Journal of neurotrauma
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Journal of neurotrauma · Apr 2009
Serial changes in the white matter diffusion tensor imaging metrics in moderate traumatic brain injury and correlation with neuro-cognitive function.
Diffuse axonal injury (DAI) that follows traumatic brain injury (TBI) is thought to be a major contributor to neurocognitive dysfunction that sometimes follows TBI. Conventional magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) and neuropsychological tests (NPT) were performed on 38 TBI patients [hemorrhagic DAI (H-DAI, n=8), non-hemorrhagic (Nh-DAI, n=7), with no apparent DAI on conventional MRI (NA-DAI, n=23)] with a Glasgow Coma Scale score ranging between 9 and 13. The fractional anisotropy (FA) and mean diffusivity (MD) were quantified from different regions of the corpus callosum (CC), and peri-ventricular white matter (PWM) within 5-14 days and 6 months following TBI. ⋯ In patients without abnormalities on conventional MRI and DTI in the initial phase, a significant decrease in FA and increase in MD were observed in a few regions of the CC at 6 months, which was suggestive of demyelination/gliosis. The changes in FA and MD in the CC and PWM at 6 months follow-up showed significant correlation with some of the NPT performed in the three groups. DTI demonstrates axonopathy in the acute stage, as well as at secondary stages, at 6 months post-injury in the CC and PWM in regions of normal-appearing white matter on conventional MRI.
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Journal of neurotrauma · Apr 2009
Comparative StudyStrain differences in response to traumatic brain injury in Long-Evans compared to Sprague-Dawley rats.
The selected strain of rodent used in experimental models of traumatic brain injury is typically dependent upon the experimental questions asked and the familiarity of the investigator with a specific rodent strain. This archival study compares the injury responsiveness and recovery profiles of two popular outbred strains, the Long-Evans (LE) and the Sprague-Dawley (SD), after brain injury induced by lateral fluid percussion injury (LFPI). ⋯ Cortical volume loss was not significantly different, but close inspection of the data suggests the possibility that LE rats may be more susceptible to damage in the hemisphere contralateral to the injury site than are SD rats. It is hoped that the information provided here encourages greater attention to the subtle differences and similarities between strains in future pre-clinical efficacy studies of traumatic brain injury.
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Journal of neurotrauma · Apr 2009
Locomotor recovery after spinal cord lesions in the lamprey is associated with functional and ultrastructural changes below lesion sites.
While axonal regeneration continues to be the major focus of research into spinal injury, there is growing evidence for changes in functional properties below lesion sites. In this study we have used the lamprey, a model system for studying axonal regeneration after spinal injury, to examine whether functional and ultrastructural changes below lesion sites might also contribute to the recovery of locomotor function in this system. In the current study, the majority of the animals showed good functional recovery 10 weeks after lesioning, even when there was no physiological evidence for regeneration across the lesion site (although animals that recovered poorly always lacked regeneration). ⋯ There were also changes in synaptic ultrastructure, including a reduction of the synaptic gap and an increase in synaptic vesicle pools at asymmetric (putative excitatory) synapses. These results provide the first evidence for functional changes below lesion sites in the lamprey, and suggest that locomotor recovery reflects an interaction between regenerated axons and altered networks below lesion sites. The lamprey offers a tractable model system in which to investigate how interactions between altered locomotor networks and regenerated axons are organized to promote locomotor recovery.
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Spinal cord injury (SCI) launches a complex cascade of events that leads to progressive damage and loss of function. Compromise of plasma membrane integrity due to the mechanical impact is an acute event that may contribute to cellular dysfunction. Therefore, the objective of this study was to better understand the extent of acute plasma membrane damage associated with SCI as a function of injury severity and membrane defect size. ⋯ In addition, after moderate injury, cell bodies and axons (located up to 2 mm and 3 mm from the epicenter, respectively) took up significantly more of the 3-kDa and 10-kDa dextran permeability marker compared to sham controls. Permeable neuronal cell bodies exhibited a morphological appearance characterized by pericellular blebbing, suggesting that plasma membrane compromise is associated with pathophysiological cellular alterations. Collectively, these results enhance our understanding of acute SCI and provide targets for developing novel treatment strategies.