Altered Motor Unit Acrivity Corresponds with Weakness and Locomotor Disability in Post-stroke Hemipareses

Patten, C., Gardner, M.C., Dickinson, L.M. & McGill, K.C. Rehabilitation Research & Development Center, VA Palo Alto Health Care System & Stanford University School of Medicine, Palo Alto, CA.

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Introduction: Weakness is a prominent sequela of post-stroke hemiparesis (CVA). Impaired neuromuscular control is thought to contribute to motor disabilities including locomotor dysfunction. However, impairments of neuromuscular control mechanisms resulting from stroke are poorly understood. The present research was conducted in an effort to better understand impairments of neuromuscular control and their potential contribution to locomotor disability following CVA.

Methods: Two groups of chronic hemiparetic subjects (mean duration of CVA: 39 mos) demonstrating near complete (CVA-I, Brunnstrom 5-6, mean Fugl-Meyer=93) and moderate recovery (CVA-II, Brunnstrom 3-4, mean Fugl-Meyer=73) from CVA were compared with control subjects. Leg extension force and motor unit (MU) discharge activity were simultaneously measured from the vastus medialis during isometric (ISO) contractions to 40% of non-paretic leg maximal voluntary force and during isometric contractions facilitated with either flexion (FF) or extension (FE) of the contralateral leg. Leg extension forces were obtained using strain gauge force transducers housed in the pedals of an instrumented bicycle ergometer. Motor unit discharge activity was obtained using a quadrifilar needle electrode and identified using custom-written spike recognition software. MU discharge rates (MUDR) were measured and instances of recruitment and derecruitment identified. Three-dimensional kinematic data were obtained during gait at self-selected (SSWS) and fast walking speeds using a Qualisys digital motion analysis system. Gait data were reduced and analyzed using Qgait software.

Results: Motor unit (MU) discharge rates during isometric leg extension to 40% of non-paretic leg maximal voluntary force were increased in CVA subjects relative to controls (11.5 pps) (p < .05). Asymmetry of MU discharge rates while producing the same absolute force was evident in CVA-II (P leg: 15.3 pps vs NP leg: 19.0 pps) but not CVA-I (P: 13.7 pps vs. NP: 11.9 pps) subjects (p < .05).

Excitatory or inhibitory Influences of contralateral limb flexion or extension on MU discharge activity were similar and relatively symmetric in control and CVA-I subjects. In CVA-II, however, remarkable asymmetries were evidenced with the P limb exerting only modest influences on the NP limb while the NP limb exerted profound effects on the P limb.

Gait velocity at SSWS was reduced in both CVA-I (.95m/s ± .2) and CVA-II (.79 m/s ± .2) relative to controls (1.44 m/s ± .1). During fast gait all subject groups increased gait velocity (CVA-I: 1.21 m/s ± .3, CVA-II: 1.07 m/s ± .4, controls: 1.94 m/s ± .1), however only the CVA-I group approached normal gait velocity in the fast condition. Stance phase symmetry (paretic (P) leg/non-paretic (NP) leg) was reduced in hemiparetic subjects (CVA-I: .97, CVA-II: .83) during SSWS and became exaggerated during fast gait (CVA-I: .86, CVA-II: .88).

Conclusions: Fundamental force regulation mechanisms are clearly altered in CVA and appear to correspond with the severity of locomotor disability. Increased MU discharge rates in persons with CVA at moderate, functional force levels are inefficient and may lead to rapid fatigue. The asymmetry of contralateral limb influences in less recovered CVA subjects suggests chronic alteration in the spinal segmental system which may occur as a compensatory adaptation.