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The next step: a common neural mechanism for freezing of gait

Simon J. G. Lewis*, James M. Shine

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)72-82
Number of pages11
JournalNeuroscientist
Volume22
Issue number1
DOIs
Publication statusPublished - 1 Feb 2016
Externally publishedYes

Keywords

  • conflict
  • freezing
  • Parkinson's disease
  • subthalamic nucleus

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