Neurocognitive basis and treatment of self-blaming emotional biases in major depressive disorder

Student thesis: Doctoral ThesisDoctor of Philosophy


The revised learned helplessness model postulates a critical role for self-blaming biases in the development and perpetuation of clinical symptoms of major depressive disorder (MDD). Causing persistent and excessive feelings of guilt and other self-blaming emotions, a maladaptive attributional style is thought to contribute to depressive symptoms. Current therapeutic approaches are limited in addressing self-blame in MDD, and often patients do not achieve symptom remission or the prevention of recurrent episodes. This is particularly true for MDD patients of the anxious distress subtype. 
The work presented in this thesis tested the clinical benefits of a novel self-blame-targeting treatment protocol, employing a self-guided psychological intervention with and without additional real-time functional magnetic resonance imaging (rtfMRI) neurofeedback in early treatment-resistant MDD. Based on the recent finding of guilt-specific hyper-connectivity between the right superior anterior temporal lobe (rSATL) and the posterior subgenual cortex (SC) as a neural signature of recurrence risk in MDD, the single-blind randomised trial presented in this thesis aimed at rebalancing rSATL-SC functional connectivity in MDD, while investigating neurocognitive underpinnings of self-blame. For this purpose, a novel experimental task was developed and tested in anxious and non-anxious MDD patients and healthy control participants. 
Both interventions, rtfMRI neurofeedback training and the solely psychological intervention, were found to be safe and therapeutically effective approaches, with response rates of more than 55% in both treatment groups. MDD patients of the anxious distress subtype were found to benefit less from rtfMRI neurofeedback training and did not present with self-blaming emotional biases compared with non-anxious MDD. Further, despite resulting in a reduction in functional connectivity between the rSATL and the posterior SC, this change was not associated with a reduction in depressive symptoms. 
Ultimately, the findings presented in this thesis are only in partial support of the revised learned helplessness model with clearer evidence for its applicability in non-anxious MDD, whereas there was experimental evidence contrary to its predictions in MDD patients of the anxious distress subtype by showing their increased levels of anger directed at others.
Date of Award1 Jul 2019
Original languageEnglish
Awarding Institution
  • King's College London
SupervisorRoland Zahn (Supervisor) & Steven Williams (Supervisor)

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