• Neurosurgery · Mar 2012

    Internal jugular vein compression mitigates traumatic axonal injury in a rat model by reducing the intracranial slosh effect.

    • David W Smith, Julian E Bailes, Joseph A Fisher, Javier Robles, Ryan C Turner, and James D Mills.
    • Department of Neurosurgery, West Virginia University, Morgantown, West Virginia, USA.
    • Neurosurgery. 2012 Mar 1;70(3):740-6.

    BackgroundTraumatic brain injury (TBI) remains a devastating condition for which extracranial protection traditionally has been in the form of helmets, which largely fail to protect against intracranial injury.ObjectiveTo determine whether the pathological outcome after traumatic brain injury can be improved via slosh mitigation by internal jugular vein (IJV) compression.MethodsTwo groups of 10 adult male Sprague-Dawley rats were subjected to impact-acceleration traumatic brain injury. One group underwent IJV compression via application of a collar before injury; the second group did not. Intracranial pressure and intraocular pressure were measured before and after IJV compression to assess collar performance. All rats were killed after a 7-day recovery period, and brainstem white matter tracts underwent fluorescent immunohistochemical processing and labeling of β-amyloid precursor protein, a marker of axonal injury. Digital imaging and statistical analyses were used to determine whether IJV compression resulted in a diminished number of injured axons.ResultsCompression of the IJV resulted in an immediate 30% increase in intraocular and intracranial pressures. Most notably, IJV compression resulted in > 80% reduction in the number of amyloid precursor protein-positive axons as indicated by immunohistochemical analysis.ConclusionUsing a standard acceleration-deceleration laboratory model of mild traumatic brain injury, we have shown successful prevention of axonal injury after IJV compression as indicated by immunohistochemical staining of amyloid precursor protein. We argue that IJV compression reduces slosh-mediated brain injury by increasing intracranial blood volume, which can be indirectly measured by intracranial and intraocular pressures.

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