The long-term goal of this research project is to understand the complicated origins of muscle weakness after a hemispheric stroke, and also to explore the origins of the associated muscle fiber loss, contracture, and other key intrinsic property changes of the spastic-paretic muscles. Specifically, we seek to use the most recent advances in high density surface electromyogram (EMG) recording and processing techniques to determine whether these features involve alterations in different motor unit components after an upper motoneuron lesion. The basic clinical and research questions will be addressed via four specific aims.
Aim 1 is to assess whether there is active motoneuron degeneration or signs of impending motoneuron death, by examining the patterns of spontaneous discharge in resting paretic muscles of stroke survivors.
Aim 2 is to assess whether there is evidence for spinal motoneuron degeneration by estimating the motor unit number loss in paretic muscles of stroke survivors.
Aim 3 is to examine alterations in motor unit control properties post stroke using recent advances in high density surface EMG decomposition.
Aim 4 is to examine muscle fiber atrophy, denervation/reinnervation changes post stroke using a range of novel quantitative motor unit action potential (MUAP) analyses. Beyond the major scope of the proposal, several pilot studies are planned as well to extract as much useful information as possible for an improved understanding of motor unit property in stroke. The proposed research using novel high density surface EMG techniques will enhance our understanding of the pathophysiology of muscle weakness and other associated changes after stroke, thus providing guidance for the development of rehabilitation strategies and devices for restoration of normal muscle functions. The findings from the novel high density surface EMG techniques will also have important clinical value to diagnosis, examination and medication/therapy study of stroke.
The proposed research using novel surface EMG techniques will enhance our understanding of the complicated origins of stroke induced muscle weakness and the associated muscle fiber loss, contracture, intrinsic mechanical property changes of the spastic-paretic muscles. This will provide guidance for the development of rehabilitation strategies and devices for restoration of normal muscle functions. The findings of the proposed research also have important clinical value to diagnosis, examination and medication/therapy study of stroke.
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