Erratum to: Epidemiology of traumatic brain injury in Austria
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ABSTRACT:
SUBMITTER: Mauritz W
PROVIDER: S-EPMC4714017 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundTraumatic brain injury (TBI) is a critical public health and socio-economic problem throughout the world, making epidemiological monitoring of incidence, prevalence and outcome of TBI necessary. We aimed to describe the epidemiology of traumatic brain injury in Europe and to evaluate the methodology of incidence studies.MethodWe performed a systematic review and meta-analyses of articles describing the epidemiology of TBI in European countries. A search was conducted in the PubMed electronic database using the terms: epidemiology, incidence, brain injur*, head injur* and Europe. Only articles published in English and reporting on data collected in Europe between 1990 and 2014 were included.ResultsIn total, 28 epidemiological studies on TBI from 16 European countries were identified in the literature. A great variation was found in case definitions and case ascertainment between studies. Falls and road traffic accidents (RTA) were the two most frequent causes of TBI, with falls being reported more frequently than RTA. In most of the studies a peak TBI incidence was seen in the oldest age groups. In the meta-analysis, an overall incidence rate of 262 per 100,000 for admitted TBI was derived.ConclusionsInterpretation of published epidemiologic studies is confounded by differences in inclusion criteria and case ascertainment. Nevertheless, changes in epidemiological patterns are found: falls are now the most common cause of TBI, most notably in elderly patients. Improvement of the quality of standardised data collection for TBI is mandatory for reliable monitoring of epidemiological trends and to inform appropriate targeting of prevention campaigns.
| S-EPMC4569652 | biostudies-literature
Project description:OBJECTIVES:To characterize admission patterns, treatments, and outcomes among patients with moderate traumatic brain injury. DESIGN:Retrospective cohort study. SETTING:National Trauma Data Bank. PATIENTS:Adults (age > 18 yr) with moderate traumatic brain injury (International Classification of Diseases, Ninth revision codes and admission Glasgow Coma Scale score of 9-13) in the National Trauma Data Bank between 2007 and 2014. INTERVENTIONS:None. MEASUREMENT AND MAIN RESULTS:Demographics, mechanism of injury, hospital course, and facility characteristics were examined. Admission characteristics associated with discharge outcomes were analyzed using multivariable Poisson regression models. Of 114,066 patients, most were white (62%), male (69%), and had median admission Glasgow Coma Scale score of 12 (interquartile range, 10-13). Seventy-seven percent had isolated traumatic brain injury. Concussion, which accounted for 25% of moderate traumatic brain injury, was the most frequent traumatic brain injury diagnosis. Fourteen percent received mechanical ventilation, and 66% were admitted to ICU. Over 50% received care at a community hospital. Seven percent died, and 32% had a poor outcome, including those with Glasgow Coma Scale score of 13. Compared with patients 18-44 years, patients 45-64 years were twice as likely (adjusted relative risk, 1.97; 95% CI, 1.92-2.02) and patients over 80 years were five times as likely (adjusted relative risk, 4.66; 95% CI, 4.55-4.76) to have a poor outcome. Patients with a poor discharge outcome were more likely to have had hypotension at admission (adjusted relative risk, 1.10; 95% CI, 1.06-1.14), lower admission Glasgow Coma Scale (adjusted relative risk, 1.37; 95% CI, 1.34-1.40), higher Injury Severity Score (adjusted relative risk, 2.97; 95% CI, 2.86-3.09), and polytrauma (adjusted relative risk, 1.05; 95% CI, 1.02-1.07), compared with those without poor discharge outcomes. CONCLUSIONS:Many patients with moderate traumatic brain injury deteriorate, require neurocritical care, and experience poor outcomes. Optimization of care and outcomes for this vulnerable group of patients are urgently needed.
