Factors Underpinning Posttraumatic Stress Disorder in Pediatric Traumatic Injury: The effects of Memory and Attentional Control Impairments

Abstract

The phenomenon of comorbid Posttraumatic Stress Disorder (PTSD) in Traumatic Brain Injury (TBI) has not been fully investigated, especially in the paediatric population. Various mechanisms for the development of PTSD have been proposed, with theories suggesting aetiological importance in the presence of trauma memories, and neurocognitive deficits in working memory and attentional control functions. To address the gap in the literature, the present study sets out to examine the potential factors underpinning the development of PTSD post-TBI in children, with prime interest in the contribution from post-injury neurocognitive outcomes. The present study recruited 166 children (from 6 to 14 years old) immediately after TBI. Injury severity, demographic information, and intellectual capacity were assessed within 2 months of the injury. Neurocognitive functions and PTSD severity were assessed at 3, and 6-months post-injury, with PTSD severity re-assessed at 18-months post-injury. Regression analyses used demographic, injury-related, and neurocognitive factors to predict PTSD severity at a later stage. Results showed that children presented with substantial neurocognitive impairments in sustained attention and verbal learning functions and greater TBI severity resulted in higher deficit rates in verbal learning, selective attention, and processing efficiency. Although presented with some degree of impairments, working memory performance did not worsen with injury severity. At 3-months post-injury, 9.5% of the children warranted a PTSD diagnosis, with the percentage dropping to 4.4%, and below at 6 and 18-months post-injury. Comorbid PTSD in paediatric TBI demonstrated similar risk factors to PTSD following non-injury related emotional trauma, for instance age at injury, sex, and intelligence. Socio-economic status, however, did not predict PTSD severity post-TBI. Paediatric TBI severity also correlated positively and significantly with post-injury PTSD severity. Neurocognitive functions emerged as the key outcome predictors for future PTSD severity. In particular, poorer attentional control and better memory encoding outcomes following injury predicted greater symptom severity in children. Unexpected by the study, post-TBI working memory deficits correlated positively with subsequent symptom severity. Evidence indicates that TBI may simultaneously facilitate and inhibit the development of subsequent PTSD symptoms in children, via the ability to encode memory and the ability to regulate these memories. As memory encoding becomes increasingly impaired with injury severity, fewer recollections of injury-related events protected children from PTSD symptoms after injury. Impaired sustained attention across injury severity post-TBI, however, gives rise to general difficulties in disinhibiting or regulating trauma memories, and emotional/physiological arousal. In conclusion, supporting the Neurobiological Theory, the present study demonstrated significant neurocognitive contributions, and highlighted the role of attentional control and memory functions in the development of PTSD. Findings suggest that the neurological mechanisms involve in PTSD and paediatric TBI are distinct, yet intertwined. A number of potential mechanisms underpinning the development of PTSD in the context of paediatric TBI are discussed. Theoretical, research, and clinical implications are also provided.