Helmchen Christoph, Kirchhoff Jan-Birger, Göttlich Martin, Sprenger Andreas
Department of Neurology, University of Lübeck, Lubeck, Germany.
Institute of Psychology II, University of Lübeck, Lubeck, Germany.
PLoS One. 2017 Jan 5;12(1):e0168808. doi: 10.1371/journal.pone.0168808. eCollection 2017.
The cerebellum integrates proprioceptive, vestibular and visual signals for postural control. Cerebellar patients with downbeat nystagmus (DBN) complain of unsteadiness of stance and gait as well as blurred vision and oscillopsia.
The aim of this study was to elucidate the differential role of visual input, gaze eccentricity, vestibular and proprioceptive input on the postural stability in a large cohort of cerebellar patients with DBN, in comparison to healthy age-matched control subjects.
Oculomotor (nystagmus, smooth pursuit eye movements) and postural (postural sway speed) parameters were recorded and related to each other and volumetric changes of the cerebellum (voxel-based morphometry, SPM).
Twenty-seven patients showed larger postural instability in all experimental conditions. Postural sway increased with nystagmus in the eyes closed condition but not with the eyes open. Romberg's ratio remained stable and was not different from healthy controls. Postural sway did not change with gaze position or graviceptive input. It increased with attenuated proprioceptive input and on tandem stance in both groups but Romberg's ratio also did not differ. Cerebellar atrophy (vermal lobule VI, VIII) correlated with the severity of impaired smooth pursuit eye movements of DBN patients.
Postural ataxia of cerebellar patients with DBN cannot be explained by impaired visual feedback. Despite oscillopsia visual feedback control on cerebellar postural control seems to be preserved as postural sway was strongest on visual deprivation. The increase in postural ataxia is neither related to modulations of single components characterizing nystagmus nor to deprivation of single sensory (visual, proprioceptive) inputs usually stabilizing stance. Re-weighting of multisensory signals and/or inappropriate cerebellar motor commands might account for this postural ataxia.
小脑整合本体感觉、前庭和视觉信号以进行姿势控制。患有下跳性眼球震颤(DBN)的小脑疾病患者会抱怨站立和步态不稳,以及视力模糊和视振荡。
本研究的目的是阐明视觉输入、注视偏心率、前庭和本体感觉输入在一大群患有DBN的小脑疾病患者中对姿势稳定性的不同作用,并与年龄匹配的健康对照受试者进行比较。
记录动眼神经(眼球震颤、平稳跟踪眼球运动)和姿势(姿势摆动速度)参数,并将它们相互关联以及与小脑的体积变化(基于体素的形态测量学,SPM)相关联。
27名患者在所有实验条件下均表现出更大的姿势不稳定性。在闭眼条件下,姿势摆动随眼球震颤增加,但睁眼时不增加。罗姆伯格比率保持稳定,与健康对照无差异。姿势摆动不随注视位置或重力感受输入而变化。两组在本体感觉输入减弱和串联站立时姿势摆动均增加,但罗姆伯格比率也无差异。小脑萎缩(蚓部小叶VI、VIII)与DBN患者平稳跟踪眼球运动受损的严重程度相关。
患有DBN的小脑疾病患者的姿势性共济失调不能用视觉反馈受损来解释。尽管存在视振荡,但小脑姿势控制的视觉反馈控制似乎得以保留,因为在视觉剥夺时姿势摆动最强。姿势性共济失调的增加既与表征眼球震颤的单个成分的调节无关,也与通常稳定姿势的单个感觉(视觉、本体感觉)输入的剥夺无关。多感觉信号的重新加权和/或不适当的小脑运动指令可能是这种姿势性共济失调的原因。