Mild Traumatic Brain Injury (mTBI) has been described as a ‘silent epidemic’ and is a significant health burden to the global population. New Zealand specific data estimates mTBI to occur 749 in 100,000 person-years. While the majority of patients that suffer mTBI make a complete recovery between 3 and 12 months following the injury, approximately 15% of all mTBI will have ongoing symptoms one year after initial injury. This condition is known as Post Concussion Syndrome (PCS).
The sheer scale and cost of PCS, not just in terms of acute care and rehabilitation costs, but the emotional and financial costs to the patient and their family are significant; this makes injury prevention, detection and care a significant health priority. At present, no robust or reliable radiological or biochemical markers have been developed to diagnose mTBI. Moving forward, injury prevention, early diagnosis, treatment and identification of people at risk of developing PCS would mean better patient education and resource allocation for rehabilitation; this in turn may ease the burden of this condition.
The objective with this thesis is to identify potential brain differences associated with full or poor recovery post mTBI and to determine whether differences existed with a group of participants with chronic pain and a group of healthy controls.
This study used both structural (grey matter volume and cortical thickness) and DTI techniques to investigate the brains of participants who had experienced an mTBI and two control groups. Data previously collected from 138 participants were used for this study; forty-two subjects comprised the PCS group. Thirty subjects deemed fully recovered from mTBI comprised the non-PCS group. The two control groups were healthy controls (n=41) and those with a chronic pain condition (CP; n=25). The PCS, non-PCS and CP groups were all matched for age, gender, education, injury, severity and pre-injury work status. The healthy control group was matched for mean age and sex distribution.
There were no significant differences in brain volume, cortical thickness, or DTI metrics along the centres of principal white matter tracts between the PCS and non-PCS groups, nor when these two mTBI groups were compared to controls. However, the CP participants exhibited reduced cerebellar grey matter volume relative to all three groups (PCS, non-PCS, and healthy controls) and significant reduction in FA and increased MD in several white matter tracts; there were no cortical thickness differences between any of the groups.
Overall the heterogeneity of the literature help to frame my results within the larger field. Lack of significant differences is not an uncommon finding. In my hands, PCS and non-PCS were indistinguishable on T1-weighted images, as well as DTI. A prospective study following mTBI from acute to chronic state with serial imaging or other study techniques such as HARDI or diffusion kurtosis should be used in future research to evaluate mTBI.||