High velocity transient visual processing deficits diminish ability of patients with schizophrenia to recognize objects.

B D Schwartz, B A Maron, W J Evans, D K Winstead
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Abstract

Objective: Early information processing deficits are consistently reported for patients with schizophrenia. A growing number of studies have applied a transient (magnocellular) or sustained (parvocellular) explanation to account for deficient processing of briefly presented visual stimuli, moving stimuli, and stimuli requiring eye movements in patients with schizophrenia. This reasoning is based on research that makes the distinction between a magnocellular channel, which primarily responds to low spatial frequency and moving or rapidly presented visual information, and a parvocellular channel, which is primarily responsive to high spatial frequency and detailed information.

Background: Although the preponderance of findings offer support for transient ("where is it") as opposed to sustained ("what is it") deficit in patients with schizophrenia, there remains a need for more specific depiction of the deficit.

Method: The present study evaluated normal control subjects and patients with schizophrenia recruited from in-patient and out-patient settings. A Motion Defined Letter task was used, owing to its sensitivity to transient (magnocellular) activation.

Results: Twenty-three patients with schizophrenia and sixteen normal control subjects were tested on eight dot velocity levels, ranging from 88 arc min/sec to 0.69 arc min/sec. A repeated measures analysis of variance indicated that the performance of patients with schizophrenia was significantly poorer than that of their normal counterparts on the three fastest dot velocity conditions (88 arc min/sec, p < 0.0001, 44 arc min/sec, p < 0.00001, and 22 arc min/sec, p < 0.00003), but performance did not differ on the five slower dot velocity conditions. A regression analysis revealed that the dosage of medication was positively associated with performance on three middle range dot velocity conditions (11 arc min/sec F (1,22) = 6.99; p < 0.025; 5.5 arc min/sec, F (2,20) = 0.379; p = 0.05, and 2.25 arc min/sec F (2,20) = 7.37; p < 0.005).

Conclusions: The findings afford support for an early information processing deficit in schizophrenics. These data also support the neurophysiologic model that explains the poor performance of patients with schizophrenia as it relates to a transient channel deficiency.

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高速瞬态视觉处理缺陷降低了精神分裂症患者识别物体的能力。
目的:精神分裂症患者的早期信息加工缺陷一直被报道。越来越多的研究应用瞬时(大细胞)或持续(细细胞)的解释来解释精神分裂症患者对短暂呈现的视觉刺激、移动刺激和需要眼球运动的刺激的处理缺陷。这一推理是基于对主要响应低空间频率和移动或快速呈现的视觉信息的大细胞通道和主要响应高空间频率和详细信息的副细胞通道进行区分的研究。背景:尽管多数研究结果支持精神分裂症患者短暂性(“它在哪里”)而非持续性(“它是什么”)缺陷,但仍需要对缺陷进行更具体的描述。方法:本研究评估了从住院和门诊招募的正常对照和精神分裂症患者。由于其对瞬态(巨细胞)激活的敏感性,使用了运动定义字母任务。结果:对23例精神分裂症患者和16例正常人进行了88 ~ 0.69弧分/秒的8个点速度水平测试。重复测量方差分析表明,精神分裂症患者在3种最快点速度条件下(88弧分/秒,p < 0.0001, 44弧分/秒,p < 0.00001,和22弧分/秒,p < 0.00003)的表现明显低于正常人,但在5种较慢点速度条件下的表现没有差异。回归分析显示,在3个中速点速度条件下(11弧分/秒F (1,22) = 6.99;P < 0.025;5.5弧分/秒,F (2,20) = 0.379;p = 0.05, 2.25弧分/秒F (2,20) = 7.37;P < 0.005)。结论:这些发现为精神分裂症患者早期信息加工缺陷提供了支持。这些数据也支持了神经生理学模型,该模型解释了精神分裂症患者的不良表现,因为它与短暂的通道缺陷有关。
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