Invited Symposium: Neural Bases of Hypnosis


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Brain Mechanisms and Attentional Processes in Hypnosis

Contact Person: Vilfredo De Pascalis (depascal@giannutri.caspur.it)


It is generally accepted that one purpose of an hypnotic induction procedure is to assist the subject in eliminating sources of irrelevant stimulation and in focalizing the attentional resources to the most relevant source of information. Tellegen and Atkinson (1974) defined the construct of "absorption" as the individual's disposition to experience episodes of "total" attention on a certain type of event which becomes particularly relevant. Absorption in no way fully explains hypnotizability, but this ability may still be relevant to the facilitation of dissociation.

This presentation reviews a number of investigations conducted in our laboratory in which is supported that (a) highly hypnotizable individuals possess stronger abilities in the focussing of attention on relevant stimuli and this ability is associated to task-related hemisphere functioning; and (b) hypnotic absorption is a mechanism facilitating dissociation and essential to describe hypnotic phenomena. Both attentional and absorption mechanisms involve the activity of a supervisory attentional control system in the frontal cortex interacting with posterior cortical and subcortical brain regions. Our previous research (De Pascalis et al., 1987, 1989, 1998) indicated that high hypnotizable persons, compared to low hypnotizables, both in waking and to a greater extent in hypnosis condition, have a greater capacity to access positive and negative life-emotional experiences and this ability was associated to task-related hemispheric shifts of fast EEG activity in the 36-44 Hz band (40-Hz EEG). High hypnotizables, during positive emotions (gladness and happiness), showed a left and right hemisphere increase of 40-Hz EEG density, while, during negative affects (anger and fear), showed a density increase in the right and a density decrease in the left. These differential hemispheric activity across emotional types in high subjects were more pronounced in hypnotic condition than in waking state. Low hypnotizables did not show differential hemispheric patterns among emotional types. In another study (De Pascalis, 1993) the EEG spectral analysis was carried out during the administration of an hypnotic induction. It was found that 40-Hz EEG spectral amplitude increases as a function of hypnotizability and hypnosis. Since it has been suggested that 40-Hz EEG activity is the physiological expression of focused arousal (Sheer, 1989), the increase of 40-Hz activity in high hypnotizables during hypnosis was interpreted as indicating the greater capacity of these subjects in focussing of attention on relevant stimuli. The beta3 (20-36 Hz) amplitude in the early hypnotic induction was found greater in the left compared to the right hemisphere and as the induction proceeded, the activity of the left hemisphere was inhibited resulting in the hemispheres becoming similar. This finding supported the validity of the frontal inhibition model suggested by Gruzelier et al. (1984).

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The phenomena of perceptual alterations in hypnosis as those of positive and negative hallucinations are some of the most compelling experiences of highly hypnotizable subjects. Spiegel et al. (1985) and Barabasz et al. (1995, 1996) examined the influence of obstructive hypnotic hallucination over event-related potentials (ERPs). They reported that among high hypnotizable subjects there were significant amplitude reductions in the P300 component of the ERPs during obstructive hallucination of visual stimuli. These results were confirmed in a study carried out in our laboratory (De Pascalis, 1994). Highly susceptible subjects, in hypnosis condition, were able to experience obstructive hallucination of train-flash stimuli when they were suggested to visualize a cardboard box that would prevent from viewing flash stimuli. High hypnotizables, while experiencing stimulus elimination, showed significant attenuation of P1 (70 ms), N2 (240 ms) and to a less extent of P3 (290 ms) ERP peak amplitudes. The effect, for the P1 component, was greater at the posterior regions as compared to the anterior and central region of the scalp. A relative increase of P1 and N1 ERP peaks were also observed in highly hypnotizables when they were suggested to enhance the brightness of the flash stimuli. These findings suggested the operation of a top-down inhibitory process that started from frontal cerebral cortex and cooperate in the regulation of talamocortical activity. This process may have attenuated or amplifyed the sensory component of the incoming input.

