Different strategies of modulation can be operative during hypnotic analgesia: a neurophysiological study.

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.

Comparative effects of electroacupuncture and transcutaneous nerve stimulation on the human blink reflex.

The effects of low frequency (2 Hz) high intensity (10-12 mA) (electroacupuncture, EA) and of high frequency (100 Hz) low intensity (2 mA) (transcutaneous nerve stimulation, TNS) conditioning stimuli were studied on the nociceptive component (R2) of the blink reflex in normal volunteers. EA induced a progressive and moderate partially naloxone-reversible depression in the R2 response. In contrast, TNS induced a rapid and major depression in this reflex. In this latter case, naloxone failed to produce any reversal effect. These two patterns of data are discussed and further electrophysiological studies provide some evidence for two different mechanisms in the depressive effects of EA and TNS upon the nociceptive component of the blink reflex in man.