Anatomy of hypnosis?

Some people don’t “believe in” hypnosis (#hypnosis) as a unique state. But if it could be shown that hypnosis is “real” in a clearly identifiable way, that could explain hypnotic analgesia, hypnotic anesthesia, hypnotic recall, and many other benefits that are seen to arise from what appears to be a therapeutic state. The brain produces signature behavior for anxiety, depression, and cognitive processes. If hypnosis is “real,” then can hypnosis similarly be seen in the brain?

About 10% of clients who present for hypnosis will continuously monitor their own internal state while secretly nursing reservations and doubts. These clients tend to come out of session with “hopes” that "it worked." Another 10% will enter deep trance at the word "sleep." Often they won't recall having been hypnotized. Most clients will just hang out with the hypnotist, effortlessly focused on, and responding to, the clinician’s voice. These clients will often exit trance surprised that so much time passed, or with claims that their experiences were “amazing,” while eyes were closed.

David Spiegel MD's lab at Stanford University School of Medicine, (Jiang et al., 2016), screened 545 healthy adults on reliable and valid tests of hypnotizability. The team found 36 people who scored very high, and 21 ‘controls’ who scored very low. The study used fMRI (which measures brain activity by increases in local blood flow) to look at the brains of the participants under 3 conditions: (1) While resting, (2) in memory recall, and (3) during 2 hypnosis sessions. By using a control group and these 3 treatment conditions, the researchers could understand which findings were due only to hypnosis.

The team identified 3 unique effects of hypnosis in the high scoring group.

But first, just a quick review of the anatomy needed to understand the results…

There is an ancient structure buried in the midline of the brain that connects what we call executive function to body sensations, perceptions, and sense of self. It is THE mind-body organ, if you will. This is the cingulate. The cingulate is so important that it has evolved to be naturally protected from stroke and impact. People who have trouble with the anterior cingulate (ACC) tend to have focus problems as in ADD or OCD (Fitzgerald et al., 2005; Maia, Cooney & Peterson, 2008; Yücel et al., 2003), problems with the mid-cingulate (MCC) tend to involve fear or pain perception (Vogt, Berger & Derbyshire, 2008). The posterior cingulate (PCC) is attributed with “internally-directed cognition” (self-talk) as well as retrieval of autobiographical memory, and participation in allocation of attention (Leech & Sharp, 2013).

The cingulate acts as a switching station between 3 major neural networks. The executive network (ECN) basically governs mood control, thinking, attention, working memory, and planning. The salience network (SN) notices things – sensory inputs, and participates in selecting what is important. It also activates during perceived threat. The default mode network (DMN) manages memory, reverie, rumination, and reflection. Overuse or underuse of any circuit is correlated with behavioral health issues (Arden, 2019). [Arden’s book is a great introduction to psychophysiology! (#psychophysiology)

Ok. Back to Spiegal’s team found that there were 3 changes in high hypnotizables during hypnosis.

• The dorsal anterior cingulate (dACC) activity showed a decrease in activity. The dACC is active during stress or worry. Reduced activity in the dACC may explain feelings of peace and calm experienced during hypnosis.

• The team found increased connectivity between the dorsolateral prefrontal cortex (DLPFC) and the insula. The DLPFC is part of the executive network which participates in cognition, planning, organization, and self-regulation of mood. The insula is part of the salience network, which attends to sensations, perceptions, and pain processing. Connectivity between these networks means that hypnosis increases the mind-body connection in the moment – it puts awareness into the present. This finding may also explain the effects of hypnotic analgesia and hypnotic anesthesia. The DLPFC is part of the ECN, and the insula are part of the SN. High hypnotizables who reported deepest states showed the greatest connectivity between the left DLPFC and the left insula.

• Finally, Spiegel and his researchers found that decreased connectivity between the left frontal lobe (DLPFC) and the posterior part of the cingulate provided the greatest indication of hypnosis in high hypnotizables. The authors speculate that this “likely reflects engagement in the hypnotic state and associated detachment from internal mental processes such as mind wandering and self-reflection” (p.4091).

Why are these findings interesting? This is a way to deal with naysayers. When challenged by skeptics, it can be useful to have scientific evidence that hypnotic trance is a distinct neurological state.

But perhaps there’s second, and more practical, use of this information: I find that using "hard" science (or math) in session, causes most people to go into trance. They stop tracking content, and attend to prosody. Much like White Coat trance formation, there is authority and diminishment of skepticism when science is used to persuade.

Dr. Lorrie R. Fisher, PhD, LMFT, BCN, NBCFCH

Posted April, 2023

References:

Arden, J. (2019). Mind-Brain-Gene: Toward Psychotherapy Integration. W. W. Norton & Company. Retrieved from Kindle Version at https://www.amazon.com/Mind-Brain-Gene-Psychotherapy-Integration-John-Arden/dp/0393711846

Cardeña, E., Jönsson, P., Terhune, D. B., & Marcusson-Clavertz, D. (2013). The neurophenomenology of neutral hypnosis. Cortex, 49(2), 375–385. https://doi.org/10.1016/j.cortex.2012.04.001

Cojan, Y., Waber, L., Schwartz, S., Rossier, L., Forster, A., & Vuilleumier, P. (2009). The Brain under Self-Control: Modulation of Inhibitory and Monitoring Cortical Networks during Hypnotic Paralysis. Neuron, 62(6), 862–875. https://doi.org/10.1016/j.neuron.2009.05.021

Fitzgerald, K. D., Welsh, R. C., Gehring, W. J., Abelson, J. L., Himle, J. A., Liberzon, I., & Taylor, S. F. (2005). Error-related hyperactivity of the anterior cingulate cortex in obsessive-compulsive disorder. Biological Psychiatry, 57(3), 287–294. https://doi.org/10.1016/j.biopsych.2004.10.038

Jiang, H., White, M. P., Greicius, M. D., Waelde, L. C., & Spiegel, D. (2016). Brain Activity and Functional Connectivity Associated with Hypnosis. Cerebral Cortex. https://doi.org/10.1093/cercor/bhw220

Leech, R., & Sharp, D. J. (2014). The role of the posterior cingulate cortex in cognition and disease. Brain, 137(1), 12–32. https://doi.org/10.1093/brain/awt162

Maia, T. V., Cooney, R. E., & Peterson, B. S. (2008). The neural bases of obsessive-compulsive disorder in children and adults. Development and Psychopathology, 20(4), 1251–1283. https://doi.org/10.1017/S0954579408000606

Vogt, B. A., Berger, G. R., & Derbyshire, S. W. G. (2003). Structural and functional dichotomy of human midcingulate cortex. The European Journal of Neuroscience, 18(11), 3134–3144. https://doi.org/10.1111/j.1460-9568.2003.03034.x

Yücel, M., Wood, S. J., Fornito, A., Riffkin, J., Velakoulis, D., & Pantelis, C. (2003). Anterior cingulate dysfunction: Implications for psychiatric disorders? Journal of Psychiatry & Neuroscience: JPN, 28(5), 350–354. PMID: 14517578