Myofascial pain syndrome (MPS) is characterized by myofascial trigger points and fascial constrictions. At present, domestic and foreign scholars have not reached a consensus on the etiology and pathogenesis of MPS. Due to the lack of specific laboratory indicators and imaging evidence, there is no unified diagnostic criteria for MPS, making it easy to confuse with other diseases. The Chinese Association for the Study of Pain organized domestic experts to formulate this Chinese Pain Specialist Consensus on the diagnosis and treatment of MPS. This article reviews relevant domestic and foreign literature on the definition, epidemiology, pathogenesis, clinical manifestation, diagnostic criteria and treatments of MPS. The consensus is intended to normalize the diagnosis and treatment of MPS and be used by first-line doctors, including pain physicians to manage patients with MPS.

Cortical mechanisms that regulate acute or chronic pain remain poorly understood. The prefrontal cortex (PFC) exerts crucial control of sensory and affective behaviors. Recent studies show that activation of the projections from the PFC to the nucleus accumbens (NAc), an important pathway in the brain’s reward circuitry, can produce inhibition of both sensory and affective components of pain. However, it is unclear whether this circuit is endogenously engaged in pain regulation. To answer this question, we disrupted this circuit using an optogenetic strategy. We expressed halorhodopsin in pyramidal neurons from the PFC, and then selectively inhibited the axonal projection from these neurons to neurons in the NAc core. Our results reveal that inhibition of the PFC or its projection to the NAc, heightens both sensory and affective symptoms of acute pain in naïve rats. Inhibition of this corticostriatal pathway also increased nociceptive sensitivity and the aversive response in a chronic neuropathic pain model. Finally, corticostriatal inhibition resulted in a similar aversive phenotype as chronic pain. These results strongly suggest that the projection from the PFC to the NAc plays an important role in endogenous pain regulation, and its impairment contributes to the pathology of chronic pain.

A variety of pain conditions have been found to be associated with depressed mood in clinical studies. Depression-like behaviors have also been described in animal models of persistent or chronic pain. In rodent chronic neuropathic pain models, elevated levels of GluA1 subunits of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the nucleus accumbens (NAc) have been found to inhibit depressive symptoms. However, the effect of reversible post-surgical pain or inflammatory pain on affective behaviors such as depression has not been well characterized in animal models. Neither is it known what time frame is required to elicit AMPA receptor subunit changes in the NAc in various pain conditions. In this study, we compared behavioral and biochemical changes in three pain models: the paw incision (PI) model for post-incisional pain, the Complete Freund’s Adjuvant (CFA) model for persistent but reversible inflammatory pain, and the spared nerve injury (SNI) model for chronic postoperative neuropathic pain. In all three models, rats developed depressive symptoms that were concurrent with the presentation of sensory allodynia. GluA1 levels at the synapses of the NAc, however, differed in these three models. The level of GluA1 subunits of AMPA-type receptors at NAc synapses was not altered in the PI model. GluA1 levels were elevated in the CFA model after a period (7 d) of persistent pain, leading to the formation of GluA2-lacking AMPA receptors. As pain symptoms began to resolve, however, GluA1 levels returned to baseline. Meanwhile, in the SNI model, in which pain persisted beyond 14 days, GluA1 levels began to rise after pain became persistent and remained elevated. In addition, we found that blocking GluA2-lacking AMPA receptors in the NAc further decreased the depressive symptoms only in persistent pain models. Our study shows that while both short-term and persistent pain can trigger depression-like behaviors, GluA1 upregulation in the NAc likely represents a unique adaptive response to minimize depressive symptoms in persistent pain states.

