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Down the Rabbit Hole
Paul Kiritsis, PsyD Clinical Psychology, DPhil., MA (History)


Hypnosis and Pain Perception: Neuroimaging Studies

Paul Kiritsis - Thursday, June 04, 2015

Chronic pain conditions constitute a medical conundrum of our times. Their resistance to standard medical treatments (Turk, Wilson, & Cahana, 2011) is burdensome to patients, doctors, and society as a whole because they initiate deleterious cycles involving costly treatments that amount to nothing but inadequate pain relief, an overreliance and abuse of analgesic medications, adverse side effects, addiction, diversion, and valuable time squandered racking up medical bills. This leaves much to be desired, and foremost of what is or should be desired by chronic pain sufferers are vigorous and efficacious treatment options backed by solid empirical evidence. Interestingly, there is contracted awareness surrounding the fact that the sole cross-cultural modality which has been used to treat a multifarious array of pain conditions over the centuries is hypnosis (Pyntar & Lynn, 2008).

Given that the mechanistic components of hypnosis are sometimes confused, this paper shall begin with a lucid definition of the phenomenon itself. Despite lack of consensus, most researchers and clinicians agree that hypnosis is a harmonious confluence of one or more of the following: imagery, focal attention, cognitive processing, relaxation, trance, and suggestion (probably its most renowned feature). Incorporating many of these features, Kihlstrom’s condensed summa describes it as, “a social interaction in which one person designated the subject, responds to suggestions offered by another person, designated the hypnotist, for experiences involving alterations in perception, memory, and voluntary action. (Kihlstrom, 1985, pp. 385).”  

            The history of hypnosis dates back to the late eighteenth century when Franz Anton Mesmer introduced it into the prevailing medical fraternity as a neurophysiological innovation to treat “nervous” diseases (Green, Lawrence, & Lynn, 2014). In fact, he’s something of an ancillary pioneer, having stumbled upon the technique completely by chance. Fascination with the phenomenon has not wavered, and the last two decades have been rife with compelling theoretical, clinical, and experimental research vindicating its efficacy and mechanistic underpinnings. Failure of some clinical and experimental studies in adopting stringent methodological criteria such as adequate sample sizes and randomized controlled trials has not dampened the appeal of hypnosis as a medical and psychotherapeutic adjunct. This sentiment is reflected in contemporary research, where the efficacy of hypnotic analgesia has been scrutinized for its propensities in alleviating acute pain in laboratory settings (Chaves, 1994; Ewin, 1986); chronic pain (Montgomery, Du-Hamel, & Redd, 2000; Stoelb, Molton, Jensen, & Patterson, 2009; Tomé-Pires & Miró, 2012); and acute pain linked to medical procedures (Patterson, Wiechman, Jensen, & Sharar, 2006). On reflection, perhaps the most important and authoritative advances, at least the ones likely to spur widespread medical and professional acceptance, have come from recent neuroimaging studies attempting to substantiate correlations between hypnosis modulated pain conditions and activation-deactivation neural patterns in the brain (Del Casale et al., 2015).

A stimulating meta-analytic review by Montgomery et al. (2000) found a medium to large effect size in seventy-five percent of all clinical and experimental cases where hypnotic analgesia was used to treat chronic, acute, or induced pain, illuminating hypnosis’s effectiveness in pain management despite outcome variances from individual to individual. Moreover, their aggregation and analysis of data demonstrated that hypnosis is superlatively operative over and above psychological placebos, pharmaceuticals, and other pain treatment options. In reviewing the clinical literature on randomized controlled trials where hypnotic analgesia was used to treat acute procedural pain, Patterson and Jensen (2003) also ranked hypnosis as superior to standard care, attention, or no treatment at all but concurrently stressed its therapeutic equivalence to autogenic training and relaxation. On a similar note, another review of controlled trials focusing on the induction of hypnotic analgesia in chronic pain patients (Elkins, Jensen, & Patterson, 2007) also determined statistically significant finds when comparing hypnosis with non-hypnotic interventions and non-treatment options. Their beneficial effects, in particular, were recognized as superior in the context of longevity, lasting for several months or more after the initial intervention. In a different experimental study examining hypnosis with fifty-five fibromyalgic patients, Castel, Pérez, Sala, Padrol, and Rull (2007) revealed that sensorial pain and its associative intensity were more effectually dampened by an amalgam of hypnosis and analgesic suggestions rather than an amalgam of hypnosis and relaxation or relaxation alone.

