a1 Department of Psychiatry and Psychology, School for Mental Health and Neuroscience, EURON, Maastricht University Medical Center, Maastricht, The Netherlands
a2 Department of Radiology, Maastricht University Medical Center, Maastricht, The Netherlands
a3 King's College London, King's Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, UK
Background Hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, associated with increased pituitary volume, may mediate observed alterations in stress reactivity in patients with psychotic disorder. We examined the association between pituitary volume, real-life stress reactivity and genetic liability for psychotic disorder.
Method Pituitary volumes were derived from magnetic resonance imaging (MRI) scans of 20 patients with psychotic disorder, 37 non-psychotic siblings of these patients, and 32 controls. The Experience Sampling Method (ESM) was used to measure emotional stress reactivity [changes in negative affect (NA) associated with daily life stress] in the three groups, and biological stress reactivity (changes in cortisol associated with daily life stress) in siblings and controls. Interactions between group, stress and pituitary volume in models of NA and cortisol were examined.
Results Groups did not differ in pituitary volume. Patients showed significantly higher emotional stress reactivity than siblings and controls. In addition, emotional stress reactivity increased with increasing pituitary volume to a greater degree in patients than in controls and siblings. Siblings had higher cortisol levels than controls but did not show increased cortisol reactivity to stress. There was no interaction between pituitary volume, stress and group in the model of cortisol.
Conclusions Higher pituitary volume was associated with increased emotional stress reactivity in patients with psychotic disorder, siblings and controls. The association was significantly stronger in the patient group, suggesting a process of progressive sensitization mediating clinical outcome.
(Received March 11 2011)
(Revised August 22 2011)
(Accepted November 01 2011)
(Online publication December 01 2011)
c1 Address for correspondence: M. Marcelis, M.D., Ph.D., Department of Psychiatry and Psychology, Maastricht University Medical Center, PO Box 616 (Vijv1), 6200 MD Maastricht, The Netherlands. (Email: M.Marcelis@maastrichtuniversity.nl)
† These authors contributed equally to this work.