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Abstract
Posttraumatic stress disorder (PTSD) is an anxiety disorder in which there are disturbances in arousal, fear regulation, and concentration and attention. Prominent neural models have focused on the fear-based phenomena of the disorder, but do not account for neuropsychological disturbances, of which reduced working memory is an example. Reduced working memory in PTSD has been observed previously and may be a cognitive cost of the processing load imposed by disorder symptomatology (the cognitive cost hypothesis). This thesis aimed to understand the neural correlates of disturbed working memory in PTSD. Studies used a 1-back working memory updating task in conjunction with behavioural and functional neural measures via event-related potential (ERP) and functional magnetic resonance imaging (fMRI) paradigms in PTSD, trauma-exposed control, and non-trauma-exposed control participants. The potential confounding contributions of trauma exposure, depressive symptoms and psychotropic medication use were also controlled. Study 1 found degraded working memory processing on ERP measures (reduced amplitude of the P3b) specific to PTSD, which was also related to severity of re-experiencing symptoms (P3b latency). Using fMRI, Study 2 found reduced activation in bilateral dorsolateral prefrontal cortex (dlPFC) and left anterior cingulate cortex (ACC) during the task that was specific to PTSD. PTSD symptom clusters were generally inversely associated with activation in dlPFC and ACC during the task. These findings are consistent with the proposed importance of these brain regions to normal working memory. They are also consistent with the cognitive cost hypothesis. Positive associations were observed between precuneus activation and avoidance and arousal symptoms, possibly reflecting disturbed operation of the default mode brain network. Study 3 found (via fMRI) that greater pre-treatment task-concurrent activation in dlPFC, ACC and inferior parietal cortex was associated with better PTSD response to cognitive behavioural therapy, a treatment proposed by researchers to require working memory integrity. This was independent of depressive symptoms and psychotropic medication use. Together, these studies provide evidence of neural dysfunction in working memory updating in PTSD, independent of contributions from depressive symptoms and medication to these deficits. The current findings point to extensions of fear-based neural models to capture the array of PTSD phenomena.