Journal of neurotrauma
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Journal of neurotrauma · Aug 2013
Randomized Controlled TrialThe effect of varied test instructions on neuropsychological performance following mild traumatic brain injury: an investigation of "diagnosis threat".
Diagnosis threat is a psychosocial factor that has been proposed to contribute to poor outcomes following mild traumatic brain injury (mTBI). This threat is thought to impair the cognitive test performance of individuals with mTBI because of negative injury stereotypes. University students (N=45, 62.2% female) with a history of mTBI were randomly allocated to a diagnosis threat (DT; n=15), reduced threat (DT-reduced; n=15), or neutral (n=15) group. ⋯ The only significant result was for the 2 × 3 ANOVA on an objective test of attention/working memory, Digit Span (p<0.05), such that the DT-reduced group performed better than the other groups, which were not different from each other. Although not consistent with predictions or earlier DT studies, the absence of group differences on most tests fits with several recent DT findings. The results of this study suggest that it is timely to reconsider the role of DT as a unique contributor to poor mTBI outcome.
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Journal of neurotrauma · Aug 2013
Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat.
Excessive extracellular glutamate after traumatic brain injury (TBI) contributes to excitotoxic cell death and likely to post-traumatic epilepsy. Glutamate transport is the only known mechanism of extracellular glutamate clearance, and glutamate transporter 1 (GLT-1) is the major glutamate transporter of the mammalian brain. We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated β-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. ⋯ However, the loss of GLT-1 expression was reversed by treatment with ceftriaxone (200 mg/kg, daily, intraperitoneally). We found that ceftriaxone treatment also decreased the level of regional GFAP expression by 43% in the lesioned cortex, relative to control treatment with saline (n=7 per group; p<0.05), and, 12 weeks after injury, reduced cumulative post-traumatic seizure duration (n=6 rats in the ceftriaxone treatment group and n=5 rats in the saline control group; p<0.001). We cautiously conclude that our data suggest a potential role for ceftriaxone in treatment of epileptogenic TBI.
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Journal of neurotrauma · Aug 2013
Influence of combat blast-related mild traumatic brain injury acute symptoms on mental health and service discharge outcomes.
Assessment of acute mild traumatic brain injury (mTBI) symptoms after a combat blast could aid diagnosis and guide follow-up care. Our objective was to document acute mTBI symptoms following a combat blast and to examine associations between acute symptoms and mental health and service discharge outcomes. A retrospective cohort study was conducted with 1656 service personnel who experienced a combat blast-related mTBI in Iraq. ⋯ While no acute mTBI symptoms were associated with discharge outcomes, injury severity was associated with disability discharge. LOC after blast-related mTBI was associated with PTSD and PCS, and injury severity was predictive of disability discharge. The assessment of cognitive status immediately after a blast could assist in diagnosing mTBI and indicate a need for follow-up care.
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Journal of neurotrauma · Aug 2013
Arginine vasopressin V1a receptor-deficient mice have reduced brain edema and secondary brain damage following traumatic brain injury.
The formation of brain edema and subsequent intracranial hypertension are major predictors of unfavorable outcome following traumatic brain injury (TBI). Previously, we reported that arginine vasopressin (AVP) receptor antagonists reduce post-traumatic and post-ischemic brain edema in mice. The aim of the current study was to investigate further the contribution of arginine vasopressin V1a receptors to TBI-induced secondary brain damage in V1a receptor knock-out mice. ⋯ Furthermore, the V1a receptor knock-out mice had less neurological dysfunction (3.2±0.8 vs. 7.0±1.4 in wild-type mice) and weight loss (1.0±1.0% vs. 4.9±1.8% in wild-type mice) seven days after CCI. Our data show that mice lacking V1a receptors have less secondary brain damage following experimental traumatic brain injury. We therefore conclude that V1a receptors may represent a novel drug target for preventing post-traumatic brain edema.
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Journal of neurotrauma · Aug 2013
Review Case Reports Multicenter StudyIncreased mortality associated with cerebral contusions following trauma in the elderly: bad patients or bad management?
Age has been identified as an independent risk factor for poor outcome following head injury in the elderly, and postulated reasons for this include nature, nurture, and variations in management. Do elderly head injuries do worse because of a self-fulfilling prophecy of poorer management? The aim of this study was to review the management of patients with cerebral contusions according to age to identify any trends. We retrospectively reviewed prospectively collected national data on cerebral contusion admissions between March 14, 1988, and May 4, 2012, to UK hospitals held in the Trauma Audit and Research Network database. ⋯ However, time from admission to CT head imaging (p=0.003) and the likelihood of not being transferred to a center with acute neurosurgical care facilities (p<0.001) increased with increasing age, too. Further, there was a significant trend for the most senior grade of doctor to review more younger patients and for only the most junior grade of doctor to review more older patients (both, p<0.001). To conclude, our data suggest differences in management practice may contribute to the observed differences in mortality between younger and older patients suffering brain contusions.