Articles: traumatic-brain-injuries.
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Traumatic brain injury (TBI) is a worldwide leading cause of mortality and disability. Among TBI complications, agitation is a frequent behavioural problem. Agitation causes potential harm to patients and caregivers, interferes with treatments, leads to unnecessary chemical and physical restraints, increases hospital length of stay, delays rehabilitation, and impedes functional independence. Pharmacological treatments are often considered for agitation management following TBI. Several types of agents have been proposed for the treatment of agitation. However, the benefit and safety of these agents in TBI patients as well as their differential effects and interactions are uncertain. In addition, animal studies and observational studies have suggested impaired cognitive function with the use of certain antipsychotics and benzodiazepines. Hence, a safe and effective treatment for agitation, which does not interfere with neurological recovery, remains to be identified. ⋯ PROSPERO CRD42016033140.
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Traumatic brain injury (TBI) affects millions yearly, and is increasingly associated with chronic neuropsychiatric symptoms. We assessed the long-term effects of different bilateral frontal controlled cortical impact injury severities (mild, moderate, and severe) on the five-choice serial reaction time task, a paradigm with relatively independent measurements of attention, motor impulsivity, and motivation. Moderately- and severely injured animals exhibited impairments across all cognitive domains that were still evident 14 weeks postinjury, while mild-injured animals only demonstrated persistent deficits in impulse control. ⋯ Analysis of brain tissue revealed that generalized neuroinflammation was associated with impulsivity even when accounting for the degree of brain damage. This is one of the first studies to characterize psychiatric-like symptoms in experimental TBI. Our data highlight the importance of testing pharmacotherapies in TBI models in order to predict efficacy, and suggest that neuroinflammation may represent a treatment target for impulse control problems following injury.
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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
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.