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With the advent of susceptibility-weighted imaging (SWI), the ability to identify cerebral microbleeds (CMBs) associated with mild traumatic brain injury (mTBI) has become increasingly commonplace. Nevertheless, the clinical significance of post-traumatic CMBs remains controversial partly because it is unclear whether mTBI-related CMBs entail brain circuitry disruptions which, although structurally subtle, are functionally significant. This study combines magnetic resonance and diffusion tensor imaging (MRI and DTI) to map white matter (WM) circuitry differences across 6 months in 26 healthy control volunteers and in 26 older mTBI victims with acute CMBs of traumatic etiology. Six months post-mTBI, significant changes (p < 0.001) in the mean fractional anisotropy of perilesional WM bundles were identified in 21 volunteers, and an average of 47% (σ = 21%) of TBI-related CMBs were associated with such changes. These results suggest that CMBs can be associated with lasting changes in perilesional WM properties, even relatively far from CMB locations. Future strategies for mTBI care will likely rely on the ability to assess how subtle circuitry changes impact neural/cognitive function. Thus, assessing CMB effects upon the structural connectome can play a useful role when studying CMB sequelae and their potential impact upon the clinical outcome of individuals with concussion.

Background: The relationship between the acute clinical presentation of patients with traumatic brain injury (TBI), long-term changes in brain structure prompted by injury and chronic functional outcome is insufficiently understood. In this preliminary study, we investigate how acute Glasgow coma score (GCS) and epileptic seizure occurrence after TBI are statistically related to functional outcome (as quantified using the Glasgow Outcome Score) and to the extent of cortical thinning observed 6 months after the traumatic event. Methods: Using multivariate linear regression, the extent to which the acute GCS and epileptic seizure occurrence (predictor variables) correlate with structural brain changes (relative cortical atrophy) was examined in a group of 33 TBI patients. The statistical significance of the correlation between relative cortical atrophy and the Glasgow Outcome Score was also investigated. Results: A statistically significant correlative relationship between cortical thinning and the predictor variables (acute GCS and seizure occurrence) was identified in the study sample. Regions where the statistical model was found to have highest statistical reliability in predicting both gray matter atrophy and neurological outcome include the frontopolar, middle frontal, postcentral, paracentral, middle temporal, angular and lingual gyri. Additionally, relative atrophy and GOS were also found to be significantly correlated over large portions of the cortex. Conclusion: This study contributes to our understanding of the relationship between clinical descriptors of acute TBI, the extent of injury-related chronic brain changes and neurological outcome. This is partly because the brain areas where cortical thinning was found to be correlated with GCS and with seizure occurrence are implicated in executive control, sensory function, motor acuity, memory and language, all of which may be affected by TBI. Thus, our quantification suggests the existence of a statistical relationship between acute clinical presentation, on the one hand, and structural/functional brain features which are particularly susceptible to post-injury degradation, on the other hand.

Available approaches to the investigation of traumatic brain injury (TBI) are frequently hampered, to some extent, by the unsatisfactory abilities of existing methodologies to efficiently define and represent affected structural connectivity and functional mechanisms underlying TBI-related pathology. In this paper, we describe a patient-tailored framework which allows mapping and characterization of TBI-related structural damage to the brain via multimodal neuroimaging and personalized connectomics. Specifically, we introduce a graphically driven approach for the assessment of trauma-related atrophy of white matter (WM) connections between cortical structures, with relevance to the quantification of TBI chronic case evolution. This approach allows one to inform the formulation of graphical neurophysiological and neuropsychological TBI profiles based on the particular structural deficits of the affected patient by relating the findings supplied by our workflow to the existing body of research that focuses on the functional roles of the cortical structures being targeted. Having a graphical means for representing patient TBI status is relevant to the emerging field of personalized medicine as well as to the investigation of human neural atrophy in response to brain trauma.