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                                 NEUROPHYSIOLOGICAL CORRELATES OF HYPNOTIC ANALGESIA

 

 Audrey Vanhaudenhuyse¹, Mélanie Boly¹, Steven Laureys¹ and
Marie-Elisabeth Faymonville²
¹ Coma Science Group, Cyclotron Research Centre and Neurology Department,
University of Liege, Belgium, ² Department of Anaesthesia and Intensive Care
Medicine, Pain Centre, University Hospital of Liege, Belgium

    

Abstract
This short review describes recent advances in understanding hypnotic modulation of
pain. Our current understanding of pain perception is followed by a critical review of
the hypnotic analgesia studies using EEG, evoked potential and functional imaging
methodologies. Copyright © 2008 British Society of Experimental & Clinical Hypnosis.
Published by John Wiley & Sons, Ltd.
Key words: pain, hypnosis, fMRI, PET-scan, EEG
After 200 years of inquiry and with varying popularity, the interest in hypnosis has more
recently been on the upswing. The phenomena that comprise the domain of ‘hypnosis'
have attracted the curiosity of researchers and clinicians who have witnessed the changes
in hypnotized subjects' behaviour and subjective experience. Evidence for the increasing
interest in hypnosis in medical health care is demonstrated in the literature, where hypnosis
can have an effective and cost-saving role (Holroyd 1996; Montgomery, DuHamel
and Redd, 2000; Stewart 2005). However, there still remains controversy over how
hypnosis should be defi ned. Some researchers (Hilgard 1965; Gruzelier 2000; Kallio and
Revonsuo 2003) state that hypnotic phenomena cannot be explained without positing a
special psychological state - an altered or dissociated state of consciousness, while others
(Barber, 1969; Spanos, 1986; Kirsch, 1991) regard all phenomena seen in association
with hypnosis as being explainable by using ordinary psychological concepts such as
expectations or role playing.
The notion of consciousness is at the core of an ongoing debate on the nature of
hypnosis. Consciousness is a multifaceted concept that can be conceived as having two
major components: awareness of environment and of self (i.e. the content of consciousness)
and wakefulness (i.e. the level of vigilance or arousal) (Laureys, 2005). The brain
is functionally in a constant state of fl ux and alteration. There are now attempts to systematically
explore and conceptualize the so-called altered states of consciousness within
the context of neuroscience (Jamieson, 2007). At present, given the absence of a thorough
understanding of the neural correlates of consciousness, results from neuroimaging
studies should however be used with appropriate caution.
Contemporary scientifi c theories of hypnosis emphasize the changes in phenomenal
experience where subjects interact in a larger sociocultural context that facilitates modifi
cations in basic cognitive mechanisms underlying perception, memory and thought.
16 Vanhaudenhuyse et al.
Copyright © 2008 British Society of Experimental & Clinical Hypnosis Contemp. Hypnosis 26: 15-23 (2009)
Published by John Wiley & Sons, Ltd DOI: 10.1002/ch
Although still viewed with scepticism, hypnosis has gained respectability in medicine,
in large part due to its demonstrated effects on analgesia (Montgomery, David, Winkel,
Silverstein and Bobbjerg, 2002; Patterson and Jensen, 2003). Hypnosis can profoundly
alter sensory awareness and cognitive processing and has been used for years to alleviate
pain perception in many different clinical circumstances (Faymonville, Mambourg, Joris,
Vrijens, Fissette, Albert and Lamy, 1997; Lang, Benotsch, Fick, Lutgendorf, Berbaum,
Berbaum, Logan and Spiegel, 2000).
