Vestibular and pulse-related modulation of skin sympathetic nerve activity during sinusoidal galvanic vestibular stimulation in human subjects

We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), a means of a selectively modulating vestibular afferent input without affecting other inputs, can cause partial entrainment of muscle sympathetic nerve activity (MSNA). Given that motion sickness causes sweating and pal...

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Veröffentlicht in:Experimental brain research 2010-04, Vol.202 (2), p.291-298
Hauptverfasser: James, Cheree, Stathis, Alexandra, Macefield, Vaughan G
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Sprache:eng
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Zusammenfassung:We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), a means of a selectively modulating vestibular afferent input without affecting other inputs, can cause partial entrainment of muscle sympathetic nerve activity (MSNA). Given that motion sickness causes sweating and pallor, we tested the hypothesis that sGVS also entrains skin sympathetic nerve activity (SSNA), but that the optimal frequencies are closer to those associated with slow postural changes (0.2 Hz). SSNA was recorded via tungsten microelectrodes inserted into the common peroneal nerve in 11 awake-seated subjects. Bipolar binaural sinusoidal GVS (±2 mA, 200 cycles) was applied to the mastoid processes at frequencies of 0.2, 0.5, 0.8, 1.1, 1.4, 1.7 and 2.0 Hz. All subjects reported strong postural illusions of ‘rocking in a boat' or ‘swaying in a hammock'. Sinusoidal GVS caused a marked entrainment of SSNA at all frequencies. Measured as the modulation index, vestibular modulation ranged from 81.5 ± 4.0% at 0.2 Hz to 76.6 ± 3.6% at 1.7 Hz; it was significantly weaker at 2.0 Hz (63.2 ± 5.4%). Interestingly, pulse-related modulation of SSNA, which is normally weak, increased significantly during sGVS but was stronger at 0.8 Hz (86.2 ± 2.0%) than at 0.2 Hz (69.3 ± 8.3%), the opposite of the pattern seen with vestibular modulation of MSNA. We conclude that vestibular inputs can entrain the firing of cutaneous sympathetic neurones and increase their normally weak pulse-related rhythmicity.
ISSN:0014-4819
1432-1106
DOI:10.1007/s00221-009-2131-8