Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2001
Enhanced associated movements in the contralateral limbs elicited by brisk voluntary contraction in choreic disorders.
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Hashimoto T, Shindo M, Yanagisawa N
Аннотация
OBJECTIVES: To study the deficit of inhibition of excessive motor drive generated in the central nervous system in chorea.
METHODS: Identical associated movements in the contralateral limb elicited by rapid hand squeezing were measured in 6 patients with Huntington's disease, 7 patients with peak-dose dyskinesia, 10 patients with Parkinson's disease, 8 patients with spinocerebellar degeneration and in 8 normal subjects. The intensity of associated movements was assessed by the EMG amplitude ratio of associated contractions to active contractions.
RESULTS: The associated movement ratios were larger in Huntington's disease and peak-dose dyskinesia as compared to other groups. The ratios in akinetic "off" phase were smaller than those in dyskinetic "on" phase in all peak-dose dyskinesia patients.
CONCLUSIONS: Enhanced associated movements support a possible common mechanism that chorea may result from failure in inhibition of phasic neural activity pathologically generated in the brain.
METHODS: Identical associated movements in the contralateral limb elicited by rapid hand squeezing were measured in 6 patients with Huntington's disease, 7 patients with peak-dose dyskinesia, 10 patients with Parkinson's disease, 8 patients with spinocerebellar degeneration and in 8 normal subjects. The intensity of associated movements was assessed by the EMG amplitude ratio of associated contractions to active contractions.
RESULTS: The associated movement ratios were larger in Huntington's disease and peak-dose dyskinesia as compared to other groups. The ratios in akinetic "off" phase were smaller than those in dyskinetic "on" phase in all peak-dose dyskinesia patients.
CONCLUSIONS: Enhanced associated movements support a possible common mechanism that chorea may result from failure in inhibition of phasic neural activity pathologically generated in the brain.