Project Details
Description
Stroke is a debilitating condition arising from ischemic or hemorrhagic damage to (motor) cortices and/or pathways, with symptoms including weakness (decreased muscle tone), increased muscle stiffness, spasticity (increased reflex sensitivity), and muscle synergies (loss of independent joint control). Previous work has investigated the origins of spasticity and the flexion synergy, and their contributions to movement impairments, mainly in postural tasks. Studying these phenomena quantitatively, especially during volitional movement, requires specialized robotic devices. We propose to use the NACT3D, which is capable of modulating shoulder abduction loading, applying high-velocity perturbations in multiple planes, and recording kinematic and dynamic participant data. By applying perturbations during movement, previously unseen mechanisms underlying spasticity post stroke can be elucidated.
A multi-faceted investigation is proposed that 1) investigates elbow reflex activity in response to velocity perturbations at various time points during volitional movement, and 2) investigates the influence of the flexion synergy on elbow reflex hyperexcitability. The first aim is a step forward from previous work, which has focused on perturbations during postural tasks, or has relied on volitional movement to investigate reflex excitability. The aim second makes use of the new capabilities of the NACT3D compared to previous robotic devices used for quantification of the neuromuscular system post-stroke, by looking at reflex excitability during movement in response to the flexion synergy, elicited by shoulder abduction loading.
With the proposed study, insight can be gained into the neurological control of the upper limb following a stroke, and how reflex excitability is modulated by volitional movement as well as synergistic muscle activation. The results of this study can improve our understanding of stretch reflex hyperexcitability during perturbed reaching, and how spa
Status | Finished |
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Effective start/end date | 1/1/20 → 12/31/21 |
Funding
- American Heart Association (20PRE35210339)
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