Articles: traumatic-brain-injuries.
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Severe traumatic brain injury (TBI) often initiates a systemic inflammatory response syndrome, which can potentially culminate into multiorgan dysfunction. A central player in this cascade is endotheliopathy, caused by perturbations in homeostatic mechanisms governed by endothelial cells due to injury-induced coagulopathy, heightened sympathoadrenal response, complement activation, and proinflammatory cytokine release. Unique to TBI is the potential disruption of the blood-brain barrier, which may expose neuronal antigens to the peripheral immune system and permit neuroinflammatory mediators to enter systemic circulation, propagating endotheliopathy systemically. This review aims to provide comprehensive insights into the "neuroendothelial axis" underlying endothelial dysfunction after TBI, identify potential diagnostic and prognostic biomarkers, and explore therapeutic strategies targeting these interactions, with the ultimate goal of improving patient outcomes after severe TBI.
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Journal of neurotrauma · Mar 2024
Metabotropic glutamate receptor 2 expression is chronically elevated in male rats with post-traumatic stress disorder related behavioral traits following repetitive low-level blast exposure.
Many military veterans who experienced blast-related traumatic brain injuries in the conflicts in Iraq and Afghanistan currently suffer from chronic cognitive and mental health problems that include depression and post-traumatic stress disorder (PTSD). Male rats exposed to repetitive low-level blast develop cognitive and PTSD-related behavioral traits that are present for more than 1 year after exposure. We previously reported that a group II metabotropic receptor (mGluR2/3) antagonist reversed blast-induced behavioral traits. ⋯ Immunohistochemical staining revealed no changes in the principally presynaptic localization of mGluR2 by blast exposure. Administering the mGluR2/3 antagonist LY341495 after behavioral traits had emerged rapidly reversed blast-induced effects on novel object recognition and cued fear responses 10 months following blast exposure. These studies support alterations in mGluR2 receptors as a key pathophysiological event following blast exposure and provide further support for group II metabotropic receptors as therapeutic targets in the neurobehavioral effects that follow blast injury.
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Traumatic brain injuries (TBIs) can be difficult to diagnose and are often marginalized when compared to more obvious physical injuries. Despite this, recognition and early treatment can lead to improved outcomes. Even mild TBIs have the potential to cause significant long-term consequences for patients, which may affect their physical recovery from orthopaedic injuries. The objective of this study was to examine the incidence and treatment of TBI within the orthopaedic trauma population. ⋯ Patients presenting after an acute trauma with orthopaedic injuries have high rates of TBI, but low rates of diagnosis and treatment. This lack of diagnosis and treatment can negatively impact recovery from orthopaedic injuries. Orthopaedic providers should be aware of the diagnostic criteria and initial treatment steps for TBI to ensure prompt and effective treatment, which has been shown to improve outcomes.
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Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glucose levels by reducing glucose reabsorption in the kidneys, which can lead to ketogenesis. Euglycemic diabetic ketoacidosis (DKA) is a rare but potentially life-threatening complication of SGLT2 inhibitors that can be triggered by trauma. ⋯ Delayed recognition of euglycemic DKA in this case led to progressive metabolic deterioration. This report emphasizes the importance of promptly suspecting, diagnosing, and treating euglycemic DKA in patients with traumatic injuries who exhibit high anion-gap metabolic acidosis, ketonuria, and glucosuria-even if they do not have significant hyperglycemia.