Facilitatory conditioning of the supplementary motor area in humans enhances the corticophrenic responsiveness to transcranial magnetic stimulation

Raux M, Xie H, Similowski T, Koski L. Facilitatory conditioning of the supplementary motor area in humans enhances the corticophrenic responsiveness to transcranial magnetic stimulation. J Appl Physiol 108: 39-46, 2010. First published November 5, 2009; doi:10.1152/japplphysiol.91454.2008.-Inspiratory loading in awake humans is associated with electroencephalographic signs of supplementary motor area (SMA) activation. To provide evidence for a functional connection between SMA and the diaphragm representation in the primary motor cortex (M1(DIA)), we tested the hypothesis that modulating SMA activity using repetitive transcranial magnetic stimulation (rTMS) would alter M1DIA excitability. Amplitude and latency of diaphragm motor evoked potentials (MEP(DIA)), evoked through single pulse M1DIA stimulation, before and up to 16 min after SMA stimulation, were taken as indicators of M1DIA excitability. MEPs from the first dorsal interosseous muscle (FDI, MEP(FDI)) served as a control. Four SMA conditioning sessions were performed in random order at 1-wk intervals. Two aimed at increasing SMA activity (5 and 10 Hz, both at 110% of FDI active motor threshold; referred to as 5Hz and 10Hz, respectively), and two aimed at decreasing it (1 Hz either at 110% of FDI active or resting motor threshold, referred to as aMT or rMT, respectively). The 5Hz protocol increased MEPDIA and MEPFDI amplitudes with a maximum 11-16 min post-stimulation (P = 0.04 and P = 0.02, respectively). The 10Hz protocol increased MEPFDI amplitude with a similar time course (P = 0.03) but did not increase MEPDIA amplitude (P = 0.32). Both aMT and rMT failed to decrease MEPDIA or MEPFDI amplitudes (P = 0.23 and P = 0.90, respectively, for diaphragm and P = 0.48 and P = 0.14 for FDI). MEPDIA and MEPFDI latencies were unaffected by rTMS. These results demonstrate that 5-Hz rTMS over the SMA can increase the excitability of M1DIA. These observations are consistent with the hypothesis of a functional connection between SMA and M1DIA.