OBJECTIVE: The objective of this study is to summarize and analyze the brain signal patterns of empathy for pain caused by facial expressions of pain utilizing activation likelihood estimation, a meta-analysis method....OBJECTIVE: The objective of this study is to summarize and analyze the brain signal patterns of empathy for pain caused by facial expressions of pain utilizing activation likelihood estimation, a meta-analysis method. DATA SOURCES: Studies concerning the brain mechanism were searched from the Science Citation Index, Science Direct, PubMed, DeepDyve, Cochrane Library, SinoMed, Wanfang, VIP, China National Knowledge Infrastructure, and other databases, such as SpringerLink, AMA, Science Online, Wiley Online, were collected. A time limitation of up to 13 December 2016 was applied to this study. DATA SELECTION: Studies presenting with all of the following criteria were considered for study inclusion: Use of functional magnetic resonance imaging, neutral and pained facial expression stimuli, involvement of adult healthy human participants over 18 years of age, whose empathy ability showed no difference from the healthy adult, a painless basic state, results presented in Talairach or Montreal Neurological Institute coordinates, multiple studies by the same team as long as they used different raw data. OUTCOME MEASURES: Activation likelihood estimation was used to calculate the combined main activated brain regions under the stimulation of pained facial expression. RESULTS: Eight studies were included, containing 178 subjects. Meta-analysis results suggested that the anterior cingulate cortex(BA32), anterior central gyrus(BA44), fusiform gyrus, and insula(BA13) were activated positively as major brain areas under the stimulation of pained facial expression. CONCLUSION: Our study shows that pained facial expression alone, without viewing of painful stimuli, activated brain regions related to pain empathy, further contributing to revealing the brain's mechanisms of pain empathy.展开更多
Knee osteoarthritis(KOA)represents one of the most common causes of chronic pain.The high prevalence and disability rates of KOA impose a severe burden on both individuals and society.In contrast to cutaneous pain,KOA...Knee osteoarthritis(KOA)represents one of the most common causes of chronic pain.The high prevalence and disability rates of KOA impose a severe burden on both individuals and society.In contrast to cutaneous pain,KOA-induced joint pain is characterized as a deep tissue pain that potentially involves distinct subgroups of peripheral sensory neurons and central processing mechanisms.Furthermore,KOA pain is closely related to locomotion activity.Impaired sensorimotor integration and pain mutually reinforce each other in KOA,forming a vicious cycle that exacerbates disease progression.In this review,we highlight the key differences between KOA pain and cutaneous pain,and the latter has been extensively studied in the pain field.We hope to offer new insights into the central mechanisms and development of new treatment strategies for KOA based on the interactions between impaired sensorimotor integration and chronic joint pain.展开更多
Cancer pain is one of the most prevalent and debilitating symptoms in patients with advanced malignancies,arising from multifactorial mechanisms involving peripheral,central,and systemic pathways.Conventional analgesi...Cancer pain is one of the most prevalent and debilitating symptoms in patients with advanced malignancies,arising from multifactorial mechanisms involving peripheral,central,and systemic pathways.Conventional analgesics,including opioids and nonsteroidal anti-inflammatory drugs,are often limited by their insufficient efficacy,tolerance,and risk of dependence.Traditional Chinese Medicine(TCM),characterized by its multi-component,multi-target,and systemic regulatory properties,has shown promising potential in cancer pain management.This review provides a comprehensive overview of the clinical classification and underlying mechanisms of cancer pain(including nerve infiltration,dysregulation of inflammatory mediators and ion channels,central sensitization,neuro-immune crosstalk,metabolic reprogramming,and gut-brain axis impairment),as well as the analgesic effects of representative TCM agents in cancer pain management.For example,bioactive components such as tetrahydroberberine,levo-tetrahydropalmatine,and piperine exert analgesic effects,thereby improving the quality of life of patients by inhibiting inflammatory cascades,regulating neurotransmitter systems,and preserving neural integrity.Commonly used preclinical models,including bone cancer pain,pancreatic cancer pain,and chemotherapy-induced peripheral neuropathy models,are summarized for their utility in mechanistic studies and efficacy evaluations.This review also discusses the current limitations of clinical evidence,such as small sample sizes,short follow-up periods,and limited translation from animal models,alongside major challenges in standardization,mechanistic elucidation,and clinical trial design.Future directions should focus on precise pain phenotyping,integrated multi-target interventions,rigorous efficacy safety validation,and innovations in drug delivery to facilitate the standardization and global adoption of TCM in cancer pain management.展开更多
