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Proprioceptive neuropathy affects normalization of the H-reflex by exercise after spinal cord injury
Journal article   Open access   Peer reviewed

Proprioceptive neuropathy affects normalization of the H-reflex by exercise after spinal cord injury

Karen Ollivier-Lanvin, Benjamin E Keeler, Rachel Siegfried, John D Houlé and Michel A Lemay
Experimental neurology, v 221(1), pp 198-205
Jan 2010
DOI: https://doi.org/10.1016/j.expneurol.2009.10.023
PMID: 19913536
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https://doi.org/10.1016/j.expneurol.2009.10.023View
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Abstract

H-Reflex - physiology Rats, Wistar Spinal Cord Injuries - pathology Pyridoxine - adverse effects Neurotoxicity Syndromes - pathology Nerve Fibers, Myelinated - pathology Reaction Time - drug effects Nerve Fibers, Myelinated - physiology Female Neurons - drug effects Electric Stimulation - methods Disease Models, Animal Pyridoxine - pharmacology Exercise Therapy - methods Proprioception - physiology Nerve Fibers, Myelinated - drug effects Rats Reaction Time - physiology Rats, Sprague-Dawley Neurotoxicity Syndromes - etiology Animals Analysis of Variance Ganglia, Spinal - pathology Neurotoxicity Syndromes - physiopathology Spinal Cord Injuries - rehabilitation Spinal Cord Injuries - physiopathology Electromyography - methods
The H-reflex habituates at relatively low frequency (10 Hz) stimulation in the intact spinal cord, but loss of descending inhibition resulting from spinal cord transection reduces this habituation. There is a return towards a normal pattern of low-frequency habituation in the reflex activity with cycling exercise of the affected hind limbs. This implies that repetitive passive stretching of the muscles in spinalized animals and the accompanying stimulation of large (Group I and II) proprioceptive fibers has modulatory effects on spinal cord reflexes after injury. To test this hypothesis, we induced pyridoxine neurotoxicity that preferentially affects large dorsal root ganglia neurons in intact and spinalized rats. Pyridoxine or saline injections were given twice daily (IP) for 6 weeks and half of the spinalized animals were subjected to cycling exercise during that period. After 6 weeks, the tibial nerve was stimulated electrically and recordings of M and H waves were made from interosseous muscles of the hind paw. Results show that pyridoxine treatment completely eliminated the H-reflex in spinal intact animals. In contrast, transection paired with pyridoxine treatment resulted in a reduction of the frequency-dependent habituation of the H-reflex that was not affected by exercise. These results indicate that normal Group I and II afferent input is critical to achieve exercise-based reversal of hyper-reflexia of the H-reflex after spinal cord injury.

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