Now we move into the crux of this investigation. Even though the neural correlates of hypnosis modulated pain perception are only partially understood, there are functional neuroimaging studies which have adopted numerous hypnotic procedures–suggestions to amend a physically induced pain condition, suggestions to amend a chronic pain condition, and the deliberate hypnotic induction of pain–and demonstrated, beyond a shadow of doubt, an existing correlational relationship between hypnosis and neural activation-deactivation patterns in the brain (Del Casale et al., 2015).

The majority of these fall into the first category, the use of hypnotic suggestions to alter a nociceptive induced pain condition. In a study conducted by Rainville et al. (1997) using positron emission tomography (PET), the left hands of 5 male and 3 female highly hypnotizable and moderately hypnotizable subjects between the ages of 19-53 were immersed in neutral (35ºC) or excruciatingly hot (47ºC) water. Scans were then recorded for each condition where the subject was alert, hypnotized, under hypnotic suggestions for perceived pleasantness (analgesia), and under hypnotic suggestions for perceived unpleasantness (hyperalgesia). Subjects were given the opportunity to rate the degree of intensity and unpleasantness on two separate scales. Results indicated that both pain affect and activity in the associated occipital cortical regions were altered when the experimenters made suggestions for increased or decreased unpleasantness. Specifically, a comparison between the hypnosis control and hypnotic suggestion conditions revealed significant increases in regional cerebral blood flow (rCBF) in the primary somatosensory cortex (SI), the ventral part of the anterior cingulate cortex (ACC), and the insular cortex (IC) when suggestions were deployed.

Two years later an analogous study using the same technique, experimental design, and number of participants was published (Rainville et al, 1999) with stimulus order being randomized within sessions and across trials to diminish order effects. During hypnotic induction, the PET scans showed correlated increases in delta EGG activity and rCBF in bilateral regions of the inferior frontal gyri and in the caudal section of the right anterior cingulate cortex along with decreases in rCBF in the left precuneus, the right inferior parietal lobule, and the posterior cingulate cortex (PCC). Interestingly, suggestions resulted in further increases of rCBF in the frontal cortices of the left hemisphere, and in areas of the medial and lateral posterior prefrontal cortex (PPC) which overlapped with hypnotic-associated reductions. At this point in the neuroscientific discourse, we know that brain regions activated by painful stimuli are the primary SI and secondary (SII) somatosensory cortices,  the ACC which mediates the relationship between cognition, sensory perception, and motor control, the IC, and the thalamic nuclei (Apkarian, Bushnell, Treede, & Zubieta, 2005; Tracey & Mantyh, 2007). The aforesaid discoveries all indicate that hypnotic analgesia might work by increasing functional connectivity between prefrontal areas, the SI, and the subcortical IC (Vanhaudenhuyse et al., 2009), spurring a state-dependent, top-down modulation of sorts whereby perceived deleterious stimuli are depotentiated and precluded from conscious awareness.

Alternatively, some experimental studies have clarified the relation of hypnosis to particular neurophysiological effects by looking at the manner in which chronic pain conditions (i.e. fibromyalgia, phantom limb pain, and low-back pain) are moderated by hypnotic suggestions. In a fascinating fMRI study examining alterations in the experience of pain with and without hypnosis (Derbyshire et al., 2009), 13 fibromyalgic and highly hypnotizable female patients with a mean age of 51.4 years were hypnotized upon entering an fMRI scanner and subsequently instructed to experience augmentations and reductions in subjective levels of their pain. To assist in the subjective representation of fibromyalgia pain, patients were advised to visualize a dial enumerating to ten. The researchers gathered two blocks of fMRI data for both the hypnotic and non-hypnotic states, occasionally reversing the order of the suggestions as to facilitate variable control. When hypnotic or nonhypnotic changes in pain perception were induced, the midbrain, midcingulate, thalamus, inferior parietal cortex (IPC), IC, prefrontal cortex (PFC), and SI and SII all became activated. Compared with the unhypnotized controls, blood oxygenation levels in the anterior medial cingulate cortex (MCC), the cerebellum, and anterior and posterior IC soared further in response to hypnotic suggestibility.

In another PET study (Nusbaum et al., 2011), 14 right-handed males suffering from chronic low-back pain were assigned to two groups and exposed to five sequential experimental conditions incorporating three 20-minute periods of rest and two 30-minute periods of analgesic suggestion. The first group received very direct suggestions regarding the nature and location of the pain, whilst the second received indirect suggestions about complacency and wellbeing without reference to the former. Findings illuminated increased neural activity in the superior temporal cortex (STC), inferior frontal cortex (IFC), medial PFC, and the orbitofrontal cortex (OFC) for analgesic suggestions offered during ordinary wakefulness, and in the ACC and anterior IC for analgesic suggestions offered during the hypnotic state. Moreover, the hypnoanalgesic condition also correlated with activations in the lenticular, caudate, and accumbens nuclei. It came to light that the cognitive processes of conscious awareness required direct suggestions to impact chronic pain perception, whereas the privilege of hypnosis lay in its uniform efficacy across all suggestion types. Despite different designs and techniques, both Derbyshire (2009) and Nusbaum (2011) implicate the PFC as a neural network manipulator and the IC as a conspiring modulator of pain perception.

