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04-04 Treatment response and post-traumatic stress disorder: neuroimaging findings

Published online by Cambridge University Press:  24 June 2014

RA Bryant
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia School of Psychology, University of New South Wales
KL Felmingham
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia Psychological Medicine, Western Clinical School, University of Sydney
EM Falconer
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia School of Psychology, University of New South Wales
AH Kemp
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia Psychological Medicine, Western Clinical School, University of Sydney
P Das
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia Neuroscience Institute of Schizophrenia and Allied Disorders (NISAD), New South Wales, Australia
A Peduto
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia Department of Radiology, Westmead Hospital, Westmead, Australia
LM Williams
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia Psychological Medicine, Western Clinical School, University of Sydney
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Abstract

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Copyright
Copyright © 2006 Blackwell Munksgaard

Biological models propose that post-traumatic stress disorder (PTSD) reflects a failure of extinction of the conditioned fear response. Animal models and recent human imaging studies suggest that ventromedial prefrontal (vmPFC) regions inhibit amygdala fear networks during fear extinction (Rauch et al. 2006; Phelps et al. 2004). Accordingly, PTSD is associated with a failure of vmPFC activity in response to threat. Exposure-based treatments are thought to facilitate the extinction of conditioned fear. No imaging studies have examined the neural correlates of symptom improvement following exposure-based treatment in PTSD. Eight individuals with PTSD underwent functional magnetic resonance imaging (fMRI) scanning while viewing fearful and neutral facial expressions in a passive viewing task adapted to a 1.5T scanner. fMRI assessments were conducted before and after treatment. Amygdala and vmPFC (anterior cingulate) activity was examined before and after treatment in a repeated-measures, fixed-effects ANOVA and changes in these regions were correlated with changes in PTSD severity. Consistent with predictions, findings show that anterior cingulate activity increased and amygdala activity reduced to fear following exposure treatment in PTSD, and symptom improvement was correlated with increased anterior cingulate activity and reduced amygdala activity to fear. These findings provide initial support for a role of reduced vmPFC activity in PTSD that recovers following exposure treatment.