Aging is a pivotal risk factor for intervertebral disc degeneration(IVDD)and chronic low back pain(LBP).The restoration of aging nucleus pulposus cells(NPCs)to a youthful epigenetic state is crucial for IVDD treatment...Aging is a pivotal risk factor for intervertebral disc degeneration(IVDD)and chronic low back pain(LBP).The restoration of aging nucleus pulposus cells(NPCs)to a youthful epigenetic state is crucial for IVDD treatment,but remains a formidable challenge.Here,we proposed a strategy to partially reprogram and reinstate youthful epigenetics of senescent NPCs by delivering a plasmid carrier that expressed pluripotency-associated genes(Oct4,Klf4 and Sox2)in Cavin2-modified exosomes(OKS@M-Exo)for treatment of IVDD and alleviating LBP.The functional OKS@M-Exo efficaciously alleviated senescence markers(p16^(INK4a),p21^(CIP1)and p53),reduced DNA damage and H4K20me3 expression,as well as restored proliferation ability and metabolic balance in senescent NPCs,as validated through in vitro experiments.In a rat model of IVDD,OKS@M-Exo maintained intervertebral disc height,nucleus pulposus hydration and tissue structure,effectively ameliorated IVDD via decreasing the senescence markers.Additionally,OKS@MExo reduced nociceptive behavior and downregulated nociception markers,indicating its efficiency in alleviating LBP.The transcriptome sequencing analysis also demonstrated that OKS@M-Exo could decrease the expression of age-related pathways and restore cell proliferation.Collectively,reprogramming by the OKS@M-Exo to restore youthful epigenetics of senescent NPCs may hold promise as a therapeutic platform to treat IVDD.展开更多
Background Tactile and mechanical pain are crucial to our interaction with the environment,yet the underpinning molecular mechanism is still elusive.Endophilin A2(EndoA2)is an evolutionarily conserved protein that is ...Background Tactile and mechanical pain are crucial to our interaction with the environment,yet the underpinning molecular mechanism is still elusive.Endophilin A2(EndoA2)is an evolutionarily conserved protein that is documented in the endocytosis pathway.However,the role of EndoA2 in the regulation of mechanical sensitivity and its underlying mechanisms are currently unclear.Methods Male and female C57BL/6 mice(8–12 weeks)and male cynomolgus monkeys(7–10 years old)were used in our experiments.Nerve injury-,inflammatory-,and chemotherapy-induced pathological pain models were established for this study.Behavioral tests of touch,mechanical pain,heat pain,and cold pain were performed in mice and nonhuman primates.Western blotting,immunostaining,co-immunoprecipitation,proximity ligation and patch-clamp recordings were performed to gain insight into the mechanisms.Results The results showed that EndoA2 was primarily distributed in neurofilament-200-positive(NF200+)medium-to-large diameter dorsal root ganglion(DRG)neurons of mice and humans.Loss of EndoA2 in mouse NF200+DRG neurons selectively impaired the tactile and mechanical allodynia.Furthermore,EndoA2 interacted with the mechanically sensitive ion channel Piezo2 and promoted the membrane trafficking of Piezo2 in DRG neurons.Moreover,as an adaptor protein,EndoA2 also bound to kinesin family member 5B(KIF5B),which was involved in the EndoA2-mediated membrane trafficking process of Piezo2.Loss of EndoA2 in mouse DRG neurons damaged Piezo2-mediated rapidly adapting mechanically activated currents,and re-expression of EndoA2 rescued the MA currents.In addition,interference with EndoA2 also suppressed touch sensitivity and mechanical hypersensitivity in nonhuman primates.Conclusions Our data reveal that the KIF5B/EndoA2/Piezo2 complex is essential for Piezo2 trafficking and for sustaining transmission of touch and mechanical hypersensitivity signals.EndoA2 regulates touch and mechanical allodynia via kinesin-mediated Piezo2 trafficking in sensory neurons.Our findings identify a potential new target for the treatment of mechanical pain.展开更多
