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Objectives: Stroke and resultant hemiparesis involves over 500,000 new cases in America each year and is a frequently encountered clinical problem in the VA Health Care System. A prominent characteristic of post-stroke hemiparesis is weakness. Consequently, a primary focus of rehabilitation is improvement of muscular strength and task dependent control of muscular force. To date, no particular therapeutic approach has produced superior functional outcomes. Importantly, the neuromuscular mechanisms impaired in post-stroke hemiparesis have not been well characterized. Thus, a sound, scientific basis for effective rehabilitation approaches is lacking. In an effort to develop more effective rehabilitation interventions, the aim of this research is to characterize the physiologic basis of impaired muscle function in persons with post-stroke hemiparesis.
Methods: Leg extension force and motor unit (MU) discharge activity are simultaneously measured from the vastus medialis during isometric (ISO) contractions to 40% of maximal voluntary force and during isometric contractions facilitated with either flexion (FF) or extension (FE) of the contralateral leg. Two groups of hemiparetic subjects demonstrating near complete (Brunnstrom 5-6, CVA-I) and moderate recovery (Brunnstrom 3-4, CVA-II) from hemiparesis are compared with young control subjects. Forces are obtained using strain gauge force transducers. Motor unit discharge activity is obtained using a quadrifilar needle electrode and identified using custom-written spike recognition software. MU discharge rates (MUDR) are measured and instances of recruitment and derecruitment identified.
Results: For isometric contractions, CVA-II subjects demonstrate significantly higher MUDRs than control and CVA-I subjects (20 pps vs 10 pps, p<.05). With contralateral flexion, control and CVA-I subjects increase ipsilateral force, primarily by recruiting additional MUs. In contrast, CVA-II subjects reduce ipsilateral force, primarily by reducing MUDR. With contralateral extension, control and CVA-I subjects reduce ipsilateral force, primarily by reducing MUDR. CVA-II subjects also reduce ipsilateral force and MUDR, but with a longer latency.
Conclusions: Results to date demonstrate remarkable impairment in force regulation mechanisms in hemiparetic individuals attributable to both supraspinal and spinal segmental levels of the neuraxis. These data will serve to identify impaired physiologic mechanisms to be targeted in future studies developing more effective rehabilitation interventions.
Acknowledgments: Department of Veterans Affairs - Rehabilitation R&D Career Development Award, Foundation for Physical Therapy - NIFTI Fellowship