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Brain, Vol. 116, No. 5, 1177-1190, 1993
© 1993 Guarantors of Brain


research-article

Vestibular induced postural responses in Parkinson's disease

M. A. Pastor, B. L. Day and C. D. Marsden

MRC Human Movement and Balance Unit, Institute of Neurology, National Hospital for Neurology and Neurosurgery London, UK

Correspondence to: Correspondence to Dr B L Day, MRC Human Movement and Balance Unit, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.

We have tested the hypothesis that dysfunction of the vestibular control of posture is a principal cause of parkinsonian instability by measuring the body sway response induced by galvanic vestibular stimulation (0.5 mA for 2 s) in a group of patients with Parkinson's disease (n = 15). Responses were compared with those obtained from a group of age-matched control subjects (n = 10). Subjects were stimulated (randomized polarity) whilst standing with feet together, eyes closed and maintaining one of five head yaw angles. The motion of the body and the ground reaction forces were measured in three dimensions. There was no significant difference between patients and controls in the speed or direction of the induced body sway response. When the patients were subdivided into two groups according to a clinical assessment of postural deficit, the more disabled group was found to respond with significantly greater body speed than either the control group or the mildly affected patient group. However, the baseline speed of spontaneous body sway was also greater in these patients and it was found that response speed was linearly related to baseline body sway even for the control group. There were no significant differences between any of these groups in the latency to onset, latency to peak or peak amplitude of the initial horizontal ground reaction force response to the stimulus. We conclude that vestibular dysfunction does not explain the postural deficits of patients who are mildly or moderately affected by Parkinson's disease.

Received February 17, 1993. Revised May 26, 1993. Accepted June 28, 1993.


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