Emotion brain alterations in anorexia nervosa: a candidate biological marker and implications for treatment

Emotion brain alterations in anorexia nervosa: a candidate biological marker and implications for treatment


J Psychiatry Neurosci 2010; 35(4): 267-274

Ainslie Hatch, BA; Sloane Madden, MBBS; Michael R. Kohn, MBBS; Simon Clarke, MBBS; Stephen Touyz, PhD; Evian Gordon, PhD; Leanne M. Williams, PhD

Hatch, Kohn, Clarke, Gordon, Williams — The Brain Dynamics Center, Westmead Millennium Institute and University of Sydney at Westmead Hospital; Hatch, Touyz — School of Psychology, University of Sydney, Camperdown; Madden — Psychological Medicine, Children’s Hospital at Westmead; Kohn, Clarke — Center for Research into Adolescents’ Health, Adolescent Medicine, Children’s Hospital at Westmead and Westmead Hospital; Gordon, Williams — Psychological Medicine, University of Sydney, Westmead Hospital, Sydney, Australia; Gordon — Brain Resource International Database, Brain Resource, Ultimo, Australia and San Francisco, Calif.


Background: Identification of the biological markers of anorexia nervosa (AN) is crucial for the development of new treatments. We aimed to determine whether AN is associated with disturbances in the nonconscious neural processing of innate signals of emotion and whether these disturbances persist after weight gain.

Methods: In a retest design, 28 adolescent females with AN were tested at first admission to hospital and again after they had gained weight. Matched healthy control participants were tested at the same times. We assessed emotion-elicited event-related potentials (ERPs) during overt and covert presentation of emotion expressions, scores on an emotion-identification behavioural task, and symptom measures. We performed between and within group analyses.

Results: Individuals with AN had a marked alteration in ERPs relative to healthy controls. Irrespective of the form of stimulus, early and late ERP components were significantly reduced in AN patients at baseline (when underweight) and on retest (after weight gain), especially in the temporo-occipital regions, suggesting a persistent disruption of the early automatic appraisal of salient emotional signals.

Limitations: This study could have been improved with a longer standardized retest interval.

Conclusions: There is likely a core, generic disturbance in AN in the early “automatic” neural processing of emotion irrespective of weight or nutritional status. New innovative emotion-based psychologic or pharmacologic treatments targeting these nonconscious processes may prove beneficial.

Preliminary data for a subset of patients included in this article were presented at the 6th International Congress of Neuropsychiatry, Sydney, Sept. 10–14, 2006 (oral presentation), and at the 14th Annual Meeting of the Organization for Human Brain Mapping in Melbourne, Australia, June 15–19, 2008 (poster).

Submitted June 26, 2009; Revised Dec. 21, 2009; Accepted Jan. 12, 2010.

Acknowledgments: We acknowledge the support of the Brain Resource International Database (under the auspices of Brain Resource; www.brainresource.com) for support in data acquisition and quantification. Brain Resource had no role in the design or implementation of the project. All scientific decisions are made independently of Brain Resource operations via the scientific division, BRAINnet (www.brainnet.net). Dr. Williams holds a Pfizer Senior Research Fellowship. Ms. Hatch was supported by a University Postgraduate Award (UPA) (University of Sydney) and The Millennium Foundation Research Scholarship Stipend Enhancement.

Competing interests: None declared for Drs. Madden, Kohn, Clarke and Touyz and Ms. Hatch. Dr. Gordon is CEO of Brain Resource, with significant financial interest in the company. Dr. Williams is a minor shareholder (< 1%) in Brain Resource and has received fees from them for work unrelated to this study. Contributors: Ms. Hatch and Drs. Kohn, Clarke, Touyz, Gordon and Williams designed the study. Ms. Hatch and Dr. Kohn acquired the data. Ms. Hatch and Drs. Madden, Kohn and Touyz analyzed the data. Ms. Hatch and Drs. Madden, Kohn, Clarke, Gordon and Williams wrote the article, which Ms. Hatch and Drs. Kohn, Touyz and Gordon reviewed. All authors approved publication.

DOI: 10.1503/jpn.090073

Correspondence to: Ms. A. Hatch, Acacia House, Hawkesbury Rd., Westmead Hospital, Westmead, Sydney, NSW, Australia 2145; fax 612 9845 8190; ainslieh@psych.usyd.edu.au