Journal of neurotrauma
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Journal of neurotrauma · Jan 1990
Characterization of axonal injury produced by controlled cortical impact.
Axonal injury and behavioral changes were evaluated 3-7 days after traumatic brain injury. Previous research from this laboratory demonstrated that clinical central nervous pathology is produced by dynamic brain compression using a stroke-constrained impactor. We wanted to determine if the technique also would produce diffuse axonal injury after recovery from the procedure. ⋯ Axonal injury also was evident in the white matter of the cerebellar folia and the region of the deep cerebellar nuclei. Behavioral assessment showed functional coma lasting up to 36 h following 8.0 m/sec impacts, with impaired movement and control of the extremities over the duration of the postinjury monitoring time. These experiments confirm that the cortical impact model of traumatic brain injury mimics all aspects of traumatic brain injury in humans and can be used to investigate mechanisms of axonal damage and prolonged behavioral suppression.
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Journal of neurotrauma · Jan 1990
Edema development and ion changes in rat spinal cord after impact trauma: injury dose-response studies.
Changes in the total tissue content of water, sodium, potassium, and magnesium were measured in spinal cord from pentobarbital-anesthetized rats subjected to impact trauma (T9) of varying severity (low, 25 g-cm; moderate, 50 g-cm; severe, 100 g-cm). Laminectomized animals served as controls. Spinal cord samples were taken from rats in the high injury group at 15 min, 60 min, 4 hr, 24 hr, 3 days, or 7 days posttrauma. ⋯ Although potassium decreases did correlate with injury severity, alterations in magnesium levels had a much higher degree of correlation. Thus, reductions in magnesium content may contribute to the development of irreversible tissue damage. In contrast, edema formation after spinal cord trauma may be an epiphenomenon, since it was found to an equal degree in low, moderate, and severe injuries.