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Among the hypnotic obstructive phenomena, hypnotic analgesia is a well documented and reliable phenomenon. But despite that neurophysiological research has pointed out mechanisms involved in the reduction of pain perception, the basic mechanisms responsible of hypnotic analgesia are still unknown. Studies using positron emission tomography (PET) (e.g., Casey et al., 1994; Talbot et al., 1991) and functional magnetic resonance imagic (fMRI) (e.g., Davise et al., 1995) found that anterior cingulate cortex was engaged in the processing of pain. Recently, Crawford et al. (1998a, b) found that hypnotic analgesia, compared to wake-attend condition, produces reductions of activity in the right hemisphere for somatosensory supplementary motor area, cingulate cortex, insular and thalamus. These authors proposed that hypnotic analgesia requires inhibitory effort dissociated from conscious awareness and that anterior frontal cortex was part of an inhibitory feedback circuit that modulate thalamocortical activities.

While these studies were successful in evidencing the basic neurophysiological inhibitory mechanism involved in hypnotic analgesia, it remains still unknown how cortical activity induced by an hypnotic suggestion of hypnotic analgesia prime the frontal inhibitory processing of incoming painful stimuli. For example, neuro-psychophysiological studies have not still pointed out how different suggestions involving different cognitive activities (and, therefore, generate different configuration patterns of cortical activation and inhibition) may prime the uppermentioned inhibitory mechanism. An answer to this question is also an answer to the validity of ‘dissociated control’ model proposed by Bowers (1992, 1994). According to this model, hypnotic analgesia is the product of dissociated control, and mental imagery is a concomitant rather than a mediator of suggested analgesia. Results obtained from a study carried out in our laboratory (De Pascalis & Perrone, 1995) supported Bower’s point of view. In this study hypnotic analgesia was obtained, in highly hypnotizable subjects, by simply suggesting that they could have perceived no pain during the deliveration of nociceptive stimuli. No specific mental imagery activity was suggested to help subjects to reduce pain. Highly hypnotizable subjects significantly reduced pain and distress levels during hypnotic analgesia. They reported that the analgesic effect happened involuntarily. During hypnotic analgesia there were significant reductions in the total (0.5-31.75 Hz), delta (0.5-3.75 Hz), and beta1 (13-15.75 Hz) EEG amplitudes over left and, to a greater extent, over the right posterior recording areas. The asymmetric amplitude reductions produced an EEG hemispheric asymmetry in favor of the left hemisphere. These EEG hemispheric effects during hypnotic analgesia were paralleled by significant reductions in sympathetic activity. Since during hypnotic analgesia, pain reductions correlated significantly with right-hemisphere decreases in total EEG amplitude, it was deduced that the inhibition of the right hemisphere may play an important role in the relief of pain.

Thus hypnotic analgesia was explained with the fact that a reduced activity in the right hemisphere produces a reduced activity of the sustained attentional component which has been suggested to be responsible for the negative emotional state (Tucker & Williamson, 1984).

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In a very recent study of our own (De Pascalis et al., 1998), the effects of different hypnotic analgesia suggestions on pain reduction and changes on cognitive and physiological responses were evaluated. Aim of this study was to validate and extend Zachariae and Bjerring (1994) findings. This study was carried out to help in understanding if hypnotic analgesia is the product of a single phenomenon in the brain and if a successful hypnotic suggestion is one of the possible keys to have access to it. Somatosensory event-related potential (SERP) and skin conductance response (SCR) changes during hypnotic suggestions of Deep Relaxation, Dissociated Imagery, Focused Analgesia, and Placebo, as compared to a Waking baseline condition, were evaluated. SERPs were recorded from frontal, temporal, central, and parietal scalp sites. 10 high, 9 mid, and 10 low hypnotizable right-handed women participated in the experiment. The following measures were obtained:

(a) pain and distress tolerance ratings;

(b) sensory and pain thresholds to biphasic electrical stimulation delivered to the right wrist; N280 and P400 peak amplitudes of SERPs to target stimuli delivered using an odd-ball paradigm;

(c) number of evoked SCRs and phasic electrodermal orienting responses (ORs);

(d) phasic heart rate changes;

(e) respiratory frequency and amplitude;

