺陷相关（P
Background: Patients with schizophrenia show deficits in early-stage visual processing, potentially reflecting dysfunction of the magnocellular visual pathway. The magnocellular system operates normally in a nonlinear amplification mode mediated by glutamatergic (N-methyl-D-aspartate) receptors. Investigating magnocellular dysfunction in schizophrenia therefore permits evaluation of underlying etiologic hypotheses.Objectives: To evaluate magnocellular dysfunction in schizophrenia, relative to known neurochemical and neuroanatomical substrates, and to examine relationships between electrophysiological and behavioral measures of visual pathway dysfunction and relationships with higher cognitive deficits.Design, Setting, and Participants: Between-group study at an inpatient state psychiatric hospital and outpatient county psychiatric facilities. Thirty-three patients met DSM-IV criteria for schizophrenia or schizoaffective disorder, and 21 nonpsychiatric volunteers of similar ages composed the control group.Main Outcome Measures: (1) Magnocellular and parvocellular evoked potentials, analyzed using nonlinear (Michaelis-Menten) and linear contrast gain approaches; (2) behavioral contrast sensitivity measures; (3) white matter integrity; (4) visual and nonvisual neuropsychological measures, and (5) clinical symptom and community functioning measures.Results: Patients generated evoked potentials that were significantly reduced in response to magnocellularbiased, but not parvocellular-biased, stimuli (P = .001). Michaelis-Menten analyses demonstrated reduced contrast gain of the magnocellular system (P = .001). Patients showed decreased contrast sensitivity to magnocellular-biased stimuli (P < .001). Evoked potential deficits were significantly related to decreased white matter integrity in the optic radiations (P < .03). Evoked potential deficits predicted impaired contrast sensitivity (P = .002), which was in turn related to deficits in complex visual processing (P