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Clinical evidence of inflammation driving secondary brain injury: a systematic review.

ABSTRACT: Despite advances in both prevention and treatment, traumatic brain injury (TBI) remains one of the most burdensome diseases; 2% of the US population currently lives with disabilities resulting from TBI. Recent advances in the understanding of inflammation and its impact on the pathophysiology of trauma have increased the interest in inflammation as a possible mediator in TBI outcome.The goal of this systematic review is to address the question: "What is the evidence in humans that inflammation is linked to secondary brain injury?" As the experimental evidence has been well described elsewhere, this review will focus on the clinical evidence for inflammation as a mechanism of secondary brain injury.Medline database (1996-Week 1 June 2014), Pubmed and Google Scholar databases were queried for relevant studies.Studies were eligible if participants were adults and/or children who sustained moderate or severe TBI in the acute phase of injury, published in English. Studies published in the last decade (since 2004) were preferentially included. Trials could be observational or interventional in nature.To address the quality of the studies retrieved, we applied the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) criteria to assess the limitations of the included studies.Trauma initiates local central nervous system as well as systemic immune activation. Numerous observational studies describe elevation of pro-inflammatory cytokines that are associated with important clinical variables including neurologic outcome and mortality. A small number of clinical trials have included immunomodulating strategies, but no intervention to date has proven effective in improving outcomes after TBI.Inclusion of studies not initially retrieved by the search terms may have biased our results. Additionally, some reports may have been inadvertently excluded due to use of non-search term key words. Conclusions and Implications of Key Findings Clinical evidence of inflammation causing secondary brain injury in humans is gaining momentum. While inflammation is certainly present, it is not clear from the literature at what juncture inflammation becomes maladaptive, promoting secondary injury rather than facilitating repairand identifying patients with maladaptive inflammation (neuro-inflammation, systemic, or both) after TBI remains elusive. Direct agonism/antagonism represents an exciting target for future study.Systematic review, level III.

SUBMITTER: Hinson HE

PROVIDER: S-EPMC4297199 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature

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Clinical evidence of inflammation driving secondary brain injury: a systematic review.

Hinson Holly E HE Rowell Susan S Schreiber Martin M

The journal of trauma and acute care surgery 20150101 1

<h4>Background</h4>Despite advances in both prevention and treatment, traumatic brain injury (TBI) remains one of the most burdensome diseases; 2% of the US population currently lives with disabilities resulting from TBI. Recent advances in the understanding of inflammation and its impact on the pathophysiology of trauma have increased the interest in inflammation as a possible mediator in TBI outcome.<h4>Objectives</h4>The goal of this systematic review is to address the question: "What is the ...[more]

PMID: 25539220

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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.

Project description:Traumatic brain injury (TBI) is a leading cause of death worldwide and is increasing exponentially particularly in low and middle income countries (LMIC). To inform the development of a standard Clinical Practice Guideline (CPG) for the acute management of TBI that can be implemented specifically for limited resource settings, we conducted a systematic review to identify and assess the quality of all currently available CPGs on acute TBI using the AGREE II instrument. In accordance with PRISMA guidelines, from April 2013 to December 2015 we searched MEDLINE, EMBASE, Google Scholar and the Duke University Medical Center Library Guidelines for peer-reviewed published Clinical Practice Guidelines on the acute management of TBI (less than 24 hours), for any level of traumatic brain injury in both high and low income settings. A comprehensive reference and citation analysis was performed. CPGs found were assessed using the AGREE II instrument by five independent reviewers and scores were aggregated and reported in percentage of total possible score. An initial 2742 articles were evaluated with an additional 98 articles from the citation and reference analysis, yielding 273 full texts examined. A total of 24 final CPGs were included, of which 23 were from high income countries (HIC) and 1 from LMIC. Based on the AGREE II instrument, the best score on overall assessment was 100.0 for the CPG from the National Institute for Health and Clinical Excellence (NIHCE, 2007), followed by the New Zealand Guidelines Group (NZ, 2006) and the National Clinical Guideline (SIGN, 2009) both with a score of 96.7. The CPG from a LMIC had lower scores than CPGs from higher income settings. Our study identified and evaluated 24 CPGs with the highest scores in clarity and presentation, scope and purpose, and rigor of development. Most of these CPGs were developed in HICs, with limited applicability or utility for resource limited settings. Stakeholder involvement, Applicability, and Editorial independence remain weak and insufficiently described specifically with piloting, addressing potential costs and implementation barriers, and auditing for quality improvement.