Toll-like receptors （TLRs） are germline-encoded pattern-recognition receptors that initiate innate immune re- sponses by recognizing molecular structures shared by a wide range of pathogens, known as pathogen-associ...Toll-like receptors （TLRs） are germline-encoded pattern-recognition receptors that initiate innate immune re- sponses by recognizing molecular structures shared by a wide range of pathogens, known as pathogen-associated molecular patterns （PAMPs）. After tissue injury or cellular stress, TLRs also detect endogenous ligands known as danger-associated molecular patterns （DAMPs）. TLRs are expressed in both non-neuronal and neuronal cell types in the central nervous system （CNS） and contribute to both infectious and non-infectious disorders in the CNS. Following tissue insult and nerve injury, TLRs （such as TLR2, TLR3, and TLR4） induce the activation of microglia and astrocytes and the production of the proinflammatory cytokines in the spinal cord, leading to the development and maintenance of inflammatory pain and neu- ropathic pain. In particular, primary sensory neurons, such as nociceptors, express TLRs （e.g., TLR4 and TLR7） to sense exogenous PAMPs and endogenous DAMPs released after tissue injury and cellular stress. These neuronal TLRs are new players in the processing of pain and itch by increasing the excitability of primary sensory neurons. Given the prevalence of chronic pain and itch and the suffering of affected people, insights into TLR signaling in the nervous system will open a new avenue for the management of clinical pain and itch.展开更多
Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain...Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain follow- ing intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID （a caspase-6 inhibitor） and the astroglial inhibitors L-α-aminoadipate （L-AA, an astroglial toxin） and car- benoxolone （a connexin 43 inhibitor）, as well as U0126 （an ERK kinase inhibitor） and D-JNKI-1 （a c-Jun N-terminal kinase inhibitor）. We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast, intrathecal L-AA reduced neuropathic pain but not inflam- matory pain in both sexes. Intrathecal U0126 and D-JNKI- 1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain.展开更多
Considerable clinical evidence has demonstrated that the prevalence and severity of many chronic pain syndromes differ across sex,and are more predominant in womenthan inmen[l]But most preclinical research on chronic ...Considerable clinical evidence has demonstrated that the prevalence and severity of many chronic pain syndromes differ across sex,and are more predominant in womenthan inmen[l]But most preclinical research on chronic pain mechanisms has been performed primarily in male animals.It is generally understood that inflammatory responses in the peripheral and central nervous systems are critical for chronic pain[2,3],Given that sex dimorphism influences immunity in various diseases[4].展开更多
Low back pain(LBP),as a leading cause of disability,is a common musculoskeletal disorder that results in major social and economic burdens.Recent research has identified inflammation and related signaling pathways as ...Low back pain(LBP),as a leading cause of disability,is a common musculoskeletal disorder that results in major social and economic burdens.Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration,a significant contributor to LBP.Inflammatory mediators also play an indispensable role in discogenic LBP.The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies.Here,an overview of the advances in inflammation-related pain in disc degeneration is provided,with a discussion on the role of inflammation in IVD degeneration and pain induction.Puncture models,mechanical models,and spontaneous models as the main animal models to study painful disc degeneration are discussed,and the underlying signaling pathways are summarized.Furthermore,potential drug candidates,either under laboratory investigation or undergoing clinical trials,to suppress discogenic LBP by eliminating inflammation are explored.We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.展开更多
Abstract The voltage-gated Na＋ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody （SVmab） reduces Na＋ currents and pain an...Abstract The voltage-gated Na＋ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody （SVmab） reduces Na＋ currents and pain and itch responses in mice. Here, we investigated whether recom- binant SVmab （rSVmab） binds to and blocks Nav1.7 similar to SVmab. ELISA tests revealed that SVmab was capable of binding to Nav1.7-expressing HEK293 cells, mouse DRG neurons, human nerve tissue, and the voltagesensor domain II of Nav1.7. In contrast, rSVmab showed no or weak binding to Nav1.7 in these tests. Patch-clamp recordings showed that SVmab, but not rSVmab, markedly inhibited Na＋ currents in Nav1.7-expressing HEK293 cells. Notably, electrical field stimulation increased the blocking activity of SVmab and rSVmab in Nav1.7- expressing HEK293 cells. SVmab was more effective than rSVmab in inhibiting paclitaxel-induced mechanical allodynia. SVmab also bound to human DRG neurons and inhibited their Na＋ currents. Finally, potential reasons for the differential efficacy of SVmab and rSVmab and future directions are discussed.展开更多
