Modeling Mechanisms of Long–Term Stroke Risk After Traumatic Brain Injury Using Fluorescent Microspheres

Presenters/Authors(s)

Dara Althouse, Mikaela Barbour , Zachary Weil, Kate Weil, Deborah Corbin, Allison Platt

Abstract or Description

Over 69 million individuals suffer traumatic brain injuries (TBI) annually around the world. While many individuals go on to recover, recent studies have shown a long term elevated risk of hemorrhagic and ischemic strokes in individuals with a history of TBI. We hypothesized that dysfunction in cerebral microvasculature after TBI could increase micro-clot formation and lead to changes in cerebral blood flow. To investigate the mechanisms leading to this increased stroke risk, we induced a moderate close-head TBI or a sham-injury in male and female Swiss Webster mice. At one week or 28-days after injury, 4 m fluorescent microspheres were systemically injected intravascularly at the 1-hour and 72-hour timepoints before euthanasia. Different colors of microspheres were injected at each time point to allow us to differentiate between them. Imaging was done using Nikon Elements, where spheres were quantified in the striatum, sensorimotor cortex, thalamus, and hippocampus. Following TBI, mice showed decreased washout efficiency of microspheres compared to sham-injured animals, suggesting hemodynamic changes or an increase in capillary clotting. Future directions include using this model to determine which cells or coagulation components are causing these occlusions and how they might lead to larger ischemic strokes and hemorrhage.