Finally, hypnotic suggestions for pain induction in adults has been the subject of three important fMRI studies, all of which reported changes in the pain matrix of the brain, otherwise known as the “homeostatic afferent processing network.” Derbyshire et al. (2004) conducted an interesting fMRI block design study with 8 highly hypnotizable subjects which involved delivering noxious heat pulses to their right palms through fitted thermal stimulators. Subjects were informed that pulses would be administered over six minutes and be accompanied by thirty seconds of repose; that a single tap to the foot would signal stimulus activation; and that rest periods would be inaugurated with two taps to the foot. However, experimenters used deception and delivered noxious heat pulses on only three of the six occasions (to stimulate psychological pain). The two blocks of 6-minute long functional data gathered reflected 3 minutes of hypnotically induced pain, 3 minutes of physically induced pain, and 6 minutes of rest. After data crunching, it came to light that the ipsilateral parietal cortex (IPC), OFC, the contralateral ACC, the perigenual ACC and the thalamus showed stronger blood-oxygenation-level-dependent activations during the nociceptive induced rather than the hypnotically induced conditions. Experimental hypnotically induced pain, on the other hand, correlated more strongly with PFC activation.   

Published the following year, a different block design fMRI study (Raij et al., 2005) subjected 11 females and 3 males to three sessions of painful stimulation induced in three different ways: hypnotic suggestion; laser stimulation to the left hand without hypnotic induction; and then laser stimulation to the left hand during a hypnotic state. Each of the three sessions was characterized by periods of pain and repose. The results supported an active role for the middle insula and ACC in the emotional nuances of pain, given that there was no discrimination or qualitative difference in their physically induced and psychologically-induced activations. As one might expect, nociceptive induced pain registered more strongly in the posterior IC and SII and psychologically-induced pain more prominently in the highly connected and metabolically active PCC. A follow-up block design fMRI study by the same experimenters but with a different design revealed a positive correlation between suggestions for pain activating the right dorsolateral PFC and the intensity of subjective pain experience induced through verbal suggestibility, along with positive correlations of the former with the highest pain-related activations of the SII. The experimental data clarified another part of the hypnosis-pain matrix puzzle, indicating that ACC and IC activations serve as true harbingers for pain-related SII activation. At any rate the all-encompassing feature of hypnotic pain modification phenomena mobilized through pleasurable recollections and subjective mental experiences is left-biased PFC hyperactivation, meaning that the PFC downregulates emotional pain. What should be blatantly clear from the abovementioned neuroimaging data is that hypnosis trumps placebo treatments because it induces quantifiable effects in specific neural networks of the brain implicated in pain processing, making it a potent and commanding tool for the clinical management and alleviation of psychological and physical pain.

Overall, significant challenges faced by the professional medical and clinical arena in their inability to effectively manage chronic and acute procedural pain through conventional treatment methods may be addressed, in part, by clinical hypnosis. On the whole, the clinical and experimental literature presented make a solid, convincing case for the official induction of hypnosis into the realm of conventional well-established and efficacious treatments. Over and above the fact that hypnosis trumps the psychological placebo, conventional treatments, and non-action in assisting with the management of pain, it exhibits minimal (if any) adverse side effects typical of conventional pharmacological treatments, making it both cost-efficient and attractive by comparison. Most importantly, promising empirical finds for the efficacy of hypnosis and analgesic suggestions have hitherto been found in neuroimaging studies which point to top-down regulation of the brain’s cortical and subcortical pain matrix (the PFC affecting SI, SII, IC, ACC, and thalamic nuclei) . From the aggregated PET and fMRI data, it also appears that the effectiveness of hypnosis modulated pain perception may be contingent on the wording of the specific analgesic suggestions themselves. On the downside lack of unanimous agreement and sanction amongst clinicians regarding the constitutional elements of hypnosis has bred ambiguity surrounding the theoretical underpinnings of hypnotic pain relief, nonetheless this shouldn’t stop receptive clinicians from amalgamating it into their professional practice as a psychotherapeutic adjunctive where pain management is concerned.






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