, 1990, 1993; Bisiach et al., 1991). Arousal effects due to the subjective feelings www.selleckchem.com/hydroxysteroid-dehydrogenase-hsd.html induced by vestibular stimulation, such as vertigo and dizziness, would be expected to be short-lived, and to generalise across modalities, while spatial effects would be expected to predominantly influence processing of stimuli to the left hand. Our results instead suggest that the vestibular system directly, and differentially modulates the activity in individual sensory submodality pathways for a period of at least several minutes. Variability in CVS
effects across individuals probably reflects differences in effectiveness of irrigation. Our correlation results are consistent with the view that vestibular stimulation, though more successful in some participants than in others, had linked effects on both touch and pain. Inference from these correlations should be cautious,
given the small size of our sample, hence low statistical power. However, the pattern of correlations p38 inhibitors clinical trials suggested a single underlying factor loading both on standard oculomotor measures of vestibular stimulation, and on both touch and pain measures. Future research with larger samples might usefully investigate whether vestibular inputs have dissociable effects on spatial representation and on somatic sensation. However, these results are consistent with either of two possible neural models of vestibular-somatosensory interaction ( Fig. 3A). In the first model, a common vestibular input has effects on independent
systems coding for touch and pain. Crucially, on this model there is no direct interaction between touch and pain: they are simply driven by a single input. In a second model, vestibular input has a direct effect on touch, but only an indirect effect on pain. The indirect effect could be due to inhibitory links between cortical areas coding for touch and pain. In particular, increased activation of somatosensory areas due to vestibular input could, in turn, cause decreased afferent transmission in pain pathways, because of the known tactile ‘gating’ of pain ( Melzack and Wall, 1965). We also considered a third model with reverse causality, in which vestibular inputs would directly influence pain, with only indirect effects on touch through click here a pain–touch link. However, we have found little evidence in the literature for such pain–touch interactions ( Ploner et al., 2004). Moreover, our results demonstrated a CVS-induced inhibition of pain. Inhibition of pain would predict reduced influence of a pain–touch link after CVS, implying reduced facilitation of tactile perception. In fact, vestibular enhancement of touch was found, ruling out this third model. To compare the first and second models, we performed a further experiment to measure CVS effects on thresholds for detecting radiant heat-pain, evoked by laser stimulation of Aδ afferents, without touching the skin.