Neurocritical care
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Traumatic brain injury (TBI) is the leading cause of mortality and disability among trauma-related injuries. Neuromonitoring plays an essential role in the management and prognosis of patients with severe TBI. Our bibliometric study aimed to identify the knowledge base, define the research front, and outline the social networks on neuromonitoring in severe TBI. ⋯ Neuromonitoring constitutes an area of active research. The present findings indicate that intracranial pressure monitoring plays a pivotal role in the management of severe TBI. Scientific interest shifts to magnetic resonance imaging and individualized patient care on the basis of optimal cerebral perfusion pressure.
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Trauma-induced coagulopathy in traumatic brain injury (TBI) remains associated with high rates of complications, unfavorable outcomes, and mortality. The underlying mechanisms are largely unknown. Embedded in the prospective multinational Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study, coagulation profiles beyond standard conventional coagulation assays were assessed in patients with isolated TBI within the very early hours of injury. ⋯ This more in-depth analysis beyond routine conventional coagulation assays suggests a counterbalanced regulation of coagulation and fibrinolysis in patients with iTBI with hemostatic abnormalities. We observed distinct patterns involving key pathways of the highly complex and dynamic coagulation system that offer windows of opportunity for further research. Whether the changes observed on factor levels may be relevant and explain the worse outcome or the more severe brain injuries by themselves remains speculative.
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Our objective was to evaluate the use of event-related potentials and the middle-latency somatosensory evoked potential (MLSEP) for the prediction of awakening in coma, determine the evaluation day that evoked potentials (EPs) best predict an awakening outcome, and determine whether the mismatch negativity (MMN) combined with the MLSEP, when recorded at 7 days after coma, improved the prediction of awakening from coma. ⋯ The N60 and MMN were the strongest prognostic factors for an awakening outcome. Furthermore, at 7 days after coma onset, the combination of the N60 and MMN improved the prediction of an awakening outcome in patients who were comatose.
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The present study explores the frequency, diagnostic approach, and therapeutic management of cerebral vasospasm in a cohort of children with moderate-to-severe traumatic and nontraumatic subarachnoid hemorrhage (SAH). ⋯ These findings indicate that cerebral vasospasm exists in pediatrics, particularly after nontraumatic SAH. The use of TCD and milrinone may help in the diagnostic and therapeutic management of cerebral vasospasm.
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Spreading depolarizations (SDs) are self-propagating waves of neuronal and glial depolarizations often seen in neurological conditions in both humans and animal models. Because SD is thought to worsen neurological injury, the role of SD in a variety of cerebral insults has garnered significant investigation. Anoxic SD is a type of SD that occurs because of anoxia or asphyxia. Although asphyxia leading to a severe drop in blood pressure may affect cerebral hemodynamics and is widely known to cause anoxic SD, the effect of anoxic SD on peripheral blood pressure in the extremities has not been investigated. This relationship is especially important to understand for conditions such as circulatory shock and cardiac arrest that directly affect both peripheral and cerebral perfusion in addition to producing anoxic SD in the brain. ⋯ To our knowledge, this is the first study to quantify the relationship between peripheral blood pressure, cerebral hemodynamics and metabolism, and neurological outcome in anoxic SD. These results indicate that the characteristics of SD may not be limited to cerebral hemodynamics and metabolism but rather may also encompass changes in peripheral blood flow, possibly through a brain-heart connection, providing new insights into the role of anoxic SD in global ischemia and recovery.