Journal of neurotrauma
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Journal of neurotrauma · Feb 2018
Meta AnalysisPrognostic value of S-100ß protein for prediction of post-concussion symptoms following a mild traumatic brain injury: systematic review and meta-analysis.
This systematic review and meta-analysis aimed to determine the prognostic value of S-100β protein to identify patients with post-concussion symptoms after a mild traumatic brain injury (mTBI). A search strategy was submitted to seven databases from their inception to October 2016. Individual patient data were requested. ⋯ Overall risk of bias was considered moderate. Results suggest that the prognostic biomarker S-100β protein has a low clinical value to identify patients at risk of persistent post-concussion symptoms. Variability in injury to S-100ß protein sample time, mTBI populations, and outcomes assessed could potentially explain the lack of association and needs further evaluation.
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Journal of neurotrauma · Feb 2018
Correlation of Concussion Symptom Profile with Head Impact Biomechanics: A Case for Individual-Specific Injury Tolerance.
Concussion is a brain injury induced by biomechanical forces that is broadly defined as a complex pathophysiological process affecting the brain. The intricate link between biomechanical input and concussion injury response is poorly understood. We aimed to test the hypothesis that greater biomechanical forces would result in the presentation of more concussion-related symptoms that would take longer to resolve. ⋯ While concussive impacts did not stand out relative to impacts that did not result in injury, concussive impacts were among the most severe for each individual player. This suggests tolerance to head acceleration might be individual-specific, meaning similar biomechanical inputs can produce different injury presentations between individuals. Future investigations should consider individual-specific analyses of tolerance to head acceleration and injury response.
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Journal of neurotrauma · Feb 2018
Exacerbation of Acute Traumatic Brain Injury by Circulating Extracellular Vesicles.
Inflammatory lesions in the brain activate a systemic acute-phase response (APR), which is dependent on the release of extracellular vesicles (EVs) into the circulation. The resulting APR is responsible for regulating leukocyte mobilization and subsequent recruitment to the brain. Factors that either exacerbate or inhibit the APR will also exacerbate or inhibit central nervous system (CNS) inflammation as a consequence and have the potential to influence ongoing secondary damage. ⋯ By manipulating the circulating EV population, we were able to demonstrate that each population of transferred EVs increased the APR. However, the characteristics of the response were dependent on the nature of the EVs; specifically, it was significantly increased when animals were challenged with macrophage-derived EVs, suggesting that the cellular origins of EVs may determine their function. Selectively targeting EVs from macrophage/monocyte populations is likely to be of value in reducing the impact of the systemic inflammatory response on the outcome of traumatic CNS injury.
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Journal of neurotrauma · Feb 2018
Erythropoietin Attenuates the Brain Edema Response after Experimental Traumatic Brain Injury.
Erythropoietin (EPO) has neuroprotective effects in multiple central nervous system (CNS) injury models; however EPO's effects on traumatic brain edema are elusive. To explore EPO as an intervention in traumatic brain edema, male Sprague-Dawley (SD) rats were subjected to blunt, controlled traumatic brain injury (TBI). Animals were randomized to EPO 5000 IU/kg or saline (control group) intraperitoneally within 30 min after trauma and once daily for 4 consecutive days. ⋯ Animals treated with EPO demonstrated conserved levels of aquaporin 4 (AQP4) protein expression in the perilesional area, whereas control animals showed a reduction of AQP4. We show that post TBI administration of EPO decreases early cytotoxic brain edema and preserves structural and functional properties of the BBB, leading to attenuation of the vasogenic edema response. The data support that the mechanisms involve preservation of the tight junction protein ZO-1 and the water channel AQP4, and indicate that treatment with EPO may have beneficial effects on the brain edema response following TBI.
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Journal of neurotrauma · Feb 2018
Hyperbaric Oxygen Therapy in the Treatment of Acute Severe Traumatic Brain Injury: a Systematic Review.
There has been no major advancement in a quarter of a century for the treatment of acute severe traumatic brain injury (TBI). This review summarizes 40 years of clinical and pre-clinical research on the treatment of acute TBI with hyperbaric oxygen therapy (HBO2) in the context of an impending National Institute of Neurologic Disorders and Stroke-funded, multi-center, randomized, adaptive Phase II clinical trial -the Hyperbaric Oxygen Brain Injury Treatment (HOBIT) trial. Thirty studies (eight clinical and 22 pre-clinical) that administered HBO2 within 30 days of a TBI were identified from PubMed searches. ⋯ These studies provided evidence that HBO2 significantly improves physiologic measures without causing cerebral or pulmonary toxicity and can potentially improve clinical outcome. These results were consistent across the other four reviewed clinical studies, thus providing preliminary clinical data supporting the HOBIT trial. This comprehensive review demonstrates that HBO2 has the potential to be the first significant treatment in the acute phase of severe TBI.