Abstract
The aim of the research presented is to gain a better understanding of the processes underlying the persistent report of somatic, cognitive and affective symptoms (known as post-concussion syndrome, PCS) after a mild brain injury (mTBI), and to elucidate whether there are any replicable biological factors contributing towards this syndrome. The results demonstrate that although PCS-like symptoms are present to a similar degree in the non-head injured population, individuals with mTBI and persistent PCS have significantly worse working memory, attention and information processing speed performance. Individuals who suffer an MTBI but do not report continued PCS perform these cognitive tasks to the same level as non-head injured controls. Following on from this, the research presented evidence that individuals with greater PCS severity had greater white matter damage, and greater attention related activity during cognitive tasks. Metabolic differences were also observed in the prefrontal cortex of individuals with mTBI, with a reduction in creatine suggesting some residual energy impairment in chronic mTBI. Combining the structural, metabolic and functional MRI data, we suggested that the increased attentional regulation observed during cognitive tasks may be compensating for reduced working memory capacity and a variation in white matter transmission caused by the structural and metabolic changes after injury. This compensation may in turn underlie some PCS symptoms such as fatigue, headache and insomnia. Therefore, the research as a whole suggests that there may be a neurophysiological basis for persistent PCS.