Abstract
Mild traumatic brain injury (mTBI) can induce persistent somatic, affective and cognitive symptoms, collectively known as post-concussion syndrome (PCS). Standard structural imaging only detects lesions in a small proportion of those with mTBI, and these lesions are not associated with PCS. However, subtle changes in structure have been observed with imaging techniques such as diffusion tensor imaging (DTI). Furthermore, these changes have been shown to correlate with cognitive and behavioural outcome in mTBI participants. This study aims to further this research by investigating the relationship between changes in neural structure and function, cognitive outcome and PCS symptomatology in the long term (>1 year) after mTBI. DTI and functional magnetic resonance imaging (fMRI) data were acquired from participants with chronic (>1 year) mTBI and persistent PCS (n=10), participants with mTBI and no on-going PCS (n=8) and non-head injured controls (n=10). Fractional Anisotropy (FA) and cortical thickness were calculated from DTI and standard structural data acquisitions. Two cognitive tasks were presented to participants in the fMRI study, one assessing working memory (n-Back) and the other assessing information processing speed (paced visual serial addition task [PVSAT]). We hypothesised that participants with mTBI would show greater structural damage and larger BOLD response during the cognitive tasks. In addition, these changes should be related to the persistent PCS symptoms reported. Preliminary analysis demonstrates a reduction in cortical (cingulate, frontal and temporal cortex) and white matter (corpus callosum, internal capsule) integrity in participants with mTBI compared to controls. Reductions in similar areas were associated with higher PCS symptom report (figure A and B). The fMRI analysis revealed little difference between groups for the n-Back, but evidence of increased prefrontal activity (figure C) in participants with mTBI and persistent PCS during PVSAT performance. This early analysis supports the hypothesis that persistent PCS symptoms may have a biological element, with those reporting greater symptoms having greater structural damage and functional changes.