Hypnotherapy

There are less commonly used psychotherapy methods that can work independently of psychotropic medication. Hypnotherapy produces an altered state of consciousness that places an individual in a state of inner absorption, which reduces an individual’s focus of attention to only a few inner realities (Erickson & Rossi, 1976b; Erickson et al., 1976). A hypnotized person has relaxed muscular tonus, reduced respiration rate, which often falls to a minimum of 13-15 respirations per minute, a general body flush, and reduced reactivity to outer sensory stimulation (Christenson, 1968). A hypnotized person’s eyes are fixed and vacant in appearance; pupils are dilated (Erickson and Erickson, 1941; Erickson, 1944). Without hypnotherapist influence, the hypnotized person lacks emotionality, arousal, and awareness of one’s typical sense of self (Erickson, 1968). The hypnotherapist’s voice replaces the hypnotized person’s inner state words. This seems to compensate for the hypnotized person’s disconnect from higher executive levels (and corticolimbic locus) of control (Bowers, 1992). The hypnotized person is highly suggestive to the verbal direction embedded in and in the execution of the hypnotic suggestion (Christenson, 1968). The hypnotized person’s readiness for encoding instructions relating to the hypnotic suggestion and its later retrieval facilitates one’s implementation of the hypnotic suggestion. This is illustrative of hypnotherapy’s role in state dependent learning (Hilgard and Hilgard, 1975).

Current hypnotherapy methods help individuals to resolve and relieve the unpleasant experience of maladaptive and painful symptoms. Hypnotherapy has been shown to be efficacious at eliminating pain that has been associated with many different types of medical conditions, such as chronic and cancer pain (Hilgard and Hilgard, 1975; Hilgard & LeBaron, 1984). It works by altering the nature and degree of adversity typically associated with the painful experience. The hypnotherapist helps the individual to associate unpleasant emotion, or aversive physical sensation, or habit with an experience that is more pleasant to stop symptom reoccurrence. For example, hypnotic suggestions can offer relief of physical pain by hypnotherapist suggestion to 1.) indirectly abolish or diminish the experience of pain; 2.) associate it with amnesia, time distortion, or numbness; 3.) replace or substitute pain for other more pleasant sensations; 4.) displace pain from one innocuous area of the body to another; 5.) associate pain with age regression that would return the individual to an earlier time when the pain was not experienced; 6.) dissociate it from the rest of the person’s body; and 7.) reinterpret pain as a sensation of warmth and comfort (Erickson & Rossi, 1976a). This associative process is state dependent learning (Hilgard & Hilgard, 1975) and relieves the experience of pain by altering its aversive quality.

The hypnotic state is typically associated with the production of theta (Crawford & Guzelier, 1992). Individuals demonstrating greater basal theta power (5.5-7.5 Hz) in the frontal cortex (including the perigenual anterior cingulate (pACC)), highly hypnotizables, tend to hypnotize quicker and with greater ease than those who present a different EEG composite (Graffin et al., 1995; Crawford et al. 1993a).

As noted above, hypnotic analgesia substitutes the aversive experience of pain with a more pleasant experience. It is this substitution that offers pain relief. Post-hypnotic suggestion for pain analgesia can significantly reduce the intensity of chronic low back pain (Crawford et al., 1998) and provide relief from chronic pain from fibromyalgia (Wik et al., 1999). These findings demonstrate that electroencephalography (E.E.G.) electrical activity and Positron Emission Tomography (P.E.T.) regional cerebral blood flow (rCBF) center in the anterior frontal cortex and present rostroventral shifts from the posterior (PCC)-midcingulate (MCC) to the subgenual cingulate and orbitofrontal cortices from states of pain toward hypnotic analgesia and pain relief, respectively. (Studying the activities of these two cortical structures are of critical importance due to their role in modulating chronic and acute psychological stress.) Event-related paradigms that measure acute responses to painful heat demonstrate rather vividly that painful rCBF activations center, in part, in the caudal MCC (Hofbauer et al., 2001) and thalamus (Faymonville et al., 2000). Rainville and colleagues (1999) have referenced a negative correlation between pain-related MCC activity and the hippocampus. They have also cited a positive correlation between pain-related MCC activity and the thalamus and a negative correlation between these structures during the hypnotic state. The hypnotic state and hypnotic analgesia are mediated by the rostral MCC (Rainville et al., 1997), pACC, and orbitofrontal cortices (Maquet, 1999; Faymonville et al., 2000). In addition, pain from ischemia (Crawford et al., 1993b) and cutaneous stimuli (Kropotov et al., 1997) has been relieved by hypnotic analgesia. Analgesia produced rCBF increases in the anterior frontal and temporal cortices in the former and a significant reduction of the positive SERP (somatosensory event-related potential) component in the anterior cingulate cortex and a significant enhancement of the negative SERP in the anterior temporal cortex in the latter.

