Date of Award

Summer 2013

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Biomedical Engineering

First Advisor

Schindler-Ivens, Sheila Marie

Second Advisor

Johnson, Michelle J.

Third Advisor

Wang, Jinsung

Abstract

The differences in the neural mechanisms contributing to upper and lower extremity movement have not been fully elucidated, and this might be a factor that leads to the ineffectiveness of rehabilitation techniques for most stroke survivors. It is unclear whether therapies designed for upper extremities should also be used for the lower extremities, and vice versa. In this study, fMRI was used to examine the supraspinal control of UE and LE movement in both neurologically intact individuals and people with post-stroke hemiparesis. We compared the location, volume, and intensity of brain activity associated with upper and lower extremity pedaling and unilateral flexion/extension of the hand and ankle. We hypothesized that if the supraspinal control strategies were the same for upper and lower extremities, then the pattern of brain activity would be the same across upper and lower limb movement.

Alternatively, if the strategies were not the same, then brain activation would differ for each task. We found movement related brain activity in three cortical regions (S1, M1, and Brodmann Area 6) among healthy subjects. The location of activity complied with the somatotopic order in the sensorimotor cortex, but upper extremity produced greater activities during both pedaling and flexion/extension movement compared to the lower extremities. These observations suggested that the general brain activation strategies were similar between upper and lower extremities, while the involvement of cortical structures was more substantial for upper than lower limb movements. The four stroke subjects showed activity in the same regions as compared to the healthy group, yet the volume, intensity and symmetry of activation varied across the subjects and motor tasks. These observations suggested that there were multiple strategies for cortical reorganization after stroke and the controlling strategies for the effectors differed.

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