Articles: traumatic-brain-injuries.
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Approximately, 275,000 American service members deployed to Iraq or Afghanistan have sustained a mild traumatic brain injury (mTBI), with 75% of these incidents involving an explosive blast. Visual processing problems and cognitive dysfunction are common complaints following blast-related mTBI. ⋯ These are the first published results that directly illustrate the relationship between blast-related mTBI severity, visual pathway neural networks, and executive dysfunction - results that highlight the detrimental relationship between blast-related brain injury and the integration of visual sensory input and executive processes.
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To investigate the frequency and risk factors of contralateral epidural hematoma (CEDH) following decompressive craniectomy (DC) in patients with calvarial skull fracture contralateral to the craniectomy site. ⋯ Age and number of fracture-involved bone plate are significant risk factors for CEDH development following DC. Involvement of 2 or more bone plates of contralateral calvarial skull fracture in young adult may prompt an immediate postoperative computed tomography scan to detect the occurrence of CEDH, irrespective of the operative findings and neurologic status. This may prevent devastating neurologic consequences of CEDH and improve therapeutic outcome.
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Neurosci Biobehav Rev · May 2016
ReviewSocial dysfunction after pediatric traumatic brain injury: A translational perspective.
Social dysfunction is common after traumatic brain injury (TBI), contributing to reduced quality of life for survivors. Factors which influence the development or persistence of social deficits after injury remain poorly understood, particularly in the context of ongoing brain maturation during childhood and adolescence. Aberrant social interactions have recently been modeled in adult and juvenile rodents after experimental TBI, providing an opportunity to gain new insights into the underlying neurobiology of these behaviors. ⋯ Modulators of social outcomes are discussed, including injury-related and environmental risk and resilience factors. Disruption of social brain network connectivity and aberrant neuroendocrine function are identified as potential mechanisms of social impairments after pediatric TBI. Throughout, we highlight the overlap and disparities between outcome measures and findings from clinical and experimental approaches, and explore the translational potential of future research to prevent or ameliorate social dysfunction after childhood TBI.
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Multicenter Study
Guideline Adherence and Outcomes in Severe Adult Traumatic Brain Injury for the CHIRAG (Collaborative Head InjuRy and Guidelines) Study.
We examined the effect of early intensive care unit (ICU) adherence to 2007 Brain Trauma Foundation Guideline indicators after traumatic brain injury (TBI) on inpatient mortality at a level 1 trauma center in India (Jay Prakash Narayan Apex Trauma Center [JPNATC]) and Harborview Medical Center (HMC) in U. S. among adults older than 18 years with severe TBI. At each site, ICU Guideline adherence in first 72 hours for 17 indicators was determined and expressed as a percentage. ⋯ Achieving early ICU adherence to guideline indicators was feasible and associated with significantly lower in-hospital mortality at JPNATC. Although the intracranial pressure (ICP) monitoring rates varied, in-hospitals deaths were similar between the two institutions. Although long-term outcomes generally improved, patients discharged with favorable GOS score often deteriorated at home.
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Brain Behav. Immun. · May 2016
Cognitive deficits develop 1month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge.
Traumatic brain injury (TBI) elicits immediate neuroinflammatory events that contribute to acute cognitive, motor, and affective disturbance. Despite resolution of these acute complications, significant neuropsychiatric and cognitive issues can develop and progress after TBI. We and others have provided novel evidence that these complications are potentiated by repeated injuries, immune challenges and stressors. A key component to this may be increased sensitization or priming of glia after TBI. Therefore, our objectives were to determine the degree to which cognitive deterioration occurred after diffuse TBI (moderate midline fluid percussion injury) and ascertain if glial reactivity induced by an acute immune challenge potentiated cognitive decline 30 days post injury (dpi). In post-recovery assessments, hippocampal-dependent learning and memory recall were normal 7 dpi, but anterograde learning was impaired by 30 dpi. Examination of mRNA and morphological profiles of glia 30 dpi indicated a low but persistent level of inflammation with elevated expression of GFAP and IL-1β in astrocytes and MHCII and IL-1β in microglia. Moreover, an acute immune challenge 30 dpi robustly interrupted memory consolidation specifically in TBI mice. These deficits were associated with exaggerated microglia-mediated inflammation with amplified (IL-1β, CCL2, TNFα) and prolonged (TNFα) cytokine/chemokine expression, and a marked reactive morphological profile of microglia in the CA3 of the hippocampus. Collectively, these data indicate that microglia remain sensitized 30 dpi after moderate TBI and a secondary inflammatory challenge elicits robust microglial reactivity that augments cognitive decline. ⋯ Traumatic brain injury (TBI) is a major risk factor in development of neuropsychiatric problems long after injury, negatively affecting quality of life. Mounting evidence indicates that inflammatory processes worsen with time after a brain injury and are likely mediated by glia. Here, we show that primed microglia and astrocytes developed in mice 1 month following moderate diffuse TBI, coinciding with cognitive deficits that were not initially evident after injury. Additionally, TBI-induced glial priming may adversely affect the ability of glia to appropriately respond to immune challenges, which occur regularly across the lifespan. Indeed, we show that an acute immune challenge augmented microglial reactivity and cognitive deficits. This idea may provide new avenues of clinical assessments and treatments following TBI.