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04-01 Abnormal recruitment of brain networks during trauma-neutral verbal working memory processing in PTSD

Published online by Cambridge University Press:  24 June 2014

KA Moores ,
CR Clark ,
AC McFarlane ,
GC Brown ,
A Puce  and
DJ Taylor
KA Moores
Affiliation:
Cognitive Neuroscience Laboratory, School of Psychology, Flinders University, Adelaide, South Australia, Australia
CR Clark
Affiliation:
Cognitive Neuroscience Laboratory, School of Psychology, Flinders University, Adelaide, South Australia, Australia
AC McFarlane
Affiliation:
The Centre of Military and Veterans' Health and Department of Psychiatry, The University of Adelaide, Adelaide, South Australia, Australia
GC Brown
Affiliation:
MRI Suite, Department of Radiology, Royal Adelaide Hospital, Adelaide, South Australia, Australia
A Puce
Affiliation:
Center for Advanced Imaging, Departments of Radiology, Neurobiology & Anatomy, West Virginia University School of Medicine, Morgantown, West Virginia, USA
DJ Taylor
Affiliation:
MRI Suite, Department of Radiology, Royal Adelaide Hospital, Adelaide, South Australia, Australia
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Abstract

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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. 322
Copyright
Copyright © 2006 Blackwell Munksgaard

Post-traumatic stress disorder (PTSD) is characterized by disturbances in concentration and memory, symptoms that are a source of further distress for patients. Abnormalities in working memory (WM) updating have been identified in PTSD (Clark et al. 2003), indicating dysfunction in left hemisphere brain regions critically involved in WM updating. However, it remains unclear whether this finding is because of underlying abnormalities in WM systems in PTSD. Functional magnetic resonance imaging was done for 13 patients with severe PTSD and matched nontraumatized controls, during WM performance where participants either maintained or continually updated verbal stimulus material in separate conditions. The PTSD group failed to show differential activation during WM updating, instead showing abnormal recruitment of WM updating network regions during WM maintenance. These regions included bilateral dorsolateral prefrontal cortex and inferior parietal lobe. Several other regions were abnormally decreased during WM updating in PTSD including the hippocampus, anterior cingulate and brainstem pons. These results suggest compensatory recruitment of WM networks normally only deployed during updating, which may be linked to the abnormally decreased activity in PTSD during WM updating in other key regions, regions that have been consistently implicated in the neurobiology of PTSD. These abnormalities reflect the difficulty patients with PTSD have engaging with their day-to-day environment.