Nociceptive electrical stimuli were applied to the sural nerve during hypnotically-suggested analgesia in the left lower limb of 18 highly susceptible subjects. During this procedure, the verbally reported pain threshold, the nociceptive flexion (RIII) reflex and late somatosensory evoked potentials were investigated in parallel with autonomic responses and the spontaneous electroencephalogram (EEG). The hypnotic suggestion of analgesia induced a significant increase in pain threshold in all the selected subjects. All the subjects showed large changes (i.e., by 20% or more) in the amplitudes of their RIII reflexes during hypnotic analgesia by comparison with control conditions. Although the extent of the increase in pain threshold was similar in all the subjects, two distinct patterns of modulation of the RIII reflex were observed during the hypnotic analgesia: in 11 subjects (subgroup 1), a strong inhibition of the reflex was observed whereas in the other seven subjects (subgroup 2) there was a strong facilitation of the reflex. All the subjects in both subgroups displayed similar decreases in the amplitude of late somatosensory evoked cerebral potentials during the hypnotic analgesia. No modification in the autonomic parameters or the EEG was observed. These data suggest that different strategies of modulation can be operative during effective hypnotic analgesia and that these are subject-dependent. Although all subjects may shift their attention away from the painful stimulus (which could explain the decrease of the late somatosensory evoked potentials), some of them inhibit their motor reaction to the stimulus at the spinal level, while in others, in contrast, this reaction is facilitated.

Mental stress induces endothelial dysfunction, that is a reduction of the post-occlusion brachial artery flow-mediated vasodilation (FMD). This does not occur in subjects highly susceptible to hypnosis (Highs) in either the waking or hypnotic state. The aim of the present experiment was to assess whether endothelial dysfunction is also induced by acute nociceptive stimulation and whether high hypnotisability and/or the specific instruction of analgesia prevent its occurrence in awake highly hypnotizable individuals. Thus, nine Highs and nine subjects with low susceptibility to hypnosis (Lows) underwent an experimental session including the administration of pressor pain and of pressor pain associated with the instruction of analgesia. Heart rate, basal artery diameters and brachial artery flow-mediated vasodilation were measured during stimulation and rest conditions. Heart rate exhibited slight changes not modulated by hypnotisability. During painful stimulation both Highs and Lows showed a decrease of FMD, but it was significantly less pronounced in Highs. During the administration of painful stimulation together with the instruction of analgesia, only Highs reported analgesia and their FMD no longer decreased. This study provides the first evidence of pain-related endothelial dysfunction and extends previous findings concerning a sort of natural protection of Highs against the vascular effects of mental stress to acute pain.

Purpose: The cerebellum is involved in a wide number of integrative functions, but its role in pain experience and in the nociceptive information processing is poorly understood. In healthy volunteers we evaluated the effects of transcranial cerebel