(f) reaction time and number of omitted responses. High hypnotizable subjects exhibited significantly greater pain intensity reductions than did mid and low hypnotizables during Dissociated Imagery and Focused Analgesia, while, in the other conditions, there were no pain differences between groups. High, mid, and low groups showed significant reductions in P3 peak amplitudes across all hypnosis conditions, and to a less degree during Placebo. The temporal cortical region was the most sensitive in differentiating SERP responses among hypnotizability groups. On this recording area the highly hypnosis susceptible subjects displayed significantly smaller P3 and greater N2 peaks during Focused Analgesia than did the other hypnotizable groups. In this condition highly susceptible subjects also reported the highest number of omitted responses and the shortest RTs. These subjects also showed smaller ORs, as compared to mid and low hypnotizables. During Dissociated Imagery and Focused Analgesia, high subjects also disclosed a smaller total number of evoked SCRs than did mid and low hypnotizable subjects. No relationship was found between hypnotizability and vividness of mental imagery and between the latter and measures of reported pain.

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The present findings suggest that common to all hypnotic suggestions used in this study were the mechanisms of focused attention and obstructive hallucination. The first mechanism should be mainly the product of the operation of frontal cortical activity, while the second mechanism should be mainly the product of the operation of posterior cortical systems which modulate mental imagery and, according to Chapman’s and Nakamura’s (1988) model, could lead to the creation of a new ‘schema’ that assumes a dominant position in the contents of consciousness and simultaneously forced normal perception into the background of consciousness. Both mechanisms, that coesist and may have additive effects, are more effective in highly hypnotizable persons mainly when focused analgesia suggestions are used.

These findings, however, did not yield direct answers to the fact that the hypnotic responses are accompained by the experience of non-volition (Bowers, 1992), but RT and SC changes, obtained in highly hypnotizable subjects during Dissociated Imagery and Focused Analgesia, suggested that automaticity and involuntariness of SCRs were characteristics of these subjects. It is not clear, however, if it is the imaginative involvement usually included in the suggestions of analgesia that prime the automaticity of hypnotic responses or, viceversa, the phenomenon of dissociated control primes hypnotic analgesia and facilitates the production of mental imagery. The shorter RTs obtained during Focused Analgesia, as compared to Dissociated Imagery (that consisted of a more demanding imagery task), however, tend to support the latter hypothesis.

The condition of Focused Analgesia, in highly hypnotizable subjects, was the most effective in producing the greatest reductions in subjective ratings of pain and distress intensities and this effect was accompained by more significant task-related changes in P3 and N2 peaks on temporal sites. This condition also displayed higher pain thresholds and faster RTs that were paralleled by a smaller number of phasic Ors (SCR). Dissociated Imagery and to a less extent Deep Relaxation conditions also displayed reductions in distress levels and significant task-related changes in N2 and P3 peaks and SCRs, but these changes were not paralleled by shorter RTs and were less pronounced than that observed for Focused Analgesia. Therefore, the present findings confirm those previously reported by Zachariae and Bjerring (1994) and suggested that different processes at cortical level may be operating among Focused Analgesia, Dissociated Imagery and Deep Relaxation conditions. Common effect among conditions appears to be an enhancement of inhibitory processing. Since the suggestion to divert attention from the body contained in the Dissociated Imagery condition was effective in reducing the subjective rating of distress and it cannot be ruled out that distraction may be an important element of hypnotic analgesia. But, on the other hand, in terms of behavioral and physiological measures, Focused Analgesia, which requires to focus attention on the hand receiving painful stimulations, and not to divert attention from it, was the most effective in reducing pain. Therefore, the hypothesis that distraction of attention from painful stimuli is the main component of hypnotic analgesia is not supported by our results. The suggestion of Focused Analgesia seems to require less processing capacity in its operation and hence that executive initiative and effort are less involved in its production (Bowers, 1994). Further investigations are needed to shed light on this question.

