• J Neurosurg Spine · Mar 2007

    Contusion, dislocation, and distraction: primary hemorrhage and membrane permeability in distinct mechanisms of spinal cord injury.

    • Anthony M Choo, Jie Liu, Clarrie K Lam, Marcel Dvorak, Wolfram Tetzlaff, and Thomas R Oxland.
    • Division of Orthopaedic Engineering Research, Department of Orthopaedics and Mechanical Engineering, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, British Columbia, Canada.
    • J Neurosurg Spine. 2007 Mar 1;6(3):255-66.

    ObjectIn experimental models of spinal cord injury (SCI) researchers have typically focused on contusion and transection injuries. Clinically, however, other injury mechanisms such as fracture-dislocation and distraction also frequently occur. The objective of the present study was to compare the primary damage in three clinically relevant animal models of SCI.MethodsContusion, fracture-dislocation, and flexion-distraction animal models of SCI were developed. To visualize traumatic increases in cellular membrane permeability, fluorescein-dextran was infused into the cerebrospinal fluid prior to injury. High-speed injuries (approaching 100 cm/second) were produced in the cervical spine of deeply anesthetized Sprague-Dawley rats (28 SCI and eight sham treated) with a novel multimechanism SCI test system. The animals were killed immediately thereafter so that the authors could characterize the primary injury in the gray and white matter. Sections stained with H & E showed that contusion and dislocation injuries resulted in similar central damage to the gray matter vasculature whereas no overt hemorrhage was detected following distraction. Contusion resulted in membrane disruption of neuronal somata and axons localized within 1 mm of the lesion epicenter. In contrast, membrane compromise in the dislocation and distraction models was observed to extend rostrally up to 5 mm, particularly in the ventral and lateral white matter tracts.ConclusionsGiven the pivotal nature of hemorrhagic necrosis and plasma membrane compromise in the initiation of downstream SCI pathomechanisms, the aforementioned differences suggest the presence of mechanism-specific injury regions, which may alter future clinical treatment paradigms.

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