International Handbook of Clinical Hypnosis - E-Lib FK UWKS

NEUROPSYCHOPHYSIOLOGY OF HYPNOSIS 71
overall right hemisphere involvement at the bipolar parieto-occipital derivation.In
an EEG study of cold pressor pain, with and without hypnotic analgesia, Crawford
1990) found hemispheric shifts in theta power production during hypnotic
analgesia only among highs, while lows showed no hemispheric asymmetries.In
the temporal region the highs were signi®cantly more left hemisphere dominant
during the pain dip while concentrating on the pain, but during hypnotic analgesia
there was a shift to right hemisphere theta power dominance.This was interpreted
as further evidence for the involvement of the frontal attentional system and
possibly the hippocampal region during pain inhibition Crawford, 1990; 1994a,b).
Typically there is continuing autonomic reactivity increases in galvanic skin
responses, blood pressure and pulse) to acute pain during hypnotic analgesia,
although some exceptions have been noted in well-trained, highly hypnotizable
persons Hilgard & Hilgard, 1994).Dynamic pupillary measurements revealed that
the reduction of pain through hypnotic suggestions was accompanied by an
autonomic deactivation Grunberger, Linzmayer, Walter et al., 1995).
Biochemical studies of hypnotic analgesia are thus far very limited, but encouraging.The
role of endorphins in hypnotic analgesia has been explored since these
endogenous substances were implicated in analgesia effects produced by acupuncture
e.g., Kisser et al., 1983) and placebo Grevert, Albert & Goldstein, 1983). The
opiate antagonist naloxone typically does not reverse hypnotic alleviation of
chronic Spiegel & Albert, 1983) or acute Goldstein & Hilgard, 1975; Joubert &
van Os, 1989; Moret, Forster, Laverriere et al., 1991) pain. Yet, Stevenson 1978)
reported such a reversal in a single subject and Hilgard personal communication,
1976) observed a reversal in a pilot subject.Only under conditions of environmental
stress did Frid and Singer 1980) ®nd naloxone could signi®cantly reverse
hypnotic analgesia levels.
Preliminary research e.g., Domangue, Margolis, Lieberman & Kaji, 1985;
Sternbach, 1982) suggests other neurochemical processes may be involved in
hypnosis.Arthritic patients who reported signi®cant reductions in pain after
hypnoanalgesia showed signi®cant posttreatment enhancement of the mean plasma
level of beta-endorphin-immunoreactivity but no changes in plasma levels of
epinephrine, dopamine or serotonin Domangue et al., 1985). There is recent
neurophysiological evidence that some descending inhibitory control systems are
responsive to naloxone while others are not.Noradrenaline, acetylcholine and
dopamine are non-opioid transmitters that are involved in analgesia and possibly
hypnotic analgesia.Which of these non-opioid transmitters and descending inhibitory
systems may be affected by hypnotic analgesia is worthy of investigation.
At the peripheral nervous system, the effect of hypnosis per se and hypnotic
analgesia on re¯ex activity has been considered.Motor-neuron excitability, as
measured by the Hoffman re¯ex amplitude of the soleus muscle, was decreased
signi®cantly during hypnosis in high but not low hypnotizables, yet manipulations
of suggested analgesia or paralysis had no further effect Santarcangelo, Busse &
Carli, 1989).Kiernan, Dane, Phillips and Price 1995) found that hypnotic