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  • The Selective Vulnerability of Foramen Magnum to Blast-TBI

    Final Number:

    Adam Pampori BS; Kaspar Keledjian; Çigdem Tosun; Volodymyr Gerzanich MD, PhD; J. Marc Simard MD, PhD

    Study Design:
    Laboratory Investigation

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2013 Annual Meeting

    Introduction: More than half of all injuries in military combat are caused by explosive munitions, with blast-induced traumatic brain injury (blast-TBI) being one of the most serious wounds suffered. The structure of the skull suggests that certain regions may be less protective, serving as portals of entry for a blast wave. We hypothesized that the foramen magnum is such an area of vulnerability.

    Methods: Using our recently described rodent cranium-only blast injury apparatus, which delivers a collimated blast wave, we compared brain injury when a blast wave is delivered to the region of the foramen magnum by centering it over the occipital crest (caudal position) vs. when centered anteriorly and delivered to the full thickness skull (rostral position). Sham-injured animals (anesthesia only) were used as controls. In the first series, survivors of blast exposure were sacrificed at 24 hours and the brains were studied with immunohistochemistry for Iba1, GFAP, and stained for FluoroJadeC. In the second series, animals were followed out to 28 days with neurobehavioral testing, including vertical rearing, accelerating rotarod, beam walk, beam balance, and Morris water maze.

    Results: In the caudal blast group, the LD50 was 785 kPa peak overpressure, while the rostral group had zero mortality up to 1880 kPa. Caudal blast injury was characterized by: 1) massive subdural hemorrhages; 2) significant oxygen saturation abnormalities up to 5 minutes after blast; 3) accelerating rotarod deficits up to 7 days post-blast; 4) beam walk deficits up to 3 days post-blast; and 5) spatial learning deficits in Morris water maze testing. Caudal blast exposure resulted in: 1) widespread microglia/macrophage activation in the brainstem, cerebellum, and hippocampus; 2) reactive astrocytosis in the brainstem and cerebellum; and 3) neurodegeneration in the brainstem.

    Conclusions: Our results suggest that the foramen magnum region is selectively vulnerable to blast wave exposure.

    Patient Care: This work identifies a novel mechanism of morbidity and mortality to blast injury in a rodent model, which may suggest new preventative treatments for military personnel and civilians in combat zones.

    Learning Objectives: By the conclusion of this session, participants should be able to 1) Describe the importance of exposure of the foramen magnum to blast waves in the morbidity and mortality of primary blast injury, and 2) Discuss the impact of foramen magnum vulnerability in military and civilian populations.


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