Bondar R L, Sharpe J A, Lewis A J
Ann Neurol. 1984 May;15(5):474-7. doi: 10.1002/ana.410150512.
Rebound nystagmus was recorded in a patient with cerebellar dysfunction. Neuropathological examination showed degeneration of the inferior olivary nuclei and the cerebellar cortex. The basis pontis and the brainstem tegmentum were spared. Rebound nystagmus is attributed to a smooth eye movement bias that is generated within intact vestibuloocular pathways to oppose gaze-evoked centripetal drift of the eyes. The source of the rebound bias was not visual, because rebound nystagmus normally occurs in darkness, smooth pursuit was paretic, and the olivocerebellar visual relay pathway was degenerated. An extraretinal, efference copy signal of the eye position error must detect the ocular drift and generate the rebound bias. The neuropathological findings indicate that rebound nystagmus can be a sign of involvement confined to the olivocerebellar circuit and that nonvisual signals of eye position are monitored independently of this cerebellar system.
在一名患有小脑功能障碍的患者中记录到了反弹性眼球震颤。神经病理学检查显示下橄榄核和小脑皮质发生退变。脑桥基底部和脑干被盖未受影响。反弹性眼球震颤归因于在完整的前庭眼反射通路中产生的一种平稳眼动偏差，以对抗凝视诱发的眼球向心性漂移。反弹性偏差的来源并非视觉性的，因为反弹性眼球震颤通常在黑暗中出现，平稳跟踪功能减弱，且橄榄小脑视觉中继通路已退变。眼位误差的视网膜外传出副本信号必须检测到眼球漂移并产生反弹性偏差。神经病理学发现表明，反弹性眼球震颤可能是仅累及橄榄小脑回路的一个征象，并且眼位的非视觉信号是独立于该小脑系统进行监测的。
