Articles: traumatic-brain-injuries.
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The role of cerebral pressure autoregulation (CPA) in brain injury and disorders has gained increased interest. The CPA is often disturbed as a consequence of acute brain injury, which contributes to further brain damage and worse outcome. Specifically, in severe traumatic brain injury, CPA disturbances predict worse clinical outcome and targeting an autoregulatory-oriented optimal cerebral perfusion pressure threshold may improve brain energy metabolism and clinical outcome. ⋯ In spontaneous intracerebral hemorrhage, the role of autoregulatory disturbances is less clear, but CPA disturbances correlate with worse clinical outcome. Also, in community-acquired bacterial meningitis, CPA dysfunction is frequent and correlates with worse clinical outcome, but autoregulatory management is yet to be evaluated. In this review, we discuss the role of CPA in different types of brain injury and disease, the strengths and limitations of the monitoring methods, the potentials of autoregulatory management, and future directions in the field.
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Cerebral venous injury (CVI) includes injury to a dural venous sinus or major vein and leads to poorer outcomes for patients with blunt traumatic brain injury (TBI). We sought to identify the incidence, associated factors, and outcomes associated with CVI in a large national cohort. ⋯ We identified a 0.3% incidence of CVI in all-comers with blunt TBI as well as several injury-related variables that may be used to guide investigation for dural venous sinus injury. CVI was associated with poorer outcomes, with superior sagittal sinus injury having the strongest association.
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As the most abundant neuropeptides in Central Nervous System, Substance P and Neuropeptide Y are arguably involved in the response to brain trauma. This study aims to characterize a new concept of multi-staged neuropeptide response to TBI. ⋯ A multi-staged neuropeptide response to TBI is obvious and represents a potential therapeutic strategy for the treatment of intraparenchymal lesions and cerebral edema following TBI.
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Geriatric patients (age ≥65 years) who sustain a traumatic brain injury have an increased risk of poor outcomes and higher mortality compared with younger cohorts. We aimed to evaluate the risk factors for discharge outcomes in a geriatric traumatic subdural hematoma population, stratified by age and pretraumatic medical comorbidities. This was a single-center retrospective cohort study of geriatric patients (N = 207). ⋯ Our findings suggest a need to establish unique prognostic risk factors based on patient outcomes that guide medical and surgical treatment in geriatric patients.
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Abundant findings including our previous work proved that the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome exerts a key role in the process of neuroinflammation following blast-induced traumatic brain injury (bTBI). The opening of potassium channels leads to low K+ environment in cells, which appears to be an essential requirement for NLRP3 inflammasome activation. Notably, MaxiK (BK) channel is significant for K+ transport. ⋯ In addition, paxilline could also decrease the level of pro-inflammatory cytokines and the biomarkers of brain injury and alleviate brain edema of bTBI rats. Our findings have revealed that MaxiK channel might be involved in the process of neuroinflammation of bTBI. Paxilline could depress neuro-inflammation response and alleviate brain injury by blocking MaxiK channel and subsequently inhibition of NLRP3 inflammasome activation.