The neural basis of treatment-resistance in depression

  • Research type

    Research Study

  • Full title

    The neural basis of treatment-resistance in depression and anxiety

  • IRAS ID

    133616

  • Contact name

    Lindsey Marwood

  • Contact email

    lindsey.l.marwood@kcl.ac.uk

  • Sponsor organisation

    King's College London

  • Research summary

    The causes of treatment resistance in depression and anxiety are complex and poorly understood, most likely reflecting the effects of many factors. It is plausible that personality characteristics within the neuroticism domain may predispose individuals to develop anxiety and depression and also to resist treatment or to relapse. The theoretical roots of this hypothesis lie in Jeffrey Gray’s explanation of trait anxiety in terms of sensitivity to punishment. Gray based his theory on the finding that anti-anxiety drugs not only reduce clinical anxiety but also dampen punishment-related behaviour in rodents. Gray postulated that people who are naturally more sensitive to punishment will also possess personalities that are prone to anxiety. This research project aims to identify the brain systems that govern threat-avoidance behaviour and, when overactive, give rise to an anxious personality profile that elevates risk of developing clinical anxiety and/or depression and, possibly, the risk of not responding to treatment. By performing Functional Magnetic Resonance Imaging in the participants’ brains while they perform three tasks which have previously been found or proposed to be related to neuroticism: 1) joystick operated runway task to measure threat-avoidance behaviour; 2) emotional processing; and 3) a novel self-criticism task, we hope to identify shared and unique brain activity associated with anxiety and depression, and use these to predict treatment response by testing patients with anxiety and/or depression before and after a course of Cognitive Behavioural Therapy. The precise nature of the networks activated by these tasks is not predicted in detail. We expect to see greater amygdalar, hippocampal and orbitofrontal activity in response to all stimuli pre-treatment, in treatment responders and that all three tasks will show some overlap in neural activity representing the neural substrate of neuroticism.

  • REC name

    London - Bromley Research Ethics Committee

  • REC reference

    13/LO/1897

  • Date of REC Opinion

    9 Jan 2014

  • REC opinion

    Further Information Favourable Opinion