Effects of hypnosis on diffuse noxious inhibitory controls.

The neurophysiological mechanisms of hypnotic analgesia are still under debate. It is known that pain occurring in one part of the body (counterstimulation) decreases pain in the rest of the body by activating the diffuse noxious inhibitory controls (DNICs). The aim of this study was to explore the effects of hypnosis on both pain perception and heterotopic nociceptive stimulation. The A forms of both the Harward Group Scale of Hypnotic Susceptibility and the Stanford Hypnotic Susceptibility Scale were administered to 50 healthy students. Twenty subjects were selected and assigned to two groups: group A, consisting of 10 subjects with high hypnotic susceptibility; and group B, consisting of 10 subjects with low hypnotic susceptibility. The subjects were then randomly assigned first to either a control session or a session of hypnotic analgesia. The nociceptive flexion reflex (RIII) was recorded from the biceps femoris muscle in response to stimulation of the sural nerve. The subjective pain threshold, the RIII reflex threshold, and the mean area with suprathreshold stimulation were determined. Heterotopic nociceptive stimulation was investigated by the cold-pressor test (CPT). During and immediately after the CPT, the subjective pain threshold, pain tolerance, and mean RIII area were determined again. The same examinations were repeated during hypnosis. Hypnosis significantly reduced the subjective pain perception and the nociceptive flexion reflex. It also increased pain tolerance and reduced pain perception and the nociceptive reflex during the CPT. These effects were found only in highly susceptible subjects. However, the DNIC's activity was less evident during hypnosis than during the CPT effects without hypnosis. Both hypnosis and DNICs were able to modify the perception of pain. It seems likely that DNICs and hypnosis use the same descending inhibitory pathways for the control of pain. The susceptibility of the subject is a critical factor in hypnotically induced analgesia.