Iansek Robert, Danoudis Mary
Clinical Research Centre for Movement Disorders and Gait The National Parkinson Foundation Center of Excellence Kingston Centre Monash Health Cheltenham Victoria Australia.
School of Clinical Sciences Monash University Clayton Victoria Australia.
Mov Disord Clin Pract. 2016 Dec 26;4(3):290-297. doi: 10.1002/mdc3.12463. eCollection 2017 May-Jun.
Freezing of gait (FOG) in Parkinson's disease (PD) is poorly understood; however, with the established understanding of basal ganglia function, its manifestations should be more easily interpretable. This review examines freezing of gait (FOG) from such a perspective.
A search of the MEDLINE and EMBASE databases from the year 2000 onward for review articles, focused on the pathophysiology of FOG, was used to determine current concepts. A previously established model of basal ganglia function was used to determine the concepts' validities. At the core of the model are deficits in motor set maintenance and timing cue production for automatic movement. It includes the shift between attention and automation to the predominant attention control of gait in PD.
The difficulties of the found concepts to explain FOG stem from failure to characterize different FOG components, from the assumption that all components share a similar pathophysiology, from a failure to separate basic deficits from compensatory mechanisms, and from the assumption that cognitive deficits are the cause of FOG rather than representing an inadequate compensation to FOG. Pragmatic approaches to management use the attention shift, with the provision of visual information about correct amplitude of step to correct initiation deficits, and motor blocks during gait. It also emphasizes the need to prevent step length reduction on turns, environmental situations, and cognitive overload.
The concept of automatic deficits in set maintenance and cue production best describe FOG manifestations in PD and, with the use of attention, the concept also provides pragmatic strategies for management.
帕金森病（PD）中的冻结步态（FOG）目前仍未得到充分理解；然而，基于对基底神经节功能的既有认识，其表现应更易于解读。本综述从这一角度审视冻结步态（FOG）。
检索2000年起的MEDLINE和EMBASE数据库中的综述文章，重点关注FOG的病理生理学，以确定当前的概念。使用先前建立的基底神经节功能模型来确定这些概念的有效性。该模型的核心是运动定势维持和自动运动定时线索产生方面的缺陷。它包括注意力与自动化之间的转换，以及PD中对步态的主要注意力控制。
现有概念难以解释FOG，原因在于未能区分不同的FOG成分，假设所有成分具有相似的病理生理学，未能将基本缺陷与代偿机制区分开，以及假设认知缺陷是FOG的原因而非对FOG的不充分代偿。实用的管理方法利用注意力转换，提供关于正确步幅的视觉信息以纠正起始缺陷，以及步态中的运动阻滞。它还强调需要防止转弯时步长缩短、环境因素和认知过载。
运动定势维持和线索产生方面的自动缺陷概念最能描述PD中的FOG表现，并且通过利用注意力，该概念还为管理提供了实用策略。
