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Pain Mechanisms and Management

Overview

The pain phenotype serves as a window on underlying pathophysiological neural mechanisms [1] and guides the development of personalized pain medicine [1]. Identification of these mechanisms in subgroups of chronic musculoskeletal pain patients contributes to a mechanism-based subgroup classification [2], which fosters the development of mechanism-based treatments [2]. Expert consensus-derived lists of clinical indicators provide criteria for classifying nociceptive, peripheral neuropathic, and central mechanisms of musculoskeletal pain [3]. Diagnostic criteria to establish the presence of central sensitization assist in phenotyping patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity [14].

Progress in understanding the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures [4] and personalized interventions [4]. Management of neuropathic pain emphasizes the need for a multidisciplinary approach [4]. Acute pain and other types of pain (cancer-related or chronic) that are classified as distinct actually have many similarities [29]. Preventive strategies are discussed for managing the transition from acute to persistent pain [7].

Best results of block therapy require a thorough understanding of the complexities and limitations of pain physiology [10]. Combinations of drugs that provide analgesic efficacy at reduced individual doses may confer the optimal risk-benefit ratio for pain management in the long term [6]. This applies specifically to patients at increased cardiovascular risk [6]. Rigorous evidence about the potential physiological mechanisms of action and effects of dry needling is still lacking [9].

How It Works

Identification of underlying pathophysiologic mechanisms in different subgroups of chronic musculoskeletal pain patients contributes to a mechanism-based subgroup classification, fostering the development of mechanism-based treatments [2]. Expert consensus-derived lists of clinical indicators of 'nociceptive', 'peripheral neuropathic' and 'central' mechanisms of musculoskeletal pain provide criteria upon which clinicians may base mechanistic classifications [3].

Central sensitization involves hyperexcitable central neural activity, and diagnostic criteria to establish its presence assist in phenotyping patients for choosing treatments that produce analgesia by normalizing this activity [14]. Chronic pain and depression may be based on common neuroplasticity mechanism changes, providing new insights into the association between the two conditions [13]. Complex regional pain syndrome is a multifaceted disorder involving sympathetic nervous system dysfunction, neurogenic inflammation, autoimmunity, and central nervous system plasticity; understanding these mechanisms is key to developing mechanism-based treatments beyond simple symptom management [8].

Specific peripheral mechanisms include cutaneous nerve entrapment in surgical scars, which can cause deep, diffuse, poorly localized pain through peripheral and central sensitization mechanisms [20]. The painful neuroma involves pathophysiology involving fascicular escape and scarring [21].

Preventive strategies are being developed for managing the transition from acute to persistent pain [7]. The goal of preventive analgesia is to reduce central sensitization that arises from noxious inputs experienced throughout the entire perioperative period [18]. Multimodal pain management can reduce the intensity and duration of pain after knee arthroplasty by addressing pain mechanisms [12]. Best results of block therapy require a thorough understanding of the complexities and limitations of pain physiology [10].

Combinations of drugs that provide analgesic efficacy at reduced individual doses may confer the optimal risk-benefit ratio for pain management in the long term or in patients at increased cardiovascular risk [6]. Progress in understanding the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, emphasizing the need for a multidisciplinary approach to management [4].

Regarding specific modalities, the modified non-invasive shot blocking device did not reduce the pain of injection, suggesting that gate control, rather than distraction or placebo, is the mechanism of action [15]. Rigorous evidence about the potential physiological mechanisms of action and effects of dry needling is still lacking [9].

What the Evidence Shows

Identification of these mechanisms in chronic musculoskeletal pain subgroups fosters mechanism-based classification and treatment development [2]. Expert consensus-derived lists of clinical indicators for nociceptive, peripheral neuropathic, and central mechanisms provide criteria for mechanistic classification [3]. Progress in understanding neuropathic pain pathophysiology spurs new diagnostic procedures and personalized interventions, emphasizing the need for a multidisciplinary management approach [4].

Complex regional pain syndrome is a multifaceted disorder involving sympathetic nervous system dysfunction, neurogenic inflammation, autoimmunity, and central nervous system plasticity [8]. Understanding these mechanisms is key to developing treatments beyond simple symptom management [8]. Chronic pain and depression may share common neuroplasticity mechanism changes [13]. Clinical research on chronic non-specific low back pain has been limited by failure to adequately attend to sub-grouping of the population [32]. Preventive strategies are being developed for managing the transition from acute to persistent pain [7].