Neuropathic pain(NPP)is a kind of pain caused by disease or damage impacting the somatosensory system.Ion channel drugs are the main treatment for NPP;however,their irregular usage leads to unsatisfactory pain relief....Neuropathic pain(NPP)is a kind of pain caused by disease or damage impacting the somatosensory system.Ion channel drugs are the main treatment for NPP;however,their irregular usage leads to unsatisfactory pain relief.To regulate the treatment of NPP with ion channel drugs in clinical practice,the Chinese Association for the Study of Pain organized first-line pain management experts from China to write an expert consensus as the reference for the use of ion channels drugs.Here,we reviewed the mechanism and characteristics of sodium and calcium channel drugs,and developed recommendations for the therapeutic principles and clinical practice for carbamazepine,oxcarbazepine,lidocaine,bulleyaconitine A,pregabalin,and gabapentin.We hope this guideline provides guidance to clinicians and patients on the use of ion channel drugs for the management of NPP.展开更多
Chronic pain is a major health problem world-wide. According to a recent report in the New England Journal of Medicine , the prevalence of pain in the United States is striking： more than 116 million Americans have p...Chronic pain is a major health problem world-wide. According to a recent report in the New England Journal of Medicine , the prevalence of pain in the United States is striking： more than 116 million Americans have pain that persist for weeks to years. Chronic pain is characterized as inflammatory pain, cancer pain, and neuropathic pain, and can result from such conditions as arthritis, cancer, diabe- tes, low back injury, surgery, viral infection, spinal cord injury, and stroke.展开更多
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...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.展开更多
Chronic musculoskeletal pain(CMP)is a common occurrence in clinical practice and there are a variety of options for the treatment of it.However,the pharmacological therapy is still considered to be a primary treatment...Chronic musculoskeletal pain(CMP)is a common occurrence in clinical practice and there are a variety of options for the treatment of it.However,the pharmacological therapy is still considered to be a primary treatment.The recent years have witnessed the emergence of opioid crisis,yet there are no relevant guidelines on how to treat CMP with non-opioid analgesics properly.The Chinese Medical Association for the Study of Pain convened a panel meeting to develop clinical practice consensus for the treatment of CMP with non-opioid analgesics.The purpose of this consensus is to present the application of nonsteroidal antiinflammatory drugs,serotonin norepinephrine reuptake inhibitors,serotonin and norepinephrine reuptake inhibitors,muscle relaxants,ion channel drugs and topical drugs in CMP.展开更多
Cervicogenic headache(CEH)has been recognized as a unique category of headache that can be difficult to diagnose and treat.In China,CEH patients are managed by many different specialties,and the treatment plans remain...Cervicogenic headache(CEH)has been recognized as a unique category of headache that can be difficult to diagnose and treat.In China,CEH patients are managed by many different specialties,and the treatment plans remain controversial.Therefore,there is a great need for comprehensive evidence-based Chinese experts’recommendations for the management of CEH.The Chinese Association for the Study of Pain asked an expert panel to develop recommendations for a series of questions that are essential for daily clinical management of patients with CEH.A group of multidisciplinary Chinese Association for the Study of Pain experts identified the clinically relevant topics in CEH.A systematic review of the literature was performed,and evidence supporting the benefits and harms for the management of CEH was summarized.Twenty-four recommendations were finally developed through expert consensus voting for evidence quality and recommendation strength.We hope this guideline provides direction for clinicians and patients making treatment decisions for the management of CEH.展开更多
基金supported by the Ministry of Science and Technology of China(2020YFA0908900)National Natural Science Foundation of China(21935011 and 82072490)+1 种基金Shenzhen Science and Technology Innovation Commission(KQTD20200820113012029 and KJZD20230923114612025)Guangdong Provincial Key Laboratory of Advanced Biomaterials(2022B1212010003).