There has been a huge explosion in our understanding of the basic mechanisms of
pain, yet despite advances in physiology, pharmacology and psychology, surveys repeatedly
reveal that unrelieved pain remains a widespread problem. While we have long
considered neurological pathways to be hard wired, it is becoming increasingly clear that
the brain and the spinal cord are able to learn or facilitate activity in commonly utilized
pathways. Functional neuroimaging studies revealed distinct anatomical pathways that
are involved in the sensory and affective pain dimension. Pain is mediated via activation
of a network of cortical and subcortical regions (Tölle, Kaufmann, Siessmeier, Lautenbacher,
Berthele, Munz, Zieglgänsberger, Willoch, Schwaiger, Conrad and Bartenstein,
1999; Peyron, Laurent, Garcia and Larrea, 2000; Derbyshire, Jones, Creed, Starz,
Meltzer, Townsend, Peterson and Firestone, 2002) but the interpretation of these fi ndings
is complicated by processes associated to the stimulus that are incidental to the actual
sensory and emotional experience of pain. Such processes include motor inhibition,
anticipation (Ploghaus, Tracey, Gati, Clare, Menon, Matthews and Rawlins, 1999; Hsieh,
Stone-Elander and Ingvar, 1999), expectation (Carlsson, Petrovic, Skare, Petersson and
Ingvar, 2000; Sawamoto, Honda, Okada, Hanakawa, Kanda, Fukuyama, Konishi and
Shibasaki, 2000), attention (Bantick, Wise, Ploghaux, Clare, Smith and Tracey, 2002:
Brooks, Nurmikko, Bimson, Singh and Roberts, 2002), distraction (Hoffman, Richards,
Coda, Bills, Blough, Richards and Sharar, 2004) as well as the placebo effect (Petrovic,
Kalso, Peterson and Ingvar, 2002; Ploghaus, Becerra, Borras and Borsook, 2003; Kupers,
Faymonville and Laureys, 2005). Specifi c modulation of brain activity via manipulation
of affective and sensory dimensions of pain experience (Derbyshire, Vogt and Jones,
1998; Coghill, Sang, Maisog and Iadarola, 1999) supported the existence of a neural
functional pain mechanism. Derbyshire, Whalley, Stenger and Oakley in 2004 provided
the fi rst direct experimental evidence in humans linking specifi c neural activity with the
immediate generation of a pain experience. They identifi ed brain areas directly involved
in the generation of pain using hypnotic suggestion to create an experience of pain in
the absence of any noxious stimulus. In contrast to the imagined pain, fMRI revealed
signifi cant changes during this hypnotically induced pain experience within the thalamus,
anterior cingulate, insula, prefrontal and parietal cortices and these fi ndings differentiate
the activation patterns during pain from nociceptive sources. Since 1980, a new era of
methodological advances for non-invasive imaging of the human brain has forged a link
between psychology and neurosciences. Budding efforts to study psychological processing
using single photon emission computed tomography (SPECT), positron emission
tomography (PET) and more recently functional magnetic resonance imaging (fMRI)
have focused on measuring regional changes in cerebral haemodynamic activity (Laureys,
Boly and Tononi, 2008). The advent of these brain imaging techniques have permitted
to disentangle the brain mechanisms involved in pain and its cognitive modulation.
The ‘gate control' theory, proposed by Melzack and Wall in 1965, according to which
activation in large myelinated fi bers is capable of inhibiting nociceptive information,
was the fi rst model striking against the belief that pain processing is a hard-wired
process, mediated exclusively by pain dedicated pathways. Later on, Melzack and Casey
Neurophysiological correlates of hypnotic analgesia 17
Copyright © 2008 British Society of Experimental & Clinical Hypnosis Contemp. Hypnosis 26: 15-23 (2009)
Published by John Wiley & Sons, Ltd DOI: 10.1002/ch
(1968) described pain as a complex multidimensional experience comprising sensorydiscriminative,
motivational-affective and cognitive-evaluative components. This theory
added a rostral (cerebral) extension to the gate control theory where cognition, e.g.
distraction (Hoffmann et al., 2004), attention (Valet, Sprenger, Boecker, Willoch,
Rummeny, Conrad, Erhard and Tolha, 2004), expectation (Koyama, McHaffi e, Laurienti
and Coghill, 2005), catastrophizing (Seminowicz and Davis, 2006) and emotion (Ochsner,
Ludlow and Knierim, 2006) play a major role.
