Scientific basis of spasticity: insights from a laboratory model.
A variety of central nervous system injuries, diseases, and developmental deficits can lead to motor disorders that present complex mixtures of symptoms. Those that have a fundamental similarity characterized by the appearance of exaggerated velocity-dependent resistance to the lengthening of skeletal muscles are called spasticity. Reports based on clinical observations of motor disorders have and continue to provide the essential database of information regarding the range and distribution of unifying and discordant features of spasticity. Laboratory investigations employing animal models of motor disorders following experimental lesions of the central nervous system have reproduced some of the neurophysiologic changes that accompany injury of the central nervous system in humans. Those experimental lesions produced by spinal cord contusion/compression reproduce many of the histopathologic features displayed in traumatic injury of the human spinal cord as well. Studies using this model have revealed not only changes in reflex threshold and amplitude but also alterations in fundamental rate-modulation processes that regulate reflex excitability during repetitive stimulation. This report characterizes insights obtained from a laboratory investigation in search of fundamental mechanisms that contribute to the development of spasticity and provides a vantage point for understanding therapeutic strategies for treatment of spasticity.
Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville 32610, USA. Thompson@ufbi.ufl.edu
F J
FJ
Thompson
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Parmer
P J
PJ
Reier
D C
DC
Wang
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Bose
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D018756:GABA Antagonists / Q000494:pharmacology; D006801:Humans; D007395:Interneurons / Q000502:physiology; D009128:Muscle Spasticity / Q000209:etiology* / Q000503:physiopathology*; D009475:Neurons, Afferent / Q000187:drug effects / Q000378:metabolism; D009943:Organophosphorus Compounds / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D013117:Spinal Cord Compression / Q000150:complications*; D013119:Spinal Cord Injuries / Q000150:complications*
D015220:Calcium Channels; D018756:GABA Antagonists; D009943:Organophosphorus Compounds; D011963:Receptors, GABA-A; C066430:CGP 35348