Nicolas A Turpin1, Anatol G Feldman1, Mindy F Levin2. 1. Department of Neuroscience, Montreal, QC, Canada; Institute of Biomedical Engineering, University of Montreal, Montreal, QC, Canada; Center for Interdisciplinary Research in Rehabilitation of Greater Montreal (CRIR), Montreal, QC, Canada. 2. School of Physical and Occupational Therapy, McGill University, Montreal, QC, Canada; Center for Interdisciplinary Research in Rehabilitation of Greater Montreal (CRIR), Montreal, QC, Canada. Electronic address: mindy.levin@mcgill.ca.
Abstract
OBJECTIVES: Voluntary movements post-stroke are affected by abnormal muscle activation due to exaggerated stretch reflexes (SRs). We examined the ability of post-stroke subjects to regulate SRs in spastic muscles. METHODS: Elbow flexor and extensor EMGs and joint angle were recorded in 13 subjects with chronic post-stroke spasticity. Muscles were either stretched passively (relaxed arm) or actively (antagonist contraction) at different velocities. Velocity-dependent SR thresholds were defined as angles where stretched muscle EMG exceeded 3SDs of baseline. Sensitivity of SRs to stretch velocity was defined as µ. The regression through thresholds was interpolated to zero velocity to obtain the tonic SR threshold (TSRT) angle. RESULTS: Compared to passive stretches, TSRTs during active motion occurred at longer muscle lengths (i.e., increased in flexors and decreased in extensors by 10-40°). Values of μ increased by 1.5-4.0. Changes in flexor TSRTs during active compared to passive stretches were correlated with clinical spasticity (r=-0.68) and arm motor impairment (r=0.81). CONCLUSIONS: Spasticity thresholds measured at rest were modulated during active movement. Arm motor impairments were related to the ability to modulate SR thresholds between the two states rather than to passive-state values. SIGNIFICANCE: Relationship between spasticity and movement disorders may be explained by deficits in SR threshold range of regulation and modifiability, representing a measure of stroke-related sensorimotor deficits.
OBJECTIVES:Voluntary movements post-stroke are affected by abnormal muscle activation due to exaggerated stretch reflexes (SRs). We examined the ability of post-stroke subjects to regulate SRs in spastic muscles. METHODS: Elbow flexor and extensor EMGs and joint angle were recorded in 13 subjects with chronic post-stroke spasticity. Muscles were either stretched passively (relaxed arm) or actively (antagonist contraction) at different velocities. Velocity-dependent SR thresholds were defined as angles where stretched muscle EMG exceeded 3SDs of baseline. Sensitivity of SRs to stretch velocity was defined as µ. The regression through thresholds was interpolated to zero velocity to obtain the tonic SR threshold (TSRT) angle. RESULTS: Compared to passive stretches, TSRTs during active motion occurred at longer muscle lengths (i.e., increased in flexors and decreased in extensors by 10-40°). Values of μ increased by 1.5-4.0. Changes in flexor TSRTs during active compared to passive stretches were correlated with clinical spasticity (r=-0.68) and arm motor impairment (r=0.81). CONCLUSIONS:Spasticity thresholds measured at rest were modulated during active movement. Arm motor impairments were related to the ability to modulate SR thresholds between the two states rather than to passive-state values. SIGNIFICANCE: Relationship between spasticity and movement disorders may be explained by deficits in SR threshold range of regulation and modifiability, representing a measure of stroke-related sensorimotor deficits.