JOURNAL/nrgr/04.03/01300535-202508000-00002/figure1/v/2024-09-30T120553Z/r/image-tiff Traumatic brain injury is a prevalent disorder of the central nervous system. In addition to primary brain parenchymal damage, the enduring biological consequences of traumatic brain injury pose long-term risks for patients with traumatic brain injury; however, the underlying pathogenesis remains unclear, and effective intervention methods are lacking. Intestinal dysfunction is a significant consequence of traumatic brain injury. Being the most densely innervated peripheral tissue in the body, the gut possesses multiple pathways for the establishment of a bidirectional "brain-gut axis" with the central nervous system. The gut harbors a vast microbial community, and alterations of the gut niche contribute to the progression of traumatic brain injury and its unfavorable prognosis through neuronal, hormonal, and immune pathways. A comprehensive understanding of microbiota-mediated peripheral neuroimmunomodulation mechanisms is needed to enhance treatment strategies for traumatic brain injury and its associated complications. We comprehensively reviewed alterations in the gut microecological environment following traumatic brain injury, with a specific focus on the complex biological processes of peripheral nerves, immunity, and microbes triggered by traumatic brain injury, encompassing autonomic dysfunction, neuroendocrine disturbances, peripheral immunosuppression, increased intestinal barrier permeability, compromised responses of sensory nerves to microorganisms, and potential effector nuclei in the central nervous system influenced by gut microbiota. Additionally, we reviewed the mechanisms underlying secondary biological injury and the dynamic pathological responses that occur following injury to enhance our current understanding of how peripheral pathways impact the outcome of patients with traumatic brain injury. This review aimed to propose a conceptual model for future risk assessment of central nervous system-related diseases while elucidating novel insights into the bidirectional effects of the "brain-gut-microbiota axis."
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http://dx.doi.org/10.4103/NRR.NRR-D-24-00088 | DOI Listing |
G3 (Bethesda)
January 2025
Department of Neurobiology, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093.
The conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Introduction: While cerebral amyloid angiopathy is likely responsible for intracerebral hemorrhage (ICH) occurring in superficial (grey matter, vermis) cerebellar locations, it is unclear whether hypertensive arteriopathy (HA), the other major cerebral small vessel disease (cSVD), is associated with cerebellar ICH (cICH) in deep (white matter, deep nuclei, cerebellar peduncle) regions. We tested the hypothesis that HA-associated neuroimaging markers are significantly associated with deep cICH compared to superficial cICH.
Patients And Methods: Brain MRI scans from consecutive non-traumatic cICH patients admitted to a referral center were analyzed for cSVD markers.
Eur J Trauma Emerg Surg
January 2025
Delray Medical Center, Division of Trauma and Critical Care Services, 5352 Linton Boulevard, Delray Beach, FL, 33484, USA.
Purpose: Many patients originally transported to non-trauma centers (NTC) require transfer to a trauma center (TC) for treatment. The aim was to analyze injury characteristics and outcomes of transfer patients and investigate the secondary overtriage (SOT).
Methods: Study included 2,056 transfers to an urban level 1 TC between 01/2016 and 06/2020.
Eur J Trauma Emerg Surg
January 2025
Department of Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, PA, 17033, USA.
Background: The role of beta-blockers in severe, traumatic brain injury (TBI) management is debated. Severe TBI may elicit a surge of catecholamines, which has been associated with increased morbidity and mortality. We hypothesize administering propranolol, a non-selective beta-blocker, within 48 h of TBI will reduce patient mortality within 30 days of injury.
View Article and Find Full Text PDFEur J Trauma Emerg Surg
January 2025
Department of Emergency Medicine, Teikyo University of Medicine, 2- 11-1 Kaga, Itabashi-ku, Tokyo, 173-8606, Japan.
Purpose: D-dimer, a fibrinolysis indicator, may predict functional and life outcomes in traumatic brain injury (TBI) patients. We aimed to identify optimal D-dimer cutoff values for poor functional outcomes in severe TBI.
Methods: We used data from a multi-centre prospective observational cohort study that included patients with TBI with a Glasgow Coma Scale (GCS) score ≤ 8 within 48 h after injury or required neurosurgical procedures.
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