T Hashimoto1, M Shindo, N Yanagisawa. 1. Third Department of Medicine (Neurology), Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. takahhh@hsp.md.shinshu-u.ac.jp
Abstract
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.
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 dyskinesiapatients. 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.