Journal of neurotrauma
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Journal of neurotrauma · Feb 2008
Late proton magnetic resonance spectroscopy following traumatic brain injury during early childhood: relationship with neurobehavioral outcomes.
We sought to extend previous research that demonstrates reduced neurometabolite concentrations during the chronic phase of pediatric traumatic brain injury (TBI) in children injured during early childhood. We hypothesized that young children with TBI in the chronic phase post-injury would have lower N-acetyl aspartate (NAA) metabolite concentrations in gray and white matter in comparison to controls. We also hypothesized that metabolite levels would be correlated with acute TBI severity and neurobehavioral skills. ⋯ Late NAA and Cr levels in the medial frontal gray matter and NAA levels in the left frontal white matter were strongly positively correlated with initial GCS score. Metabolite levels were correlated with some neurobehavioral measures differentially for children with TBI or OI. Some neurometabolite levels differed between the TBI and OI groups more than 1 year post-injury and were related to injury severity, as well as some neurobehavioral outcomes following TBI during early childhood.
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Journal of neurotrauma · Feb 2008
Identification of serum biomarkers in brain-injured adults: potential for predicting elevated intracranial pressure.
Brain injury biomarkers may have clinical utility in stratifying injury severity level, predicting adverse secondary events or outcomes, and monitoring the effectiveness of therapeutic interventions. As a biomarker source, serum offers several advantages over cerebrospinal fluid (CSF), including ease of accessibility and reduced risk to the patient. We screened pooled serum samples obtained from 11 severely injured traumatic brain injury (TBI) patients (Glasgow Coma Scale [GCS]
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Journal of neurotrauma · Feb 2008
Nicotinamide treatment provides acute neuroprotection and GFAP regulation following fluid percussion injury.
Previous studies in our laboratory have demonstrated the preclinical efficacy of nicotinamide (NAM; vitamin B3) treatment following fluid percussion injury (FPI). At a dose of 500 or 50 mg/kg, NAM significantly facilitated recovery of function on a variety of motor and sensorimotor tasks in rodents, and the 500 mg/kg dose improved cognitive performance. The purpose of the present study was to examine the acute neuroprotective ability of NAM following FPI. ⋯ However, the inverse was observed at 7 days where NAM treatment significantly increased the number of GFAP(+) astrocytes. Both doses of NAM also significantly reduced FJ expression at the 24-h and 7-day time intervals. The results of this study suggest that NAM has strong neuroprotective abilities in the injured brain and may have therapeutic potential for brain injury.
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Journal of neurotrauma · Feb 2008
Differential neuroprotective properties of endogenous and exogenous erythropoietin in a mouse model of traumatic brain injury.
Both heat acclimation (HA) and post-injury treatment with recombinant human erythropoietin (Epo, rhEpo, exogenous Epo) are neuroprotective against traumatic brain injury (TBI). Our previous data demonstrated that HA-induced neuroprotection includes improved functional recovery and reduced cerebral edema formation. Additionally, in earlier Western-blot analyses, we found that HA mice display increased expression of the specific erythropoietin receptor (EpoR) and of hypoxia-inducible factor-1 alpha (HIF-1 alpha), the inducible subunit of the transcription factor, which regulates Epo gene expression, but not of Epo itself. ⋯ Treatment with anti-Epo antibody given to NT mice increased edema formation, whereas rhEpo induced no beneficial effect. Cognitive performance testing and immunohistochemical findings reinforced HA and rhEpo as separate protective interventions but showed no advantage to combining the two strategies. We therefore suggest that HA-induced neuroprotection is shaped by pre-existing mediators but cannot be modified by post-injury treatment aimed at increasing the levels of neuroprotective agents.