Activation impairment alters muscle torque-velocity in the knee extensors of persons with post-stroke hemiparesis

David J. Clark, Elizabeth G. Condliffe, Carolynn Patten

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Objective: To elucidate mechanisms of impaired force production in post-stroke hemiparesis. Methods: Knee extensor torque-velocity and activation-velocity relationships were examined in seventeen persons with post-stroke hemiparesis (age 57.5, ±6.9) and thirteen non-disabled (age 63.0 ±10.4) persons. Results: Velocity-dependent concentric torque impairment was exaggerated in subjects with hemiparesis relative to control subjects (p < .001). Muscle power was also less in the group with hemiparesis (p < .001), and plateaued at velocities ≥90 deg/s (p > .05). In the control group agonist EMG during concentric actions exhibited a positive linear relationship as velocity increased (R2 = .93, p < .05). The group with hemiparesis produced 34-60% less agonist EMG than controls (p < .02) and modulation was absent (p > .05). Antagonist EMG was either greater in the control (biceps femoris, p < .006) or similar between groups (semimembranosus, p = .95). Under eccentric testing conditions, torque normalized to peak isometric torque (p = .44) and rectus femoris activation (p = .33) were similar between groups, indicating a relative preservation of eccentric torque producing capacity post-stroke. Conclusions: Certain clinical perspectives assert that weakness following central nervous system injury stems from spastic antagonist restraint. Instead, absence of an antagonist restraint strongly suggests that impaired agonist activation is the principal determinant of hemiparetic weakness. Significance: These findings have important implications for promoting optimal recovery of motor function in neuro-rehabilitation.

Original languageEnglish (US)
Pages (from-to)2328-2337
Number of pages10
JournalClinical Neurophysiology
Volume117
Issue number10
DOIs
StatePublished - Oct 1 2006
Externally publishedYes

Fingerprint

Torque
Paresis
Knee
Stroke
Muscles
Nervous System Trauma
Muscle Spasticity
Recovery of Function
Quadriceps Muscle
Rehabilitation
Central Nervous System
Control Groups
Hamstring Muscles

Keywords

  • EMG
  • Hemiplegia
  • Motor control
  • Muscle
  • Post-stroke hemiparesis
  • Stroke
  • Torque-velocity
  • Weakness

ASJC Scopus subject areas

  • Sensory Systems
  • Neurology
  • Clinical Neurology
  • Physiology (medical)

Cite this

Activation impairment alters muscle torque-velocity in the knee extensors of persons with post-stroke hemiparesis. / Clark, David J.; Condliffe, Elizabeth G.; Patten, Carolynn.

In: Clinical Neurophysiology, Vol. 117, No. 10, 01.10.2006, p. 2328-2337.

Research output: Contribution to journalArticle

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AB - Objective: To elucidate mechanisms of impaired force production in post-stroke hemiparesis. Methods: Knee extensor torque-velocity and activation-velocity relationships were examined in seventeen persons with post-stroke hemiparesis (age 57.5, ±6.9) and thirteen non-disabled (age 63.0 ±10.4) persons. Results: Velocity-dependent concentric torque impairment was exaggerated in subjects with hemiparesis relative to control subjects (p < .001). Muscle power was also less in the group with hemiparesis (p < .001), and plateaued at velocities ≥90 deg/s (p > .05). In the control group agonist EMG during concentric actions exhibited a positive linear relationship as velocity increased (R2 = .93, p < .05). The group with hemiparesis produced 34-60% less agonist EMG than controls (p < .02) and modulation was absent (p > .05). Antagonist EMG was either greater in the control (biceps femoris, p < .006) or similar between groups (semimembranosus, p = .95). Under eccentric testing conditions, torque normalized to peak isometric torque (p = .44) and rectus femoris activation (p = .33) were similar between groups, indicating a relative preservation of eccentric torque producing capacity post-stroke. Conclusions: Certain clinical perspectives assert that weakness following central nervous system injury stems from spastic antagonist restraint. Instead, absence of an antagonist restraint strongly suggests that impaired agonist activation is the principal determinant of hemiparetic weakness. Significance: These findings have important implications for promoting optimal recovery of motor function in neuro-rehabilitation.

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