Movement disorders : official journal of the Movement Disorder Society
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The clinical and neurophysiologic features of 14 patients with chronic posthypoxic myoclonus are presented. Patients were first seen a mean of 2.5 years (range, 2 to 105 months) after the hypoxic event and followed up for 3.7 years (range, 7 to 84 months) thereafter. All patients had had a cardiorespiratory arrest, most caused by an acute asthmatic attack (11 cases). ⋯ Electrophysiologic investigation confirmed cortical action myoclonus in every case, although this could be combined with cortical reflex myoclonus, an exaggerated startle response, or brainstem reticular reflex myoclonus. We conclude that posthypoxic myoclonus typically consists of multifocal cortical action myoclonus that improves with time. It is only rarely associated with severe additional neurologic deficit.
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Comparative Study
Influence of dopaminergic medication on automatic postural responses and balance impairment in Parkinson's disease.
It is still unclear why balance impairment in Parkinson's disease (PD) often responds insufficiently to dopaminergic medication. We have studied this issue in 23 patients with idiopathic PD and 24 healthy controls. Our specific purposes were (a) to investigate the contribution of abnormal automatic postural responses to balance impairment in PD and (b) to assess the influence of dopaminergic medication on abnormal automatic postural responses and balance impairment. ⋯ Consequently, the increased posterior COG displacement was not ameliorated during the on phase. We conclude that (a) a combination of abnormal automatic and perhaps more voluntary postural corrections contributes to increased body sway in PD and (b) dopaminergic medication fails to improve balance impairment in PD because early automatic postural responses are only partially corrected, while later occurring postural corrections are not improved at all. These electrophysiological results support clinical observations and suggest that nondopaminergic lesions play a significant role in the pathophysiology of postural abnormalities in PD.