Journal of neurotrauma
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Electric currents of small magnitude have been used successfully to induce regrowth of injured spinal cord fibers. The purpose of this study was to determine the potentials and current density distributions on the surface, as well as within the spinal cord, after the application of exogenous electric fields. A 10 microA DC current was applied epidurally to the spinal cord using two different electrode configurations. ⋯ The current density was more localized on the dorsal surface of the spinal cord for the D-D configuration. In contrast, in the V-D configuration, the current density was greater near the anode on the ventral surface and near the cathode on the dorsal surface of the spinal cord. As a result of the anode being located ventrally, there was a more uniform current density distribution within the spinal cord.
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Journal of neurotrauma · Oct 1994
Different cerebral hemodynamic responses following fluid percussion brain injury in the newborn and juvenile pig.
The present study was designed to characterize the influence of early developmental changes on the relationship among systemic arterial pressure, cerebral hemodynamics, and cerebral oxygenation during the first 3 h following percussion brain injury. Anesthetized newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Brain injury of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. ⋯ These data show that the effects of comparable brain injury level were very different in newborn and juvenile pigs. Further, these data suggest that reductions in cerebral blood flow following brain injury are more dependent on changes in reactivity of arterioles. Finally, these data suggest that the decrease in cerebral oxygenation, an index of metabolism, coupled with reduced cerebral blood flow, could result in profound hypoperfusion after brain injury.
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Journal of neurotrauma · Oct 1994
Modification of the cortical impact model to produce axonal injury in the rat cerebral cortex.
Diffuse axonal injury (DAI) is a form of brain injury that is characterized by morphologic changes to axons throughout the brain and brainstem. Previous biomechanical studies have shown that primary axonal dysfunction, ranging from minor electrophysiologic disturbances to immediate axotomy, can be related to the rate and level of axonal deformation. Some existing rodent head injury models display varying degrees of axonal injury in the forebrain and brainstem, but the extent of axonal damage in the forebrain has been limited to the contused hemisphere. ⋯ Neurofilament immunohistochemistry revealed numerous axonal retraction balls in the subcortical white matter and overlying deep cortical layers in the right hemisphere beneath the contralateral craniotomy. Retraction balls were not seen at these positions in normals, sham controls, or animals that received cortical impact without contralateral craniotomy and dural opening. The results from these physical modeling and animal experiments indicate that opening of the contralateral dura mater permits translation of sufficient mechanical deformation across the midline to produce a more widespread pattern of axonal injury in the forebrain, a pattern that is distinct from those produced by existing fluid percussion and cortical impact techniques.
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Journal of neurotrauma · Oct 1994
Neurofilament 68 and neurofilament 200 protein levels decrease after traumatic brain injury.
We have examined the effect of lateral cortical impact injury on the levels of axonal cytoskeletal proteins in adult rats. Traumatic brain injury (TBI) causes a significant decrease in the protein levels of two prominent neurofilament (NF) proteins, NF68 and NF200. We employed quantitative immunoreactivity measurements on Western blots to examine NF68 and NF200 levels in homogenates of hippocampal and cortical tissue taken at several intervals postinjury. ⋯ This NF68 antigenicity pattern suggests the production of NF68 breakdown products caused by the pathologic activation of neuronal proteases, such as calpain. Putative NF68 breakdown products increase significantly until 1 day postinjury, suggesting that NF degradation may be ongoing until that time and indicating that a potential therapeutic window may exist within the first 24 h postinjury. In summary, these data identify specific biochemical alterations of the neuronal cytoskeleton following TBI and lay a foundation for further investigation of postinjury cytoskeletal changes in neuronal processes.
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Journal of neurotrauma · Oct 1994
Lateral cortical impact injury in rats: pathologic effects of varying cortical compression and impact velocity.
Direct lateral cortical impact through the intact leptomeninges using a pneumatically driven piston produces increasingly severe pathophysiologic derangements with increasing cortical deformation. We studied the histopathologic correlates of cortical impact injury produced by 2 mm, 2.5 mm, and 3 mm deformation in the rat at 5 m/sec. Additionally, the effect of impact velocity at a 2.5 mm deformation was assessed at 1 m/sec, 3 m/sec, and 5 m/sec. ⋯ Impact velocities of 1, 3, and 5 m/sec produced neuronal loss of 18.25%, 33.75%, and 48.3%, respectively. Hippocampal CA1 neuronal loss was also seen and paralleled cortical deformation and impact velocity. Cortical deformation and impact velocity are critical parameters in producing cortical contusion and must be considered when comparing results using this model.