• Arun Venkatesan and Steven Frucht.
• Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. avenkat2@jhmi.edu
• Neurol Clin. 2006 Feb 1;24(1):123-32.

AbstractIt is difficult to predict precisely the final neurologic outcome from cardiac arrest and accompanying cerebral hypoxia. Although rare, several movement disorders may arise as a consequence of hypoxic injury, including myoclonus, dystonia, akinetic-rigid syndromes, tremor, and chorea. Dys-function of various portions of the central nervous system, including the basal ganglia, thalamus, midbrain, and cerebellum, is implicated in the pathogenesis of these posthypoxic movement disorders. The development of animal models of posthypoxic movement disorders and of newer imaging techniques applied to human patients who have movement disorders after hypoxic episodes has improved understanding of the pathophysiology of posthypoxic movement disorders and has suggested newer treatments. Many outstanding questions remain, however. What factors promote susceptibility to the development of posthypoxic movement disorders? Why do patients who have similar clinical hypoxic insults develop markedly dis-similar movement disorders? Why are the basal ganglia especially vulnerable to cerebral hypoxia? Why do some movement disorders occur in delayed fashion and progress for years after the hypoxic insult? Is the pathogenesis of progressive posthypoxic movement disorders related to that of neurodegenerative diseases? What are the most effective medications for the various posthypoxic movement disorders? Is there a role for deep brain stimulation in the treatment of posthypoxic movement disorders? We anticipate that current and future research in the area of posthypoxic movement disorders will reveal answers to some of these important questions.

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