Multimodal analgesia protocols reduce opioid consumption and minimize side effects, with prevention of chronic pain positively affecting long-term results [16]. These protocols are effective at reducing pain and the number of opioids needed for breakthrough pain with minimal side effects and without compromising patient satisfaction [17]. Multimodal pain management can reduce the intensity and duration of pain after knee arthroplasty [12]. Combinations of drugs that provide analgesic efficacy at reduced individual doses may confer the optimal risk-benefit ratio for pain management in the long term or in patients at increased cardiovascular risk [6].

Block therapy best results require a thorough understanding of the complexities and limitations of pain physiology [10]. A modified non-invasive shot blocking device did not reduce the pain of injection, suggesting that gate control, rather than distraction or placebo, is the mechanism of action [15]. Rigorous evidence about the potential physiological mechanisms of action and effects of dry needling is still lacking [9].

The best treatment for prolonged pain and persistent opioid use is likely prevention followed by early intervention, utilizing opioid-reducing strategies within enhanced recovery pathways and customized care for outliers [31]. An intervention focusing on pain catastrophizing seems to have potential for improving pain outcome in patients prone to catastrophizing pain [30]. Consideration of mechanism-appropriate rehabilitation interventions may assist therapists to select the most appropriate and effective treatments from the body of evidence supporting rehabilitation of CRPS [33].

Cannabis-based medicines may be effective in treating the pain and symptoms of peripheral neuropathy [36]. Persistent pain is prevalent up to 84 months following traumatic injury [35]. Results from studies on pain and biomarkers in patients with hand osteoarthritis will contribute to increased knowledge about pain mechanisms and pain outcomes in hand OA [11].

Practical Considerations

Identification of these mechanisms in different subgroups of chronic musculoskeletal pain patients contributes to a mechanism-based subgroup classification, fostering the development of mechanism-based treatments [2]. Expert consensus-derived lists of clinical indicators of nociceptive, peripheral neuropathic, and central mechanisms provide criteria upon which clinicians may base mechanistic classifications [3].

Poorly controlled acute postoperative pain is associated with increased morbidity, functional and quality-of-life impairment, delayed recovery time, prolonged duration of opioid use, and higher health-care costs [24]. Acute postoperative pain can be more effectively managed if prioritized and anticipated by a well-informed care team educated regarding appropriate analgesic options and the long-term benefits of pain relief [22]. Evaluating perioperative analgesic strategies is essential for developing individualized plans [25].

Multimodal analgesia protocols are effective at reducing pain and the number of opioids needed for breakthrough pain with minimal side effects and without compromising patient satisfaction [17]. Multimodal pain management can reduce the intensity and duration of pain after knee arthroplasty [12]. Reduction of opioid consumption and minimization of side effects are primary outcomes of oral multimodal analgesia for total joint arthroplasty, with prevention of chronic pain positively affecting long-term results [16]. Minimizing opioid consumption involves the application of opioid titration, multimodal analgesia, or interventions with opioid-sparing effects [23]. Combinations of drugs that provide analgesic efficacy at reduced individual doses may confer the optimal risk-benefit ratio for pain management in the long term or in patients at increased cardiovascular risk [6].

Peripheral nerve blocks are a safe and effective way to improve pain management while decreasing opioid consumption, particularly in outpatient settings [19]. Opioids should be used cautiously and at specific times aided by tools assessing patient's risk of opioid abuse and pain chronicity [27].

Chronic pain and depression may be based on common neuroplasticity mechanism changes [13]. Psychosocial factors should be considered as possible risk and protective factors for the development of pain, as well as treatment targets that might be modulated to minimize the burden of pain [26]. Progress in understanding the pathophysiology of neuropathic pain emphasizes the need for a multidisciplinary approach to management [4]. Preventive strategies exist for managing the transition from acute to persistent pain [7].

Complex regional pain syndrome involves sympathetic nervous system dysfunction, neurogenic inflammation, autoimmunity, and central nervous system plasticity, requiring mechanism-based treatments beyond simple symptom management [8].

