Perioperative multimodal analgesia can reduce the side effects of a high concentration of opioids, improving the comfort of the patient. However, insufficient analgesia of this model has prompted researchers to explore new adjuvant analgesics. Recently, an increasing number of studies have found a low-grade analgesic effect in the clinical application of ultra-short-acting β-adrenergic receptor antagonists, which are conventionally used as pharmacologic agents in the cardiovascular system. The mechanism by which ultra-short-acting β-antagonists exert antinociceptive effects has not been clarified yet. In this review, we intend to address its potential reasons from the side of neurotransmitters, inflammatory cytokines, and signaling pathways, providing theoretical proof for the application of β-adrenergic receptor antagonists in analgesia.

Chronic pain is a major cause of suffering. This interferes with daily functioning and is often accompanied by distress. However, current therapeutic strategies for chronic pain are unsatisfactory because of poor understanding of its mechanisms. Therefore, more comprehensive therapeutic targets must be identified to improve the quality of life of these patients. Myeloid differentiation primary response protein 88 (MyD88) is an adaptor protein of the toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families. Recently, overexpression of MyD88 in the spinal and dorsal root ganglia was observed in multiple pain models, which also revealed that MyD88 plays an important role in the development and maintenance of chronic pain. In this review, we summarized the roles and mechanisms of MyD88 in the progression of different pain models, including chemotherapy-induced peripheral neuropathy (CIPN), diabetic neuropathic pain (DNP), spinal nerve ligation (SNL), chronic constriction injury (CCI), spinal cord injury (SCI) and inflammatory pain.

Rationale: Posterior percutaneous endoscopic cervical discectomy (P-PECD) is a minimally invasive procedure for cervical spine disorders. Although it is associated with less surgical trauma and faster postoperative recovery, serious perioperative thromboembolic complications may still occur. Patient concerns: A 65-year-old woman with cervical disc herniation, right upper limb pain, and multiple comorbidities underwent posterior percutaneous endoscopic cervical discectomy after unsuccessful conservative treatment. On the 2nd postoperative day, she developed dizziness and decreased oxygen saturation. On the 3rd postoperative day, she complained of chest tightness. Diagnoses: Laboratory testing revealed a markedly elevated plasma D-dimer level. Venous color Doppler ultrasound of both lower limbs demonstrated thrombosis in the bilateral calf muscular veins, and computed tomography pulmonary angiography confirmed multiple pulmonary emboli. Interventions: The patient received oxygen therapy, continuous cardiorespiratory monitoring, anticoagulation with low-molecular-weight heparin, and other supportive treatments. She was transferred to the intensive care unit for further monitoring and management. Outcomes: The patient’s respiratory and circulatory status gradually stabilized, and her chest tightness and dizziness resolved. She was subsequently transferred back to the pain ward and discharged in stable condition. Lessons: This case highlights that minimally invasive spinal surgery does not eliminate the risk of perioperative venous thromboembolism. Comprehensive preoperative thrombotic risk assessment, individualized perioperative management of antithrombotic therapy, appropriate thromboprophylaxis, early mobilization, and timely recognition and treatment of suspected APE are important for improving perioperative safety.

Chronic pain, a devastatingly prevalent condition, is increasingly understood not merely as a disorder of neuronal signaling but as a failure of the neuronal infrastructure itself. Central to this paradigm is the microtubule (MT) cytoskeleton, which functions not as a passive scaffold but as a dynamic regulatory hub and the primary railway for intracellular transport. This review provides a comprehensive mechanistic analysis of how the dysregulation of microtubule dynamics drives the initiation and maintenance of chronic pain. We dissect the change in microtubule dynamics across diverse pain etiologies, summarizing how diverse insults lead to either pathological hyper-stabilization or catastrophic disassembly of the microtubule network. Finally, we explore emerging therapeutic strategies that move beyond broad-spectrum microtubule modulators to target specific regulatory proteins such as Histone deacetylase 6 (HDAC6), Collapsin Response Mediator Protein 2 (CRMP2), Heat Shock Protein 27 (HSP27), and motor proteins (kinesins and dyneins). We propose that restoring cytoskeletal homeostasis, by which we recalibrate the tubulin code or rescue motor-driven transport, represents a paradigm-shifting approach to pain management. By moving the therapeutic focus from blocking electrical signals to repairing the structural and logistical integrity of the nociceptive neuron, these strategies hold the potential to modify the underlying disease process, offering a new frontier for analgesic development.