文摘Aging is a pivotal risk factor for intervertebral disc degeneration(IVDD)and chronic low back pain(LBP).The restoration of aging nucleus pulposus cells(NPCs)to a youthful epigenetic state is crucial for IVDD treatment,but remains a formidable challenge.Here,we proposed a strategy to partially reprogram and reinstate youthful epigenetics of senescent NPCs by delivering a plasmid carrier that expressed pluripotency-associated genes(Oct4,Klf4 and Sox2)in Cavin2-modified exosomes(OKS@M-Exo)for treatment of IVDD and alleviating LBP.The functional OKS@M-Exo efficaciously alleviated senescence markers(p16^(INK4a),p21^(CIP1)and p53),reduced DNA damage and H4K20me3 expression,as well as restored proliferation ability and metabolic balance in senescent NPCs,as validated through in vitro experiments.In a rat model of IVDD,OKS@M-Exo maintained intervertebral disc height,nucleus pulposus hydration and tissue structure,effectively ameliorated IVDD via decreasing the senescence markers.Additionally,OKS@MExo reduced nociceptive behavior and downregulated nociception markers,indicating its efficiency in alleviating LBP.The transcriptome sequencing analysis also demonstrated that OKS@M-Exo could decrease the expression of age-related pathways and restore cell proliferation.Collectively,reprogramming by the OKS@M-Exo to restore youthful epigenetics of senescent NPCs may hold promise as a therapeutic platform to treat IVDD.
基金National Natural Science Foundation of China(82271241 and 82001172 to XLZ,81801112 to MXX)Guangdong Basic and Applied Basic Research Foundation(2022A1515012389 to MXX,2022A1515012543 to RCL)+2 种基金Young Talent Support Project of Guangzhou Association for Science and Technology(QT20220101169 to XLZ)Excellent Young Talents Project of Guangdong Provincial People’s Hospital,Guangdong Academy of Medical Sciences(KY012021188 to XLZ)Science and Technology Projects in Guangzhou(202201010792 to RCL)。
文摘Background Tactile and mechanical pain are crucial to our interaction with the environment,yet the underpinning molecular mechanism is still elusive.Endophilin A2(EndoA2)is an evolutionarily conserved protein that is documented in the endocytosis pathway.However,the role of EndoA2 in the regulation of mechanical sensitivity and its underlying mechanisms are currently unclear.Methods Male and female C57BL/6 mice(8–12 weeks)and male cynomolgus monkeys(7–10 years old)were used in our experiments.Nerve injury-,inflammatory-,and chemotherapy-induced pathological pain models were established for this study.Behavioral tests of touch,mechanical pain,heat pain,and cold pain were performed in mice and nonhuman primates.Western blotting,immunostaining,co-immunoprecipitation,proximity ligation and patch-clamp recordings were performed to gain insight into the mechanisms.Results The results showed that EndoA2 was primarily distributed in neurofilament-200-positive(NF200+)medium-to-large diameter dorsal root ganglion(DRG)neurons of mice and humans.Loss of EndoA2 in mouse NF200+DRG neurons selectively impaired the tactile and mechanical allodynia.Furthermore,EndoA2 interacted with the mechanically sensitive ion channel Piezo2 and promoted the membrane trafficking of Piezo2 in DRG neurons.Moreover,as an adaptor protein,EndoA2 also bound to kinesin family member 5B(KIF5B),which was involved in the EndoA2-mediated membrane trafficking process of Piezo2.Loss of EndoA2 in mouse DRG neurons damaged Piezo2-mediated rapidly adapting mechanically activated currents,and re-expression of EndoA2 rescued the MA currents.In addition,interference with EndoA2 also suppressed touch sensitivity and mechanical hypersensitivity in nonhuman primates.Conclusions Our data reveal that the KIF5B/EndoA2/Piezo2 complex is essential for Piezo2 trafficking and for sustaining transmission of touch and mechanical hypersensitivity signals.EndoA2 regulates touch and mechanical allodynia via kinesin-mediated Piezo2 trafficking in sensory neurons.Our findings identify a potential new target for the treatment of mechanical pain.
