Motor unit activity and synaptic inputs to motoneurons in the caudal part of the injured spinal cord.
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Spinal cord injury (SCI) disrupts neuronal function below the lesion epicenter, causing disuse muscle atrophy. We investigated motor unit (MU) activity and synaptic inputs to motoneurons in the caudal region of the injured spinal cord. Participants with C4-C7 cervical injuries were studied. The extensor digitorum communis (EDC) muscle, which is mainly innervated by C8, was assessed for disuse muscle atrophy. Using advanced electromyography and signal-processing techniques, we examined the concurrent activation of a substantial population of MUs during force-tracking tasks. We found that in participants with SCI (n = 9), both MU discharge rates and the amplitudes of MU action potentials were significantly lower than in controls (n = 9). After SCI, MUs were recruited in a limited force range as the strength of muscle contractions increased, implying a disruption in the orderly MU recruitment pattern. Coherence analysis revealed reduced synaptic inputs to motoneurons in the delta band (0.5-5 Hz) for participants with SCI, suggesting diminished common synaptic inputs to the EDC muscle. In addition, participants with SCI exhibited greater muscle force variability. Using principal component analysis on low-frequency MU discharge rates, we found that the first common component (FCC) captured the most discharge variability in participants with SCI. The coefficients of variation (CV) of the FCC correlated with force signal CVs, suggesting force variability mainly results from common synaptic inputs to the EDC muscle after SCI. These results advance our understanding of the neurophysiology of disuse muscle atrophy in human SCI, paving the way for therapeutic interventions to restore muscle function.NEW & NOTEWORTHY This study analyzed motor unit (MU) function below the lesion epicenter in patients with spinal cord injury (SCI). We found reduced MU discharge rates and action potential amplitudes in participants with SCI compared with controls. The strength of common synaptic inputs to motoneurons was reduced in patients with SCI, with increased force variability primarily due to low-frequency oscillations of common inputs. This study enhances understanding of neurophysiological and behavioral changes in disuse muscle atrophy post-SCI.
