or lidocaine as evidence-informed options for selected patients); Monitor (use the PSQI and ISI for preoperative screening and longer-term assessment; use brief validated scales, supplemented by actigraphy or wearable devices where available, during the early postoperative period; and reserve polysomnography for selected high-risk patients or research settings); and Recover (implement multimodal analgesia, opioid-sparing strategies, and regional anesthesia, together with nonpharmacological interventions such as CBT-I, sleep hygiene, reduction of nighttime noise and light, environmental optimization, and early mobilization). This integrated approach is intended to improve perioperative sleep quality, alleviate pain, reduce opioid consumption, accelerate recovery, and mitigate the risk of chronic postsurgical pain. CBT-I cognitive behavioral therapy for insomnia, ISI insomnia severity index; N3 stage N3 non-rapid eye movement sleep (deep sleep), PSQI Pittsburgh Sleep Quality Index, REM rapid
Lidocaine is a well-established amide local anaesthetic and antiarrhythmic agent. Its perioperative use as an intravenous infusion has expanded rapidly, with growing evidence supporting its benefits for postoperative analgesia and recovery. However, wider adoption remains limited by three issues: heterogeneous dosing and infusion protocols, inconsistent efficacy across clinical settings, and inadequate risk stratification for vulnerable patients. To promote the safe, standardized, and evidence-based use of intravenous lidocaine, the Youth Group of the Chinese Society of Anesthesiology and the Perioperative Medicine Professional Committee of the Chinese Medical Education Association convened a multidisciplinary expert panel. Following international guideline-development methodology, the panel developed this consensus based on the best available peer-reviewed evidence and expert clinical experience. The consensus provides 12 evidence-based recommendations concerning infusion regimens and clinical indications, including the prevention of propofol injection pain, attenuation of the hemodynamic stress response to tracheal intubation, management of acute postoperative pain, opioid sparing, prevention of postoperative nausea and vomiting and postoperative pulmonary complications, improvement of the quality of recovery, and sedation during colonoscopy. It also outlines absolute and relative contraindications and key principles for safety monitoring and adverse-event management. This consensus aims to provide practical guidance on the rational use of intravenous lidocaine in adults throughout the perioperative period, including during related invasive procedures. Practice guideline registration PREPARE-2025CN653.
Pain usually resolves as tissue inflammation subsides and sensory pathways return toward their pre-injury operating range. In some patients, nociceptive output persists after the initial lesion has stabilized. This Mini Review examines whether a durable senescence-like state in dorsal root ganglion (DRG) sensory neurons may contribute to failed pain resolution. We searched PubMed, Web of Science, and Scopus for English-language articles published from January 2016 to July 2026. Earlier mechanistic studies were included when they informed the central concepts. We prioritized original studies that identified the relevant cell type, assessed multiple senescence-associated features, incorporated temporal or functional measurements, or tested reversibility. Evidence from glia and peripheral tissues was included only when it clarified the neuronal hypothesis. Aging and nerve injury are associated with senescence-like features in subsets of mouse DRG neurons. The strongest direct evidence combines multiple markers with altered firing and behavioral improvement after senolytic treatment, although the intervention was not neuron-specific. Single-cell studies identify senescence-associated transcriptional programs in nociceptor subsets. Studies of persistent excitability, local neuron-glia signaling, and mitochondrial dysfunction provide candidate links to failed pain resolution, but do not establish neuronal senescence as their cause. Senescence-like DRG neurons should be regarded as a testable contributor to failed pain resolution, not an established cause of chronic pain. Longitudinal studies must connect a composite neuronal state to sensory output, recovery trajectories, and selective reversal. Defined perioperative injuries provide a particularly observable model in which the timing of injury and divergence of recovery can be followed prospectively.
Post-infectious persistent pain (PIPP) is a common long-term outcome of infection, but the link between transient infection and persistent pain remains unclear. Traditional explanations, such as tissue injury, residual inflammation, and nerve damage, do not fully explain pain persistence after pathogen clearance. This review proposes that signaling between pathogen-associated molecular patterns and pattern recognition receptors (PAMP–PRR) is a key mechanistic bridge from acute infection to persistent pain. Microbial ligands from bacterial, viral, fungal, and parasitic pathogens activate PRRs in immune cells, sensory neurons, glia, and epithelial cells, triggering shared neuroimmune programs that include inflammatory amplification, neuron–immune crosstalk, glial activation, and sensitization of peripheral and central pain pathways. Persistent microbial products, viral latency, repeated antigen exposure, and trained immunity may maintain these circuits and promote a shift from PAMP-driven responses to damage-associated molecular pattern (DAMP)-mediated sterile neuroinflammation. These observations reframe PIPP as a dynamic neuroimmune disorder and support biomarker-informed, stage-specific therapies aimed at restoring neuroimmune homeostasis while preserving host defense.