基金supported by the US National Institutes of Health (R01-DE17794, R01-NS54362 and R01-NS67686)
文摘Toll-like receptors （TLRs） are germline-encoded pattern-recognition receptors that initiate innate immune re- sponses by recognizing molecular structures shared by a wide range of pathogens, known as pathogen-associated molecular patterns （PAMPs）. After tissue injury or cellular stress, TLRs also detect endogenous ligands known as danger-associated molecular patterns （DAMPs）. TLRs are expressed in both non-neuronal and neuronal cell types in the central nervous system （CNS） and contribute to both infectious and non-infectious disorders in the CNS. Following tissue insult and nerve injury, TLRs （such as TLR2, TLR3, and TLR4） induce the activation of microglia and astrocytes and the production of the proinflammatory cytokines in the spinal cord, leading to the development and maintenance of inflammatory pain and neu- ropathic pain. In particular, primary sensory neurons, such as nociceptors, express TLRs （e.g., TLR4 and TLR7） to sense exogenous PAMPs and endogenous DAMPs released after tissue injury and cellular stress. These neuronal TLRs are new players in the processing of pain and itch by increasing the excitability of primary sensory neurons. Given the prevalence of chronic pain and itch and the suffering of affected people, insights into TLR signaling in the nervous system will open a new avenue for the management of clinical pain and itch.
基金supported by NIH R01 grants DE17794,DE22743,and NS87988 to RRJsupported by NIH T32 2T32GM008600a Foundation of Anesthesia Education and Research Fellowship
文摘Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain follow- ing intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID （a caspase-6 inhibitor） and the astroglial inhibitors L-α-aminoadipate （L-AA, an astroglial toxin） and car- benoxolone （a connexin 43 inhibitor）, as well as U0126 （an ERK kinase inhibitor） and D-JNKI-1 （a c-Jun N-terminal kinase inhibitor）. We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast, intrathecal L-AA reduced neuropathic pain but not inflam- matory pain in both sexes. Intrathecal U0126 and D-JNKI- 1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain.
基金supported by National Natural Science Foundation of China(81771204)the Natural Science Foundation of Guangdong Province(2019A1515011838,2020A1515010204,2021A1515011742,and 2021A1515011742).
文摘Considerable clinical evidence has demonstrated that the prevalence and severity of many chronic pain syndromes differ across sex,and are more predominant in womenthan inmen[l]But most preclinical research on chronic pain mechanisms has been performed primarily in male animals.It is generally understood that inflammatory responses in the peripheral and central nervous systems are critical for chronic pain[2,3],Given that sex dimorphism influences immunity in various diseases[4].
基金the National Natural Science Foundation of China(81772386,81702191,81572175,81371984,and 81071511)the Guangdong-Hong Kong Joint Innovation Project of Guangdong Province(2017A050506019)the Natural Science Foundation of Guangdong Province,China(2020A1515011031).
文摘Low back pain(LBP),as a leading cause of disability,is a common musculoskeletal disorder that results in major social and economic burdens.Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration,a significant contributor to LBP.Inflammatory mediators also play an indispensable role in discogenic LBP.The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies.Here,an overview of the advances in inflammation-related pain in disc degeneration is provided,with a discussion on the role of inflammation in IVD degeneration and pain induction.Puncture models,mechanical models,and spontaneous models as the main animal models to study painful disc degeneration are discussed,and the underlying signaling pathways are summarized.Furthermore,potential drug candidates,either under laboratory investigation or undergoing clinical trials,to suppress discogenic LBP by eliminating inflammation are explored.We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.
