Nonnekes Jorik, de Kam Digna, Oude Nijhuis Lars B, van Geel Karin, Bloem Bastiaan R, Geurts Alexander, Weerdesteyn Vivian
Radboud University Medical Centre, Donders Institute for Brain, Cognition and Behaviour, Department of Rehabilitation, Nijmegen, The Netherlands.
Radboud University Medical Centre, Donders Institute for Brain, Cognition and Behaviour, Department of Neurology, Nijmegen, The Netherlands.
PLoS One. 2015 Mar 24;10(3):e0122064. doi: 10.1371/journal.pone.0122064. eCollection 2015.
The pathophysiology underlying postural instability in Parkinson's disease is poorly understood. The frequent co-existence with freezing of gait raises the possibility of shared pathophysiology. There is evidence that dysfunction of brainstem structures contribute to freezing of gait. Here, we evaluated whether dysfunction of these structures contributes to postural instability as well. Brainstem function was assessed by studying the StartReact effect (acceleration of latencies by a startling acoustic stimulus (SAS)).
We included 25 patients, divided in two different ways: 1) those with postural instability (HY = 3, n = 11) versus those without (HY<3, n = 14); and 2) those with freezing (n = 11) versus those without freezing (n = 14). We also tested 15 matched healthy controls. We tested postural responses by translating a balance platform in the forward direction, resulting in backward balance perturbations. In 25% of trials, the start of the balance perturbation was accompanied by a SAS.
The amplitude of automatic postural responses and length of the first balance correcting step were smaller in patients with postural instability compared to patients without postural instability, but did not differ between freezers and non-freezers. In contrast, the StartReact effect was intact in patients with postural instability but was attenuated in freezers.
We suggest that the mechanisms underlying freezing of gait and postural instability in Parkinson's disease are at least partly different. Underscaling of automatic postural responses and balance-correcting steps both contribute to postural instability. The attenuated StartReact effect was seen only in freezers and likely reflects inadequate representation of motor programs at upper brainstem level.
帕金森病姿势不稳的潜在病理生理学机制尚不清楚。姿势不稳常与步态冻结并存,提示可能存在共同的病理生理学机制。有证据表明脑干结构功能障碍与步态冻结有关。在此,我们评估这些结构的功能障碍是否也与姿势不稳有关。通过研究起始反应效应(由突发听觉刺激(SAS)加速潜伏期)来评估脑干功能。
我们纳入了25例患者,以两种不同方式分组:1)姿势不稳患者(Hoehn-Yahr分级 = 3,n = 11)与无姿势不稳患者(Hoehn-Yahr分级<3,n = 14);2)步态冻结患者(n = 11)与无步态冻结患者(n = 14)。我们还测试了15名匹配的健康对照者。通过向前平移平衡平台来测试姿势反应,从而产生向后的平衡扰动。在25%的试验中,平衡扰动开始时伴有SAS。
与无姿势不稳的患者相比,姿势不稳患者的自动姿势反应幅度和首个平衡纠正步长较小,但步态冻结患者与无步态冻结患者之间无差异。相反,姿势不稳患者的起始反应效应正常,但步态冻结患者的起始反应效应减弱。
我们认为帕金森病步态冻结和姿势不稳的潜在机制至少部分不同。自动姿势反应和平衡纠正步长不足均导致姿势不稳。起始反应效应减弱仅在步态冻结患者中出现,可能反映了上脑干水平运动程序的表征不足。