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Psychotherapy meets neuroscience

Published online by Cambridge University Press:  02 January 2018

David Nutt*
Affiliation:
University of Bristol, Psychopharmacology Unit, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 2NY
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Abstract

Type
The columns
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
Copyright © 2005. The Royal College of Psychiatrists.

I read with interest the ‘opinion and debate’ article by Peter Fonagy ‘Psychotherapy meets neuroscience’ (Psychiatric Bulletin, October 2004, 28, 357-359). While I am in agreement with the points he makes and the illustrations he uses, I think he has overlooked what is very likely to be the defining technology in the future of psychiatric treatment: neuroimaging. There is already a smattering of papers that have addressed the possible convergent brain mechanisms that underlie psychotherapeutic response and drug responses in the same disorder (for example in social anxiety disorder, e.g. Reference Furmark, Tillfors and MarteinsdottirFurmark et al, 2002). These studies are bound to increase in future years. So far, they seem to suggest that different brain regions are involved in psychotherapeutic response compared with drug response, although they may target a common final pathway such as the amygdala.

Another area of growing interest which will presumably turn into publications in the next few years is the exploration of the underlying neurochemical mechanisms of psychotherapy. For instance, our own group is currently conducting a study in which we give cognitive-behavioural therapy (CBT) for panic disorder and when patients have made a full recovery we test whether the therapeutic benefit of this intervention can be undermined by depleting brain 5-HT using the tryptophan depletion paradigm. Our preliminary data (Reference Hood, Nahs and BellHood et al, 2004) suggest that tryptophan depletion does elicit a return of vulnerability to the panicogenic actions of a flumazenil challenge. Some earlier data from the Oxford group (Reference Smith, Fairburn and CowenSmith et al, 1997) using tryptophan depletion in those recovered from depression support the view that CBT effects may be mediated through serotonergic action, since they found a depressive relapse in a couple of patients who had recovered on CBT whom had never had any drug treatment for their depression.

It was pleasing to read a psychotherapist promoting a positive view of the interaction with neuroscience and I am very happy to offer my support for any biological studies he would like to conduct in this field.

References

Furmark, T., Tillfors, M., Marteinsdottir, I., et al (2002) Common changes in cerebral blood flow in patients with social phobia treated with citalopram or cognitive–behavioral therapy. Archives of General Psychiatry, 59, 425433.CrossRefGoogle ScholarPubMed
Hood, S. D., Nahs, J. R., Bell, C. J., et al (2004) Early results from a tryptophan depletion study in panic disorder patients treated with cognitive behavioral therapy. Journal of Psychopharmacology, 18, A22, MB13.Google Scholar
Smith, K. A., Fairburn, C. G., Cowen, P. J. (1997) Relapse of depression after rapid depletion of tryptophan. Lancet, 349, 915919.CrossRefGoogle ScholarPubMed
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