Journal of neurotrauma
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Journal of neurotrauma · Oct 2016
Ultrastructure of diaschisis lesions following traumatic brain injury.
We used controlled cortical impact in mice to model human traumatic brain injury (TBI). Local injury was accompanied by distal diaschisis lesions that developed within brain regions anatomically connected to the injured cortex. At 7 days after injury, histochemistry documented broadly distributed lesions, particularly in the contralateral cortex and ipsilateral thalamus and striatum. ⋯ Cell bodies and processes that were silver positive at the light microscopy level showed hydropic disintegration consisting of: loss of nuclear heterochromatin; dilated somal and neuritic processes with a paucity of filaments, tubules, and mitochondria; and increased numbers of electron-dense membranous structures. Importantly the cell membrane itself was still intact 3 weeks after injury. Although the full biochemical nature of these lesions remains to be deciphered, the morphological preservation of damaged neurons and processes raises the question of whether this is a reversible process.
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Journal of neurotrauma · Oct 2016
Serum Neurofilament Light in American Football Athletes Over the Course of a Season.
Despite being underreported, American football boasts the highest incidence of concussion among all team sports, likely due to exposure to head impacts that vary in number and magnitude over the season. This study compared a biological marker of head trauma in American football athletes with non-contact sport athletes and examined changes over the course of a season. Baseline serum neurofilament light polypeptide (NFL) was measured after 9 weeks of no contact and compared with a non-contact sport. ⋯ Over the course of the season, an increase (effect size [ES] = 1.8; p < 0.001) was observed post-camp relative to baseline (1.52 ± 1.18 pg•mL-1), which remained elevated until conference play, when a second increase was observed (ES = 2.6; p = 0.008) over baseline (4.82 ± 2.64 pg•mL-1). A lack of change in non-starters resulted in substantial differences between starters and non-starters over the course of the season. These data suggest that a season of collegiate American football is associated with elevations in serum NFL, which is indicative of axonal injury, as a result of head impacts.
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Journal of neurotrauma · Oct 2016
Mechanisms of Head and Neck Injuries Sustained by Helmeted Motorcyclists in Fatal Real-World Crashes: Analysis of 47 In-Depth Cases.
Despite an improved understanding of traumatic head and neck injury mechanisms, the impact tests required by major motorcycle helmet standards have remained unchanged for decades. Development of new test methods must reflect the specific impact loads causing injury in real crashes as well as test criteria appropriate for the observed injury profiles. This study analysed a collection of in-depth crash investigations of fatally injured helmeted riders in the Adelaide metropolitan region between 1983 and 1994 inclusive to review the head and neck injury patterns that resulted from specific types of impact. ⋯ Motorcycle helmets are effective for preventing local skull fractures in impacts for which they are designed, whereas other serious injuries such as basilar skull fracture (BSF) and inertial brain injury persist despite helmet protection. Further impact test procedures should be developed for injurious impact types not currently assessed by major helmet standards, in particular facial impacts, and using test criteria based on commonly observed injuries. This study provides the necessary link, from impact load to injury, for guiding impact test development.
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Journal of neurotrauma · Oct 2016
Role of Pre-Morbid Factors and Exposure to Blast Mild Traumatic Brain Injury on Post-Traumatic Stress in United States Military Personnel.
Mild traumatic brain injury (mTBI), the signature injury of the recent wars in Afghanistan and Iraq, is a prevalent and potentially debilitating condition that is associated with symptoms of post-traumatic stress/post-traumatic stress disorder (PTS/PTSD). Prior mTBI, severity and type of injury (blast vs. non-blast), and baseline psychiatric illness are thought to impact mTBI outcomes. It is unclear if the severity of pre-morbid PTS/PTSD is a risk factor of post-injury levels of PTS and mTBI symptoms. ⋯ Pre-morbid PTS symptoms are associated with an increased risk for clinical levels of PTS following a subsequent mTBI. Symptom severity and positive radiologic findings may amplify this risk. At-risk personnel may benefit from early identification and intervention.
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Journal of neurotrauma · Oct 2016
Microglial/macrophage polarization dynamics following traumatic brain injury.
Activated microglia and macrophages exert dual beneficial and detrimental roles after central nervous system injury, which are thought to be due to their polarization along a continuum from a classical pro-inflammatory M1-like state to an alternative anti-inflammatory M2-like state. The goal of the present study was to analyze the temporal dynamics of microglia/macrophage polarization within the lesion micro-environment following traumatic brain injury (TBI) using a moderate-level controlled cortical impact (CCI) model in mice. We performed a detailed phenotypic analysis of M1- and M2-like polarized microglia/macrophages, as well as nicotinamide adenine dinucleotide phosphate oxidase (NOX2) expression, through 7 days post-injury using real-time polymerase chain reaction (qPCR), flow cytometry and image analyses. ⋯ In a follow up study, we administered a selective NOX2 inhibitor, gp91ds-tat, to CCI mice starting at 24 h post-injury to investigate the relationship between NOX2 and M1-like/Mtran phenotypes. Delayed gp91ds-tat treatment altered M1-/M2-like balance in favor of the anti-inflammatory M2-like phenotype, and significantly reduced oxidative damage in neurons at 7 days post-injury. Therefore, our data suggest that despite M1-like and M2-like polarized microglia/macrophages being activated after TBI, the early M2-like response becomes dysfunctional over time, resulting in development of pathological M1-like and Mtran phenotypes driven by increased NOX2 activity.