Persistent postsurgical pain is a major clinical concern,especially in the aging population,who represent a growing proportion of surgical patients.Although age is a known pain risk factor,the mechanisms driving age-r...Persistent postsurgical pain is a major clinical concern,especially in the aging population,who represent a growing proportion of surgical patients.Although age is a known pain risk factor,the mechanisms driving age-related vulnerability to chronic postoperative pain remain poorly understood.This study aims to investigate how aging influences the resolution of postoperative pain and to elucidate the roles of microglial activation and synaptic remodeling in the spinal dorsal horn.A plantar incision model in young(3-month-old)and aged(18-month-old)male and female mice was used to mimic postoperative pain conditions.Mechanical and thermal hypersensitivity at various postoperative intervals were assessed by von Frey and Hargreaves tests.Microglial activation and inhibitory/excitatory synaptic densities in the spinal dorsal horn were evaluated using immunofluorescence and 3D reconstruction with Imaris software.On postoperative day(POD)3,both age groups exhibited reduced pain thresholds on the ipsilateral side,along with microglial activation in the dorsal horn.On POD 7,pain thresholds in young mice had returned to baseline with no significant microglial activation,while aged mice showed sustained reduction in pain thresholds,continuous microglial activation,and significant loss of inhibitory synapses without detectable changes in excitatory synapse density.These findings are consistent across both sexes,with no sex-related differences.Collectively,these results suggest that aging is associated with persistent postoperative pain,which correlates with microglial activation and inhibitory synapse loss.These insights advance our understanding of age-related pain vulnerability and may inform the development of more effective,targeted,and age-specific therapeutic strategies to prevent or alleviate persistent postoperative pain in elderly patients.展开更多
Pseudounipolar neurons in the dorsal root ganglia(DRG),as the central nodes of primary sensory afferents,possess a distinctive T-junction that is not merely a morphological peculiarity but also performs complex roles ...Pseudounipolar neurons in the dorsal root ganglia(DRG),as the central nodes of primary sensory afferents,possess a distinctive T-junction that is not merely a morphological peculiarity but also performs complex roles in rapid,multiplexed shunting and regulation of sensory signals.This specialized geometry enables separation,filtering,and feedback regulation of neuronal signals,thereby coordinating peripheral and central responses at multiple levels.Recent advances,including spatial transcriptomics,single-cell sequencing,super-resolution microscopy,organoid models,and novel electrophysiological methods,have permitted more precise dissection of the T-junction's molecular composition,ion-channel distribution,and electrophysiological properties.Here,we review current knowledge of the T-junction's developmental regulation and multilayered molecular networks,and we detail its functional alterations in both physiological signaling and pathological pain states,with particular emphasis on ion-channel modulation,signal attenuation,and selective transmission mechanisms.Finally,we discuss contemporary pain-intervention approaches and prospects for precision-targeted therapies,aiming to provide a theoretical foundation for future studies in pain physiology and clinical translation.展开更多
While acute nociceptive pain is a crucial warning system that protects us from injury or disease,chronic pain is not protective,but a pathological condition.As such,it is now recognized as a disease in its own right,w...While acute nociceptive pain is a crucial warning system that protects us from injury or disease,chronic pain is not protective,but a pathological condition.As such,it is now recognized as a disease in its own right,which major classes refer to inflammatory,neuropathic,and idiopathic pain.It is frequent,with up to a third of the population that may suffer at one point from chronic pain.It is often associated with other pathologies,including sleep disorders,anxiety,depression,and is still difficult to treat.It thus represents a significant burden in terms of health and societal impact(Tracey et al.,2019).The mechanisms of chronic pain involve multiple diverse pathways in both the peripheral and central nervous systems(CNS),reflecting its multifaceted biology.Indeed,research over the past decades has established that central sensitization(enhancement in the function of neurons and circuits in central nociceptive pathways),in particular within the dorsal horn,the first central relay of nociceptive inputs plays a key role in the chronicity of pain(Latremoliere and Woolf,2009).展开更多
