Abstract

Cognitive behavioural therapy (CBT) for psychosis (CBTp) aims to lower the stress of psychotic symptoms. Given that the pituitary is involved in stress regulation, CBT-led stress reduction may be accompanied by a change in pituitary volume. This study aimed to determine whether CBTp reduces pituitary volume in schizophrenia. The relation between pre-therapy memory and CBTp-led pituitary volume change was also examined given that poor memory relates to a blunted cortisol awakening response, denoting impaired stress response, in schizophrenia. Pituitary volume was measured at baseline in 40 schizophrenia or schizoaffective disorder patients and 30 healthy participants before therapy. Pituitary volume was measured again 6–9months after patients had either received CBTp in addition to standard care (CBTp+SC, n=24), or continued with standard care alone (SC, n=16). CBTp+SC and SC groups were compared on pituitary volume change from baseline to follow-up. Pre-therapy memory performance (Hopkins Verbal Learning and Wechsler Memory Scale – Logical memory) was correlated with baseline-to-follow-up pituitary volume change. Pituitary volume reduced over time in CBTp+SC patients. Additionally, pre-therapy verbal learning correlated more strongly with longitudinal pituitary volume reduction in the CBTp+SC group than the SC group. To conclude, CBTp reduces pituitary volume in schizophrenia most likely by enhancing stress regulation and lowering the distress due to psychotic symptoms.

Highlights

  • The pituitary plays a key role in physiological stress regulation

  • The study aimed to examine whether pituitary volume decreases following cognitive behavioural therapy for psychosis (CBTp) in schizophrenia patients, as pituitary volume is a potential marker of HPA axis function

  • We hypothesized that pituitary volume would decrease, because Cognitive behavioural therapy (CBT)-led stress reduction lowers cortisol levels (Rosnick et al, 2016) and lower cortisol relates to lower pituitary volume (Axelson et al, 1992)

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Summary

Introduction

The pituitary plays a key role in physiological stress regulation. Stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis to release corticosteroids from the hypothalamus and anterior pituitary (Appiah-Kusi et al, 2015). The hypothalamus and anterior pituitary stimulate cortisol release from the adrenal glands that lowers stress reactivity. The neural diathesis-stress model of schizophrenia posits that a genetic predisposition to schizophrenia combines with an accumulation of environmental factors, including psychosocial stress, that disturb the homeostasis of the HPA axis (Pruessner et al, 2017; Walker et al, 2008). This disturbance results in HPA axis hyperactivity and elevated cortisol level that affect glucocorticoid receptors in the hippocampus and medial prefrontal cortex, and increases dopamine release and prominent psychotic symptoms

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