The advance in our understanding of pain mechanisms had lead to improved methods
of management by allowing more effi cient usage of other therapies like hypnosis. Hypnosis
researchers have long sought for physiological indicators of the hypnotic analgesia.
Such studies have monitored the effect of hypnosis on autonomous responses such as
changes in heart rate, galvanic skin responses (Pascalis and Perrone 1996; Balocchi,
Varanini, Menicucci, Santarcangelo, Migliorini, Fontani and Carli, 2005; Santarcangelo,
Carli, Migliorini, Fontani, Varanini and Balocchi, 2008) and endothelial function
(Jambrik, Carli, Rudish, Varga, Forster and Santarcangelo, 2005). These aspects of hypnotic
analgesia have become particularly intriguing due to the evidence that the autonomic
activity is monitored in cerebral areas and this information is integrated at higher
levels where it contributes to the construction of the experience (Damasio, 1999; Critchley,
Wiens, Rotshtein, Ohman and Dolan, 2004; Pollatos, Schandry, Auer and Kaufmann,
2007). As recently suggested by Carli, Huber and Santarcangelo (2008), the peculiar
autonomic control observed in highly hypnotizable individuals might account for possible
differences in the likelihood of low and high susceptible subjects to suffer with
chronic pain as well as for possible differences between the two groups in the cardiovascular
damage associated with chronic pain.
There is also evidence that hypnotic analgesia is associated with changes in the RIII
component of the nociceptive refl exes (Kiernan, Dane, Philips and Price, 1995), although
heat detection and heat-pain thresholds were increased under hypnosis, whereas heat
pain tolerance and cold detection thresholds were not statistically changed (Langlade,
Jussiau, Lamonerie, Marret and Bonnet, 2002). In addition, hypnotic suggestions alter
pain sensation in both high and low susceptible subjects, but the changes are selective
and somatotopically organized only in highly susceptible subjects (Benhaiem, Attal,
Chauvi, Brasseur and Bouhassira, 2001)
Electroencephalographic (EEG) and evoked potential (EP) studies done since the late
1970s have shown some physiological correlates refl ecting hypnotic analgesia (Halliday
and Mason 1964; Meszaros, Banyai and Greguss, 1980; Barabasz and Lonsdale 1983;
Spiegel, Bierre and Rootenberg, 1989; Arendt-Nielsen, Zachariae and Bjerring, 1990;
Meier, Klucken, Soyka and Bromm, 1993; Zachariae and Bjerring 1994; Crawford,
Knebel, Kaplan, Vendemia, Xie, Jamison and Pribram, 1998; De Pascalis, Magurano
and Bellusci, 1999). In summary, these studies observed reductions in late somatosensory
potentials evoked by nociceptive stimuli during hypnosis, linked to perceived pain
intensity changes which seem not to be under conscious control. Unfortunately, these EP
experiments did not disentangle the infl uence of suggestion from the hypnotic context.
De Pascalis, Magurano, Bellusci and Chen (2001) tested somatosensory event-related
potentials to noxious stimuli varying cognitive strategies - deep relaxation dissociative
imagery and focuses analgesia. They observed that the effect of pain modulation is
limited to high hypnotizable subjects rather than low, and that higher frontal - temporal
N2 and smaller posterior parietal P3 may indicate active inhibitory processes during
cognitive strategies in hypnotic analgesia. These inhibitory processes may also regulate
the autonomic activities on pain perception. Hypnotically induced analgesia was also
