The main aim of this dissertation was to investigate cognitive function in victims of secondary traumatic stress. In particular, the research program was designed to investigate whether ambulance officers, who have been exposed to work-related traumatic/critical incidents and subsequently develop PTSD, suffer impairment in cognitive functioning, and if so what is the nature of that impairment?
deficits in PTSD have been related to the effects of chronic stress on the hippocampus. However, if this were true one would assume similar deficits in those exposed to high levels of stress, regardless of whether they also developed PTSD. Consequently, cognitive functioning was compared in those ambulance officers who had developed PTSD and in those exposed to similar levels of critical incident stress but who had not gone on to develop PTSD. Cognitive impairment may also be related to the effects of disrupted neurochemical systems, another possible sequelae of PTSD. The literature relating to both morphological and neurochemical explanations for cognitive deficits are reviewed in this dissertation.
Firstly, a series of preliminary studies established that ambulance officers report high levels of PTSD symptomatology and that exposure to critical incident stress has a compounding effect. Officers were also found to be
affected by a range of organizational stressors not simply those of a clinical nature, however, the importance of coping strategy in the relationship between critical incident exposure and PTSD was highlighted.
Ambulance officers with a diagnosis of PTSD, officers without PTSD and a group of student officers (not yet exposed to critical incident stress) were compared on a battery of neuropsychological tests. Results of the research indicated that officers with PTSD performed more poorly than both officers without PTSD and student officers in the areas of general cognitive ability, verbal memory and attention. Furthermore, officers without PTSD performed similarly to student officers indicating that it is PTSD, not exposure to critical incident stress, which is associated with cognitive dysfunction.
A further aim was to elucidate the role of IQ in the development of PTSD. Higher IQ may serve to buffer the effects of exposure to trauma. The cognitive performance of trauma-exposed officers without PTSD was compared to non-traumatised student controls on tests of cognitive functioning. No differences in performance were observed leading to the conclusion that higher IQ does not act as a buffer or protective factor in the development of PTSD. Alternatively, low IQ may predict the development of PTSD via the relationship with coping strategy and in a subsequent study it was hypothesised that lower premorbid IQ would be positively associated with more severe PTSD symptoms. However, there was no evidence of such a relationship. Interestingly, results indicated that there had been a decline in general cognitive function after exposure to critical incident stress
exclusively amongst the subset of officers who developed PTSD lending support to the view that deficits in cognitive functioning are a product of PTSD rather than a premorbid characteristic of the individual.
Cognitive deficits were examined in more detail than has generally been attempted in the previous literature. Results indicated that compared to Non-PTSD officers, those with PTSD demonstrated significantly poorer total recall of new learning in the context of similar consolidation and retrieval abilities indicating some form of encoding difficulty and attentional impairment. The examination of attentional processes
demonstrated that officers with PTSD exhibit a specific profile of attentional dysfunction, including impaired performance in the ability to focus, shift and encode information in the context of preserved ability to sustain attention. Overall then, evidence presented in this dissertation uncovered attention or executive deficits associated with PTSD consistent with the pattern of a frontal rather than medial temporal lobe pathology.