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The Next Step: A Common Neural Mechanism for Freezing of Gait
Simon J G Lewis1, James M Shine2
1Parkinson's Disease Research Clinic, Brain and Mind Research Institute, The University of Sydney, Sydney, New South Wales, Australia simon.lewis@sydney.edu.au.
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.
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