Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Apr 2016
Time Course of Coagulation and Fibrinolytic Parameters in Patients with Traumatic Brain Injury.
Traumatic brain injury (TBI) has long been associated with coagulopathy; however, the time course of coagulation/fibrinolytic parameters in the acute phase of TBI remains unclear. The purpose of the study was to analyze the time course of coagulation/fibrinolytic parameters in the acute phase of TBI and to elucidate parameter relationships to prognosis. We retrospectively evaluated 234 patients with severe isolated TBI with initial blood samples obtained no more than 1 h after injury. ⋯ An upward trend of aPTT on admission and 3 h after injury was also a significant negative prognostic indicator (admission: p = 0.0011; 3 h after injury: p = 0.013). On multivariate logistic regression analysis, which included all initial variables, independent risk factors for poor prognosis included older age (p = 0.0005), low Glasgow Coma Scale score (p < 0.0001), high Abbreviated Injury Score (p = 0.015), aPTT >30.2 sec (p = 0.019), and elevated D-dimer level (p = 0.0005). We concluded that D-dimer is the best coagulation/fibrinolytic parameter to monitor for prediction of outcome.
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Combined central diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury (TBI) is rare, is characterized by massive polyuria leading to severe water and electrolyte disturbances, and usually is associated with very high mortality mainly as a result of delayed diagnosis and improper management. ⋯ For combined diabetes insipidus and cerebral salt wasting syndrome after traumatic brain injury, massive polyuria is a major typical presentation, and intensive monitoring of fluid and sodium status is key for timely diagnosis. To achieve a favorable outcome, proper sodium chloride supplementation and cortisone acetate and vasopressin coadministration are key.
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Journal of neurotrauma · Apr 2016
How stable is coping in patients with neuropsychiatric symptoms after acquired brain injury? Changes in coping styles and their predictors in the chronic phase.
The objective of the study was to examine changes in coping and their predictors in patients in the chronic phase after an acquired brain injury with prominent neuropsychiatric symptoms. Patients with brain injury were recruited from consecutive admissions to the outpatient clinics of four mental health centers in the Netherlands. Patients received psychoeducation and/or one or more individual treatment sessions that were not targeting coping styles. ⋯ Self-reported executive functioning at T1 was not associated with changes in coping. In conclusion, avoidance coping increased in the chronic phase after brain injury. The changes in coping could partially be explained by the level of neuropsychiatric symptoms and the level of self-awareness but not by self-reported executive functioning, which should be considered in treatment programs.
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Head Trauma (HT) is a major cause of death, disability and important public health problem. HT is also the main cause of hyperglycaemia that can increase mortality. ⋯ Hyperglycaemia after severe TBI (RBS ≥ 200) is associated with poor outcome. It can be a predictive factor for mortality rate, ICU stay, GCS arrival, VAP & RDS, hospital stay and ISS. Management of hyperglycaemia with insulin protocol in cases with value >200mg/dl, is critical in improving the outcome of patients with TBI.
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Journal of neurotrauma · Apr 2016
Altered neuroinflammation and behavior following traumatic brain injury in a mouse model of Alzheimer's disease.
Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. ⋯ Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator.