Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Nov 2016
Observational StudyCerebrovascular signal complexity six hours after ICU admission correlates with outcome following severe traumatic brain injury.
Disease states are associated with a breakdown in healthy interactions and are often characterized by reduced signal complexity. We applied approximate entropy (ApEn) analysis to investigate the correlation between the complexity of heart rate (ApEn-HR), mean arterial pressure (ApEn-MAP), intracranial pressure (ApEn-ICP), and a combined ApEn-product (product of the three individual ApEns) and outcome after traumatic brain injury. In 174 severe traumatic brain injured patients, we found significant differences across groups classified by the Glasgow Outcome Score in ApEn-HR (p = 0.007), ApEn-MAP (p = 0.02), ApEn-ICP (p = 0.01), ApEn-product (p = 0.001), and pressure reactivity index (PRx) (p = 0.004) in the first 6 h. ⋯ Patients in the lowest quartile for ApEn-product were over four times more likely to die (39.5% vs. 9.3%, p < 0.001) than those in the highest quartile. ApEn-ICP was inversely correlated with PRx (r = -0.39, p < 0.000001) indicating unique information related to impaired cerebral autoregulation. Our results demonstrate that as early as 6 h into monitoring, complexity measures from easily attainable vital signs, such as HR and MAP, in addition to ICP, can help triage those who require more intensive neurological management at an early stage.
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Journal of neurotrauma · Nov 2016
Establishing a TBI Program of Care - Benchmarking Outcomes after Institutional Adoption of Evidence-based Guidelines.
Traumatic brain injury (TBI) is a widespread global disease, often with widely varying outcomes. Standardization of care and adherence to established guidelines are central to the effort to improve outcomes. At our level I urban trauma center, we developed and implemented a Joint Commission-certified TBI Program of Care in 2011 and compared our post-implementation patient data set with historical controls, using the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) prognostic model. ⋯ The greatest reductions in mortality were observed in the group of patients with IMPACT-predicted mortality ≤50%. Significant progress has been made in reducing the percentage of unexpected deaths in TBI patients. It is likely that major factors include more aggressive management and tracking of compliance with the implementation of guidelines for the management of TBI patients.
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Journal of neurotrauma · Nov 2016
Post-injury treatment of 7,8-dihydroxyflavone promotes neurogenesis in the hippocampus of the adult mouse.
Traumatic brain injury (TBI) at the moderate level of impact induces massive cell death and results in extensive dendrite degeneration in the brain, leading to persistent cognitive, sensory, and motor dysfunction. Our previous reports have shown that adult-born immature granular neurons in the dentate gyrus are the most vulnerable cell type in the hippocampus after receiving a moderate TBI with a controlled cortical impact (CCI) device. There is no effective approach to prevent immature neuron death or degeneration following TBI. ⋯ In the present study, we systemically treated moderate CCI-TBI mice or sham surgery mice with DHF once a day for 2 weeks via intraperitoneal injection, and then assessed the immature neurons in the hippocampus the 2nd day after the last DHF injection. We found that post-injury treatment of DHF for 2 weeks not only increased the number of adult-born immature neurons in the hippocampus, but also promoted their dendrite arborization in the injured brain following TBI. Thus, DHF may be a promising compound that can promote neurogenesis and enhance immature neuron development following TBI.
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Journal of neurotrauma · Nov 2016
Glucose-dependent insulinotropic polypeptide ameliorates mild traumatic brain injury-induced cognitive and sensorimotor deficits and neuroinflammation in rats.
Mild traumatic brain injury (mTBI) is a major public health issue, representing 75-90% of all cases of TBI. In clinical settings, mTBI, which is defined as a Glascow Coma Scale (GCS) score of 13-15, can lead to various physical, cognitive, emotional, and psychological-related symptoms. To date, there are no pharmaceutical-based therapies to manage the development of the pathological deficits associated with mTBI. ⋯ GIP was well tolerated and ameliorated mTBI-induced memory impairments, poor balance, and sensorimotor deficits after initiation in the post-injury period. In addition, GIP mitigated mTBI-induced neuroinflammatory changes on GFAP, APP, and BMX protein levels. These findings suggest GIP has significant benefits in managing mTBI-related symptoms and represents a novel strategy for mTBI treatment.
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Journal of neurotrauma · Nov 2016
Tau oligomers derived from Traumatic Brain Injury cause cognitive impairment and accelerate onset of pathology in Htau mice.
Tau aggregation is a pathological feature of numerous neurodegenerative disorders and has also been shown to occur under certain conditions of traumatic brain injury (TBI). Currently, no effective treatments exist for the long-term effects of TBI. In some cases, TBI not only induces cognitive changes immediately post-injury, but also leads to increased incidence of neurodegeneration later in life. ⋯ Additionally, these oligomers accelerated onset of cognitive deficits when injected into brains of Htau mice. Tau oligomer levels increased in the hippocampal injection sites and cerebellum, suggesting that tau oligomers may be responsible for seeding the spread of pathology post-TBI. Our results suggest that tau oligomers play an important role in the toxicity underlying TBI and may be a viable therapeutic target.