Mobilization in traumatic brain injury (TBI) have shown the improvement of length of stay, infection, long term weakness, and disability. Primary damage as a result of trauma's direct effect (skull fracture, hematoma, contusion, laceration, and nerve damage) and secondary damage caused by trauma's indirect effect (microvasculature damage and pro-inflammatory cytokine) result in reduced tissue perfusion & edema. These can be facilitated through mobilization, but several precautions must be recognized as mobilization itself may further deteriorate patient's condition. Very few studies have discussed in detail regarding mobilizing patients in TBI cases. Therefore, the scope of this review covers the detail of physiological effects, guideline, precautions, and technique of mobilization in patients with TBI.
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http://dx.doi.org/10.4266/acc.2023.00640 | DOI Listing |
J 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.
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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.
J Neurotrauma
January 2025
Regenerative Bioscience Center, University of Georgia, Athens, Georgia, USA.
Human neural stem cells (hNSCs) possess significant therapeutic potential for the treatment of traumatic brain injury (TBI), a leading cause of global death and disability. Recent pre-clinical studies have shown that hNSCs reduce tissue damage and promote functional recovery through neuroprotective and regenerative signaling and cell replacement. Yet the overall efficacy of hNSCs for TBI indications remains unclear.
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