Attentional bias modification is associated with fMRI response toward negative stimuli in individuals with residual depression: a randomized controlled trial

Attentional bias modification is associated with fMRI response toward negative stimuli in individuals with residual depression: a randomized controlled trial

J Psychiatry Neurosci 2020;45(1):23-33 | PDF | Appendix

Eva Hilland, MSc; Nils I. Landrø, PhD; Catherine J. Harmer, DPhil; Michael Browning, MB BS, DPhil; Luigi A. Maglanoc, MSc; Rune Jonassen, PhD

Background: Attentional bias modification (ABM) may lead to more adaptive emotion perception and emotion regulation. Understanding the neural basis of these effects may lead to greater precision for the development of future treatments. Task-related functional MRI (fMRI) after ABM training has not been investigated in depression so far. The main aim of this randomized controlled trial was to explore differences in brain activity after ABM training, in response to emotional stimuli.

Methods: A total of 134 people with previous depression, who had been treated for depression and had various degrees of residual symptoms, were randomized to 14 days of active ABM or a closely matched placebo training, followed by an fMRI emotion regulation task. The training procedure was a classical dot–probe task with emotional face stimuli. In the active ABM condition, the probes replaced the more positively valenced face of a given pair. As participants implicitly learned to predict the probe location, this would be likely to induce a more positive attentional bias. The placebo condition was identical, except for the contingency of the probe, which appeared equally behind positive and negative stimuli. We compared depression symptoms and subjective ratings of perceived negativity during fMRI between the training groups. We explored brain activation in predefined regions of interest and across the whole brain. We explored activation in areas associated with changes in attentional bias and degree of depression.

Results: Compared with the placebo group, the ABM group showed reduced activation in the amygdala and the anterior cingulate cortex when passively viewing negative images. We found no group differences in predefined regions of interest associated with emotion regulation strategies. Response in the temporal cortices was associated with the degree of change in attentional bias and the degree of depressive symptoms in ABM versus placebo.

Limitations: These findings should be replicated in other samples of patients with depression, and in studies using fMRI designs that allow analyses of within-group variability from baseline to follow-up.

Conclusion: Attentional bias modification training has an effect on brain function in the circuitry associated with emotional appraisal and the generation of affective states.

Clinicaltrials.gov identifier: NCT02931487.


Submitted Jul. 23, 2018; Revised Aug. 6, 2018; Revised Dec. 22, 2018; Accepted Mar. 26, 2019; Published online Aug. 9, 2019

Acknowledgements: The authors thank their fMRI research assistant Dani Beck; the Division of Psychiatry, Diakonhjemmet Hospital, for help and support during the recruiting period; the Intervention Centre, OUS, for radiological assistance in MRI protocols, data acquisitions and screening for unexpected neuropathological findings; Tor Endestad for establishing invaluable infrastructure for MRI research in the department; and the external recruitment sites Unicare, Coperiosenteret AS, Torgny Syrstad, MD, Synergi Helse AS and Lovisenberg Hospital. This project is supported by the Southeastern Norway Regional Health Authority, grant number 2015052 (to NIL); the Research Council Norway, grant number 229135 (to NIL); and the Department of Psychology, University of Oslo. CJH is supported by the NIHR Oxford Health Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.

Affiliations: From the Clinical Neuroscience Research Group, Department of Psychology, University of Oslo, Oslo, Norway (Hilland, Landrø, Harmer, Maglanoc, Jonassen); the Division of Psychiatry, Diakonhjemmet Hospital, Oslo, Norway (Hilland, Landrø); the Psychopharmacology and Emotional Research Lab, University Department of Psychiatry, University of Oxford, Oxford, United Kingdom (Harmer); the Computational Psychiatry Laboratory, Department of Psychiatry, University of Oxford, Oxford, United Kingdom (Browning); the Oxford Health NHS Trust, Oxford, United Kingdom (Browning); the NORMENT, KG Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Norway (Maglanoc); and the Division of Psychiatry, Akerhus University Hospital, Oslo, Norway (Jonassen).

Competing interests: N. Landrø has received consultancy fees and travel expenses from Lundbeck. C. Harmer has received consultancy fees from Johnson and Johnson Inc, P1 vital and Lundbeck. M. Browning holds a part-time position at P1 vital Ltd. and owns shares in P1 vital products Ltd. M. Browning has also received travel expenses from Lundbeck and has acted as a consultant for J&J. No other competing interests declared.

Contributors: E. Hilland, N. Landrø, C. Harmer, M. Browning and R. Jonassen designed the study. E. Hilland, L. Maglanoc and R. Jonassen acquired the data, which E. Hilland, N. Landrø, C. Harmer, M. Browning and R. Jonassen analyzed. E. Hilland and R. Jonassen wrote the article, which all authors reviewed. All authors approved the final version to be published and can certify that no other individuals not listed as authors have made substantial contributions to the paper.

DOI: 10.1503/jpn.180118

Correspondence to: E. Hilland, Department of Psychology, University of Oslo, P.O. Box 1094, Blindern 0317 Oslo, Norway; eva.hilland@psykologi.uio.no