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Prog Brain Res. 2011;188:167-80. doi: 10.1016/B978-0-444-53825-3.00016-4.

Chapter 11--novel mechanism for hyperreflexia and spasticity.

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  • 1Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.

Abstract

We established that hyperreflexia is delayed after spinal transection in the adult rat and that passive exercise could normalize low frequency-dependent depression of the H-reflex. We were also able to show that such passive exercise will normalize hyperreflexia in patients with spinal cord injury (SCI). Recent results demonstrate that spinal transection results in changes in the neuronal gap junction protein connexin 36 below the level of the lesion. Moreover, a drug known to increase electrical coupling was found to normalize hyperreflexia in the absence of passive exercise, suggesting that changes in electrical coupling may be involved in hyperreflexia. We also present results showing that a measure of spasticity, the stretch reflex, is rendered abnormal by transection and normalized by the same drug. These data suggest that electrical coupling may be dysregulated in SCI, leading to some of the symptoms observed. A novel therapy for hyperreflexia and spasticity may require modulation of electrical coupling.

Copyright © 2011 Elsevier B.V. All rights reserved.

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