Traumatic brain injury: relationships between brain structural abnormalities and cognitive function

Traumatic brain injury (TBI) is the leading cause of disability in young adults and a major public health problem. Persistent cognitive impairments are common, and constitute a significant source of long-term disability. The specific pathophysiological mechanisms underlying these impairments remain poorly understood. As it disconnects brain networks, white matter damage can be a key determinant of cognitive impairment after TBI. Neuroimaging and neuropsychological methods were employed to explore the relationships between indices of brain structure and cognitive function. The participants were 40 TBI patients and 40 healthy controls. First, relationships between focal lesions and cognitive performance were investigated using structural magnetic resonance imaging (MRI) and a battery of neuropsychological tests. The results demonstrated that lesion location and load are not good indices of the cognitive deficits - probably because diffuse axonal injury is poorly assessed by standard MRI. By contrast, diffusion tensor imaging (DTI) can be used to quantify the microstructure of white matter. A ‘whole-brain’ technique, tract-based spatial statistics (TBSS), was used to flexibly analyse the structure of white matter tracts. Despite only small amounts of focal damage observed using standard MRI, TBSS revealed widespread white matter abnormalities after TBI. White matter damage was found in patients with no evidence of focal damage, and in patients classified as ‘mild’ clinically. Relationships between white matter tract structure and specific cognitive functions were then explored. The structure of the fornix, an important white matter pathway of the hippocampus, correlated with verbal associative memory across the patient and control groups. By contrast, structure of frontal lobe connections showed distinct relationships with executive function in these two groups. The results emphasise the importance of white matter pathology after TBI and suggest that disruption to specific white matter tracts is associated with particular patterns of cognitive impairment, but also highlight the complexity of these relationships