Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Jul 2023
ADAM17 aggravates the inflammatory response by modulating microglia polarization through the TGF-β1/Smad pathway following experimental traumatic brain injury.
Microglia-mediated neuroinflammatory responses play important roles in secondary neurological injury after traumatic brain injury (TBI). The TGF-β pathway participates in the regulation of M1/M2 phenotype transformation of microglia. TGF-β can activate the Smad pathway by binding to TGF-βRs, which is regulated by the cleavage function of A disintegrin and metalloproteinase 17 (ADAM17). ⋯ The neuroprotective effect of ADAM17 inhibition was related to a shift from the M1 microglial phenotype to the M2 microglial phenotype, thus reducing TBI-induced neuroinflammation. ADAM17 inhibition increased expression of TGF-βRs on the microglia membrane, promoted formation of TGF-β1/TGF-βRII complexes, and induced intranuclear translocation of Smads, which activated the TGF-β/Smad pathway. In conclusion, our study suggested that ADAM17 inhibition regulated microglia M1/M2 phenotype polarization through the TGF-β1/Smad pathway and influenced the neuroinflammatory response after TBI.
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J Neurosurg Anesthesiol · Jul 2023
Predicting Mortality Following Traumatic Brain Injury or Subarachnoid Hemorrhage: An Analysis of the Validity of Standardized Mortality Ratios Obtained From the APACHE II and ICNARCH-2018 Models.
Standardized mortality ratios (SMRs), calculated using the Acute Physiology, Age, Chronic Health Evaluation II (APACHE II) and Intensive Care National Audit and Research Centre H-2018 (ICNARC H-2018 ) risk prediction models, are widely used in UK intensive care units (ICUs) to measure and compare the quality of critical care delivery. Both models incorporate an assumption of Glasgow Coma Score (GCS) if an actual GCS without sedation is not recordable in the first 24 hours after ICU admission. This study assesses the validity of the APACHE II and ICNARC H-2018 models to predict mortality in ICU patients with traumatic brain injury (TBI) or aneurysmal subarachnoid hemorrhage (aSAH) in whom GCS is related to outcomes. ⋯ The APACHE II and ICNARC H-2018 models predicted mortality well for the overall TBI/aSAH ICU population but underpredicted mortality when GCS was ≤8 or "unrecordable." This raises questions about the accuracy of these risk prediction models in TBI/aSAH patients and their use to evaluate treatments and compare outcomes between centers.
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Journal of neurotrauma · Jul 2023
ReviewPutting the mind to rest: a historical foundation for rest as a treatment for traumatic brain injury.
Rest after traumatic brain injury (TBI) has been a part of clinical practice for more than a century but the use of rest as a treatment has ancient roots. In contemporary practice, rest recommendations have been significantly reduced but are still present. This advice to brain injured patients, on the face of it makes some logical sense but was not historically anchored in either theory or empirical data. ⋯ The goals and theoretical explanations for this approach have evolved and in modern conception include avoiding reinjury and reducing the metabolic demands on injured tissue. Moreover, as cellular and molecular understanding of the physiology of TBI developed, scientists and clinicians sometimes retroactively cited these new data in support of rest recommendations. Here, we trace the history of this approach and how it has been shaped by new understanding of the underlying pathology associated with brain injury.
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Journal of neurotrauma · Jul 2023
ReviewGrowth Hormone Deficiency Following Traumatic Brain Injury in Pediatric and Adolescent Patients: Presentation, Treatment, and Challenges of Transitioning From Pediatric to Adult Services.
Abstract Traumatic brain injury (TBI) is increasingly recognized, with an incidence of approximately 110 per 100,000 in pediatric populations and 618 per 100,000 in adolescent and adult populations. TBI often leads to cognitive, behavioral, and physical consequences, including endocrinopathies. Deficiencies in anterior pituitary hormones (e.g., adrenocorticotropic hormone, thyroid-stimulating hormone, gonadotropins, and growth hormone [GH]) can negatively impact health outcomes and quality of life post-TBI. ⋯ We place particular emphasis on the ways in which testing and dosage recommendations may change during the transition phase. We conclude with a review of the challenges faced by transition-age patients and how these may be addressed to improve access to adequate healthcare. Little information is currently available to help guide patients with TBI and GHD through the transition phase and there is a risk of interrupted care; therefore, a strength of this review is its emphasis on this critical period in a patient's healthcare journey.
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Journal of neurotrauma · Jul 2023
Lifetime Traumatic Brain Injury and Cognitive Domain Deficits in Late Life: The PROTECT-TBI Cohort Study.
Traumatic brain injury (TBI) causes cognitive impairment but it remains contested regarding which cognitive domains are most affected. Further, moderate-severe TBI is known to be deleterious, but studies of mild TBI (mTBI) show a greater mix of negative and positive findings. This study examines the longer-term cognitive effects of TBI severity and number of mTBIs in later life. ⋯ The most sensitive cognitive domains are attention and executive function, with approximately double the effect compared with processing speed and working memory. Post-TBI cognitive rehabilitation should be targeted appropriately to domain-specific effects. Significant long-term cognitive deficits were associated with three or more lifetime mTBIs, a critical consideration when counseling individuals post-TBI about continuing high-risk activities.