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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