Neural and Biomechanical Mechanisms of Movement Impairment in Stroke Survivors

摘要

Many stroke survivors are left with residual movement impairments. Treating these impairments has proven difficult, because it is often unclear which mechanisms drive movement impairment. While the exact mechanisms are still uncertain, at present, evidence suggests that neuromuscular function is disrupted in two key domains following stroke: muscle biomechanics, and neural control of movement.;Regarding muscle biomechanics, recent shear wave elastography evidence has demonstrated that stroke affected muscle is stiffer than contralateral muscle. However, two key questions remain: (i) "How do we interpret shear wave elastography experiments in terms of variability - what factors could introduce variability into shear wave elastography (SWE) experiments, and how important is each factor?" and (ii) "Do changes in muscle biomechanics depend on muscle length?";Regarding neural control of movement, it is clear that the function of individual motor neurons is disrupted in stroke survivors' muscles. However, it is still not clear how the motor unit pool changes in the biceps brachii, and if changes in motor unit function are reflected in surface electromyogram (EMG) signals. Finally, it is unknown which disruptions are most closely linked with muscle weakness.;Thus, in this thesis, I aimed to investigate key mechanisms that may be related to movement impairments in stroke survivors. Specifically, I aimed to: 1) Establish the repeatability of shear wave elastography and quantify the experimental sources of variability in shear wave elastography. 2) Quantify muscle biomechanics by estimating muscle's stiffness/length curve in stroke survivors. 3) Quantify the organization of the motor neuron pool and the electrical properties of stroke survivors' biceps brachii. Correlate abnormalities in muscle and motor unit function with muscle weakness.;Each aim yielded a noteworthy result. In the first study, we found that shear wave elastography was repeatable across days, and within-day. In addition, we found that muscle activation was the strongest confounding influence on the results from shear wave elastography. Following muscle activation, elbow flexion, shoulder abduction angle, and probe indentation were also significant influences on shear wave velocity. In the second study, we found that muscle elasticity was not strongly altered across the entire range of motion in most stroke survivors. In the third study, we found consistent disruptions of motor unit function. However, the only disruption that correlated with muscle weakness was a lateralized deficit in maximum voluntary EMG activity.;Overall, these results represent an advancement in stroke pathophysiology research for several reasons. First, we have quantified the variability in SWE experiments, leading to better ability to interpret SWE experiments in human muscle. Second, we have demonstrated that most stroke survivors do not have profound alterations in muscle biomechanics. This result suggests that other factors, such as low levels of muscle activity, may play a role in stroke survivors' resting muscle tone. Finally, our results demonstrate consistent abnormalities in motor neuron and muscle function. These results were most consistent with decreased descending drive. In sum, we see these studies as a step forward towards answering the question, "What mechanisms play significant roles in post-stroke movement impairments?"