Correlative electrophysiological and behavioral evaluation following L5 lesions in the cat: a model of spasticity

The present work developed an animal model of hindlimb spasticity by analyzing the electrophysiological and behavioral consequences of L5 spinal cord lesions in cats. In chronically lesioned animals (1 to 6 months), the L7-S1 dorsal roots were stimulated and evoked potentials were recorded from hind...

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Veröffentlicht in:Experimental neurology 1991-11, Vol.114 (2), p.206-215
Hauptverfasser: Carter, R L, Ritz, L A, Shank, C P, Scott, E W, Sypert, G W
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Sprache:eng
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Zusammenfassung:The present work developed an animal model of hindlimb spasticity by analyzing the electrophysiological and behavioral consequences of L5 spinal cord lesions in cats. In chronically lesioned animals (1 to 6 months), the L7-S1 dorsal roots were stimulated and evoked potentials were recorded from hindlimb flexor and extensor motor nerves. Following lateral hemisection, the monosynaptic responses were 2-5 times larger (for voltage-time integral and for amplitude) on the ipsilateral side than those from the contralateral side or from control animals. Half-widths, rise-times, and latencies of the monosynaptic responses were the same on both sides. Behavioral signs of spasticity, including hypertonia and increased deep tendon reflexes, were displayed from the ipsilateral hindlimb following lateral hemisection. With lateral hemisection or with extensive dorsal quadrant lesions, hopping and proprioceptive placing reflexes were abolished; these behavioral observations impart functional significance to physiological and anatomical studies of a mid-lumbar center considered to be important for movement control. The present model represents the first demonstration of a statistically significant correlation between electrophysiological and behavioral observations of spasticity for animals with a lateral hemisection. These correlations demonstrate the utility of behavioral screening of animals for subsequent neurophysiological analyses. This facilitates the investigation of cellular events underlying spasticity and of strategies for its relief with tissue repair techniques affecting local circuitry involved in spasticity.
ISSN:0014-4886
DOI:10.1016/0014-4886(91)90037-D