Even though interlimb coordination is critical in bipedal locomotion, the role of muscle afferent mediated feedback is unknown. The aim of this study was to establish if ipsilateral muscle generated afferent feedback can influence contralateral muscle activation patterns in the human lower limb and to elucidate the mechanisms involved. The effect of ipsilateral tibial nerve stimulation on contralateral soleus (cSOL) responses were quantified. Three interventions were investigated, 1) electrical stimulation applied to the tibial nerve at stimulation intensities from 0 to 100% of maximal M-wave (M-max) with the cSOL contracted from 5 to 15% of maximal voluntary contraction (MVC) and 15 to 30% MVC, 2) ispsilateral tibial nerve stimulation at 75% M-max prior to, during, and following the application of ischemia to the ipsilateral thigh. 3) Electrical stimulation applied to the ipsilateral sural (SuN) and medial plantar nerves at stimulation intensities from 1 to 3 times perceptual threshold. A short-latency depression in the cSOL electromyogram (EMG; onset: 37-41 ms) was observed following ipsilateral tibial nerve stimulation. The magnitude of this depression increased (P = 0.0005 and P = 0.000001) with increasing stimulus intensities. Ischemia delayed the time of the minimum of the cSOL depression (P = 0.04). SuN and medial plantar nerve stimulation evoked a longer latency depression [average; 91.2 ms (SuN); 142 ms (medial plantar nerve)] and therefore do not contribute to the response. This is the first study to demonstrate a short-latency depression in the cSOL following ipsilateral tibial nerve stimulation. Due to its short latency, the response is spinally mediated. The involvement of crossed spinal interneurons receiving input from low-threshold muscle afferents is discussed.

Short-latency spinally mediated interlimb reflex pathways were recently reported between the left and right soleus muscles in the human lower-limb during sitting. The aim of the current study was to establish if these pathways were observed during a functional motor task such as human gait and modulated by the gait cycle phase and/or electrical stimulation intensity. The second aim was to elucidate on the afferents involved. Two interventions were investigated. First was ipsilateral tibial nerve (iTN) stimulation at motor threshold (MT), 35% of the maximal peak-to-peak M-wave(M-Max) and 85% M-Max (85M-Max) with stimuli applied at 60%, 70%, 80%, 90%, and 100%of the gait cycle of the ipsilateral leg. Second was ipsilateral sural nerve (SuN) and medial plantar nerve (MpN) stimulation at 1, 2, and 3X perceptual threshold at 90% of the gait cycle [corrected]. The root mean squared (RMS) of the contralateral soleus (cSOL) responses were analyzed in a time window, 40-55 ms (or 45-60 ms for subjects >50 y/o) following iTN stimulation. The most consistent responses occurred at 90 and 100% of the gait cycle at higher stimulation intensities of the iTN. Significantly inhibitory responses (P = 0.006) were reported at 60 versus 80% (P = 0.03), 90% (P = 0.006), and 100% (P = 0.002) and 70 versus 90% (P = 0.02) and 100% (P = 0.009) of the gait cycle at 85M-Max. The responses became more inhibitory with increasing stimulation intensities at 80% (P = 0.01), 90% (P = 0.001), and 100% (P = 0.004) of the gait cycle. Stimulation of the MpN and SuN at all stimulation intensities demonstrated no short-latency responses. Therefore, it is unlikely that afferents within these nerves contribute to the response. This is the first study to show short-latency spinally mediated responses in the cSOL following iTN stimulation, during walking. It provides evidence for a new spinal pathway contributing to motor control and demonstrates that the response likely has functional relevance.

The activity of this spinal pathway can be quantified using H-reflex conditioning to provide a controlled model for further studies of this response.

The current study indicates microstructural changes in the thalamus and corpus callosum from within 14 days to 3 months after mTBI and suggests MKT as a potential biomarker after mTBI.