A variety of central nervous system injuries, diseases, and developmental d
eficits can lead to motor disorders that present complex mixtures of sympto
ms. Those that have a fundamental similarity characterized by the appearanc
e of exaggerated velocity-dependent resistance to the lengthening of skelet
al muscles are called spasticity. Reports based on clinical observations of
motor disorders have and continue to provide the essential database of inf
ormation regarding the range and distribution of unifying and discordant fe
atures of spasticity. Laboratory investigations employing animal models of
motor disorders following experimental lesions of the central nervous syste
m have reproduced some of the neurophysiologic changes that accompany injur
y of the central nervous system in humans. Those experimental lesions produ
ced by spinal cord contusion/compression reproduce many of the histopatholo
gic features displayed in traumatic injury of the human spinal cord as well
. Studies using this model have revealed not only changes in reflex thresho
ld and amplitude but also alterations in fundamental rate-modulation proces
ses that regulate reflex excitability during repetitive stimulation. This r
eport characterizes insights obtained from a laboratory investigation in se
arch of fundamental mechanisms that contribute to the development of spasti
city and provides a vantage point for understanding therapeutic strategies
for treatment of spasticity.