Date of Award
Spring 2025
Document Type
Thesis
Degree Name
Master of Science (MS)
Department
Biomedical Engineering
First Advisor
Allison Hyngstrom
Second Advisor
Brian Schmit
Third Advisor
Francesco Negro
Abstract
Stroke causes deficits in regulating submaximal forces, which are essential for maintaining postural control and performing coordinated motor tasks. These deficits are often attributed to stroke related damage in the motor cortex and corticospinal tract, which disrupts descending neural drive to motor neuron pools, and can influence force steadiness and motor unit (MU) firing behavior. Stroke survivors also experience greater neuromuscular fatiguability than neurotypical controls, which is closely linked to impaired motor unit function. However, the extent to which disruptions in descending neural input impacts MU firing behavior has not been well documented in stroke at baseline, nor when fatigued. Therefore, the primary purpose of this study was to quantify stroke related changes in fluctuations in common synaptic drive (CSD) and relate them to force steadiness in stroke survivors during a fatiguing contraction. Nineteen chronic stroke survivors and 15 age and sex matched neurotypical controls performed a sustained submaximal fatiguing contraction at 30% of their maximum voluntary isometric contraction. We examined the role of fluctuations in CSD to motor neuron pools on force steadiness by using a multichannel convolutive blind source separation technique to extract individual motor units in the vastus lateralis from high-density surface electromyography (EMG) recordings during the first and last 10% of the fatigue. Stroke survivors exhibited greater relative magnitudes of fluctuations in CSD and decreased force steadiness at baseline and during fatigue compared to controls. Reduced force steadiness at baseline and during fatigue correlated with increased baseline variability in CSD in stroke, but not in controls. Additionally, we found that decreased force steadiness correlated with greater variability in motor unit discharge rates at baseline and during fatigue. Our findings suggest that increased baseline variability in CSD in stroke may contribute to the impaired motor control often seen in stroke survivors and their motor systems may be more vulnerable to fatigue related disruptions in CSD, as CSD variability also increased as a result of time. Furthermore, stroke survivors may rely more heavily on CSD to activate muscles and generate movement.
