Date of Award

Fall 2003

Document Type

Thesis - Restricted

Degree Name

Master of Science (MS)

Department

Biomedical Engineering

First Advisor

Schmit, Brian D.

Second Advisor

Brown, David A.

Third Advisor

Harris, Gerald F.

Abstract

Stroke causes a number of functional problems in the neuromuscular system, including muscle spasticity and poor motor control during locomotion. One hypothesis for this loss of muscular control is that the normal locomotor response to hip proprioception is modified following a stroke. The hip position is believed to play an important role in the peripheral regulation of gait. To determine the role hip proprioceptors play during gait, a single-limbed pedaling study that alters the sensorimotor input from hip proprioceptors by changing hip and knee phasing was developed. The normal phasic hip and knee motion was converted to anti-phasic motion such that hip flexion and knee extension occurred simultaneously, and vice versa. Non-impaired and post-stroke subjects performed these pedaling tasks while electromyography (EMG) data was being collected from four lower limb muscles: vastus medialis, rectus femoris, biceps femoris, and semimembranosus. The results from this study showed that the muscle activity of paretic uniarticular knee extensors, such as the vastus medialis, was anti-phased with respect to controls in that the activity was more strongly correlated with hip extension rather than physiologic knee extension. The rectus femoris, a biarticular knee extensor/hip flexor, acted like the vastus medialis and was also correlated with hip extension rather than physiologic knee extension, but with greater variability. The hamstrings were anti-phased with respect to non-impaired subjects (i.e. activity occurred during hip flexion and knee extension rather than during hip extension and knee flexion). The muscles of the non-paretic leg showed variable results. Half of the subjects showed muscle patterns similar to that of controls and the other half similar to that of the paretic leg. This may be due to cortical reorganization of the unaffected side. The changes in hip and knee phasing caused changes in afferent information sent to the spinal pattern networks in the spinal cord, which in turn produced abnormal muscle activation patterns in the post-stroke locomotor system. Further studies are needed to explore which specific hip afferents may be responsible for the modified control of locomotion in the post-stroke nervous system.

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