<p>We have shown that single-pulse transcranial magnetic stimulation (TMS) of the dorsolateral prefrontal cortex (dlPFC) inhibits muscle sympathetic nerve activity. However, this was likely due to arousal caused by the TMS pulses themselves, rather than altering the underlying neuronal circuitry. In extension, we have aimed to explore the effects of single-pulse TMS on skin sympathetic nerve activity (SSNA), which is more sensitive to arousal. It was hypothesised that TMS-evoked arousal would increase SSNA but would not generate <i>de novo</i> bursts from the dlPFC. Microneurographic recordings were taken from the right common peroneal nerve in 10 participants. TMS pulses were then delivered to the ipsilateral dlPFC at resting motor threshold (MT) of the finger, at stimulator output intensities 20% and 10% below MT, and at 110% and 120% of MT. The MT and 110% of MT intensities were also used in stimulating the right motor cortex and shoulder. Reductions in SSNA from baseline were seen at almost all intensities, and these mostly did not differ between intensities or sites despite the appearance of SSNA bursts after each pulse. This suggests that TMS is simply generating an arousal response, leading to initial excitation of SSNA followed by a period of sympathoinhibition.</p>

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Cortical excitation does not drive changes in skin sympathetic nerve activity during single-pulse transcranial magnetic stimulation in humans

  • Brendan McCarthy,
  • Donggyu Rim,
  • Gianni Sesa-Ashton,
  • Luke A. Henderson,
  • Vaughan G. Macefield

摘要

We have shown that single-pulse transcranial magnetic stimulation (TMS) of the dorsolateral prefrontal cortex (dlPFC) inhibits muscle sympathetic nerve activity. However, this was likely due to arousal caused by the TMS pulses themselves, rather than altering the underlying neuronal circuitry. In extension, we have aimed to explore the effects of single-pulse TMS on skin sympathetic nerve activity (SSNA), which is more sensitive to arousal. It was hypothesised that TMS-evoked arousal would increase SSNA but would not generate de novo bursts from the dlPFC. Microneurographic recordings were taken from the right common peroneal nerve in 10 participants. TMS pulses were then delivered to the ipsilateral dlPFC at resting motor threshold (MT) of the finger, at stimulator output intensities 20% and 10% below MT, and at 110% and 120% of MT. The MT and 110% of MT intensities were also used in stimulating the right motor cortex and shoulder. Reductions in SSNA from baseline were seen at almost all intensities, and these mostly did not differ between intensities or sites despite the appearance of SSNA bursts after each pulse. This suggests that TMS is simply generating an arousal response, leading to initial excitation of SSNA followed by a period of sympathoinhibition.