Evaluation of spinal-cortical excitability by transcranial magnetic stimulation during and after the mixed nerve silent period generated by peripheral nerve stimulation

Mixed nerve silent period (MNSP) and cortical silent period (CoSP) both defined as the suppression periods in the EMG activity recorded from the voluntary contracting muscle; occur as a result of electrical stimulation of the peripheral mixed nerve and a single stimulation over the primary motor cortex respectively. At the end of each supression period returning to the baseline occurs with an increased EMG activity (facilitation). In our study, it was aimed to elucidate the physiological mechanisms of CoSP, MNSP and the facilitation periods. For this purpose; silent period, latency of facilitation, area of facilitation and latency of peak amplitude parameters were measured in test MNSP and test CoSP experiments by using only electrical stimulation and only TMS, in 9 healthy volunteers. The variation of these parameters by conditioning with coinciding the facilitation period of MNSP with the onset of CoSP and coinciding the facilitation period of CoSP with the onset of MNSP were analysed. In addition, a short latency afferent inhibition (SAI) test measurement was recorded from the muscle both at the rest and voluntary contraction. Conditional-SAI studies in which SAI was coincided with the onset and facilitation periods of MNSP, compared with the SAI test measurements. In the analysis of the data; CoSP facilitation did not occur while matching the facilitation period of CoSP with the onset of MNSP, and the facilitation period which occurred lately was at a similar latency with the test-MNSP facilitation period (88.3±6.07 ms and 86.11±4.84 ms, p= 0.401). While matching the facilitation period of MNSP with the onset of CoSP, a significant shortening was observed in the duration of CoSP (84.44±7.78 ms and 54.78 ± 13.53ms, p= 0.014) and latency of facilitation (266.78±17.3 and 220.13±19.82, p=0.049). In addition, latency of MNSP facilitation was significantly prolonged-delayed (151.78±10.99 vs 220.13±19.82p=0.000). Compared to test stimulation, when SAI was coincided with the MNSP facilitation period during rest; an increase in SAI numerical values (disinhibition) was observed. These results; 1) supported the hypothesis that the early inhibition period of the MNSP with electrical stimulation occurs at the spinal level and with inhibitory effects on the final output motor neuron 2) new findings have been obtained as the facilitation that occurs after the MNSP mainly occurs at the cortical level and that spinal mechanisms also contribute 3) also new findings promote the hypothesis of cortical facilitating mechanisms are mainly involved in the facilitation period after CoSP. The findings obtained in this study, in which two different stimulus paradigms that cause inhibitory and then facilitator effects on voluntary activity in healthy individuals were examined, provided new information on the physiological mechanisms of CoSP and MNSP. In different neurological diseases such as dystonia, in which disinhibition is involved in the pathophysiology, these findings related to MNSP and CoSP in healthy individuals may provide a diagnostic contribution with further studies. It is thought that the findings obtained in our study may contribute to the development of treatment strategies targeting different inhibitory mechanisms. Keywords: Mixed Nerve Silent Period, Cortical Silent Period, Transcranial Magnetic Stimulation