Journal of neurotrauma
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Journal of neurotrauma · Apr 2012
Glial neuronal ratio: a novel index for differentiating injury type in patients with severe traumatic brain injury.
Neurobiochemical marker levels in blood after traumatic brain injury (TBI) may reflect structural changes detected by neuroimaging. This study evaluates whether correlations between neuronal (ubiquitin carboxy-terminal hydrolase-L1 [UCH-L1]) and glial (glial fibrillary acidic protein [GFAP]) biomarkers may be used as an indicator for differing intracranial pathologies after brain trauma. In 59 patients with severe TBI (Glasgow Coma Scale [GCS] score≤8) serum samples were obtained at the time of hospital admission and analyzed for UCH-L1 and GFAP. ⋯ GNR was significantly higher in patients who died, but was not an independent predictor of death. The data from the present study indicate that GNR provides valuable information about different injury pathways, which may be of diagnostic significance. In addition, GNR may help to identify different pathophysiological mechanisms following different types of brain trauma, with implications for therapeutic interventions.
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Journal of neurotrauma · Apr 2012
Validity of a pediatric version of the Glasgow Outcome Scale-Extended.
The Glasgow Outcome Scale (GOS) and its most recent revision, the GOS-Extended (GOS-E), provide the gold standard for measuring traumatic brain injury (TBI) outcome. The GOS-E exhibits validity when used with adults and some adolescents, but validity with younger children is not established. Because the GOS-E lacks the developmental specificity necessary to evaluate children, toddlers, and infants, we modified the original version to create the GOS-E Pediatric Revision (GOS-E Peds), a developmentally appropriate structured interview, to classify younger patients. ⋯ The GOS-E Peds is sensitive to severity of injury and is associated with changes in TBI sequelae over time. This pediatric revision provides a valid outcome measure in infants, toddlers, children, and adolescents through age 16. Findings support using the GOS-E Peds as the primary outcome variable in pediatric clinical trials.
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Journal of neurotrauma · Apr 2012
Randomized Controlled TrialCerebral microdialysis effects of propofol versus midazolam in severe traumatic brain injury.
Propofol, an anesthetic agent acting as an analogue of vitamin E, has been advocated to be an ideal neuroprotective agent both in animal models and in clinical practice, due to its positive effects on oxidative stress. Nevertheless, no studies have compared this agent to another sedative agent used for sedation after traumatic brain injury (TBI). The objective was to compare the effects of propofol to midazolam on cerebral biomarkers at the acute phase of severe TBI patients. ⋯ No difference between groups was observed for the L:P ratio (time effect p=0.201, treatment effect p=0.401, time×treatment interaction p=0.101). Similarly, no difference was observed for glutamate (time effect p=0.930, treatment effect p=0.651, time×treatment interaction p=0.353), glycerol (time effect p=0.223, treatment effect p=0.922, time×treatment interaction p=0.308), or glucose (time effect p=0.116, treatment effect p=0.088, time×treatment interaction p=0.235). These results do not support a difference between propofol and midazolam for sedation for the cerebral metabolic profile in severe TBI.
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Journal of neurotrauma · Apr 2012
Case ReportsFrontal cortex neuropathology in dementia pugilistica.
Dementia pugilistica (DP) is associated with chronic traumatic brain injury (CTBI), and leads to a "punch drunk" syndrome characterized by impairments in memory and executive function, behavioral changes, and motor signs. Microscopic features include the accumulation of neurofibrillary tangles (NFTs), beta-amyloid (Aβ), and TAR DNA binding protein 43 (TDP-43) pathology. Here we describe detailed clinical and neuropathological data about a 55-year-old retired boxer (ApoE3/4), who presented with executive dysfunction and behavioral impairments. ⋯ Inflammation was another key feature, including microglial activation and significant C1q labeling of neurons, along with NFTs. TDP-43-positive pathology was also observed. Inflammation may be a key inciting as well as propagating feature of DP neuropathology.
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Journal of neurotrauma · Apr 2012
Modulation of transcription factor Nrf2 in an in vitro model of traumatic brain injury.
Traumatic brain injury (TBI) afflicts approximately 1.4 million people in the United States and TBIs have been labeled a major cause of death and disability on a global scale. Regulatory responses in a variety of neuronal loss conditions have supported the protective involvement of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor. Nrf2 regulates antioxidant enzyme genes, and an increase in Nrf2 expression may counteract oxidative damage that results from TBI. ⋯ We confirmed that Trx and HSP70 were upregulated by treatment with tBHQ. We observed that tBHQ protected neurons from either insult, and that this was evident by different measures of cell viability and a decrease in annexin V binding. Neuronal health after insult was improved approximately 50% by tBHQ, indicating that neurons exposed to TBI in vitro can be protected.