{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T19:01:40Z","timestamp":1792522900875,"version":"4.5.0"},"reference-count":95,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2014,11,14]],"date-time":"2014-11-14T00:00:00Z","timestamp":1415923200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Neuroscientist"],"published-print":{"date-parts":[[2016,2]]},"abstract":"<jats:p>Freezing of gait is a disabling symptom of Parkinson\u2019s 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\u2019s disease.<\/jats:p>","DOI":"10.1177\/1073858414559101","type":"journal-article","created":{"date-parts":[[2014,11,14]],"date-time":"2014-11-14T22:58:14Z","timestamp":1416005894000},"page":"72-82","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":154,"title":["The Next Step"],"prefix":"10.1177","volume":"22","author":[{"given":"Simon J. 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