Gygli Jan, Romano Fausto, Bockisch Christopher J, Feddermann-Demont Nina, Straumann Dominik, Bertolini Giovanni
Faculty of Medicine, University of Zurich, Zurich, Switzerland.
Department of Neurology, University Hospital Zurich, Zurich, Switzerland.
Front Neurol. 2021 Mar 31;12:518133. doi: 10.3389/fneur.2021.518133. eCollection 2021.
Observing a rotating visual pattern covering a large portion of the visual field induces optokinetic nystagmus (OKN). If the lights are suddenly switched off, optokinetic afternystagmus (OKAN) occurs. OKAN is hypothesized to originate in the velocity storage mechanism (VSM), a central processing network involved in multi-sensory integration. During a sustained visual rotation, the VSM builds up a velocity signal. After the lights are turned off, the VSM discharges slowly, with OKAN as the neurophysiological correlate. It has been reported that the initial afternystagmus in the direction of the preceding stimulus (OKAN-I) can be followed by a reversed one (OKAN-II), which increases with stimulus duration up to 15 min. In 11 healthy adults, we investigated OKAN following optokinetic stimulus lasting 30 s, 3-, 5-, and 10-min. Analysis of slow-phase cumulative eye position and velocity found OKAN-II in only 5/11 participants. Those participants presented it in over 70% of their trials with longer durations, but only in 10% of their 30 s trials. While this confirms that OKAN-II manifests predominantly after sustained stimuli, it suggests that its occurrence is subject-specific. We also did not observe further increases with stimulus duration. Conversely, OKAN-II onset occurred later as stimulus duration increased ( = 0.02), while OKAN-II occurrence and peak velocity did not differ between the three longest stimuli. Previous studies on OKAN-I, used negative saturation models to account for OKAN-II. As these approaches have no foundation in the OKAN-II literature, we evaluated if a simplified version of a rigorous model of OKAN adaptation could be used in humans. Slow-phase velocity following the trials with 3-, 5-, and 10-min stimuli was fitted with a sum of two decreasing exponential functions with opposite signs (one for OKAN-I and one for OKAN-II). The model assumes separate mechanisms for OKAN-I, representing VSM discharge, and OKAN-II, described as a slower adaptation phenomenon. Although the fit was qualitatively imperfect, this is not surprising given the limited reliability of OKAN in humans. The estimated adaptation time constant seems comparable to the one describing the reversal of the vestibulo-ocular reflex during sustained rotation, suggesting a possible shared adaptive mechanism.
观察覆盖大部分视野的旋转视觉模式会诱发视动性眼球震颤（OKN）。如果灯光突然关闭，则会出现视动性眼震后效（OKAN）。据推测，OKAN起源于速度存储机制（VSM），这是一个参与多感官整合的中枢处理网络。在持续的视觉旋转过程中，VSM会建立一个速度信号。灯光关闭后，VSM会缓慢放电，OKAN即为其神经生理相关表现。据报道，先前刺激方向的初始眼震后效（OKAN-I）之后可能会出现反向的眼震后效（OKAN-II），且OKAN-II会随着刺激持续时间增加至15分钟而增强。在11名健康成年人中，我们研究了持续30秒、3分钟、5分钟和10分钟的视动刺激后的OKAN。对慢相累积眼位和速度的分析发现，只有5/11的参与者出现了OKAN-II。这些参与者在超过70%的较长持续时间试验中出现了OKAN-II，但在30秒试验中只有10%出现。虽然这证实了OKAN-II主要在持续刺激后出现，但表明其发生具有个体特异性。我们也未观察到随着刺激持续时间进一步增加OKAN-II有增强。相反，随着刺激持续时间增加，OKAN-II的起始时间延迟（=0.02），而在三个最长刺激中，OKAN-II的出现和峰值速度并无差异。先前关于OKAN-I的研究使用负饱和模型来解释OKAN-II。由于这些方法在OKAN-II文献中并无依据，我们评估了是否可以在人类中使用简化版的OKAN适应严格模型。用两个符号相反的递减指数函数之和（一个用于OKAN-I，一个用于OKAN-II）拟合3分钟、5分钟和10分钟刺激试验后的慢相速度。该模型假设OKAN-I有单独的机制，代表VSM放电，而OKAN-II被描述为一种较慢的适应现象。尽管拟合在定性上并不完美，但考虑到OKAN在人类中的可靠性有限，这并不奇怪。估计的适应时间常数似乎与描述持续旋转期间前庭眼反射反转的时间常数相当，这表明可能存在共同的适应机制。
