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04-03 The neural networks of inhibitory control in post-traumatic stress disorder

Published online by Cambridge University Press:  24 June 2014

EM Falconer ,
R Bryant ,
K Felmingham ,
AH Kemp ,
G Olivieri ,
A Peduto ,
E Gordon  and
LM Williams
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
R 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
K Felmingham
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
AH Kemp
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
G Olivieri
Affiliation:
Department of Radiology, Westmead Hospital
A Peduto
Affiliation:
Department of Radiology, Westmead Hospital
E Gordon
Affiliation:
The Brain Resource International Database, Brain Resource Company, Sydney, Australia
LM Williams
Affiliation:
The Brain Dynamics Centre, Westmead Millennium Institute, Westmead Hospital and Western Clinical School, University of Sydney, Australia
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Abstract

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Information

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006 , pp. 323
Copyright
Copyright © 2006 Blackwell Munksgaard

Post-traumatic stress disorder (PTSD) is associated with information-processing deficits and a reduction of selective attention, along with hyperarousal and hyper-reactivity to threat- and emotion-related stimuli. PTSD may involve an enhancement in automatic processing and an inability to inhibit automatic processing when required. The predominant neurophysiological model of PTSD has focused on medial prefrontal disruptions during the processing of fear-related stimuli and does not include potential alterations in the explicit inhibitory control of automatic responding. We investigated executive inhibitory control in PTSD during an emotionally neutral (go/no go) response inhibition task in individuals with PTSD (n = 23) and matched healthy controls (n = 23) using functional magnetic resonance imaging. PTSD was associated with diminished inhibitory control and reduced activation of a cortical inhibitory network (particularly right ventrolateral prefrontal cortex), as well as an increase in areas associated with sensory processing (somatosensory and visual cortices) and increased inhibitory task demand (striatum). These findings are consistent with diminished executive inhibitory control in PTSD and may reflect increased stimulus processing, which undermines cortical control mechanisms.