18 Vanhaudenhuyse et al.
Copyright © 2008 British Society of Experimental & Clinical Hypnosis Contemp. Hypnosis 26: 15-23 (2009)
Published by John Wiley & Sons, Ltd DOI: 10.1002/ch
studied by recording intracranial somatosensory event-related potentials (SEPs) to
painful cutaneous stimuli during hypnotically suggested analgesia. Kropotov, Crawford
and Polyakov (1997) found that the hypnotically responsive patient reduced pain perception
during suggested hypnotic analgesia and observed a reduction of the positive SEP
component within the range of 140-160 ms post-stimulus in the left anterior cingulate
cortex and an enhancement of the negative SEP component occurring after 200-260 ms
in the left anterior temporal cortex (Brodman area (BA) 21). Their study was the fi rst to
demonstrate the involvement of the anterior cingulate cortex and the anterior temporal
cortex in the inhibitory control of pain during hypnotically suggested analgesia.
Surface EEG recordings during hypnotic induced analgesia in volunteers with high
versus low hypnotic suggestibility scores have subsequently shown greater theta activity
among those subjects with high scores, especially in the anterior temporal region (Crawford
1990). These volunteers also showed greater left hemisphere dominance during the
pain condition and a reversal in hemispheric dominance during hypnotic analgesia
(Crawford, 1990; De Pascalis and Perrone, 1996). These results were interpreted as
refl ecting greater cognitive fl exibility and abilities to shift from left to right anterior brain
functioning. It was proposed that hypnosis may operate via attention fi ltering with a
central role for the frontal limbic system. Attempts to summarize the EEG differences
in terms of frequency dominance and coherence (alpha, beta, theta power for hemispheric
lateralization), together (Spiegel and Barabasz 1988; Crawford and Gruzelier, 1992)
showed such methodological differences that it seems not possible to propose a common
physiological substrate (Barabasz, Barabasz, Jensen, Calvin, Trevisan and Warner, 1999).
De Pascalis, Marucci and Penna (1989) presented a wide range of studies in support of
the modulation of gamma oscillations in the construction of hypnotic changes of consciousness.
More recently, Trippe, Weiss and Miltner (2004) reported a breakdown in
EEG functional connectivity in the gamma band between somatosensory and frontal
cortical regions. They hypothesized that hypnosis may result from inhibitory infl uences
on the secondary somatosensory cortex (S2)/insula regions from the right lateral prefrontal
cortex. They argue that hypnosis is characterized by a breakdown on coherent
large-scale cortical oscillations organized and controlled by regions in the frontal cortex.
Fractal analysis of EEG in hypnosis and its relationship with hypnotizability was studied
by Lee, Spiegel, Kim, Lee, Kim, Yang, Choi, Kho and Nam in 2007. They found that
the application of this analysis technique can demonstrate the electrophysiological correlations
with hypnotic infl uence on cerebral activity.
Neuroimaging techniques also facilitate efforts for an improved understanding of the
brain mechanisms involved in pain experience and hypnosis. Hypnosis induced changes
in pain perception and the underlying brain mechanisms were studied by Rainville,
Duncan, Price, Carrier and Buschnell (1997). They used the PET scan technique to study
brain activity of volunteers exposed to hot water induced pain during hypnotically
induced analgesia inducing changes in perceived unpleasantness, but not in the intensity
of the noxious stimulation. They found that hypnosis related changes of the affective
dimension of pain were associated with changes in activity in anterior and mid-cingulate
cortices, but not with activity in primary somatosensory cortex. Faymonville, Laureys,
Degueldre, DelFiore, Luxen, Franck, Lamy and Maquet (2000) investigated brain mechanisms
underlying the modulation of pain perception without specifi c suggestion for
hypnotic pain reduction. Their hypnotic protocol relied on their clinical experience where
patients were invited to have revivication of pleasant autobiographic experiences without
any instruction of analgesia (Faymonville, Meurisse and Fissette, 1999). This technique
lowers both the affective and the sensory component of the noxious stimuli. Hypnosis
Neurophysiological correlates of hypnotic analgesia 19
