Citation

Douglas KM, Groves S, Porter RJ, Jordan J, Wilson L, Melzer TR, Wise RG, Bisson JI, Bell CJ. Aust. N. Zeal. J. Psychiatry 2019; ePub(ePub): 4867419851860.

Affiliation

Department of Psychological Medicine, University of Otago, Christchurch, Christchurch, New Zealand.

Copyright

(Copyright © 2019, Royal Australian and New Zealand College of Psychiatrists, Publisher SAGE Publishing)

DOI

10.1177/0004867419851860

PMID

31146540

Abstract

OBJECTIVE: Post-traumatic stress disorder involves excessive retrieval of traumatic memories. Glucocorticoids impair declarative memory retrieval. This preliminary study examined the effect of acute hydrocortisone administration on brain activation in individuals with earthquake-related post-traumatic stress disorder compared with earthquake-exposed healthy individuals, during retrieval of traumatic memories.

METHOD: Participants exposed to earthquakes with ( n = 11) and without post-traumatic stress disorder ( n = 11) underwent two functional magnetic resonance imaging scans, 1-week apart, in a double-blind, placebo-controlled, counter-balanced design. On one occasion, they received oral hydrocortisone (20 mg), and on the other, placebo, 1 hour before scanning. Symptom provocation involved script-driven imagery (traumatic and neutral scripts) and measures of self-reported anxiety.

RESULTS: Arterial spin labelling showed that both post-traumatic stress disorder and trauma-exposed controls had significantly reduced cerebral blood flow in response to retrieval of traumatic versus neutral memories in the right hippocampus, parahippocampal gyrus, calcarine sulcus, middle and superior temporal gyrus, posterior cingulate, Heschl's gyrus, inferior parietal lobule, angular gyrus, middle occipital gyrus, supramarginal gyrus, lingual gyrus and cuneus, and the left prefrontal cortex. Hydrocortisone resulted in non-significant trends of increasing subjective distress and reduced regional cerebral blood flow in the left inferior frontal gyrus, left anterior cingulate gyrus, middle temporal gyrus, cerebellum, postcentral gyrus and right frontal pole, during the trauma script.

CONCLUSION: Findings do not fit with some aspects of the accepted neurocircuitry model of post-traumatic stress disorder, i.e., failure of the medial prefrontal cortex to quieten hyperresponsive amygdala activity, and the potential therapeutic benefits of hydrocortisone. They do, however, provide further evidence that exposure to earthquake trauma, regardless of whether post-traumatic stress disorder eventuates, impacts brain activity and highlights the importance of inclusion of trauma-exposed comparisons in studies of post-traumatic stress disorder.

Language: en

Keywords

Post-traumatic stress disorder; neuroimaging; trauma exposure