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- W2050447588 abstract "command as spastic cocontraction. While spastic cocontraction is really the main antagonistic mechanism impeding movement, in particular leg movements during gait, muscle overactivity is often assumed to be represented by mere measurements of resistance to passive movement. A five-step clinical assessment, including a quantitative assessment of active range of motion, may better serve the clinician to reflect the amount of cocontraction. Another critical phenomenon is stretch-sensitive paresis, which is the aggravation of paresis of agonist command by the stretched position of the antagonist. The physiological underpinnings of spastic cocontraction and stretch-sensitive paresis probably involve neuronal rarefaction in agonist command, hypo-excitabilty of the remaining upper motor neurons, hyperexcitability of the lower motor neurons subserving the more shortened muscles and reduction or reversal into facilitation of Ia and groups II reciprocal inhibition. Considering its determinants (agonist effort and muscle position), treatment of spastic cocontraction and stretch-sensitive paresis – and management of deforming spastic paresis in general – should logically involve a combination of: – prolonged stretching postures for the more overactive and shortened antagonists, potentially in association with focal weakening agents such as botulinum toxin; – intensive motor training (e.g. non assisted maximal amplitude rapid alternating movements and task-related exercises) of the less overactive muscles." @default.
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- W2050447588 date "2012-10-01" @default.
- W2050447588 modified "2023-09-30" @default.
- W2050447588 title "Spasticity treatment by botulinum toxin in multiple sclerosis" @default.
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- W2050447588 doi "https://doi.org/10.1016/j.rehab.2012.07.824" @default.
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