J Psychiatry Neurosci 2017;42(3):200-209
Daniela Mier, PhD; Josef Bailer, PhD; Julia Ofer, PhD; Tobias Kerstner, PhD; Vera Zamoscik, MSc; Fred Rist, PhD; Michael Witthöft, PhD; Carsten Diener, PhD
Background: An attentional bias to health-threat stimuli is assumed to represent the primary pathogenetic factor for the development and maintenance of pathological health anxiety (PHA; formerly termed “hypochondriasis”). However, little is known about the neural basis of this attentional bias in individuals with PHA.
Methods: A group of patients with PHA, a group of depressed patients and a healthy control group completed an emotional Stroop task with health-threat (body symptom and illness) words and neutral control words while undergoing functional MRI.
Results: We included 33 patients with PHA, 28 depressed patients and 31 controls in our analyses. As reflected in reaction times, patients with PHA showed a significantly stronger attentional bias to health-threat words than both control groups. In addition, patients with PHA showed increased amygdala and rostral anterior cingulate cortex activation for body symptom, but not for illness words. Moreover, only in patients with PHA amygdala activation in response to symptom words was positively associated with higher arousal and more negative valence ratings of the body symptom word material.
Limitations: A control group of patients with an anxiety disorder but without PHA would have helped to define the specificity of the results for PHA.
Conclusion: The attentional bias observed in patients with PHA is associated with hyperactivation in response to body symptom words in brain regions that are crucial for an arousal-related fear response (e.g., the amygdala) and for resolving emotional interference (e.g., the rostral anterior cingulate cortex). The findings have important implications for the nosological classification of PHA and suggest the application of innovative exposure-based interventions for the treatment of PHA.
Submitted Apr. 26, 2016; Revised Aug. 29, 2016; Accepted Sept. 25, 2016; Early-released Feb. 7, 2017
Acknowledgements: This study was supported by the Deutsche Forschungsgemeinschaft (DFG BA1597/5-1). The authors thank the colleagues who helped with study organization, clinical ratings and data acquisition.
Affiliations: From the Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany (Mier, Bailer, Ofer, Kerstner, Zamoscik, Diener); the University of Münster, Münster, Germany (Rist); the Johannes Gutenberg University, Mainz, Germany (Witthöft); and the SRH University of Applied Sciences Heidelberg, Germany (Diener).
Competing interests: None declared.
Contributors: J. Bailer, F. Rist, M. Witthöft and C. Diener designed the study. D. Mier, J. Bailer, J. Ofer, T. Kerstner and V. Zamoscik acquired the data, which D. Mier, J. Bailer, V. Zamoscik, F. Rist, M. Witthöft and C. Diener analyzed. D. Mier, J. Bailer, M. Witthöft and C. Diener wrote the article, which all authors reviewed and approved for publication.
Correspondence to: D. Mier, Department of Clinical Psychology, Central Institute of Mental Health, J5, 68159 Mannheim, Germany; Daniela.Mier@zi-mannheim.de