Hypnosis and Pain Control

Now back to our irregularly scheduled neuroscience programming!

It's been so long since The Neurocritic began a plodding series on hypnosis (June 6 to be exact), that the in press articles are now in print in the Journal of Physiology (Paris). The final topic for discussion is the use of hypnosis to control pain.

Functional neuroanatomy of the hypnotic state
Pages 463-469
Marie-Elisabeth Faymonville, Mélanie Boly and Steven Laureys
SummaryPlus | Full Text + Links | PDF (283 K)

. . . Second, we looked at the anti-nociceptive effects of hypnosis. Compared to the resting state, hypnosis reduced pain perception by approximately 50%. The hypnosis-induced reduction of affective and sensory responses to noxious thermal stimulation were modulated by the activity in the midcingulate cortex (area 24a′). Finally, we assessed changes in cerebral functional connectivity related to hypnosis. Compared to normal alertness (i.e., rest and mental imagery), the hypnotic state, significantly enhanced the functional modulation between midcingulate cortex and a large neural network involved in sensory, affective, cognitive and behavioral aspects of nociception. These findings show that not only pharmacological but also psychological strategies for pain control can modulate the cerebral network involved in noxious perception.

What are some of the brain regions involved in the perception of pain? A meta-analysis of 35 imaging studies is illustrated below.






By way of explanation, back in January, I became addicted to BrainMap,

an online database of published functional neuroimaging experiments with coordinate-based (Talairach) activation locations. The goal of BrainMap is to provide a vehicle to share methods and results of brain functional imaging studies. It is a tool to rapidly retrieve and understand studies in specific research domains, such as language, memory, attention, reasoning, emotion, and perception, and to perform meta-analyses of like studies.

where one can do

coordinate-based meta-analyses according to the activation likelihood estimation (ALE) method.

That's when I did the ALE meta-analysis for imaging studies of physical pain, for comparison to "empathy for pain" and the "social rejection of being excluded from Pong" (which, of course, feels exactly like being cut open with a scalpel).

Eisenberger NI, Lieberman MD, Williams KD. (2003). Does rejection hurt? An FMRI study of social exclusion. Science 302: 290-2.

A neuroimaging study examined the neural correlates of social exclusion and tested the hypothesis that the brain bases of social pain are similar to those of physical pain. Participants were scanned while playing a virtual ball-tossing game in which they were ultimately excluded. Paralleling results from physical pain studies, the anterior cingulate cortex (ACC) was more active during exclusion than during inclusion and correlated positively with self-reported distress. Right ventral prefrontal cortex (RVPFC) was active during exclusion and correlated negatively with self-reported distress. ACC changes mediated the RVPFC-distress correlation, suggesting that RVPFC regulates the distress of social exclusion by disrupting ACC activity.

More on that topic later.

[But I think I might actually like this study -- relatively speaking -- since it doesn't equate social rejection with physical pain.

Somerville LH, Heatherton TF, Kelley WM. (2006). Anterior cingulate cortex responds differentially to expectancy violation and social rejection. Nat Neurosci. Jul 2 [Epub ahead of print]

This study investigated human anterior cingulate cortex (ACC) involvement during a task that dissociated expectancy violation from social rejection. Across two studies, participants underwent functional magnetic resonance imaging while making social judgments and receiving fictitious feedback that was either positive or negative and consistent or inconsistent with their expectations. The results demonstrate that the dorsal ACC is sensitive to expectancy violations, whereas the ventral ACC is differentially responsive to social feedback.]

Now back to physical pain. OK, here's another ALE map that shows clusters of activation (below). In this map, different clusters of activation are coded with different colors. The first map (above) was color-coded for significance level.



Technical details: ALE is a quantitative meta-analysis method (Turkeltaub et al., 2002) that can be used to infer function-location relationships from the functional neuroimaging literature. At the time of this analysis, BrainMap, a Java software application developed at the Research Imaging Center in San Antonio, contained 35 papers reporting activations in studies that delivered painful stimuli to the participants, and 34 of these were included in the meta-analysis. The Talairach coordinates of all pain-related activations were used to estimate voxel-wise activation likelihoods. A false discovery rate threshold of p less than .05 and a cluster extent threshold of 100 mm³ were applied to the ALE map. The resulting map identified the regions of activation common to all studies comprising the meta-analysis. Sixteen clusters were identified, with the largest being centered in the thalamus, insula, and cerebellum.

So there's evidence (Kulkarni et al., 2005) for a lateral pain system (ventral lateral nucleus of the thalamus, primary and secondary somatosensory cortices), a medial pain system (medial thalamic nuclei, anterior cingulate cortex, other prefrontal regions, and the fearful amygdala), and the intermediate insula, which sits between them. The lateral system is related to the sensory aspects of pain, while the medial is related to more "perceptual/affective" components of pain. What hypnosis does is to increase activity in the ACC, which may then downregulate activity in the sensory regions (see also Faymonville et al., 2000). 1

Would I have surgery under hypnosis?

Meurisse M, Defechereux T, Hamoir E, Maweja S, Marchettini P, Gollogly L, Degauque C, Joris J, Faymonville ME. (1999). Hypnosis with conscious sedation instead of general anaesthesia? Applications in cervical endocrine surgery. Acta Chir Belg. 99:151-8.

Uh, NO!

1 Functional connectivity analysis methods DO NOT prove causality, although some practitioners might want to believe otherwise.

References

Derbyshire SW, Whalley MG, Stenger VA, Oakley DA. (2004). Cerebral activation during hypnotically induced and imagined pain. Neuroimage 23:392-401.

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 92:1257-67.

Kulkarni B, Bentley DE, Elliott R, Youell P, Watson A, Derbyshire SW, Frackowiak RS, Friston KJ, Jones AK. (2005). Attention to pain localization and unpleasantness discriminates the functions of the medial and lateral pain systems. Eur J Neurosci. 21:3133-42.

Raij TT, Numminen J, Narvanen S, Hiltunen J, Hari R. (2005). Brain correlates of subjective reality of physically and psychologically induced pain. PNAS 102:2147-51.

Turkeltaub PE, Eden GF, Jones KM, Zeffiro TA (2002) Meta-analysis of the functional neuroanatomy of single-word reading: Method and validation. NeuroImage 16:765-780.

ADDENDUM: Interestingly, the opposite manipulation has also been examined (Raij et al., 2004; Derbyshire et al., 2004). Hypnotically-induced pain activates the same pain matrix as real pain, but with less activity in the sensory areas.