Date of Award
Doctor of Philosophy (PhD)
Clinical and Translational Rehabilitation Health Sciences
Hyperreflexia that causes muscle spasticity may contribute to limitations in force regulation and walking ability post stroke. Additionally, neuromuscular fatigue may reduce force regulation, which is important because fatigue can assist to strengthen muscles that control walking. Hyperreflexia may be caused by cortical disinhibition that allows Ia afferents to amplify excitatory synaptic inputs to motoneuron pools. Cortical disinhibition is presumably caused by stroke-related motor cortex damage. Although, other excitatory synaptic sources to motoneurons contribute to motor control, hyperreflexia may be one contributor that affects stroke survivors. However, hyperreflexia is reported infrequently to effect force regulation post stroke. The goal was to quantify stroke related hyperreflexia with (out) a fatiguing condition and relate the findings to clinical function. To investigate how hyperreflexia affected force regulation in a non-fatiguing condition, stimulus frequency was examined in the soleus H-reflex response of stroke survivors and healthy controls. The H-reflex is an electrical analog of the stretch reflex and gives insight into the monosynaptic sensory pathway. After repetitive stimulation, stroke survivors had less H-reflex depression as compared to controls. Additionally, the slowest walking stroke survivors had less H-reflex depression. These results may indicate hyperreflexia contributes to rate depression and walking speed post stroke. Further implications on how hyperreflexia affected force regulation were investigated with patellar tendon tap (TT) responses during a fatiguing knee extensor task in stroke survivors and healthy controls. Additionally, the contributions of voluntary muscle strength, neural drive and involuntary muscle property responses were probed. Central mechanisms may primarily affect force regulation after fatigue because stroke survivors had less muscle property and maximal voluntary contraction reductions, along with greater voluntary activation reduction as compared to controls. Likewise, stroke survivors had higher post TT responses and less TT change after fatigue, which may suggest hyperreflexia with paresis may contribute to decreased force regulation. Additionally, stroke survivors with fewer baseline central impairments had less clinical dysfunctions. Hyperreflexia and impairments in the nervous system may decrease force regulation post stroke. Moreover, quantitative metrics of neuromuscular impairments may relate to clinical function measures, which may reveal central mechanisms need to be treated to improve force regulation.