基金supported by National Institutes of Health Grants R01NS89479,R01NS045594 and ROINS055860
文摘Abstract The voltage-gated Na＋ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody （SVmab） reduces Na＋ currents and pain and itch responses in mice. Here, we investigated whether recom- binant SVmab （rSVmab） binds to and blocks Nav1.7 similar to SVmab. ELISA tests revealed that SVmab was capable of binding to Nav1.7-expressing HEK293 cells, mouse DRG neurons, human nerve tissue, and the voltagesensor domain II of Nav1.7. In contrast, rSVmab showed no or weak binding to Nav1.7 in these tests. Patch-clamp recordings showed that SVmab, but not rSVmab, markedly inhibited Na＋ currents in Nav1.7-expressing HEK293 cells. Notably, electrical field stimulation increased the blocking activity of SVmab and rSVmab in Nav1.7- expressing HEK293 cells. SVmab was more effective than rSVmab in inhibiting paclitaxel-induced mechanical allodynia. SVmab also bound to human DRG neurons and inhibited their Na＋ currents. Finally, potential reasons for the differential efficacy of SVmab and rSVmab and future directions are discussed.
基金Supported by Sichuan Science and Technology Program,No.2018SZ0386。
文摘Neuropathic pain(NPP)is a kind of pain caused by disease or damage impacting the somatosensory system.Ion channel drugs are the main treatment for NPP;however,their irregular usage leads to unsatisfactory pain relief.To regulate the treatment of NPP with ion channel drugs in clinical practice,the Chinese Association for the Study of Pain organized first-line pain management experts from China to write an expert consensus as the reference for the use of ion channels drugs.Here,we reviewed the mechanism and characteristics of sodium and calcium channel drugs,and developed recommendations for the therapeutic principles and clinical practice for carbamazepine,oxcarbazepine,lidocaine,bulleyaconitine A,pregabalin,and gabapentin.We hope this guideline provides guidance to clinicians and patients on the use of ion channel drugs for the management of NPP.
文摘Chronic pain is a major health problem world-wide. According to a recent report in the New England Journal of Medicine , the prevalence of pain in the United States is striking： more than 116 million Americans have pain that persist for weeks to years. Chronic pain is characterized as inflammatory pain, cancer pain, and neuropathic pain, and can result from such conditions as arthritis, cancer, diabe- tes, low back injury, surgery, viral infection, spinal cord injury, and stroke.
文摘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.
文摘Chronic musculoskeletal pain(CMP)is a common occurrence in clinical practice and there are a variety of options for the treatment of it.However,the pharmacological therapy is still considered to be a primary treatment.The recent years have witnessed the emergence of opioid crisis,yet there are no relevant guidelines on how to treat CMP with non-opioid analgesics properly.The Chinese Medical Association for the Study of Pain convened a panel meeting to develop clinical practice consensus for the treatment of CMP with non-opioid analgesics.The purpose of this consensus is to present the application of nonsteroidal antiinflammatory drugs,serotonin norepinephrine reuptake inhibitors,serotonin and norepinephrine reuptake inhibitors,muscle relaxants,ion channel drugs and topical drugs in CMP.
文摘Cervicogenic headache(CEH)has been recognized as a unique category of headache that can be difficult to diagnose and treat.In China,CEH patients are managed by many different specialties,and the treatment plans remain controversial.Therefore,there is a great need for comprehensive evidence-based Chinese experts’recommendations for the management of CEH.The Chinese Association for the Study of Pain asked an expert panel to develop recommendations for a series of questions that are essential for daily clinical management of patients with CEH.A group of multidisciplinary Chinese Association for the Study of Pain experts identified the clinically relevant topics in CEH.A systematic review of the literature was performed,and evidence supporting the benefits and harms for the management of CEH was summarized.Twenty-four recommendations were finally developed through expert consensus voting for evidence quality and recommendation strength.We hope this guideline provides direction for clinicians and patients making treatment decisions for the management of CEH.
