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
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.
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Journal of neurotrauma · Apr 2012
Psychiatric disorders and health-related quality of life after severe traumatic brain injury: a prospective study.
Traumatic brain injury (TBI) is a major cause of death and disability and impairs health-related quality of life (HRQOL). Psychiatric disorders have been recognized as major components of TBI morbidity, yet few studies have addressed the relationship between these outcomes. Sample size, selection bias, and retrospective design, are methodological limitations for TBI-related psychiatric studies. ⋯ In comparison to patients without personality changes, patients with personality changes experienced a decline in general health and impairments in physical and social functioning. Patients with MDD showed impairment in all SF-36 domains compared to non-depressed patients. This prospective TBI-related psychiatric study is the first to demonstrate a significant association between MDD, personality changes, and HRQOL, following severe TBI in a well-defined sample of patients.
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Journal of neurotrauma · Apr 2012
Polymorphisms in the brain-derived neurotrophic factor gene influence memory and processing speed one month after brain injury.
Brain-derived neurotrophic factor (BDNF) plays a role in cognition, as well as neural survival and plasticity. There are several common polymorphisms in the BDNF gene, one of which (rs6265) is an extensively studied non-synonymous coding polymorphism (Val66Met) which has been linked to cognitive performance in healthy controls and some clinical populations. We hypothesized that the Met allele of rs6265 would be associated with poorer cognitive performance in individuals with mild-to-moderate traumatic brain injury, and that other polymorphisms in the BDNF gene would also affect cognition. ⋯ These associations were not affected by adjustment for rs6265 status. Polymorphisms in BDNF influence cognitive performance shortly after mTBI. The results raise the possibility that a functional polymorphism other than rs6265 may contribute to memory function after mTBI.
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Journal of neurotrauma · Apr 2012
Use of serum biomarkers to predict cerebral hypoxia after severe traumatic brain injury.
The management of severe traumatic brain injury (TBI) focuses on prevention and treatment of secondary insults such as cerebral hypoxia (CH). There are a number of biomarkers that are thought to play a part in secondary injury following severe TBI. This study evaluates the association between S100β, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP), detected in the serum of severe TBI patients and CH as measured by brain tissue oxygen partial pressure (Pbo(2)). ⋯ S100β, NSE, and GFAP demonstrate promise as candidate serum markers of impending CH. The fact that these biomarker elevations occur prior to the onset of clinical manifestations suggests that we may be able to predict imminent events following TBI. Given the morbidity of CH, early intervention and prevention may have a significant impact on outcomes and help guide decisions about the timing of interventions.