EVIDENCE THAT ALTERATIONS IN PRESYNAPTIC INHIBITION CONTRIBUTE TO SEGMENTAL HYPOEXCITABILITY AND HYPEREXCITABILITY AFTER SPINAL-CORD INJURYIN MAN

Citation
B. Calancie et al., EVIDENCE THAT ALTERATIONS IN PRESYNAPTIC INHIBITION CONTRIBUTE TO SEGMENTAL HYPOEXCITABILITY AND HYPEREXCITABILITY AFTER SPINAL-CORD INJURYIN MAN, Electroencephalography and clinical neurophysiology, 89(3), 1993, pp. 177-186
Citations number
56
Categorie Soggetti
Neurosciences
ISSN journal
00134694
Volume
89
Issue
3
Year of publication
1993
Pages
177 - 186
Database
ISI
SICI code
0013-4694(1993)89:3<177:ETAIPI>2.0.ZU;2-L
Abstract
We examined Hoffmann (H) and tendon (T) reflexes in 3 populations of a dult subjects: acute SCI ( < 2 weeks post injury), controls, and chron ic SCI ( > 1 year post injury). We further investigated the effects of continuous tendon vibration and different stimulus rates on the size of evoked H reflexes in these,subject populations. All reflex amplitud es were expressed as a function of the maximum direct muscle response (M wave), to allow comparison between subjects. Both H and T reflexes were successfully-elicited from all subjects examined, including those in 'spinal shock.' Tendon vibration caused a marked attenuation of H reflexes in acute SCI subjects, intermediate attenuation in controls, and relatively little effect in the chronic SCI group. H reflexes show ed greatest attenuation for a given stimulus rate in acute SCI subject s compared to controls (intermediate attenuation) or chronic SCI (limi ted attenuation) subjects.Both rate sensitivity and vibration influenc e have been linked to presynaptic inhibitory mechanisms. We suggest th at spinal cord injury disrupts the supraspinal influence over segmenta l interneurons mediating presynaptic inhibition, and that the hyporefl exia associated with 'spinal shock' is due in part to a substantial in crease in the efficacy of presynaptic inhibition. Conversely, over tim e the level of presynaptic inhibition of ankle extensor Ia input in SC I subjects declines to levels less than those of control subjects, con tributing to the enhancement of spinal reflexes consistent with the cl inical state of 'spasticity' seen in chronic SCI.