Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man.

We examined Hoffmann (H) and tendon (T) reflexes in 3 populations of adult subjects: acute SCI (< 2 weeks post injury), controls, and chronic 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 amplitudes 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 showed greatest attenuation for a given stimulus rate in acute SCI subjects compared to controls (intermediate attenuation) or chronic SCI (limited attenuation) subjects. Both rate sensitivity and vibration influence have been linked to presynaptic inhibitory mechanisms. We suggest that spinal cord injury disrupts the supraspinal influence over segmental interneurons mediating presynaptic inhibition, and that the hyporeflexia associated with 'spinal shock' is due in part to a substantial increase in the efficacy of presynaptic inhibition. Conversely, over time the level of presynaptic inhibition of ankle extensor Ia input in SCI subjects declines to levels less than those of control subjects, contributing to the enhancement of spinal reflexes consistent with the clinical state of 'spasticity' seen in chronic SCI.