Journal of neurotrauma
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Journal of neurotrauma · Oct 2006
Impact of additional extracranial injuries on outcome after mild traumatic brain injury.
Many patients with mild traumatic brain injury (MTBI) concurrently sustain extracranial injuries; however, little is known about the impact of these additional injuries on outcome. We assessed the impact of additional injuries on the severity of postconcussional symptoms (PCS) and functional outcome 6 months post-injury. A questionnaire (including the Rivermead Post-Concussion Questionnaire and SF-36) was sent to consecutive MTBI patients (hospital admission Glasgow Coma Score 13-15; age range 18-60 years) admitted to the emergency department of a level-I trauma center, and, to serve as a baseline for PCS, a control group of minor-injury patients (ankle or wrist distortion). ⋯ Regardless of the presence of additional injuries, patients that were still in treatment reported significantly more severe PCS, with highest rates in patients with isolated MTBI. In conclusion, many patients with additional extracranial injuries are still in the process of recovery at 6 months after injury. However, despite more severe impact to the head and inferior functional outcomes, these patients do not report more severe PCS.
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Journal of neurotrauma · Oct 2006
Nicotinamide treatment reduces behavioral impairments and provides cortical protection after fluid percussion injury in the rat.
This study examined the ability of nicotinamide (vitamin B3) to improve functional outcome in a dose-dependent manner following fluid percussion injury (FPI). Injured (duration of unconsciousness mean = 85.8 sec; apnea = 9.9 sec), rats were administered nicotinamide (500 or 50 mg/kg; ip) or saline at 15 min and 24 h. Serum analysis of nicotinamide concentrations were conducted 1 h following the last injection. ⋯ Both doses significantly reduced tissue loss and glial fibrillary acid protein (GFAP) expression in the cortex. The 500 mg/kg dose reduced GFAP expression in the hippocampus. This data suggests that nicotinamide has substantial preclinical efficacy for TBI, and there appears to be some differences in the ability of the doses to improve performance in the MWM.
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Journal of neurotrauma · Oct 2006
Recovery of function after vagus nerve stimulation initiated 24 hours after fluid percussion brain injury.
Recent evidence from our laboratory demonstrated in laboratory rats that stimulation of the vagus nerve (VNS) initiated 2 h after lateral fluid percussion brain injury (FPI) accelerates the rate of recovery on a variety of behavioral and cognitive tests. VNS animals exhibited a level of performance comparable to that of sham-operated uninjured animals by the end of a 2-week testing period. The effectiveness of VNS was further evaluated in the present study in which initiation of stimulation was delayed until 24 h post-injury. ⋯ On day 14, the FPI-VNS animals did not differ in the latency to find the platform from sham controls, whereas the injured controls did; however, the FPI-VNS animals and injured controls were not significantly different. Despite the lack of significant histological differences between the FPI groups, VNS, when initiated 24 h following injury, clearly attenuated the ensuing behavioral deficits and enhanced acquisition of the cognitive task. The results are discussed with respect to the norepinephrine hypothesis.
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Journal of neurotrauma · Sep 2006
Neuronal response to high rate shear deformation depends on heterogeneity of the local strain field.
Many cellular models of traumatic brain injury (TBI) deform cells in a planar (2-D) configuration, a contrast from the three-dimensional (3-D) architecture of the brain, resulting in strain fields that may fail to represent the complex deformation patterns seen in vivo. Cells cultured in 3-D may more accurately represent in vivo cellular behavior than planar models due to differences in cytostructure, cell-cell/cell-matrix interactions and access to trophic factors; however, the effects of culture configuration on the response to high rate deformation have not been evaluated. We examined cell viability following a defined mechanical insult to primary cortical neurons distributed throughout a bioactive matrix (3-D) or in a monolayer sandwiched between layers of a bioactive matrix (2-D). ⋯ Computer simulations of bulk loading predicted local cellular strains, revealing that neurons in 3-D were subjected to a heterogeneous strain field simultaneously consisting of tensile, compressive and shear strains; conversely, neurons in 2-D experienced a less complex deformation regime varying mainly based on shear strains. These results show differential susceptibility to mechanical loading between neurons cultured in 2-D and 3-D that may be due to differences in cellular strain manifestation. Models of TBI that accurately represent the related cellular biomechanics and pathophysiology are important for the elucidation of cellular tolerances and the development of mechanistically driven intervention strategies.
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Journal of neurotrauma · Sep 2006
Activin a release into cerebrospinal fluid in a subset of patients with severe traumatic brain injury.
Activin A is a member of the transforming growth factor-beta superfamily and has been demonstrated to be elevated during inflammation and to have neuroprotective properties following neural insults. In this study, we examined whether traumatic brain injury (TBI) induced a response in activin A or in the concentrations of its binding protein, follistatin. Thirty-nine patients with severe TBI had daily, matched cerebrospinal fluid (CSF) and serum samples collected post-TBI and these were assayed for activin A and follistatin using specific immunoassays. ⋯ Further, activin A levels were also associated with indices of metabolism, such as lactate and pyruvate, excitotoxicity (glutamate) and membrane lipid breakdown products such as glycerol. In one of the two patients who developed a CSF infection, activin A concentrations in CSF became markedly elevated. Thus, some TBI patients have an early release of activin A into the CSF that may result from activation of inflammatory and/or neuroprotective pathways.