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Psychiatric Bulletin (2005) 29: 114. doi: 10.1192/pb.29.3.114
© 2005 The Royal College of Psychiatrists
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Psychiatric Bulletin (2005) 29: 114
© 2005 The Royal College of Psychiatrists


Correspondence

Psychotherapy meets neuroscience

David Nutt, Professor of Psychopharmacology, Head of the Department of Community Based Medicine

University of Bristol, Psychopharmacology Unit, Dorothy Hodgkin Building, Whitson Street, Bristol BS12NY

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. Furmark 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 (Hood 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 (Smith 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, 425 –433.[Abstract/Free Full Text]

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.

SMITH, K. A., FAIRBURN, C. G., COWEN, P. J. (1997) Relapse of depression after rapid depletion of tryptophan. Lancet, 349, 915 –919.[CrossRef][Medline]





This Article
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