Sweeney J A, Luna B, Srinivasagam N M, Keshavan M S, Schooler N R, Haas G L, Carl J R
Department of Psychiatry, University of Pittsburgh School of Medicine, Pennsylvania, USA.
Biol Psychiatry. 1998 Oct 15;44(8):698-708. doi: 10.1016/s0006-3223(98)00035-3.
Eye tracking deficits are robust abnormalities in schizophrenia, but the neurobiological disturbance underlying these deficits is not known.
To clarify the pathophysiology of eye tracking disturbances in schizophrenia, we tested 12 first-episode treatment-naive schizophrenic patients and 10 matched healthy individuals on foveofugal and foveopetal step-ramp pursuit tasks.
On foveopetal tasks, the initiation of pursuit eye movements was delayed in schizophrenic patients, and their steady-state pursuit gain was reduced particularly at slower target speeds (8 and 16 deg/sec). In foveofugal step-ramp tasks, their primary catch-up saccades were normal in latency and accuracy, but their postsaccadic pursuit in the first 100 msec after the primary catch-up saccade was significantly reduced even relative to their slow steady-state pursuit, especially during and immediately after an acute episode of illness.
These observations indicate that motion-sensitive areas in posterior temporal cortex provide sufficiently intact information about moving targets to guide accurate catch-up saccades, but that the sensory processing of motion information is not being used effectively for pursuit eye movements. Low-gain pursuit after the early stage of pursuit initiation suggests that the use of extraretinal signals about target motion (e.g., anticipatory prediction) only partially compensates for this deficit. The pattern of low-gain pursuit, impaired pursuit initiation, and intact processing of motion information for catch-up saccades but not pursuit eye movements, was consistent in the schizophrenic patients tested at five time points over a 2-year follow-up period, and implicates the frontal eye fields or their efferent or afferent pathways in the pathophysiology of eye tracking abnormalities in schizophrenia.
眼动追踪缺陷是精神分裂症中一种常见的异常表现，但导致这些缺陷的神经生物学紊乱尚不清楚。
为了阐明精神分裂症患者眼动追踪障碍的病理生理学机制，我们对12例首发未治疗的精神分裂症患者和10名匹配的健康个体进行了离心和向心阶梯-斜坡追踪任务测试。
在向心任务中，精神分裂症患者追踪眼动的起始延迟，其稳态追踪增益降低，尤其是在较低目标速度（8和16度/秒）时。在离心阶梯-斜坡任务中，他们的初级追赶扫视的潜伏期和准确性正常，但在初级追赶扫视后的前100毫秒内，其扫视后追踪明显减少，甚至相对于其缓慢的稳态追踪也是如此，尤其是在急性发病期间和之后。
这些观察结果表明，颞叶后部皮质中的运动敏感区域能够提供关于移动目标的足够完整信息，以指导准确的追赶扫视，但运动信息的感觉处理未有效地用于追踪眼动。追踪起始早期后的低增益追踪表明，利用关于目标运动的视网膜外信号（例如预期预测）仅部分补偿了这一缺陷。在为期2年的随访期间的五个时间点对精神分裂症患者进行测试，结果显示低增益追踪、追踪起始受损以及用于追赶扫视而非追踪眼动的运动信息处理完整这一模式是一致的，这表明额叶眼区或其传出或传入通路与精神分裂症患者眼动追踪异常的病理生理学有关。
