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Mild traumatic brain injury (mTBI) is a debilitating but extremely common form of brain injury that affects a substantial number of people each year. mTBI is especially common in children and adolescents. Our understanding of mTBI pathophysiology is limited, and there is currently no accepted marker for disease severity. A potential marker for disease severity may be cerebrovascular dysfunction. Recent findings have implicated cerebrovascular alteration as an important component of mTBI and suggest it contributes to the development of persistent, long-term symptoms. In this paper, we conducted two studies to investigate whether mTBI affects venous drainage patterns in the central nervous system using alterations in the size of venous sinuses as a marker of changes in drainage. Using a closed head vertical weight-drop model and a lateral impact injury model of mTBI, we imaged and quantified the size of three major draining vessels in the adolescent rat brain using 9.4T MRI. Areas and volumes were quantified in the superior sagittal sinus and left and right transverse sinuses using images acquired from T2w MRI in one study and post-gadolinium T1w MRI in another. Our results indicated that the three venous sinuses were significantly larger in mTBI rats as compared to sham rats 1-day post injury but recovered to normal size 2 weeks after. Acutely enlarged sinuses post-mTBI may indicate abnormal venous drainage, and this could be suggestive of a cerebrovascular response to trauma.

Brain hypoxia is present in multiple sclerosis, a condition associated with inflammation. Hypoxia may be related to inflammation. Quantitative susceptibility mapping (QSM) is sensitive to deoxyhemoglobin and so hypoxia. Here, we combined perfusion MRI with QSM to assess hypoxia and cerebral blood flow (CBF) in the lipopolysaccharide (LPS) inflammatory model. We report a reduction in susceptibility, as well as a significant reduction in CBF, in the cortex of the LPS model. As reduced tissue susceptibility was observed in more hypoxic subjects, this could be consistent with hypoxia in the inflammatory model, and QSM might be a possible biomarker.

Systemic inflammation is linked to a range of neurological diseases. Reductions in cerebral blood flow (CBF) and the presence of brain hypoxia have been detected in animal models of inflammation and in multiple sclerosis, a disease with significant inflammation. Reduced CBF combined with hypoxia could exacerbate damage in neuroinflammatory conditions. To study this link, we used in-vivo 9.4T MRI to quantify CBF and R2*, a marker of deoxyhemoglobin, following systemic inflammation induced by bacterial lipopolysaccharide. We found reduced CBF and increased R2* in 4 regions, including the cortex and hippocampus—indicating that inflammation is accompanied by hypoxia and reduced CBF.

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