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  2. Barabasz, A.F., Barabasz, M., Jensen, S. & Calvin (1996). Alternative hypnotic suggestions alter visual and auditory EEG event related potentials. Paper presented at the 47th annual Scientific Program of the Society for Clinical and Experimental Hypnosis, November, Tampa.
  3. Bowers, K.S. (1992). Imagination and dissociation in hypnotic responding. International Journal of Clinical and Experimental Hypnosis, 40, 253-275.
  4. Bowers, K.S. (1994). Dissociated control, imagination, and the phenomenology of dissociation. In D. Spiegel (Ed.), Dissociation – Culture, Mind and Body (pp. 21-38). Washington, DC: American Psychiatric Press, Inc.
  5. Casey, K.L., Minoshima, S., Berger, K.L., Koeppe, R.A., Morrow, T.J., & Frey, K.A. (1994). Positron emission tomographic analysis of cerebral structures activated specifically by repetitive noxious heat stimuli. Journal of Neurophysiology, 4802-807.
  6. Chapman, C.R. & Nakamura, Y. (1998). Hypnotic analgesia: A constructivist framework. The International Journal of Clinical and Experimental Hypnosis, 1, 6-27.
  7. Crawford, H.J., Horton, J., Hirsch, T.B., Harrington, G.S., Plantec, M.B., Vendemia, J.M.C., Shamro, C., McClainfurmanski, D., & Downs, J.H. (1998b). Attention and disattention (hypnotic analgesia to painful somatosensory tens stimuli differentially affects brain dynamics: A functional magnetic resonance imaging study. International Journal of Psychophysiology, 30, 77.
  8. Crawford, H.J., Knebel, T., Kaplan, L. & Vendemia, J.M.C. (1998a). Hypnotic analgesia: 1. Somatosensory event-related potential changes to noxious stimuli and 2. transfer learning to reduce chronic low back pain. International Journal of Clinical and Experimental Hypnosis, 1, 92-132.
  9. Davis, K.D., Wood, M.L., Crawley, A.P., & Mikulis, D.J. (1995). FMRI of human somatosensory and cingulate cortex during painful electrical nerve stimulation.Neuroreport, 7, 321-325.
  10. De Pascalis, V. (1993). EEG spectral analysis during hypnotic induction, hypnotic dream and age-regression. International Journal of Psychophysiology, 5, 153-166.
  11. De Pascalis, V. (1994). Event-related potentials during hypnotic hallucination. The International Journal of Clinical and Experimental Hypnosis, 1, 39-55.
  12. De Pascalis, V., Magurano, M.R., and Bellusci, A. (1998). Pain perception, somatosensory event-related potentials and skin conductance responses to painful stimuli in high, mid, and low hypnotizable subjects during hypnotic suggestions involving different pain reduction strategies. Paper presented at the 9th World Congress of the International Organization of Psychophysiology (IOP), Taormina, Sicily, Italy, 14-19 September, 1998.
  13. De Pascalis, V., Marucci, F.S., & Penna M.P. (1989). 40-Hz EEG asymmetry during recall of emotional events in waking and hypnosis: differences between low and high hypnotizables. International Journal of Psychophysiology, 7, 85-96.
  14. De Pascalis, V., Marucci, F.S., Penna, M.P., & Pessa, E. (1987). Hemispheric activity of 40-Hz EEG during recall of emotional events: Differences between low and high hypnotizables. International Journal of Psychophysiology, 5, 167-180.
  15. De Pascalis, V., & Perrone, M. (1995). EEG asymmetry and heart rate during experience of hypnotic analgesia in high and low hypnotizables.International Journal of Psychophysiology, 21, 163-175.
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  17. Sheer, D.E. (1989). Sensory and cognitive 40-Hz EEG event-related potentials: Behavioral correlates, brain function and clinical application. In E. Basar, and T.H. Bullock (Eds.), Brain Dynamics (pp. 339-374). Berlin: Springer-Verlag.
  18. Spiegel, D., Cutcomb, S., Ren, C., & Pribram, K. (1985). Hypnotic hallucination alters evoked potentials. Journal of Abnormal Psychology, 3, 249-255.
  19. Talbot, J.D., Marrett, S., Evans, A.C., Meyer, E., Bushnell, M.C., & Duncan, G.H. (1991). Multiple representations of pain in human cerebral cortex. Science, 251,1355-1358.
  20. Tucker, D.M. & Williamson, P.A. (1984). Asymmetric neural control systems in human self-regulation. Psychological Review, 91, 185-215.
  21. Zachariae, R. & Bjerring, P. (1994). Laser-induced pain-related brain potentials and sensory pain ratings in high and low hypnotizable subjects during hypnotic suggestions of relaxation, dissociated imagery, focused analgesia, and placebo. The International Journal of Clinical and Experimental Hypnosis, XLII, 56-80.

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De Pascalis, V.; (1998). Brain Mechanisms and Attentional Processes in Hypnosis. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/woody/de_pascalis0311/index.html
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