Key Evidence

  • [L5] The pain phenotype serves as a window on underlying pathophysiological neural mechanisms and as a guide for developing personalized pain medicine. (10.1016/j.neuron.2012.02.008)
  • [L4] The identification of the underlying pathophysiologic mechanisms in different subgroups of chronic musculoskeletal pain patients will contribute to a mechanism-based subgroup classification, fostering the development of mechanism-based treatments. (10.1186/1471-2474-13-136)
  • [L5] Expert consensus-derived lists of clinical indicators of 'nociceptive', 'peripheral neuropathic' and 'central' mechanisms of musculoskeletal pain provide some indication of the criteria upon which clinicians may base such mechanistic classifications. (10.1016/j.math.2009.07.005)
  • [Paper] Progress in the understanding of the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain. (10.1038/nrdp.2017.2)
  • [L4] Combinations of drugs that provide analgesic efficacy at reduced individual doses may confer the optimal risk-benefit ratio for pain management in the long term or in patients at increased cardiovascular risk. (10.1007/s10067-006-0311-5)
  • [L4] The authors also discuss preventive strategies on the horizon for managing the transition from acute to persistent pain. (10.1016/j.eujps.2011.08.013)
  • [L5] Complex regional pain syndrome is a multifaceted disorder involving sympathetic nervous system dysfunction, neurogenic inflammation, autoimmunity, and central nervous system plasticity; understanding these mechanisms is key to developing mechanism-based treatments beyond simple symptom management. (10.1016/j.hcl.2015.08.003)
  • [L4] Rigorous evidence about the potential physiological mechanisms of action and effects of dry needling is still lacking. (10.1007/s11916-013-0348-5)
  • [L5] Best results of block therapy require thorough understanding of the complexities and limitations of pain physiology. (10.1016/s0749-0712(21)00368-1)
  • [L4] Results will contribute to increased knowledge about pain mechanisms and pain outcomes in hand OA. (10.1136/bmjopen-2017-016938)
  • [L4] This narrative review offers a clear overview of pain mechanism after knee arthroplasty and an understanding on how multimodal pain management can reduce the intensity and duration of pain after knee arthroplasty. (10.1007/s00167-013-2750-2)
  • [L5] It concludes that chronic pain and depression may be based on common neuroplasticity mechanism changes, providing new insights into the understanding of the association between the two conditions. (10.1155/2017/9724371)
  • [L4] Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. (10.1016/j.pain.2010.09.030)
  • [L1] The modified device did not reduce the pain of injection, suggesting that gate control, rather than distraction or placebo, is the mechanism of action. (10.1177/1558944719884655)
  • [L5] Reduction of opioid consumption and minimization of side effects are primary outcomes, and prevention of chronic pain can positively affect long-term results. (10.1016/j.arth.2017.05.002)
  • [L5] Multimodal analgesia protocols are effective at reducing pain and the number of opioids needed for breakthrough pain with minimal side effects and without compromising patient satisfaction. (10.1016/j.arthro.2020.05.003)
  • [L5] The goal of preventive analgesia is to reduce central sensitization that arises from noxious inputs experienced throughout the entire perioperative period. (10.2106/jbjs.f.00906)
  • [L5] Peripheral nerve blocks are a safe and effective way to improve pain management while decreasing opioid consumption, particularly in outpatient settings. (10.5435/jaaos-d-20-01325)
  • [L5] Cutaneous nerve entrapment in surgical scars can cause deep, diffuse, poorly localized pain through peripheral and central sensitization mechanisms; while lidocaine injection is diagnostic, no surgical standard has emerged and future research should target central nervous system responses to injury. (10.1016/j.jhsa.2009.04.003)
  • [L5] The painful neuroma is a debilitating sequela of nerve injury with poorly understood pathophysiology involving fascicular escape and scarring; treatment must be tailored to the individual patient as there are a number of approaches available. (10.1016/j.jhsa.2009.12.019)
  • [Paper] Acute postoperative pain can be more effectively managed if it is prioritised and anticipated by a well-informed care team who are educated with regard to appropriate analgesic options and understand what the long-term benefits of pain relief are. (10.1185/03007990903281059)
  • [L2] The first aspect of minimizing opioid consumption involves the application of opioid titration, multimodal analgesia, or interventions with opioid-sparing effects. (10.1111/pan.12420)
  • [L4] Poorly controlled acute postoperative pain is associated with increased morbidity, functional and quality-of-life impairment, delayed recovery time, prolonged duration of opioid use, and higher health-care costs. (10.2147/jpr.s144066)
  • [L2] Evaluating these strategies is essential for understanding their benefits and limitations to develop individualized perioperative analgesic plans. (10.1186/s13018-024-05324-4)
  • [L4] These psychosocial factors should be considered as possible risk and protective factors for the development of pain, as well as treatment targets that might be modulated to minimize the burden of pain. (10.2106/jbjs.20.00082)
  • [L5] Opioids remain useful in both acute and chronic pain management but should be used cautiously and at specific times aided by tools assessing patient's risk of opioid abuse and pain chronicity. (10.1016/j.arres.2021.100003)
  • [L5] Acute pain and other types of pain (cancer-related or chronic) that are classified as distinct actually have many similarities. (10.1016/s0140-6736(99)03313-9)
  • [L2] An intervention focusing on pain catastrophizing seems to have potential for improving pain outcome in patients prone to catastrophizing pain. (10.1007/s11999-009-0963-y)
  • [L5] The best treatment for prolonged pain and persistent opioid use is likely prevention followed by early intervention, utilizing opioid-reducing strategies within enhanced recovery pathways and customized care for outliers. (10.1016/j.arth.2018.08.005)
  • [L5] The disappointing results of clinical research are commonly explained by the failure of researchers to adequately attend to sub-grouping of the chronic non-specific low back pain population; alternatively, current approaches may be ineffective and clinicians and researchers may need to radically rethink the nature of the problem and how it should best be managed. (10.1186/1471-2474-9-11)
  • [L2] Consideration of mechanism-appropriate rehabilitation interventions may assist therapists to select the most appropriate and effective treatments from the body of evidence supporting rehabilitation of CRPS. (10.1016/j.jht.2018.01.007)
  • [L4] The evidence from the eleven studies included in this review indicates that persistent pain is prevalent up to 84 months following traumatic injury. (10.2147/jpr.s38878)
  • [L2] Our analysis of the literature shows that cannabis-based medicines may be effective in treating the pain and symptoms of peripheral neuropathy. (10.1016/j.jhsa.2024.09.015)

