• Miguel A Gama Sosa, Rita De Gasperi, Pierce L Janssen, Frank J Yuk, Pamela C Anazodo, Paul E Pricop, Alejandro J Paulino, Bridget Wicinski, Michael C Shaughness, Eric Maudlin-Jeronimo, Aaron A Hall, Dara L Dickstein, Richard M McCarron, Mikulas Chavko, Patrick R Hof, Stephen T Ahlers, and Gregory A Elder.
• General Medical Research Service, James J, Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, New York, USA. miguel.gama-sosa@mssm.edu.
• Acta Neuropathol Commun. 2014 Jan 1;2:67.

BackgroundBlast-related traumatic brain injury (TBI) is a common cause of injury in the military operations in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. The aim of the present study was to examine whether blast exposure affects the cerebral vasculature in a rodent model. We analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI. Rats were sacrificed 24 hours or between 6 and 10 months after exposure. Blast-induced cerebral vascular pathology was examined by a combination of light microscopy, immunohistochemistry, and electron microscopy.ResultsWe describe a selective vascular pathology that is present acutely at 24 hours after injury. The vascular pathology is found at the margins of focal shear-related injuries that, as we previously showed, typically follow the patterns of penetrating cortical vessels. However, changes in the microvasculature extend beyond the margins of such lesions. Electron microscopy revealed that microvascular pathology is found in regions of the brain with an otherwise normal neuropil. This initial injury leads to chronic changes in the microvasculature that are still evident many months after the initial blast exposure.ConclusionsThese studies suggest that vascular pathology may be a central mechanism in the induction of chronic blast-related injury.

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