Facilitation of descending excitatory and spinal inhibitory networks from training of endurance and precision walking in participants with incomplete spinal cord injury.

After incomplete spinal cord injury (iSCI), training of walking function that emphasizes both endurance and speed may produce different changes in spared neural pathways compared to precision training that emphasizes walking over obstacles and precise placement of the foot. To examine this, 16 participants with iSCI received 2 months of endurance or precision training, in random order, with 2 months of rest before crossing-over to the other type of training. Both forms of training increased the maximum motor-evoked potential (MEPmax) elicited by transcranial magnetic stimulation over the motor cortex, but only in tibialis anterior (TA) muscles that had small (<0.5 mV) MEPmax values before training, no matter when the specific type of training was performed. A similar pattern of training-induced increases in maximum voluntary contractions was also observed. Although walking function was improved by both forms of training, a positive correlation between MEPmax and clinical measures of walking function only occurred after endurance training. Endurance and precision training also increased the excitability of inhibitory spinal networks, as demonstrated by an increase in the suppression of TA MEPs by a prior, low-threshold stimulation to the common peroneal nerve and by increases in the inhibitory component of the cutaneomuscular reflex. The increase in the descending excitation of the spinal cord and the increase in excitability of inhibitory spinal networks may mediate the improved volitional control of walking and reduction of involuntary muscle spasticity, respectively, that are observed in response to intensive motor training in participants with incomplete spinal cord injury.

Long-latency, inhibitory spinal pathway to ankle flexors activated by homonymous group 1 afferents.

Inhibitory feedback from sensory pathways is important for controlling movement. Here, we characterize, for the first time, a long-latency, inhibitory spinal pathway to ankle flexors that is activated by low-threshold homonymous afferents. To examine this inhibitory pathway in uninjured, healthy participants, we suppressed motor-evoked potentials (MEPs), produced in the tibialis anterior (TA), by a prior stimulation to the homonymous common peroneal nerve (CPN). The TA MEP was suppressed by a triple-pulse stimulation to the CPN, applied 40, 50, and 60 ms earlier and at intensities of 0.5-0.7 times motor threshold (average suppression of test MEP was 33%). Whereas the triple-pulse stimulation was below M-wave and H-reflex threshold, it produced a long-latency inhibition of background muscle activity, approximately 65-115 ms after the CPN stimulation, a time period that overlapped with the test MEP. However, not all of the MEP suppression could be accounted for by this decrease in background muscle activity. Evoked responses from direct activation of the corticospinal tract, at the level of the brain stem or thoracic spinal cord, were also suppressed by low-threshold CPN stimulation. Our findings suggest that low-threshold muscle and cutaneous afferents from the CPN activate a long-latency, homonymous spinal inhibitory pathway to TA motoneurons. We propose that inhibitory feedback from spinal networks, activated by low-threshold homonymous afferents, helps regulate the activation of flexor motoneurons by the corticospinal tract.