Kun‐Ze Lee, Rui-Yi Chen, Stéphane Vinit, Li‐Min Liou
The current investigation aimed to establish a respiration-triggered trans-spinal magnetic stimulation configuration and examine its modulatory effect on bilateral diaphragmatic motor-evoked potentials following cervical spinal cord injury. Diaphragmatic motor-evoked potential responses were assessed during inspiration- and expiration-triggered trans-spinal magnetic stimulation under different respiratory drives (i.e., normocapnia and hypercapnia) in both spinal-intact and cervical spinal cord contused rats. The results demonstrated that inspiration-triggered trans-spinal magnetic stimulation elicited a greater bilateral diaphragmatic motor-evoked potential response compared with expiration-triggered trans-spinal magnetic stimulation in uninjured animals. Moreover, heightened respiratory drives induced by hypercapnia diminished the bilateral diaphragmatic motor-evoked potential response during respiration-triggered trans-spinal magnetic stimulation. Notably, high-intensity inspiration-triggered trans-spinal magnetic stimulation mitigated diaphragmatic bursting that occurred after motor-evoked potentials (i.e., post-motor-evoked potential activity). Cervical spinal cord contusion not only reduced inspiratory diaphragmatic activity but also influenced trans-spinal magnetic stimulation-induced diaphragmatic motor-evoked potentials. Specifically, the respiratory modulatory effect of trans-spinal magnetic stimulation on diaphragmatic motor-evoked potentials was blunted in the diaphragm ipsilateral to the lesion. Additionally, the inhibitory impact of inspiration-triggered trans-spinal magnetic stimulation on post-motor-evoked potential activity was also attenuated in contused animals. These results suggest that the effect of trans-spinal magnetic stimulation on diaphragmatic motor-evoked potentials is modulated by respiratory phases and drives. Respiration-triggered trans-spinal magnetic stimulation may serve as a tool to evaluate changes in diaphragm excitability and spinal respiratory circuits following cervical spinal cord injury.