Hypnotic analgesia provides pain relief by raising pain thresholds. The hypnotic state is mediated by a cholinergic mechanism, as atropine sulfate, a cholinergic antagonist, can delay the induction of the hypnotic state and the impair the prior effectiveness of analgesia (Sternbach, 1982) in humans and attenuate neocortical desynchronization and hippocampal RSA in spontaneously immobilized and hypnotized laboratory rabbits (Whishaw et al., 1982). Hypnotic analgesia’s antinociceptive effect may be cholinergic as well, for carbachol, a cholinergic agonist, can elevate nociceptive thresholds to thermic heat and calibrated tail-pinch (Klamt & Prado, 1991). Hypnotic analgesia’s ability for relieving pain is not degraded by an injection of the opiate antagonist, naloxone (Goldstein & Hilgard, 1975); therefore its antinociceptive qualities are not opiate in origin. Repeated deep brain stimulation of the amygdala evokes arousal from hypnosis (DeBenedittis & Sironi, 1988). Amygdala stimulation may disrupt the inhibitory role of the Ammon’s horn, a region of the hippocampus that, with stimulation, produces hypoactivity, placidity, insensitivity to environmental changes, etc. and maintenance of the hypnotic state. Hypnotic analgesia appears to be mediated by a cholinergic mechanism, without neural input from the amygdala.

Hypnotherapy has been shown to provide pain and unpleasant symptom relief. It also has been employed in clinical practice, with age regression techniques, to help patients to access repressed memory or stress or trauma memory for which the patient has amnesia. The latter is currently not a commonly used psychotherapy method.

References

Bowers KS (1992): Imagination and dissociation in hypnotic responding. Int J Clin Exp Hypn, 40: 253-75.

Christenson JA (1968): Dynamics in hypnotic induction. In: Experimental Hypnosis-A Symposium of Articles on Research by Many of the World’s Leading Authors. Ed. LM LeCron, pp. 29-54, Citadel Press, New York, New York.

Crawford HJ, Gruzelier JH (1992): A midstream view of the neuropsychophysiology of hypnosis: recent research and future directions. In: Contemporary Hypnosis Research. Eds. E Fromm, MR Nash, pp. 227-66, Guilford Press, New York, New York.

Crawford HJ (1993): Sustained attentional and disattentional abilities: differences between low and highly hypnotizable persons. J Abnorm Psycol, 102(4): 534-43.

Crawford HJ, Gur RC, Skolnick B, Gur RE, Benson DM (1993): Effects of hypnosis on regional cerebral blood flow during ischemic pain with and without suggested hypnotic analgesia. Int J Psychophysiol, 15(3): 181-95.

Crawford HJ, Knebel T, Kaplan L, Vendemia JM, Xie M, Jamison S, Pribram KH (1998): Hypnotic analgesia: 1. somatosensory event-related potential changes to noxious stimuli and 2. transfer learning to reduce chronic low back pain. Int J Clin Exp Hypn, 46(1): 92-123.