Neuropathic pain is a complex and debilitating condition caused by lesions or dysfunction within the somatosensory nervous system.Affecting an estimated 7%-10%of the global population,it presents with spontaneous pain...Neuropathic pain is a complex and debilitating condition caused by lesions or dysfunction within the somatosensory nervous system.Affecting an estimated 7%-10%of the global population,it presents with spontaneous pain,hyperalgesia,and allodynia,often accompanied by long-term emotional and cognitive consequences,such as depression and anxiety,which result in a reduced quality of life.Despite extensive research efforts,effective treatments remain limited.This limited efficacy likely stems,in part,from the heterogeneous nature of neuropathic pain,which varies widely across individuals in both clinical presentation and treatment responsiveness.展开更多
Summary Pain is not pain because people interpret symptoms differently.Neck pain is one of the most common pains and should not be missing from a study on the effects of pain.Depression does not arise solely from pain...Summary Pain is not pain because people interpret symptoms differently.Neck pain is one of the most common pains and should not be missing from a study on the effects of pain.Depression does not arise solely from pain but is multicausal and often caused by this cumulative effect.展开更多
Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability...Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.展开更多
Chronic pain following a spinal cord injury refers to pain that persists or recurs after the injury.This pain can manifest as burning,stinging,or sensations similar to electric shocks.Recent studies have shown that sp...Chronic pain following a spinal cord injury refers to pain that persists or recurs after the injury.This pain can manifest as burning,stinging,or sensations similar to electric shocks.Recent studies have shown that spinal cord stimulation is an effective way to treat chronic pain after spinal cord injury.The purpose of this review is to introduce the technique of spinal cord stimulation,the clinical manifestations of spinal cord injury,and the role of spinal cord stimulation in the treatment of spinal cord injury.The mechanism and clinical application of spinal cord stimulation in the treatment of pain after spinal cord injury are discussed.The mechanism of spinal cord stimulation primarily involves three aspects:neuromodulation,neurochemical regulation,and anti-inflammatory effects,along with nerve repair.In terms of neuromodulation,spinal cord stimulation is based on the gate control theory of pain.It activates large-diameter amyloid-βnerve fibers to promote the release of inhibitory neurotransmitters by gamma-aminobutyric acidergic inhibitory interneurons in the spinal cord,thereby blocking the transmission of pain signals from small-diameter C fibers.Neurochemical studies indicate that spinal cord stimulation can regulate the balance of neurotransmitters within the spinal cord,increasing the release of inhibitory neurotransmitters such as gamma-aminobutyric acid,serotonin,and acetylcholine while reducing the levels of excitatory neurotransmitters.Additionally,spinal cord stimulation exhibits significant anti-inflammatory and neuroprotective effects,downregulating pro-inflammatory factor levels,upregulating anti-inflammatory factor expression,alleviating neuroinflammatory responses,and repairing damaged neural circuits by promoting the secretion of neurotrophic factors and axonal regeneration.Spinal cord stimulation have demonstrated remarkable efficacy in the clinical treatment of pain after spinal cord injury,but there are still limitations such as small sample size and high heterogeneity in clinical studies,as well as insufficient long-term efficacy data.Future research should conduct multi-center large-sample randomized controlled trials,and establish long-term follow-up mechanisms to improve evidence-based medical evidence.展开更多
Chronic pain represents a significant global health challenge,and the limitations of conventional analgesics have urged a search for alternative therapeutic strategies.Cannabinoids derived from Cannabis sativa have em...Chronic pain represents a significant global health challenge,and the limitations of conventional analgesics have urged a search for alternative therapeutic strategies.Cannabinoids derived from Cannabis sativa have emerged as prominent candidates.While psychotropic cannabinoids are known for their analgesic effects,their psychoactive properties often limit their clinical utility.Consequently,interest has shifted towards non-psychotropic cannabinoids that offer potential pain relief without inducing cognitive or euphoric effects.This comprehensive review investigates the pain-modulating mechanisms of cannabinoids,encompassing interactions with the endocannabinoid system and other non-traditional pathways,and summarizes the existing preclinical and clinical evidence supporting their use in various pain states.Furthermore,it discusses the therapeutic potential,clinical considerations,significant challenges,and the need for product standardization.This review also aims to evaluate the role and prospects of non-psychotropic cannabinoids as a therapeutic option for pain management.展开更多
Exercise produces a decrease in pain sensitivity via an effect called exercise-induced hypoalgesia(EIH).Transcranial direct current stimulation(tDCS),acting on similar analgesic mechanisms as EIH,represents a potentia...Exercise produces a decrease in pain sensitivity via an effect called exercise-induced hypoalgesia(EIH).Transcranial direct current stimulation(tDCS),acting on similar analgesic mechanisms as EIH,represents a potential complementary intervention that may amplify the effects of exercise on pain.This study aimed to explore if anodal tDCS could enhance the effect of exercise on pain compared to exercise alone.A total of 35 healthy participants aged 19–37 years completed a familiarisation session followed by two separate sessions where active and sham tDCS was applied in a randomised cross-over design.The familiarisation session involved familiarisation to the pain assessment and exercise tasks,while the subsequent tDCS sessions involved pain sensitivity assessment,exercise and either anodal tDCS or sham tDCS.tDCS doses were applied at 2 mA over the primary motor cortex for 10 min,with the reference electrode placed over the contralateral supraorbital area.The exercise task involved a sustained isometric grip strength contraction at 35%of maximal voluntary contraction(MVC)until volitional exhaustion.Pain sensitivity was evaluated as pressure pain threshold before tDCS,after tDCS,and after exercise.Across both tDCS conditions,pain threshold was higher after exercise when compared to pre-and post-tDCS measurement.This increase in pain threshold did not differ between active and sham tDCS conditions.Our findings suggest that the hypoalgesic effects of active anodal tDCS over the motor cortex prior to exercise are no greater than the effects of sham tDCS prior to exercise.展开更多
基金supported by the National Natural Science Foundation of China,No.81473769(to WW),81772430(to WW)a grant from the Training Program of Innovation and Entrepreneurship for Undergraduates of Southern Medical University of Guangdong Province of China in 2016,No.201612121057(to WW)
文摘OBJECTIVE: The objective of this study is to summarize and analyze the brain signal patterns of empathy for pain caused by facial expressions of pain utilizing activation likelihood estimation, a meta-analysis method. DATA SOURCES: Studies concerning the brain mechanism were searched from the Science Citation Index, Science Direct, PubMed, DeepDyve, Cochrane Library, SinoMed, Wanfang, VIP, China National Knowledge Infrastructure, and other databases, such as SpringerLink, AMA, Science Online, Wiley Online, were collected. A time limitation of up to 13 December 2016 was applied to this study. DATA SELECTION: Studies presenting with all of the following criteria were considered for study inclusion: Use of functional magnetic resonance imaging, neutral and pained facial expression stimuli, involvement of adult healthy human participants over 18 years of age, whose empathy ability showed no difference from the healthy adult, a painless basic state, results presented in Talairach or Montreal Neurological Institute coordinates, multiple studies by the same team as long as they used different raw data. OUTCOME MEASURES: Activation likelihood estimation was used to calculate the combined main activated brain regions under the stimulation of pained facial expression. RESULTS: Eight studies were included, containing 178 subjects. Meta-analysis results suggested that the anterior cingulate cortex(BA32), anterior central gyrus(BA44), fusiform gyrus, and insula(BA13) were activated positively as major brain areas under the stimulation of pained facial expression. CONCLUSION: Our study shows that pained facial expression alone, without viewing of painful stimuli, activated brain regions related to pain empathy, further contributing to revealing the brain's mechanisms of pain empathy.
基金supported by the Natural Science Foundation of Beijing Municipality(No.F252065)the National Natural Science Foundation of China(No.32271190,32571323)the STI 2030 Major Project(No.2021ZD0203202)。
文摘Knee osteoarthritis(KOA)represents one of the most common causes of chronic pain.The high prevalence and disability rates of KOA impose a severe burden on both individuals and society.In contrast to cutaneous pain,KOA-induced joint pain is characterized as a deep tissue pain that potentially involves distinct subgroups of peripheral sensory neurons and central processing mechanisms.Furthermore,KOA pain is closely related to locomotion activity.Impaired sensorimotor integration and pain mutually reinforce each other in KOA,forming a vicious cycle that exacerbates disease progression.In this review,we highlight the key differences between KOA pain and cutaneous pain,and the latter has been extensively studied in the pain field.We hope to offer new insights into the central mechanisms and development of new treatment strategies for KOA based on the interactions between impaired sensorimotor integration and chronic joint pain.
基金supported by the National Natural Science Foundation of China(No.82360238,82071245)。
文摘Cancer pain is one of the most prevalent and debilitating symptoms in patients with advanced malignancies,arising from multifactorial mechanisms involving peripheral,central,and systemic pathways.Conventional analgesics,including opioids and nonsteroidal anti-inflammatory drugs,are often limited by their insufficient efficacy,tolerance,and risk of dependence.Traditional Chinese Medicine(TCM),characterized by its multi-component,multi-target,and systemic regulatory properties,has shown promising potential in cancer pain management.This review provides a comprehensive overview of the clinical classification and underlying mechanisms of cancer pain(including nerve infiltration,dysregulation of inflammatory mediators and ion channels,central sensitization,neuro-immune crosstalk,metabolic reprogramming,and gut-brain axis impairment),as well as the analgesic effects of representative TCM agents in cancer pain management.For example,bioactive components such as tetrahydroberberine,levo-tetrahydropalmatine,and piperine exert analgesic effects,thereby improving the quality of life of patients by inhibiting inflammatory cascades,regulating neurotransmitter systems,and preserving neural integrity.Commonly used preclinical models,including bone cancer pain,pancreatic cancer pain,and chemotherapy-induced peripheral neuropathy models,are summarized for their utility in mechanistic studies and efficacy evaluations.This review also discusses the current limitations of clinical evidence,such as small sample sizes,short follow-up periods,and limited translation from animal models,alongside major challenges in standardization,mechanistic elucidation,and clinical trial design.Future directions should focus on precise pain phenotyping,integrated multi-target interventions,rigorous efficacy safety validation,and innovations in drug delivery to facilitate the standardization and global adoption of TCM in cancer pain management.
基金supported by the National Natural Science Foundation of China(No.82401445 and 82271249)the China Postdoctoral Science Foundation(No.2024M752251)+3 种基金the Postdoctoral Fellowship Program of CPSF(No.GZC20241141)the Sichuan Science and Technology Program(No.2024NSFSC1636 and 2025ZNSFSC1645)the Postdoctoral Research Fund of West China Hospital of Sichuan University(No.2024HXBH013)1-3-5 Project for Disciplines of Excellence of West China Hospital of Sichuan University(No.ZYYC23002)。
文摘Persistent postsurgical pain is a major clinical concern,especially in the aging population,who represent a growing proportion of surgical patients.Although age is a known pain risk factor,the mechanisms driving age-related vulnerability to chronic postoperative pain remain poorly understood.This study aims to investigate how aging influences the resolution of postoperative pain and to elucidate the roles of microglial activation and synaptic remodeling in the spinal dorsal horn.A plantar incision model in young(3-month-old)and aged(18-month-old)male and female mice was used to mimic postoperative pain conditions.Mechanical and thermal hypersensitivity at various postoperative intervals were assessed by von Frey and Hargreaves tests.Microglial activation and inhibitory/excitatory synaptic densities in the spinal dorsal horn were evaluated using immunofluorescence and 3D reconstruction with Imaris software.On postoperative day(POD)3,both age groups exhibited reduced pain thresholds on the ipsilateral side,along with microglial activation in the dorsal horn.On POD 7,pain thresholds in young mice had returned to baseline with no significant microglial activation,while aged mice showed sustained reduction in pain thresholds,continuous microglial activation,and significant loss of inhibitory synapses without detectable changes in excitatory synapse density.These findings are consistent across both sexes,with no sex-related differences.Collectively,these results suggest that aging is associated with persistent postoperative pain,which correlates with microglial activation and inhibitory synapse loss.These insights advance our understanding of age-related pain vulnerability and may inform the development of more effective,targeted,and age-specific therapeutic strategies to prevent or alleviate persistent postoperative pain in elderly patients.