| S-EPMC5899009 | biostudies-literature
Project description:This review of the literature on traumatic brain injury (TBI) in older adults focuses on incident TBI sustained in older adulthood ("geriatric TBI") rather than on the separate, but related, topic of older adults with a history of earlier-life TBI. We describe the epidemiology of geriatric TBI, the impact of comorbidities and pre-injury function on TBI risk and outcomes, diagnostic testing, management issues, outcomes, and critical directions for future research. The highest incidence of TBI-related emergency department visits, hospitalizations, and deaths occur in older adults. Higher morbidity and mortality rates among older versus younger individuals with TBI may contribute to an assumption of futility about aggressive management of geriatric TBI. However, many older adults with TBI respond well to aggressive management and rehabilitation, suggesting that chronological age and TBI severity alone are inadequate prognostic markers. Yet there are few geriatric-specific TBI guidelines to assist with complex management decisions, and TBI prognostic models do not perform optimally in this population. Major barriers in management of geriatric TBI include under-representation of older adults in TBI research, lack of systematic measurement of pre-injury health that may be a better predictor of outcome and response to treatment than age and TBI severity alone, and lack of geriatric-specific TBI common data elements (CDEs). This review highlights the urgent need to develop more age-inclusive TBI research protocols, geriatric TBI CDEs, geriatric TBI prognostic models, and evidence-based geriatric TBI consensus management guidelines aimed at improving short- and long-term outcomes for the large and growing geriatric TBI population.
| S-EPMC5865621 | biostudies-literature
Project description:Traumatic brain injury (TBI) in children can result in long-lasting social, cognitive, and neurological impairments. In adults, TBI can lead to endocrinopathies (endocrine system disorders), but this is infrequently reported in children. Untreated endocrinopathies can elevate risks of subsequent health issues, such that early detection in pediatric TBI survivors can initiate clinical interventions. To understand the risk of endocrinopathies following pediatric TBI, we identified patients who had experienced a TBI and subsequently developed a new-onset hypothalamic regulated endocrinopathy (n = 498). We hypothesized that pediatric patients who were diagnosed with a TBI were at higher risk of being diagnosed with a central endocrinopathy than those without a prior diagnosis of TBI. In our epidemiological assessment, we identified pediatric patients enrolled in the Arizona Health Care Cost Containment System (AHCCCS) from 2008 to 2014 who were diagnosed with one of 330 TBI International Classification of Diseases (ICD)-9 codes and subsequently diagnosed with one of 14 central endocrinopathy ICD-9 codes. Additionally, the ICD-9 code data from over 600,000 Arizona pediatric patients afforded an estimate of the incidence, prevalence, relative risk, odds ratio, and number needed to harm, regarding the development of a central endocrinopathy after sustaining a TBI in Arizona Medicaid pediatric patients. Children with a TBI diagnosis had 3.22 times the risk of a subsequent central endocrine diagnosis compared with the general population (±0.28). Pediatric AHCCCS patients with a central endocrine diagnosis had 3.2-fold higher odds of a history of a TBI diagnosis than those without an endocrine diagnosis (±0.29). Furthermore, the number of patients with a TBI diagnosis for one patient to receive a diagnosis of a central endocrine diagnosis was 151.2 (±6.12). Female subjects were more likely to present with a central endocrine diagnosis after a TBI diagnosis compared to male subjects (64.1 vs. 35.9%). These results are the first state-wide epidemiological study conducted to determine the risk of developing a hypothalamic-pituitary disorder after a TBI in the pediatric population. Our results contribute to a body of knowledge demonstrating a TBI etiology for idiopathic endocrine disorders, and thus advise physicians with regard to TBI follow-up care that includes preventive screening for endocrine disorders.
