Articles: brain-injuries.
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Turgeon AF, Fergusson DA, Clayton L, et al; HEMOTION Trial Investigators on behalf of the Canadian Critical Care Trials Group, the Canadian Perioperative Anesthesia Clinical Trials Group, and the Canadian Traumatic Brain Injury Research Consortium. Liberal or restrictive transfusion strategy in patients with traumatic brain injury. N Engl J Med. 2024;391:722-735. 38869931.
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J Pain Symptom Manage · Nov 2024
Race and Socio-Economic Status Impact Withdrawal of Treatment in Young Traumatic Brain Injury.
Withdrawal of life-sustaining therapies (WDLST) in young individuals with traumatic brain injury (TBI) is an overwhelming situation often made more stressful by socioeconomic factors that shape health outcomes. Identifying these factors is crucial to developing equitable and goal-concordant care for patients and families. ⋯ The decision for WDLST in young patients with severe TBI may be influenced by cultural and socioeconomic factors in addition to clinical considerations.
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Observational Study
The impact of early cranioplasty on neurological function, stress response, and cognitive function in traumatic brain injury.
To analyze the efficacy of early cranioplasty in patients with traumatic brain injury and its impact on neurological function, stress response, and cognitive function. A total of 90 patients with traumatic brain injury admitted to the hospital from January 2021 to March 2024 were included in the study. The patients were divided into an observation group (45 cases) and a control group (45 cases) based on the timing of their cranioplasty. ⋯ The total incidence of postoperative complications was significantly lower in the observation group (8.70% vs 26.09%, P < .05). Early cranioplasty is beneficial for the postoperative recovery of patients with traumatic brain injury. It improves neurological function, enhances cognitive function, and reduces stress response, while also significantly lowering the incidence of postoperative complications.
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Journal of neurotrauma · Nov 2024
Bradykinin 2 receptors (B2R) mediate long term neurocognitive deficits after experimental traumatic brain injury.
The kallikrein-kinin system is one of the first inflammatory pathways to be activated following traumatic brain injury (TBI) and has been shown to exacerbate brain edema formation in the acute phase through activation of bradykinin 2 receptors (B2R). However, the influence of B2R on chronic post-traumatic damage and outcome is unclear. In the current study, we assessed long-term effects of B2R-knockout (KO) after experimental TBI. ⋯ Scar formation and astrogliosis were unaffected, but B2R deficiency led to a gene-dose-dependent attenuation of microglial activation and a reduction of CD45+ cells 3 months after TBI in cortex (p = 0.0003) and hippocampus (p < 0.0001). These results suggest that chronic hippocampal neurodegeneration and subsequent cognitive impairment are mediated by prolonged neuroinflammation and B2R. Inhibition of B2R may therefore represent a novel strategy to reduce long-term neurocognitive deficits after TBI.
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Journal of neurotrauma · Nov 2024
Evaluating the Efficacy of Chronic Galantamine on Sustained Attention and Cholinergic Neurotransmission in A Pre-Clinical Model of Traumatic Brain Injury.
Cholinergic disruptions underlie attentional deficits following traumatic brain injury (TBI). Yet, drugs specifically targeting acetylcholinesterase (AChE) inhibition have yielded mixed outcomes. Therefore, we hypothesized that galantamine (GAL), a dual-action competitive AChE inhibitor and α7 nicotinic acetylcholine receptor (nAChR) positive allosteric modulator, provided chronically after injury, will attenuate TBI-induced deficits of sustained attention and enhance ACh efflux in the medial prefrontal cortex (mPFC), as assessed by in vivo microdialysis. ⋯ In vivo microdialysis revealed no differences in basal ACh in the mPFC; however, GAL (5.0 mg/kg) significantly increased ACh efflux 30 min following injection compared to the VEH and the other GAL (0.5 and 2.0 mg/kg) treated groups (p's < 0.05). In both experiments, there were no differences in cortical lesion volume across treatment groups (p's > 0.05). In summary, albeit the higher dose of GAL increased ACh release, it did not improve measures of sustained attention or histopathological markers, thereby partially supporting the hypothesis and providing the impetus for further investigations into alternative cholinergic pharmacotherapies such as nAChR positive allosteric modulators.