Jacobs Jonathan B, Dell'Osso Louis F
Ocular Motor Neurophysiology Laboratory, Louis Stokes Cleveland Veterans Affairs Medical Center, and Department of Neurology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106, USA.
J Vis. 2004 Jul 27;4(7):604-25. doi: 10.1167/4.7.7.
Attempts to simulate dysfunction within ocular motor system (OMS) models capable of exhibiting known ocular motor behavior have provided valuable insight into the structure of the OMS required for normal visual function. The pendular waveforms of congenital nystagmus (CN) appear to be quite complex, composed of a sustained sinusoidal oscillation punctuated by braking saccades and foveating saccades followed by periods of extended foveation. Previously, we verified that these quick phases are generated by the same mechanism as voluntary saccades. We propose a computer model of the ocular motor system that simulates the responses of individuals with pendular CN (including its variable waveforms) based on the instability exhibited by the normal pursuit subsystem and its interaction with other components of the normal ocular motor control system. Fixation data from subjects with CN using both infrared and magnetic search coil oculography were used as templates for our simulations. Our OMS model simulates data from individuals with CN during fixation and in response to complex stimuli. The use of position and velocity efference copy to suppress oscillopsia is the key element in allowing for normal ocular motor behavior. The model's responses to target steps, pulse-steps, ramps, and step-ramps support the hypothetical explanation for the conditions that result in sustained pendular oscillation and the rules for the corrective saccadic responses that shape this underlying oscillation into the well-known family of pendular CN waveforms: pendular (P), pseudopendular (PP), pendular with foveating saccades (Pfs), and pseudopendular with foveating saccades (PPfs). Position error determined the saccadic amplitudes of foveating saccades, whereas stereotypical braking saccades were not dependent on visual information. Additionally, we propose a structure and method of operation for the fixation subsystem, and use it to prolong the low-velocity intervals immediately following foveating saccades. The model's robustness supports the hypothesis that the pendular nystagmus seen in CN is due to a loss of damping of the normal pursuit-system velocity oscillation (functionally, it is pursuit-system nystagmus--PSN).
在能够展现已知眼球运动行为的眼球运动系统（OMS）模型中模拟功能障碍的尝试，为正常视觉功能所需的OMS结构提供了有价值的见解。先天性眼球震颤（CN）的钟摆样波形似乎相当复杂，由持续的正弦振荡组成，其间穿插着制动性扫视和注视性扫视，随后是长时间的注视期。此前，我们证实这些快速相是由与随意性扫视相同的机制产生的。我们提出了一种眼球运动系统的计算机模型，该模型基于正常追踪子系统表现出的不稳定性及其与正常眼球运动控制系统其他组件的相互作用，模拟患有钟摆样CN的个体的反应（包括其可变波形）。使用来自患有CN的受试者的红外和磁性搜索线圈眼动图的注视数据作为我们模拟的模板。我们的OMS模型模拟了患有CN的个体在注视期间以及对复杂刺激的反应数据。使用位置和速度传出副本以抑制视振荡是实现正常眼球运动行为的关键要素。该模型对目标阶跃、脉冲 - 阶跃、斜坡和阶跃 - 斜坡的反应支持了对导致持续钟摆样振荡的条件的假设解释，以及将这种潜在振荡塑造为著名的钟摆样CN波形家族（钟摆样（P）、假钟摆样（PP）、伴有注视性扫视的钟摆样（Pfs）和伴有注视性扫视的假钟摆样（PPfs））的矫正性扫视反应规则。位置误差决定了注视性扫视的扫视幅度，而刻板的制动性扫视不依赖于视觉信息。此外，我们提出了注视子系统的结构和操作方法，并使用它来延长注视性扫视之后的低速间隔。该模型的稳健性支持了这样的假设，即CN中所见的钟摆样眼球震颤是由于正常追踪系统速度振荡的阻尼丧失（从功能上讲，它是追踪系统眼球震颤 - PSN）。
