Journal of neurotrauma
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Journal of neurotrauma · Aug 2009
Predicting outcomes of traumatic brain injury by imaging modality and injury distribution.
Early prediction of outcomes after traumatic brain injury (TBI) is often difficult. To improve prognostic accuracy soon after trauma, we compared different radiological modalities and anatomical injury distribution in a group of adult TBI patients. The four methods studied were computed tomography (CT), magnetic resonance imaging (MRI) with T2-weighted imaging (T2WI), fluid-attenuated inversion recovery (FLAIR) imaging, and susceptibility weighted imaging (SWI). ⋯ In addition, T2WI and FLAIR imaging most consistently discriminated between good and poor outcomes by zonal distribution. While SWI rarely discriminated by outcome, it was very sensitive to intraparenchymal injury and its optimal use in evaluating TBI is unclear. SWI and other new imaging modalities should be further studied to fully evaluate their prognostic utility in TBI evaluation.
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Journal of neurotrauma · Aug 2009
Cauda equina repair in the rat: part 1. Stimulus-evoked EMG for identifying spinal nerves innervating intrinsic tail muscles.
Cauda equina injuries may produce severe leg and pelvic floor dysfunction, for which no effective treatments exist. We are developing a rat cauda equina injury model to allow nerve root identification and surgical repair. One possible difficulty in implementing any repair strategy after trauma in humans involves the correct identification of proximal and distal ends of nerve roots separated by the injury. ⋯ Correctly identifying the level of origin of that root was more difficult, but for ventral roots this rate still exceeded 90%. Using the rat cauda equina model, we have shown that stimulus-evoked EMG can be used to identify ventral nerve roots innervating tail muscles with a high degree of accuracy. These findings support the feasibility of using this conceptual approach for identifying and repairing damaged human cauda equina nerve roots based on stimulus-evoked recruitment of muscles in the leg and pelvic floor.
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Journal of neurotrauma · Aug 2009
Increased cerebral uptake of [18F]fluoro-deoxyglucose but not [1-14C]glucose early following traumatic brain injury in rats.
Following experimental and clinical traumatic brain injury (TBI), the local cerebral metabolic rate of glucose (lCMR(Glc)) is commonly estimated using the 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG) method. The adequate estimation of lCMR(Glc) using FDG requires a correction factor, the lumped constant (LC), to convert FDG net uptake into lCMR(Glc). The LC, and thus lCMR(Glc) calculations, require a steady-state that may be disrupted following TBI. ⋯ At 12 h following FPI, the ipsilateral FDG and [1-(14)C]glucose uptake were decreased in the cortex and hippocampus, and the ipsilateral cortical ATP concentration was decreased in comparison to sham-injured controls (p < 0.05). Under the present experimental conditions, the rate of cerebral uptake of FDG and of [1-(14)C]glucose differed, and indicated that following TBI, regional changes in the LC may occur in the immediate, but not in the late, post-injury phase. These results should be considered when interpreting results obtained using FDG for the estimation of lCMR(Glc) early following experimental TBI.
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Journal of neurotrauma · Aug 2009
Arachidonyl trifluoromethyl ketone is neuroprotective after spinal cord injury.
In spinal cord injury (SCI), neuronal and oligodendroglial loss occurs as a result of the initial trauma and the secondary damage that is triggered by excitotoxicity, free radicals, and inflammation. There is evidence that SCI ellicits increased cytosolic phospholipase A(2) (cPLA(2)) activity. The cleavage of phospholipids by cPLA(2) leads to release of fatty acids, and in particular arachidonic acid (AA), the metabolites of which have been associated with increased inflammation and oxidative stress. ⋯ The number of surviving neurons and oligodendrocytes was significantly increased in animals treated with the cPLA(2) inhibitor compared to saline controls. The behavioral analysis mirrored the neuroprotective effects and showed that the inhibitor-treated group had better locomotor recovery compared to saline controls. Our results show that AACOCF3 has neuroprotective potential, and support the idea that cPLA(2) is critically involved in acute spinal injury.