The objective of this study is to characterize finger extension following stroke. A number of potential mechanisms have been implicated in chronic impairment of the hand. The relative impact of these various mechanisms on impairment, however, has not been fully elucidated, as understanding of even the healthy hand remains incomplete. Of special interest is the relatively greater impairment of finger extension as compared to flexion as this asymmetry may help us to better understand the changes occurring after stroke. Accordingly, the following aims are proposed: 1. Examine Effect of Joint Posture on Extension Neuromechanics. Finger extension is a complex process with tendons from 5 different muscles merging to form the extensor hood, an aponeurosis connected to the dorsal side of the finger phalanges. The effect of activation (or loss) of a given muscle is difficult to predict, especially as the finger posture changes. For this study, a finite element model of the extensor hood will be created to quantify force transmission to the finger. The effects of finger posture on extension biomechanics will be compared with its effects on neural activation patterns, recorded with intramuscular electrodes. The developed model will be used to estimate the impact of changes measured in Aims 2 and 3. 2. Compare Mechanical Tissue Changes in Periphery Following Stroke. Observed weakness in finger torque production may be attributable to changes in muscle and soft tissue. Increases in joint impedance or asymmetrical muscle atrophy could make finger extension relatively more difficult. For this study, passive joint impedance will be assessed using system identification techniques on stroke survivors. Atrophy will be measured using magnetic resonance imaging (MRI) and ultrasound techniques. 3. Examine Neural Activation Patterns Following Stroke. Extension deficits may alternatively or additionally have neurological origins. Excessive coactivation of the finger flexors and/or reduced ability to voluntarily activate the finger extensors may contribute to impaired finger extension. While excessive finger flexor coactivation has been shown following stroke, especially during activation of muscles in other limbs, it has not been determined whether this increase is cortically mediated. For this study, functional MRI will be used to examine cortical activity during finger, arm, and leg extension/flexion. The ability to voluntary activate muscles will be assessed through electromyography. Voluntary activation signals will be compared with those obtained from electrical stimulation of the innervating nerve.Chronic impairment of finger extension is the most common deficit following hemispheric stroke, with profound consequences on function, employment, and quality of life. Its origins, however, remain incompletely understood, as a number of mechanisms, with potentially conflicting treatments, may contribute. The knowledge gained from this study will facilitate hand rehabilitation by targeting specific areas for treatment.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Research Project (R01)
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Musculoskeletal Rehabilitation Sciences Study Section (MRS)
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Chen, Daofen
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Rehabilitation Institute of Chicago
United States
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