Department of Neurology, University Hospital Zurich, Frauenklinikstrasse 26, CH-8091, Zurich, Switzerland.
University of Zurich, Zurich, Switzerland.
Cerebellum. 2021 Oct;20(5):751-759. doi: 10.1007/s12311-020-01118-6.
A brain stem/cerebellar neural integrator enables stable eccentric gaze. Cerebellar loss-of-function can cause an inability to maintain gaze eccentrically (gaze-evoked nystagmus). Moreover, after returning gaze to straight ahead, the eyes may drift toward the prior eye position (rebound nystagmus). Typically, gaze-evoked nystagmus decays during continuously held eccentric gaze. We hypothesized this adaptive behavior to be prerequisite for rebound nystagmus and thus predicted a correlation between the velocity decay of gaze-evoked nystagmus and the initial velocity of rebound nystagmus. Using video-oculography, eye position was measured in 11 patients with cerebellar degeneration at nine horizontal gaze angles (15° nasal to 25° temporal) before (baseline), during, and after attempted eccentric gaze at ± 30° for 20 s. We determined the decrease of slow-phase velocity at eccentric gaze and the slow-phase velocity of the subsequent rebound nystagmus relative to the baseline. During sustained eccentric gaze, eye drift velocity of gaze-evoked nystagmus decreased by 2.40 ± 1.47°/s. Thereafter, a uniform change of initial eye drift velocity relative to the baseline (2.40 ± 1.35°/s) occurred at all gaze eccentricities. The velocity decrease during eccentric gaze and the subsequent uniform change of eye drift were highly correlated (R = 0.80, p < 0.001, slope = 1.09). Rebound nystagmus can be explained as gaze-evoked nystagmus relative to a set point (position with least eye drift) away from straight-ahead eye position. To improve detection at the bedside, we suggest testing rebound nystagmus not at straight-ahead eye position but at an eccentric position opposite of prior eccentric gaze (e.g., 10°), ideally using quantitative video-oculography to facilitate diagnosis of cerebellar loss-of-function.
脑于/小脑神经整合器可实现稳定的外展凝视。小脑功能丧失可导致无法维持外展凝视（凝视诱发眼震）。此外，在将凝视返回正前方后，眼睛可能会漂移至先前的眼位（反弹眼震）。通常，在持续外展凝视时，凝视诱发眼震会逐渐减弱。我们假设这种适应性行为是反弹眼震的前提条件，因此预测了凝视诱发眼震的速度衰减与反弹眼震初始速度之间存在相关性。使用视频眼动描记术，在 11 例小脑变性患者的 9 个水平凝视角度（鼻侧 15°至颞侧 25°）下测量眼位，分别在试图进行±30°的外展凝视前（基线）、进行时和进行后 20 s。我们确定了外展凝视时慢相速度的下降以及后续反弹眼震的慢相速度相对于基线的下降。在持续外展凝视期间，凝视诱发眼震的眼漂移速度下降了 2.40±1.47°/s。此后，所有凝视偏斜处相对于基线的初始眼漂移速度均发生了均匀变化（2.40±1.35°/s）。外展凝视期间的速度下降和随后眼漂移的均匀变化高度相关（R=0.80，p<0.001，斜率=1.09）。反弹眼震可以解释为相对于正前方眼位（眼漂移最小的位置）的凝视诱发眼震。为了在床边提高检测效果，我们建议不在正前方眼位测试反弹眼震，而是在先前外展凝视的相反位置测试（例如 10°），理想情况下使用定量视频眼动描记术来促进小脑功能丧失的诊断。