| S-EPMC6988738 | biostudies-literature
Project description:IntroductionFew studies account for prehospital deaths when estimating incidence and mortality rates of moderate and severe traumatic brain injury (msTBI). In a population-based study, covering both urban and rural areas, including also prehospital deaths, the aim was to estimate incidence and mortality rates of msTBI. Further, we studied the 30-day and 6-month case-fatality proportion of severe TBI in relation to age.MethodsAll patients aged ≥17 years who sustained an msTBI in Central Norway were identified by three sources: (1) the regional trauma center, (2) the general hospitals, and (3) the Norwegian Cause of Death Registry. Incidence and mortality rates were standardized according to the World Health Organization's world standard population. Case-fatality proportions were calculated by the number of deaths from severe TBI at 30 days and 6 months, divided by all patients with severe TBI.ResultsThe overall incidence rates of moderate and severe TBI were 4.9 and 6.7 per 100,000 person-years, respectively, increasing from age 70 years. The overall mortality rate was 3.4 per 100,000 person-years, also increasing from age 70 years. Incidence and mortality rates were highest in men. The case-fatality proportion in people with severe TBI was 49% in people aged 60-69 years and 81% in people aged 70-79 years.ConclusionThe overall incidence and mortality rates for msTBI in Central Norway were low but increased from age 70 years, and among those ≥80 years of age with severe TBI, nearly all died. Overall estimates are strongly influenced by high incidence and mortality rates in the elderly, and studies should therefore report age-specific estimates, for better comparison of incidence and mortality rates.
| S-EPMC10866178 | biostudies-literature
Project description:Traumatic brain injury (TBI) is a debilitating medical and emerging public health problem that is affecting people worldwide due to a multitude of factors including both domestic and war-related acts. The objective of this paper is to systematically review the status of TBI in Lebanon - a Middle Eastern country with a weak health system that was chartered by several wars and intermittent outbursts of violence - in order to identify the present gaps in knowledge, direct future research initiatives and to assist policy makers in planning progressive and rehabilitative policies.OVID/Medline, PubMed, Scopus databases and Google Scholar were lastly searched on April 15, 2016 to identify all published research studies on TBI in Lebanon. Studies published in English, Arabic or French that assessed Lebanese patients afflicted by TBI in Lebanon were warranting inclusion in this review. Case reports, reviews, biographies and abstracts were excluded. Throughout the whole review process, reviewers worked independently and in duplicate during study selection, data abstraction and methodological assessment using the Downs and Black Checklist.In total, 11 studies were recognized eligible as they assessed Lebanese patients afflicted by TBI on Lebanese soils. Considerable methodological variation was found among the identified studies. All studies, except for two that evaluated domestic causes such as falls, reported TBI due to war-related injuries. Age distribution of TBI victims revealed two peaks, young adults between 18 and 40 years, and older adults aged 60 years and above, where males constituted the majority. Only three studies reported rates of mild TBI. Mortality, rehabilitation and systemic injury rates were rarely reported and so were the complications involved; infections were an exception.Apparently, status of TBI in Lebanon suffers from several gaps which need to be bridged through implementing more basic, epidemiological, clinical and translational research in this field in the future.
| S-EPMC5134863 | biostudies-other
Project description:ObjectiveTo comprehensively assess recurrent traumatic brain injury (rTBI) risk and risk factors in the general population.MethodsWe systematically searched MEDLINE, EMBASE, and the references of included studies until January 16, 2017, for general population observational studies reporting rTBI risk or risk factors. Estimates were not meta-analyzed due to significant methodologic heterogeneity between studies, which was evaluated using meta-regression.ResultsTwenty-two studies reported recurrence risk and 11 reported on 27 potential risk factors. rTBI risk was heterogeneous and varied from 0.43% (95% confidence interval [CI] 0.19%-0.67%) to 41.92% (95% CI 34.43%-49.40%), with varying follow-up periods (3 days-55 years). Median time to recurrence ranged from 0.5 to 3.8 years. In studies where cases were ascertained from multiple points of care, at least 5.50% (95% CI 4.80%-6.30%) of patients experienced a recurrence after a 1-year follow-up. Studies that used administrative data/self-report surveys to ascertain cases tended to report higher risk. Risk factors measured at time of index traumatic brain injury (TBI) that were significantly associated with rTBI in more than one study were male sex, prior TBI before index case, moderate or severe TBI, and alcohol intoxication. Risk factors reported in a single study that were significantly associated with rTBI were epilepsy, not seeking medical care, and multiple factors indicative of low socioeconomic status.ConclusionsrTBI is an important contributor to the general population TBI burden. Certain risk factors can help identify individuals at higher risk of these repeated injuries. However, higher quality research that improves on rTBI surveillance methodology is needed.
