Department of Neurology, The Johns Hopkins University, Baltimore, MD, United States.
Department of Neurology, The Johns Hopkins University, Baltimore, MD, United States; Department of Neurology, Hacettepe University, Ankara, Turkey.
Prog Brain Res. 2019;249:197-209. doi: 10.1016/bs.pbr.2019.04.040. Epub 2019 Jun 8.
Rebound nystagmus, a common cerebellar sign, is a transient nystagmus that appears on returning to straight-ahead gaze after prolonged eccentric gaze. The slow phases of rebound nystagmus are in the direction of prior eccentric gaze. After eccentric gaze, healthy subjects also show rebound nystagmus when fixation is removed. Rebound nystagmus is thought to be related to the function of the oculomotor neural integrator-the circuit that ensures accurate gaze holding after any eye movement-but the exact mechanism of rebound nystagmus is unknown. Here, we combine experimental data with mathematical modeling to test several hypotheses for the generation of rebound nystagmus. We show that two mechanisms contribute, one relies on vision and the other does not. Future experiments must determine if (1) the non-visual mechanism is related to eye position or to eye velocity signals and (2) whether these signals are based on afferent (proprioception) or efferent (corollary) information.
反弹性眼球震颤，一种常见的小脑体征，是一种在长时间的外转眼注视后返回正前方注视时出现的短暂性眼球震颤。反弹性眼球震颤的慢相朝先前的外转眼注视方向。在外转眼注视后，当注视被移除时，健康受试者也会出现反弹性眼球震颤。反弹性眼球震颤被认为与眼球运动神经整合器的功能有关——该电路可确保在任何眼球运动后准确保持注视，但反弹性眼球震颤的确切机制尚不清楚。在这里，我们结合实验数据和数学模型来测试产生反弹性眼球震颤的几种假说。我们表明，有两种机制起作用，一种依赖于视觉，另一种则不依赖于视觉。未来的实验必须确定（1）非视觉机制是否与眼位或眼速度信号有关，以及（2）这些信号是基于传入（本体感觉）还是传出（传出信息）信息。