基金supported by grant from the National Key Technology Support Program of the Ministry of Science and Technology of China(No.2021ZD0203204)。
文摘Pseudounipolar neurons in the dorsal root ganglia(DRG),as the central nodes of primary sensory afferents,possess a distinctive T-junction that is not merely a morphological peculiarity but also performs complex roles in rapid,multiplexed shunting and regulation of sensory signals.This specialized geometry enables separation,filtering,and feedback regulation of neuronal signals,thereby coordinating peripheral and central responses at multiple levels.Recent advances,including spatial transcriptomics,single-cell sequencing,super-resolution microscopy,organoid models,and novel electrophysiological methods,have permitted more precise dissection of the T-junction's molecular composition,ion-channel distribution,and electrophysiological properties.Here,we review current knowledge of the T-junction's developmental regulation and multilayered molecular networks,and we detail its functional alterations in both physiological signaling and pathological pain states,with particular emphasis on ion-channel modulation,signal attenuation,and selective transmission mechanisms.Finally,we discuss contemporary pain-intervention approaches and prospects for precision-targeted therapies,aiming to provide a theoretical foundation for future studies in pain physiology and clinical translation.
基金Institut National de la Santéet de la Recherche Médicale(Inserm)UniversitéClermont Auvergne(France)+2 种基金CHU Clermont-Ferrand(to RD)the French government IDEX-ISITE initiative 16-IDEX-0001(to RD)The Fondation pour la Recherche Médicale(FRM)(to SM).
文摘While acute nociceptive pain is a crucial warning system that protects us from injury or disease,chronic pain is not protective,but a pathological condition.As such,it is now recognized as a disease in its own right,which major classes refer to inflammatory,neuropathic,and idiopathic pain.It is frequent,with up to a third of the population that may suffer at one point from chronic pain.It is often associated with other pathologies,including sleep disorders,anxiety,depression,and is still difficult to treat.It thus represents a significant burden in terms of health and societal impact(Tracey et al.,2019).The mechanisms of chronic pain involve multiple diverse pathways in both the peripheral and central nervous systems(CNS),reflecting its multifaceted biology.Indeed,research over the past decades has established that central sensitization(enhancement in the function of neurons and circuits in central nociceptive pathways),in particular within the dorsal horn,the first central relay of nociceptive inputs plays a key role in the chronicity of pain(Latremoliere and Woolf,2009).
基金Institute for Basic Science(IBS)Center for Cognition and Sociality(IBS-R001-D2 to BL).
文摘Neuropathic pain is a complex and debilitating condition caused by lesions or dysfunction within the somatosensory nervous system.Affecting an estimated 7%-10%of the global population,it presents with spontaneous pain,hyperalgesia,and allodynia,often accompanied by long-term emotional and cognitive consequences,such as depression and anxiety,which result in a reduced quality of life.Despite extensive research efforts,effective treatments remain limited.This limited efficacy likely stems,in part,from the heterogeneous nature of neuropathic pain,which varies widely across individuals in both clinical presentation and treatment responsiveness.
文摘Summary Pain is not pain because people interpret symptoms differently.Neck pain is one of the most common pains and should not be missing from a study on the effects of pain.Depression does not arise solely from pain but is multicausal and often caused by this cumulative effect.
文摘Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.
基金supported by Key Tackling Project of the Education Department of Liaoning Province,No.2024C011the Medical-Industrial Joint Innovation Funding Project of the First Hospital of Dalian Medical University and Dalian Institute of Chemical Physics,No.DMU-1&DICP UN202311(both to ZL).
