Dell'Osso L F
Ocular Motor Neurophysiology Laboratory, Veterans Affairs Medical Center, Cleveland, Ohio 44106.
J Vestib Res. 1994 Sep-Oct;4(5):335-45.
Current models of the ocular motor system are usually presented in their most reduced form, are unilateral in architecture, and precise yoking is presumed. Although this simplifies the models, it does not accurately simulate the actual neuroanatomy and limits the models to simple, stereotyped responses. Studies of normal humans and monkeys have demonstrated striking disconjugacies in normal responses. Normal saccades may be disconjugate, or 1 eye may exhibit a dynamic overshoot. Asymmetric vergence can result in disconjugate saccades, unequal magnification spectacles cause differential saccadic gain adjustment, and saccades to unequal disparities also cause unequal saccades in the 2 eyes. In strabismus, deviated eyes typically do not mimic the movements of the fixating eye nor do their latent or congenital nystagmus waveforms duplicate those of the fixating eye. In spasmus nutans, each eye oscillates independently of the other. In achiasmatic dogs, uni-ocular saccades and uni-ocular nystagmus waveforms are seen; the same may be true in human achiasma. These data from both normals and those with abnormalities suggest that current models for ocular motor control are inadequate representations of the actual system. The inability of unilateral, yoked control (or even bilateral, yoked control) system models to duplicate the ocular motor responses of binocular mammals suggests that their ocular motor systems evolved from the bilateral, independent control systems seen in chameleons. One need only postulate a yoking overlay superimposed on two independent control systems to achieve conjugacy (bilateral, yoked, independent control) of the eyes. Abnormalities producing grossly disconjugate eye movements may then be simulated using the independent control of each eye released by a deficiency in the yoking overlay. Independent control of each eye coupled with the essential bilateral brain stem architecture implies that each individual muscle is driven by independent populations of neurons (burst cells, neural integrator cells, etc.). The agonist muscles of each eye are usually coordinated (yoked) but may function independently if the task dictates or if binocularity did not develop. Models based on the above architecture would be robust and could duplicate the many responses (both normal and abnormal) possible from the neurophysiological system.
当前的眼球运动系统模型通常以其最简化的形式呈现，结构上是单侧的，并且假定存在精确的联动。尽管这简化了模型，但它并不能准确模拟实际的神经解剖结构，并且将模型限制在简单的、刻板的反应上。对正常人类和猴子的研究表明，正常反应中存在明显的非共轭现象。正常扫视可能是非共轭的，或者一只眼睛可能表现出动态过冲。不对称性集合可导致非共轭扫视，不等放大率的眼镜会引起不同的扫视增益调整，对不等视差的扫视也会导致两只眼睛的扫视不等。在斜视中，偏斜眼通常不会模仿注视眼的运动，其潜在或先天性眼球震颤波形也不会与注视眼的波形重复。在痉挛性斜颈中，每只眼睛独立振荡。在无交叉的狗中，可以看到单眼扫视和单眼眼球震颤波形；人类无交叉时可能也是如此。这些来自正常人和异常者的数据表明，当前的眼球运动控制模型并不能充分代表实际系统。单侧、联动控制系统模型无法复制双眼哺乳动物的眼球运动反应，这表明它们的眼球运动系统是从变色龙中所见的双侧、独立控制系统进化而来的。只需假设在两个独立控制系统上叠加一个联动覆盖层，就能实现眼睛的共轭（双侧、联动、独立控制）。然后可以使用因联动覆盖层缺陷而释放的每只眼睛的独立控制来模拟产生明显非共轭眼球运动的异常情况。每只眼睛的独立控制加上基本的双侧脑干结构意味着每块肌肉由独立的神经元群体（爆发细胞、神经整合细胞等）驱动。每只眼睛的主动肌通常是协调的（联动的）但如果任务需要或双眼视觉未发育，它们也可以独立运作。基于上述结构的模型将是强大的，并且可以复制神经生理系统可能产生的许多反应（正常和异常）。