Copyright © 2008 British Society of Experimental & Clinical Hypnosis Contemp. Hypnosis 26: 15-23 (2009)
Published by John Wiley & Sons, Ltd DOI: 10.1002/ch
was shown to decrease both components of pain perception by more than 50% as compared
to resting state conditions and by approximately 40% as compared to a control
distraction task based on mental imagery of autobiographical events. Both studies
(Rainville, Duncan, Price, Carrier and Buschnell, 1997 and Faymonville, Laureys, Degueldre,
DelFiore, Luxen, Franck, Lamy and Maquet, 2000) showed that the analgesic
effect of hypnosis is mediated by the anterior/mid-cingular cortex (Brodmann's area
24′a). This area is innervated by a multitude of neuromodulatory pathways including
opioidergic, noradrenergic and serotoninergic systems (Paus, 2001). The anterior cingulate
cortex (ACC) is a functionally heterogeneous region thought to modulate the interaction
between cognition, sensory perception and motor control (Vogt, 2005) in relation
to changes in attentional, motivational and emotional states (Devinsky, Morrell and Vogt,
1995). In order to further explore the antinociceptive effects of hypnosis, Faymonville,
Roediger, Del Fiore, Degueldre, Phillips, Lamy, Luxen, Maquet and Laureys (2003)
subsequently assessed the hypnosis-induced changes in functional connectivity involved
in noxious processing. The hypnosis-induced reduction of pain perception was shown to
be related to an increased functional modulation of the ACC and a network of cortical
and subcortical structures known to be involved in different aspects of pain processing
encompassing prefrontal, insular and pregenual cortices, pre-supplementary motor
cortex, thalami, striatum and brainstem. Functional brain connectivity studies suggest
that the anterior cingulated and the prefrontal cortices exert their effects by modulating
activity in the midbrain periaqueductal gray, a structure that is of utmost importance in
the descending noxious inhibitory system (DNIS) (Faymonville, Vogt, Maquet and
Laureys, in press).
Summary and conclusion
Many factors infl uence a patient's response to pain, and they are as important as the
extent of the physical damage causing it. They include personality, cultural background,
previous experience, the signifi cance of the organ involved as well as social and economic
factors. Psychologically mediated forms of pain reduction, as shown during hypnotic
procedure, not only modulate nociceptive refl exes and pain-related autonomic
activity elicited by peripherical stimulation, but also supraspinal pain-control system.
Functional imaging studies have identifi ed activation in midcingulate cortex, area 24′a
as directly mediating the changes in pain perception specifi c to hypnotic suggestion.
Hypnosis was found to enhance functional modulation between midcingulate area 24′A
and a wide network of sensory affective, cognitive and motor-related brain regions. This
short review of neurophysiological correlates of hypnotic modulation of pain reinforce
the idea, that not only pharmacological but also psychological strategies for relieving
pain can modulate the interconnected network of cortical and subcortical regions that
participate in the processing of painful stimuli.
Acknowledgments
This research was funded by the Belgian National Funds for Scientifi c Research (FNRS),
the European Commission, the James McDonnell Foundation, the Mind Science Foundation,
the French Speaking Community Concerted Research Action (ARC-06/11-340), the
Fondation Médicale Reine Elisabeth and the University of Liège. A.V. was funded by
ARC 06/11-340, M.B. is research fellow at the FNRS, S.L. are senior research associate
at the FNRS.
20 Vanhaudenhuyse et al.
Copyright © 2008 British Society of Experimental & Clinical Hypnosis Contemp. Hypnosis 26: 15-23 (2009)
Published by John Wiley & Sons, Ltd DOI: 10.1002/ch
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Marie-Elisabeth Faymonville
Pain Clinic, University Hospital of Liège
Sart-Tilman
4000 Liège
Belgium

Disclaimer: The services we render are held out to the public as non-therapeutic hypnotism, defined as the use of hypnosis to inculcate positive thinking and the capacity for self-hypnosis. Results may vary from person to person.  We do not represent our services as any form of medical, behavioral, or mental health care, and despite research to the contrary, by law we make no health claim to our services.