The Next Step: A Common Neural Mechanism for Freezing of Gait

被引：127

作者：

Lewis, Simon J. G. ^{[1
]}

Shine, James M. ^{[1
]}

机构：

[1] Univ Sydney, Brain & Mind Res Inst, Parkinsons Dis Res Clin, 94 Mallett St, Sydney, NSW 2050, Australia

来源：

NEUROSCIENTIST | 2016年 / 22卷 / 01期

关键词：

freezing; Parkinson's disease; conflict; subthalamic nucleus; PARKINSONS-DISEASE PATIENTS; DEEP BRAIN-STIMULATION; POSTURAL MUSCLE TONE; BASAL GANGLIA; PEDUNCULOPONTINE NUCLEUS; SUBTHALAMIC NUCLEUS; ORGANIZATION; DEFICITS; NETWORK; CONNECTIVITY;

D O I：

10.1177/1073858414559101

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Freezing of gait is a disabling symptom of Parkinson's disease that causes a paroxysmal cessation of normal footsteps while walking. Despite a great deal of empirical research, the pathophysiological mechanisms underlying the symptom remain unclear. In this targeted review, we synthesize recent insights from research into freezing in an effort to clarify the neurobiological basis of this phenomenon. We conclude that freezing manifests via a common neural pathway in which transient increases in inhibitory basal ganglia output lead to decreased activity within the brainstem structures that coordinate gait. This cascade may be triggered through dopaminergic depletion in the striatum and over-activity within the subthalamic nucleus. These insights may benefit both the diagnostic and therapeutic management of freezing in Parkinson's disease.

引用

页码：72 / 82

页数：11

共 95 条

[1] Deep brain stimulation of the pedunculopontine tegmental nucleus modulates neuronal hyperactivity and enhanced beta oscillatory activity of the subthalamic nucleus in the rat 6-hydroxydopamine model [J].