Bone cancer pain (BCP) is common in patients with advanced cancers when the tumors are metastasized to bone. The limited understanding of the complex pathogenesis of BCP leads to the poor effectiveness of clinical treatment. Previous studies have shown that astrocyte-specific connexin (Cx) 43, a forming protein of gap junction (GJ) and hemichannel, and N-methyl-D-aspartate receptors (NMDARs), especially the phosphorylated NMDAR 2B subunit (NR2B) phosphorylated NR2B (p-NR2B) subunit are involved in BCP. However, the relationship between Cx43 and p-NR2B in BCP remains unclear. In the present study, we investigated the expressions of Cx43, glial fibrillary acidic protein (GFAP, a marker of astrocytes), and p-NR2B in the spinal dorsal horn (SDH) in a mouse model of BCP established by intra-femural inoculation of Lewis lung carcinoma (LLC) cells via intrathecal (ith) injection of the GJ/hemichannel blocker carbenoxolone (CARB) and the NMDAR antagonist MK801, respectively. We found that the characters of BCP were mimicked by intra-femural inoculation of LLC cells in mice, and the expressions of Cx43, GFAP and p-NR2B in BCP mice were remarkably increased in a time-dependent manner from day 7 to day 21 after cell inoculation with a gradual aggravate in spontaneous pain and mechanical allodynia. Furthermore, Cx43 was predominantly expressed in the spinal astrocytes. Both CARB and MK801 inhibited the expressions of Cx43, GFAP and p-NR2B with attenuated pain hypersensitivity in BCP mice. In addition, Cx43 was co-localized with p-NR2B in the SDH, which further evidenced the presence of functional NR2B in the spinal astrocytes in BCP mice. Our findings demonstrate that inhibition of Cx43 and p-NR2B in spinal astrocytes could attenuate BCP in mice and Cx43 and p-NR2B in the astrocytes of the SDH may play an important role via their combination action in the development and maintenance of BCP in mice. These results may provide a potential therapeutic target in the prevention and/or treatment of BCP.

Objective: Peripheral nerve stimulation may be an alternative option to treat severe facial pain. We assessed the application of peripheral nerve stimulation for pain management in patients with herpes zoster ophthalmicus. Method: A retrospective analysis was conducted in patients suffering severe facial pain caused by ophthalmic herpetic lesions. We identified the change in pain severity before and after peripheral nerve stimulation for up to 12 months. Results: Eighteen patients were enrolled. Their mean age was 70.8 ± 9.5 years. Fifteen patients presented with subacute pain for 1–3 months, and three patients suffered postherpetic neuralgia. Dramatic relief from pain was achieved in 83% of patients (15 out of 18) upon initial removal of the stimulator, with pain reduction of > 50%. The long-term analgesic effect was reported at the 6- and 12-month follow-ups, with reductions in the visual analog scale of 4.8 ± 1.2 (n = 18) and 5.4 ± 1.4 (n = 11), respectively. The prevalence of postherpetic neuralgia was 7% (1 out of 15) in the subacute pain group. No obvious adverse effect was observed. Conclusion: Peripheral nerve stimulation may be an efficacious and safe approach for pain control in patients with herpes zoster ophthalmicus.

Introduction Percutaneous balloon compression (PBC) is an effective and safe option for patients with trigeminal neuralgia. A pear-shaped balloon can be used to identify the proper compression of the Gasserian ganglion during the PBC procedure. The aim of this study was to evaluate the relationship between the foramen ovale (FO) size and intraluminal pressure of the pear-shaped balloon. Methods Thirteen patients that presented with classical trigeminal neuralgia were scheduled to undertake PBC surgery at the Pain Department of the Third Xiangya Hospital, Central South University, from November 2020 to April 2021. Three-dimensional computed tomography reconstruction of the skull base was performed to capture the feature of FO preoperatively. The intraluminal pressure was continuously recorded when a pear-shaped balloon was obtained during the procedure. Correlation analysis was calculated to determine the association of the intraluminal balloon pressure with FO parameter. Results All participants reported complete relief of pain at discharge. The enduring analgesic effect of PBC was maintained in all patients with a median follow-up up to 5.5 months (range, 3–8 months). The average intraluminal balloon pressure was 161.5 ± 29.4 kPa at the initial compression (P1), and 134.8 ± 21.5 kPa at the ending of compression (P2), respectively. P1 was significantly correlated with the length (r = 0.61, P = 0.024) of FO. Similarly, a significant and positive correlation was observed between P2 and the length (r = 0.63, P = 0.022) of FO. Conclusions Preoperative assessment of FO may be a potential predictor of intraluminal pressure to reach a pear-shaped balloon during PBC treatment. Narrow FO is associated lower intraluminal balloon pressure.