Project description:BackgroundTraumatic brain injuries (TBI) are a significant cause of mortality and morbidity for children globally. Adherence to evidence-based treatment guidelines have been shown to improve TBI outcomes. To inform the creation of a pediatric TBI management guideline for a low and middle income country context, we assessed the quality of available clinical practice guidelines (CPGs) for the acute management pediatric TBI.MethodsArticles were identified and retrieved from MEDLINE, EMBASE, Cochrane Library, LILACS, Africa-Wide Information and Global Index Medicus. These articles were screened by four reviewers independently. Based on the eligibility criteria, with the exception of literature reviews, opinion papers and editor's letters, articles published from 1995 to November 11, 2016 which covered clinical recommendations, clinical practice or treatment guidelines for the acute management of pediatric TBI (within 24 hours) were included for review. A reference and citation analysis was performed. Seven independent reviewers from low, middle and high income clinical settings with knowledge of pediatric TBI management appraised the guidelines using the AGREE II instrument. Scores for the CPGs were aggregated by domain and overall assessment was determined.ResultsWe screened 2372 articles of which 17 were retained for data extraction and guideline appraisal. Except for one CPG from a middle income country, the majority (16/17) of the guidelines were developed in high income countries. Seven guidelines were developed specifically for the pediatric population, while the remaining CPGs addressed the acute management of TBI in both adult and pediatric populations. The New Zealand Guideline Group (NZGG, 2006) received the highest overall assessment score of 46/49 (93.88%) followed by the Scandinavian Neurotrauma Committee (SNC, 2016) with a score of 45/49 (91.84%) followed by the Scottish Intercollegiate Guideline Network (SIGN, 2009) and Brain Trauma Foundation (BTF 2012) both with scores of 44/49 (89.80%). CPGs from Cincinnati Children's Hospital (CCH 2006) and Sao Paulo Medical School Hospital/Brazilian Society of Neurosurgery (USP/BSN, 2001) received the lowest score of 27/49 (55.10%) subsequently followed by the Appropriateness Criteria (ACR, 2015) with 29/49 (59.18%). The domains for scope and purpose and clarity of presentation received the highest scores across the CPGs, while applicability and editorial independence domains had the lowest scores with a wider variability in score range for rigor of development and stakeholder involvement.ConclusionsTo our knowledge, this is the first systematic review and guideline appraisal for pediatric CPGs concerning the acute management of TBI. Targeted guideline creation specific to the pediatric population has the potential to improve the quality of acute TBI CPGs. Furthermore, it is crucial to address the applicability of a guideline to translate the CPG from a published manuscript into clinically relevant local practice tools and for resource limited practice settings.

Project description:IntroductionThe high failure rate of clinical trials in traumatic brain injury (TBI) may be attributable, in part, to the use of untested or insensitive measurement instruments. Of more than 1,000 clinical outcome assessment measures (COAs) for TBI, few have been systematically vetted to determine their performance within specific "contexts of use (COU)." As described in guidance issued by the U.S. Food and Drug Administration (FDA), the COU specifies the population of interest and the purpose for which the COA will be employed. COAs are commonly used for screening, diagnostic categorization, outcome prediction, and establishing treatment effectiveness. COA selection typically relies on expert consensus; there is no established methodology to match the appropriateness of a particular COA to a specific COU. We developed and pilot-tested the Evidence-Based Clinical Outcome assessment Platform (EB-COP) to systematically and transparently evaluate the suitability of TBI COAs for specific purposes.Methods and findingsFollowing a review of existing literature and published guidelines on psychometric standards for COAs, we developed a 6-step, semi-automated, evidence-based assessment platform to grade COA performance for six specific purposes: diagnosis, symptom detection, prognosis, natural history, subgroup stratification and treatment effectiveness. Mandatory quality indicators (QIs) were identified for each purpose using a modified Delphi consensus-building process. The EB-COP framework was incorporated into a Qualtrics software platform and pilot-tested on the Glasgow Outcome Scale-Extended (GOSE), the most widely-used COA in TBI clinical studies.ConclusionThe EB-COP provides a systematic methodology for conducting more precise, evidence-based assessment of COAs by evaluating performance within specific COUs. The EB-COP platform was shown to be feasible when applied to a TBI COA frequently used to detect treatment effects and can be modified to address other populations and COUs. Additional testing and validation of the EB-COP are warranted.

Project description:Schizophrenia is a psychiatric disorder which has a lifetime prevalence of ~1%. Multiple candidate mechanisms have been proposed in the pathogenesis of schizophrenia. One such mechanism is the involvement of neuroinflammation. Clinical studies, including neuroimaging, peripheral biomarkers and randomized control trials, have suggested the presence of neuroinflammation in schizophrenia. Many studies have also measured markers of neuroinflammation in postmortem brain samples from schizophrenia patients. The objective of this study was to conduct a systematic search of the literature on neuroinflammation in postmortem brains of schizophrenia patients indexed in MEDLINE, Embase and PsycINFO. Databases were searched up until 20th March 2016 for articles published on postmortem brains in schizophrenia evaluating microglia, astrocytes, glia, cytokines, the arachidonic cascade, substance P and other markers of neuroinflammation. Two independent reviewers extracted the data. Out of 5385 articles yielded by the search, 119 articles were identified that measured neuroinflammatory markers in schizophrenic postmortem brains. Glial fibrillary acidic protein expression was elevated, lower or unchanged in 6, 6 and 21 studies, respectively, and similar results were obtained for glial cell densities. On the other hand, microglial markers were increased, lower or unchanged in schizophrenia in 11, 3 and 8 studies, respectively. Results were variable across all other markers, but SERPINA3 and IFITM were consistently increased in 4 and 5 studies, respectively. Despite the variability, some studies evaluating neuroinflammation in postmortem brains in schizophrenia suggest an increase in microglial activity and other markers such as SERPINA3 and IFITM. Variability across studies is partially explained by multiple factors including brain region evaluated, source of the brain, diagnosis, age at time of death, age of onset and the presence of suicide victims in the cohort.

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Clinical evidence of inflammation driving secondary brain injury: a systematic review.

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Clinical evidence of inflammation driving secondary brain injury: a systematic review.

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