British journal of anaesthesia
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Observational Study
Association of perioperative plasma concentration of neurofilament light with delirium after cardiac surgery: a nested observational study.
Neurofilament light is a blood-based biomarker of neuroaxonal injury that can provide insight into perioperative brain vulnerability and injury. Prior studies have suggested that increased baseline and postoperative concentrations of neurofilament light are associated with delirium after noncardiac surgery, but results are inconsistent. Results have not been reported in cardiac surgery patients, who are among those at highest risk for delirium. We hypothesised that perioperative blood concentrations of neurofilament light (both baseline and change from baseline to postoperative day 1) are associated with delirium after cardiac surgery. ⋯ Baseline neurofilament light concentration, but not change from baseline to postoperative day 1, was associated with delirium after cardiac surgery.
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Delayed emergence from general anaesthesia poses a significant perioperative safety hazard. Subanaesthetic doses of ketamine not only deepen anaesthesia but also accelerate recovery from isoflurane anaesthesia; however, the mechanisms underlying this phenomenon remain elusive. Esketamine exhibits a more potent receptor affinity and fewer adverse effects than ketamine and exhibits shorter recovery times after brief periods of anaesthesia. As the paraventricular thalamus (PVT) plays a pivotal role in regulating wakefulness, we studied its role in the emergence process during combined esketamine and isoflurane anaesthesia. ⋯ Our results suggest that esketamine promotes recovery from isoflurane anaesthesia by activating PVTGlu neurones. This mechanism could explain the rapid arousability exhibited upon treatment with a low dose of esketamine.
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Administration of subanaesthetic doses of ketamine during isoflurane anaesthesia has been shown in animals to deepen the anaesthetised state, while accelerating emergence. Duan and colleagues have now shown that the addition of subanaesthetic doses of esketamine to isoflurane has a similar effect of increasing the burst suppression ratio, while accelerating emergence. Using c-Fos expression and fibre photometry, they show that esketamine activates glutamatergic neurones in the paraventricular nucleus of the thalamus, a structure that regulates wakefulness. Chemogenetic inhibition of these neurones attenuates the arousal-promoting effects, suggesting a causal role of the paraventricular nucleus of the thalamus in esketamine-mediated acceleration of recovery from anaesthesia.
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Chronic pain is a common, complex, and challenging condition, for which specialised healthcare is required. We investigated the relationship between multisite chronic pain (MCP) and different disease traits identify safe biomarker interventions that can prevent MCP. ⋯ We established that MCP has an effect on health conditions covering various physiological systems and identified six novel biomarkers for intervention. In particular, S100A6, PTN9, NEUG, and ferritin light chain represent promising targets for MCP prevention, as no significant side-effects were predicted in our study.
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Building on their known ability to influence sleep and arousal, Li and colleagues show that modulating the activity of glutamatergic pedunculopontine tegmental neurones also alters sevoflurane-induced hypnosis. This finding adds support for the shared sleep-anaesthesia circuit hypothesis. However, the expanding recognition of many neuronal clusters capable of modulating anaesthetic hypnosis raises the question of how disparate and anatomically distant sites ultimately interact to coordinate global changes in the state of the brain. Understanding how these individual sites work in concert to disrupt cognition and behaviour is the next challenge for anaesthetic mechanisms research.