文摘Chronic pain following a spinal cord injury refers to pain that persists or recurs after the injury.This pain can manifest as burning,stinging,or sensations similar to electric shocks.Recent studies have shown that spinal cord stimulation is an effective way to treat chronic pain after spinal cord injury.The purpose of this review is to introduce the technique of spinal cord stimulation,the clinical manifestations of spinal cord injury,and the role of spinal cord stimulation in the treatment of spinal cord injury.The mechanism and clinical application of spinal cord stimulation in the treatment of pain after spinal cord injury are discussed.The mechanism of spinal cord stimulation primarily involves three aspects:neuromodulation,neurochemical regulation,and anti-inflammatory effects,along with nerve repair.In terms of neuromodulation,spinal cord stimulation is based on the gate control theory of pain.It activates large-diameter amyloid-βnerve fibers to promote the release of inhibitory neurotransmitters by gamma-aminobutyric acidergic inhibitory interneurons in the spinal cord,thereby blocking the transmission of pain signals from small-diameter C fibers.Neurochemical studies indicate that spinal cord stimulation can regulate the balance of neurotransmitters within the spinal cord,increasing the release of inhibitory neurotransmitters such as gamma-aminobutyric acid,serotonin,and acetylcholine while reducing the levels of excitatory neurotransmitters.Additionally,spinal cord stimulation exhibits significant anti-inflammatory and neuroprotective effects,downregulating pro-inflammatory factor levels,upregulating anti-inflammatory factor expression,alleviating neuroinflammatory responses,and repairing damaged neural circuits by promoting the secretion of neurotrophic factors and axonal regeneration.Spinal cord stimulation have demonstrated remarkable efficacy in the clinical treatment of pain after spinal cord injury,but there are still limitations such as small sample size and high heterogeneity in clinical studies,as well as insufficient long-term efficacy data.Future research should conduct multi-center large-sample randomized controlled trials,and establish long-term follow-up mechanisms to improve evidence-based medical evidence.
文摘Chronic pain represents a significant global health challenge,and the limitations of conventional analgesics have urged a search for alternative therapeutic strategies.Cannabinoids derived from Cannabis sativa have emerged as prominent candidates.While psychotropic cannabinoids are known for their analgesic effects,their psychoactive properties often limit their clinical utility.Consequently,interest has shifted towards non-psychotropic cannabinoids that offer potential pain relief without inducing cognitive or euphoric effects.This comprehensive review investigates the pain-modulating mechanisms of cannabinoids,encompassing interactions with the endocannabinoid system and other non-traditional pathways,and summarizes the existing preclinical and clinical evidence supporting their use in various pain states.Furthermore,it discusses the therapeutic potential,clinical considerations,significant challenges,and the need for product standardization.This review also aims to evaluate the role and prospects of non-psychotropic cannabinoids as a therapeutic option for pain management.
文摘Exercise produces a decrease in pain sensitivity via an effect called exercise-induced hypoalgesia(EIH).Transcranial direct current stimulation(tDCS),acting on similar analgesic mechanisms as EIH,represents a potential complementary intervention that may amplify the effects of exercise on pain.This study aimed to explore if anodal tDCS could enhance the effect of exercise on pain compared to exercise alone.A total of 35 healthy participants aged 19–37 years completed a familiarisation session followed by two separate sessions where active and sham tDCS was applied in a randomised cross-over design.The familiarisation session involved familiarisation to the pain assessment and exercise tasks,while the subsequent tDCS sessions involved pain sensitivity assessment,exercise and either anodal tDCS or sham tDCS.tDCS doses were applied at 2 mA over the primary motor cortex for 10 min,with the reference electrode placed over the contralateral supraorbital area.The exercise task involved a sustained isometric grip strength contraction at 35%of maximal voluntary contraction(MVC)until volitional exhaustion.Pain sensitivity was evaluated as pressure pain threshold before tDCS,after tDCS,and after exercise.Across both tDCS conditions,pain threshold was higher after exercise when compared to pre-and post-tDCS measurement.This increase in pain threshold did not differ between active and sham tDCS conditions.Our findings suggest that the hypoalgesic effects of active anodal tDCS over the motor cortex prior to exercise are no greater than the effects of sham tDCS prior to exercise.
