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Brain, Vol. 113, No. 3, 691-707, 1990
© 1990 Guarantors of Brain


research-article

ABNORMAL VIBRATION-INDUCED CEREBRAL BLOOD FLOW RESPONSES IN IDIOPATHIC DYSTONIA

LEE W. TEMPEL and JOEL S. PERLMUTTER

Department of Neurology and Neurological Surgery (Neurology), Mallinckrodt Institute of Radiology (Radiation Sciences), and the McDonnell Center for Studies of Higher Brain Function, Washington University School of Medicine St Louis, Missouri, USA

Correspondence to: Correspondence to: Dr Joel S. Perlmutter, Washington University School of Medicine, Division of Radiation Sciences, 510 South Kingshighway, St Louis, MO 63110, USA.

Regional cerebral blood flow responses to vibrotactile stimulation were studied in 11 patients with predominantly unilateral idiopathic focal dystonia and 18 normal subjects using PET and H215O. Stimulation produced a consistently localized and robust peak response in primary sensorimotor cortex contralateral to hand vibration in normal subjects (averaged hemisphere response 10.97 ml/(100 g·min) ±2.53). The sensorimotor response in dystonic patients was also consistently localized to the same area, but significantly reduced in magnitude whether vibrating the affected (8.35 ml/(100 g·min)±2.29) or unaffected hand (8.40 ml/(100 g·min) ±2.15). Furthermore, vibration induced a dystonic cramp in the stimulated arm/hand in 6 patients, but not in any normal subjects. To determine whether the cocontraction of aganist and antagonist muscles could, in itself, attenuate the regional blood flow response, 10 normal subjects were studied with vibration during voluntary cocontraction of appropriate hand and forearm muscles, as well as with vibration alone. Vibration with voluntary cocontraction (mean = 12.57 ml/(100 g·min ± 2.13) produced a significantly greater response than vibration alone (mean = 10.30 ml/(100 g·min) ±2.20, P < 0.00008). This abnormal sensorimotor response may have important implications for understanding the pathophysiology of idiopathic dystonia.

Received November 15, 1988. Revised May 31, 1989. Accepted July 3, 1989.


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