Journal of neurotrauma
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Journal of neurotrauma · Oct 2018
What Can Be Learned from Diffusion Tensor Imaging from a Large Traumatic Brain Injury Cohort?: White Matter Integrity and Its Relationship with Outcome.
Traumatic axonal injury (TAI) contributes significantly to mortality and morbidity after traumatic brain injury (TBI), but its identification is still a diagnostic challenge because of the limitations of conventional imaging techniques to characterized it. Diffusion tensor imaging (DTI) can indirectly identify areas of damaged white matter (WM) integrity by detecting water molecule diffusion alterations. Therefore, DTI may improve detection and description of TAI lesions after TBI. ⋯ We found statistically significant correlation between FA metrics and some demographic, clinical, and conventional imaging characteristics. Additionally, these FA metrics were highly associated with outcome assessed at hospital discharge and at 6 and 12 months after TBI. We conclude that FA reduction in the subacute stage after TBI assessed by DTI may be a useful prognostic factor for long-term unfavorable outcome.
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Journal of neurotrauma · Oct 2018
Sarcopenia Measured Using Masseter Area Predicts Early Mortality following Severe Traumatic Brain Injury.
Sarcopenia is strongly associated with poor outcomes and mortality following injury among the geriatric population. Diagnosis using psoas area is most common but may be unavailable given limited radiographic evaluation following low-impact injuries. Masseter area has recently been identified as an available alternative and associated with 2-year mortality following injury. ⋯ Patients with sarcopenia had significantly increased rates of 30-day mortality (80.0% vs. 50.6%; p = 0.01). Sarcopenia (odds ratio [OR], 2.95; 95% confidence interval [CI] 1.03-8.49) and decreasing masseter area were significantly associated with 30-day mortality (OR, 0.66; 95% CI 0.46-0.95) in multivariate modeling. Masseter area is a readily available and objective measure to determine sarcopenia, which is significantly associated with in-creased 30-day mortality following sTBI.
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Journal of neurotrauma · Oct 2018
Post-Concussion Driving Behaviors and Opinions: A Survey of Collegiate Student-Athletes.
Post-concussion driving restrictions are eminent, but we lack understanding of current behaviors and opinions about driving following concussion among populations at risk of concussion. We aimed to describe post-concussion driving behaviors and opinions among collegiate student-athletes. Student-athletes completed a survey (response rate = 45.3%, 223/492) regarding their post-concussion driving behaviors and opinions. ⋯ Despite generally believing that driving immediately following a concussion is unsafe, a majority of student-athletes did not refrain from driving at any point following their previous concussions. Post-concussion driving restrictions may have some influence on student-athletes' decisions to report the injury to a health care provider. Health care providers play a critical role in post-concussion driving restriction, but lack standardized recommendations to guide their care.
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Journal of neurotrauma · Oct 2018
Divergent induction of branched-chain aminotransferases and phosphorylation of branched chain keto-acid dehydrogenase is a potential mechanism coupling BCKA -mediated-astrocyte activation to BCAA depletion-mediated cognitive deficit after TBI.
Deficient branched-chain amino acids (BCAAs) are implicated in cognitive dysfunction after traumatic brain injury (TBI). The mechanism remains unknown. BCAAs are catabolized by neuron-specific cytosolic and astrocyte-specific mitochondrial branched-chain aminotransferases (BCATc, BCATm) to generate glutamate and branched-chain keto-acids (BCKAs) that are metabolized by the mitochondrial branched-chain keto-acid dehydrogenase (BCKD) whose activity is regulated by its phosphorylation state. ⋯ BCKD protein expression is higher in primarily cultured cortical neurons than in astrocytes, whereas pBCKD protein level is higher in astrocytes than in cortical neurons. Transforming growth factor beta treatment (10 μg/mL for 48 h) significantly increased pBCKD protein expression in astrocytes, whereas glutamate treatment (25 μM for 24 h) significantly decreased pBCKD protein in neurons. Because increased pBCKD would lead to increased BCKA accumulation, BCKA-mediated astrocyte activation, cell death, and cognitive dysfunction as found in maple syrup urine disease; thus, TBI may potentially induce cognitive deficit through diverting BCAA from glutamate production in neurons to BCKA production in astrocytes through the pBCKD-dependent mechanism.
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Journal of neurotrauma · Oct 2018
A Mild Traumatic Brain Injury in Mice Produces Lasting Deficits in Brain Metabolism.
Metabolic uncoupling has been well-characterized during the first minutes-to-days after a traumatic brain injury (TBI), yet mitochondrial bioenergetics during the weeks-to-months after a brain injury is poorly defined, particularly after a mild TBI. We hypothesized that a closed head injury (CHI) would be associated with deficits in mitochondrial bioenergetics at one month after the injury. A significant decrease in state-III (adenosine triphosphate production) and state-V (complex-I) driven mitochondrial respiration was found at one month post-injury in adult C57Bl/6J mice. ⋯ We also found regional variations in cerebral blood flow, including both hypo- and hyperperfusion, as measured by a pseudocontinuous arterial spin labeling MR sequence. Our results highlight a chronic deficit in mitochondrial bioenergetics associated with a CHI that may lead toward a novel approach for neurorestoration after a mild TBI. MRS provides a potential biomarker for assessing the efficacy of candidate treatments targeted at improving mitochondrial bioenergetics.