DeBenedittis G, Sironi VA (1988): Arousal effects of electrical deep brain stimulation in hypnosis. Int J Clin Exp Hypn. 36(2): 96-106.

Erickson MH, Erickson, EM (1941): Concerning the nature and character of post-hypnotic behavior. J Gen Psychol, 24; 95-133.

Erickson MH (1944): An experimental investigation of the hypnotic subjects apparent ability to become aware of stimuli. J Gen Psychol, 31: 191-212.

Erickson MH (1968): Deep hypnosis and its induction. In: Experimental Hypnosis-A Symposium of Articles on Research by Many of the World’s Leading Authors. Ed. LM LeCron, pp. 70-112, Citadel Press, New York, New York.

Erickson, MH & Rossi EL (1976a): Hypnotherapy: An Exploratory Casebook. Irvington Publishers, New York, New York.

Erickson MH & Rossi EL (1976b): Two level communication and microdynamics of trance and suggestion. Am J Clinical Hypnosis, 18(3): 153-71.

Erickson MH, Rossi EL, Rossi SI (1976): Hypnotic Realities: The Induction of Clinical Hypnosis and Form of Indirect Suggestion. Irvington Pub., New York.

Faymonville ME, Laureys S, Degueldre C, DelFiore G, Luxen A, Franck G, Lamy M, Maquet P (2000): Neural mechanisms of antinociceptive effects of hypnosis. Anesthesiology, 92(5): 1257-67.

Goldstein A, Hilgard ER (1975): Failure of the opiate antagonist naloxone to modify hypnotic analgesia. Proc Natl Acad Sci USA, 72(6): 2041-3.

Graffin NF, Ray WJ, Lundy R (1995): EEG concomitants of hypnosis and hypnotic susceptibility. J Abnorm Psychol, 104(1): 123-31.

Hilgard ER, Hilgard JR (1975): Hypnosis in the Relief of Pain. William Kaufmann, Los Altos, California.

Hilgard JR, LeBaron S (1984): Hypnotherapy of Pain in Children with Cancer. William Kaufmann, Inc. Los Altos, CA.

Hofbauer RK, Rainville P, Duncan GH, Bushness MC (2001): Cortical representation of the sensory dimension of pain. J Neurophysiol, 86(1): 402-11.

Klamt JG, Prado WA (1991): Antinociception and behavioral changes induced by carbachol microinjected into identified sites of the rat brain. Brain Res, 549(1): 9-18.

Kroptov JD, Craford HJ, Polyakov YI (1997): Somatosensory event-related potential changes to painful stimulation during hypnotic analgesia: anterior cingulate cortex and anterior temporal cortex intracranial recordings. Int J Psychophysiol, 27(1): 1-8.

Maquet P, Faymonville ME, Deguildre C, Delfiore G, Franck G, Luxen A, Lamy M (1999): Functional neuroanatomy of hypnotic state. Biol Psychiatry, 45(3): 327-33.

Rainville P, Duncan GH, Price DD, Carrier B, Bushnell MC (1997): Pain affect encoded in human anterior cingulate but not somatosensory cortex. Science, 277(5328): 968-71.

Rainville P, Hofbauer RK, Paus T, Duncan GH, Bushnell MC, Price DD (1999): Cerebral mechanisms of hypnotic induction and suggestion. J Cogn Neurosci, 11(1): 110-25.

Sternbach RA (1982): On strategies for identifying neurochemical correlates of hypnotic analgesia. Int J Clin Exp Hypn, 30(3): 251-6.

Whishaw IQ, Flannigan KP, Schallert T (1982): An assessment of the state hypothesis of animal “hypnosis” through and analysis of neocortical and hippocampal EEG in spontaneous immobile and hypnotized rabbits. Electroencephalogr Clin Neurophysiol, 54(4): 365-74.

Wik G, Fischer H, Bragee B, Finer B, Fredrickson M (1999): Functional anatomy of hypnotic analgesia: a PET study of patients with fibromyalgia. Eur J Pain, 3(1): 7-12.