Articles: traumatic-brain-injuries.
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Molecular neurobiology · Dec 2016
Meta AnalysisEfficacy of Progesterone for Acute Traumatic Brain Injury: a Meta-analysis of Randomized Controlled Trials.
Progesterone, a steroid hormone, has been shown to have multifactorial neuroprotective effects in a variety of animal models of acute traumatic brain injury (TBI). Translation to humans showed positive effects in previous phase II trials, but unfortunately, negative results were observed in two recent phase III trials. The present study focuses on the efficacy of progesterone on acute TBI based on the published data of randomized controlled trials (RCTs). ⋯ Sensitivity analysis showed that all the outcomes were stable after excluding Shakeri (Clin Neurol Neurosurg 115: 2019-2022, 2013) or Wright (N Engl J Med 371: 2457-2466, 2014) trials. The quality of the evidence was varied from high to low. In conclusion, progesterone has no significant improvement in the functional recovery and mortality rate after acute TBI.
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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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Review Meta Analysis
Risk of Delayed Intracranial Hemorrhage in Anticoagulated Patients with Mild Traumatic Brain Injury: Systematic Review and Meta-Analysis.
Delayed intracranial hemorrhage is a potential complication of head trauma in anticoagulated patients. ⋯ The present study is the first published meta-analysis estimating the risk of delayed intracranial hemorrhage 24 h after head trauma in patients anticoagulated with vitamin K antagonist and normal initial CT scan. In most situations, a repeat CT scan in the emergency department 24 h later is not necessary if the first CT scan is normal. Special care may be required for patients with serious mechanism of injury, patients showing signs of neurologic deterioration, and patients presenting with excessive anticoagulation or receiving antiplatelet co-medication.
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Meta Analysis
Is APOE ε4 associated with poorer cognitive outcome following traumatic brain injury? A meta-analysis.
Cognitive impairment is a common sequelae of traumatic brain injury (TBI); however, predicting who will experience poorer outcomes remains challenging. A potential risk factor that has gained attention is the APOE gene, with the ε4 allele hypothesized to have a detrimental effect on post-TBI cognitive outcome. The aim of this meta-analysis was to evaluate the effect of APOE ε4 both in terms of general cognitive function and within specific domains known to be prone to impairment following TBI (executive function, working memory, verbal memory and visual memory). ⋯ This meta-analysis indicates that APOE ε4 does not have a detrimental effect on cognitive performance following TBI. We propose that the relationship between APOE and cognitive function following TBI is complex, and a more-nuanced exploration of APOE genotypes is needed. (PsycINFO Database Record
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Meta Analysis
A meta-analysis of working memory impairments in survivors of moderate-to-severe traumatic brain injury.
To establish the magnitude of deficits in working memory (WM) and short-term memory (STM) in those with moderate-to-severe traumatic brain injury (TBI) relative to age-matched, healthy controls and to explore the moderating effects of time since injury and age at injury on these impairments. ⋯ Evidence for WM impairments following TBI is consistent with previous research. Larger verbal STM and verbal WM deficits were related to a longer time postinjury, suggesting that these aspects of memory do not "recover" over time and instead, individuals might show increased rates of cognitive decline. Age at injury was associated with the severity of verbal WM impairments, with larger deficits evident for injuries that occurred later in life. Further research needs to chart the long-term effects of TBI on WM and to compare the effects of injury on verbal relative to visuospatial memory. (PsycINFO Database Record