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Updated: Aug 4, 2026
Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI
Published on: April 18, 2011
Locomotor-specific measure of spasticity of plantarflexor muscles after stroke
A Lamontagne1, F Malouin, C L Richards
1Jewish Rehabilitation Hospital Research Center, Gait and Posture Research Unit, Laval, Que, Canada. anouk@lamontagne.mcgill.ca
Objectives:
To study the stretch reflex excitability (spasticity) of the plantarflexor muscles during gait in patients with hemiparesis and to study the relationships of spasticity during gait with spasticity at rest and gait speed.
Design:
Cross-sectional, descriptive.
Setting:
Rehabilitation center.
Participants:
Convenience sample of 30 patients (58 +/- 11yr) with hemiparesis (<6mo poststroke) and 15 healthy controls (59 +/- 8yr).
Interventions:
Patients walked at natural speed, healthy subjects at very slow speed for 10 gait cycles. Electromyographic activation of the medial gastrocremius was recorded by using surface electrodes. A 2-dimensional video camera system with reflective markers was used to acquire kinematics of the lower limbs.
Main Outcome Measures:
Electromyography-lengthening velocity slopes, calculated from measures obtained during the lengthening periods of the medial gastrocnemius muscle during the stance and the swing phases. Measured spatisticity (Modified Ashworth Scale [MAS]), static strength (ankle clonus), and motor control (Fugl-Meyer test).
Results:
Velocity-sensitive electromyographic responses, indicative of hyperactive stretch reflexes, were found on the paretic side during the stance phase of gait (in 66% of the patients), but not on the nonparetic side or in controls. In many patients, velocity-sensitive responses coexisted with low plantarflexor activation levels during the stance phase. No clear patterns of response were measured during the swing phase in either group. Spasticity during gait in the patients was found to be positively related (r = .47, p < .01; r = .57, p < .001) to spasticity at rest (MAS; ankle clonus), whereas it was found to be negatively related to gait speed (r = -.47 to -.53, p < .01).
Conclusions:
The validity of the present method is supported by the fact that it is locomotor-specific and that it allowed for a good discrimination between spastic and nonspastic limbs, as well as between stance and swing phases of the gait cycle. The results also support plantarflexor spasticity as a factor contributing to the poor locomotor performance after stroke.