| S-EPMC5696641 | biostudies-literature
Project description:Time dependent-profiles in the gene expression level following lateral moderate fluid percussion injury in the rat brain We used microarray to elucidate relationship between the alteration of gene expression levels and the progression of brain damages following traumatic brain injury. To examine the levels of gene expression in the early phase of traumatic brain injury, we analyzed the gene expression at 3, 6, 12, and 48 h after trauma using the lateral moderate fluid percussion TBI model. The ratios of the gene expression level were compared between chips corresponding to the 3, 6 and 12 h fluid percussion groups and the sham group chips. On the other hand, the rations of gene expression level after 48 h FPI were compared with 48 h sham chip, because the gene expression levels of 48 h sham chip were distinct from sham group chips (3, 6 and 12 h) in the cluster and principal components analyses.
2010-12-07 | E-GEOD-24047 | biostudies-arrayexpress
Project description:Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite extensive preclinical research supporting the effectiveness of neuroprotective therapies for brain trauma, there have been no successful randomized controlled clinical trials to date. TBI results in delayed secondary tissue injury due to neurochemical, metabolic and cellular changes; modulating such effects has provided the basis for neuroprotective interventions. To establish more effective neuroprotective treatments for TBI it is essential to better understand the complex cellular and molecular events that contribute to secondary injury. Here we critically review relevant research related to causes and modulation of delayed tissue damage, with particular emphasis on cell death mechanisms and post-traumatic neuroinflammation. We discuss the concept of utilizing multipotential drugs that target multiple secondary injury pathways, rather than more specific "laser"-targeted strategies that have uniformly failed in clinical trials. Moreover, we assess data supporting use of neuroprotective drugs that are currently being evaluated in human clinical trials for TBI, as well as promising emerging experimental multipotential drug treatment strategies. Finally, we describe key challenges and provide suggestions to improve the likelihood of successful clinical translation.
| S-EPMC4808298 | biostudies-literature
Project description:Traumatic brain injury (TBI) represents the leading cause of death in young individuals. It triggers the accumulation of harmful mediators, leading to secondary damage, yet protective mechanisms are also set in motion. The endocannabinoid (eCB) system consists of ligands, such as anandamide and 2-arachidonoyl-glycerol (2-AG), receptors (e.g. CB1, CB2), transporters and enzymes, which are responsible for the 'on-demand' synthesis and degradation of these lipid mediators. There is a large body of evidence showing that eCB are markedly increased in response to pathogenic events. This fact, as well as numerous studies on experimental models of brain toxicity, neuroinflammation and trauma supports the notion that the eCB are part of the brain's compensatory or repair mechanisms. These are mediated via CB receptors signalling pathways that are linked to neuronal survival and repair. The levels of 2-AG, the most highly abundant eCB, are significantly elevated after TBI and when administered to TBI mice, 2-AG decreases brain oedema, inflammation and infarct volume and improves clinical recovery. The role of CB1 in mediating these effects was demonstrated using selective antagonists or CB1 knockout mice. CB2 were shown in other models of brain insults to reduce white blood cell rolling and adhesion, to reduce infarct size and to improve motor function. This review is focused on the role the eCB system plays as a self-neuroprotective mechanism and its potential as a basis for the development of novel therapeutic modality for the treatment of CNS pathologies with special emphasis on TBI.
| S-EPMC3165950 | biostudies-literature