Date of Award

Spring 2002

Document Type

Thesis

Degree Name

Master of Science in Biomedical Engineering - (M.S.)

Department

Biomedical Engineering Committee

First Advisor

Richard A. Foulds

Second Advisor

David S. Kristol

Third Advisor

Tara L. Alvarez

Abstract

It is generally accepted that spasticity results from changes in the excitability of the stretch reflex. This change lowers the threshold of the motoneurons of the spinal cord where the integration of a signal from velocity/position sensors is processed and then fed back to the contracting muscle (alphaextrafusal and gamma-intrafusal fibers). The stretch reflex depends on the initial length of the muscle, the stretch velocity and voluntary activity. The exact sequence of the triggering events remains unknown, is poorly understood and as a result is controversial. The clinical classification scales are mainly subjective and by definition, inaccurate.

This computational model of spasticity is based on the concept of the existence of a normal neuromuscular control coupling function, which ordinarily encloses the extrafusal and intrafusal fibers, and explains the spasticity as a result of the uncoupling of this normal mechanism. The model involves mechanical parameters and basic neuromuscular control theory.

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