See Also

  • Osteoarthritis

References

[1] Deconstructing the Neuropathic Pain Phenotype to Reveal Neural Mechanisms. Neuron. 2012. DOI: 10.1016/j.neuron.2012.02.008

[2] Subgroups of musculoskeletal pain patients and their psychobiological patterns – The LOGIN study protocol. BMC Musculoskeletal Disorders. 2012. DOI: 10.1186/1471-2474-13-136

[3] Clinical indicators of ‘nociceptive’, ‘peripheral neuropathic’ and ‘central’ mechanisms of musculoskeletal pain. A Delphi survey of expert clinicians. Manual Therapy. 2010. DOI: 10.1016/j.math.2009.07.005

[4] Neuropathic pain. Nature Reviews Disease Primers. 2017. DOI: 10.1038/nrdp.2017.2

[6] Pain management today—what have we learned?. Clinical Rheumatology. 2006. DOI: 10.1007/s10067-006-0311-5

[7] Preventing chronic pain following acute pain: Risk factors, preventive strategies, and their efficacy. European Journal of Pain Supplements. 2011. DOI: 10.1016/j.eujps.2011.08.013

[8] New Concepts in Complex Regional Pain Syndrome. Hand Clinics. 2016. DOI: 10.1016/j.hcl.2015.08.003

[9] Physiologic Effects of Dry Needling. Current Pain and Headache Reports. 2013. DOI: 10.1007/s11916-013-0348-5

[10] NEURAL BLOCKADE FOR UPPER-EXTREMITY PAIN. Hand Clinics. 1996. DOI: 10.1016/s0749-0712(21)00368-1

[11] A hospital-based observational cohort study exploring pain and biomarkers in patients with hand osteoarthritis in Norway: The Nor-Hand protocol. BMJ Open. 2017. DOI: 10.1136/bmjopen-2017-016938

[12] Pain after knee arthroplasty: an unresolved issue. Knee Surgery, Sports Traumatology, Arthroscopy. 2013. DOI: 10.1007/s00167-013-2750-2

[13] The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain. Neural Plasticity. 2017. DOI: 10.1155/2017/9724371

[14] Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2011. DOI: 10.1016/j.pain.2010.09.030

[15] The Effectiveness of a Non-Invasive Shot Blocking Device for Reducing Pain of In-office Injections in Hand Surgery. HAND. 2019. DOI: 10.1177/1558944719884655

[16] Oral Multimodal Analgesia for Total Joint Arthroplasty. The Journal of Arthroplasty. 2017. DOI: 10.1016/j.arth.2017.05.002

[17] Editorial Commentary : Opioids After Orthopaedic Surgery: Who Needs ‘Em?. Arthroscopy. 2020. DOI: 10.1016/j.arthro.2020.05.003

[18] Preventing the Development of Chronic Pain After Orthopaedic Surgery with Preventive Multimodal Analgesic Techniques. The Journal of Bone & Joint Surgery. 2007. DOI: 10.2106/jbjs.f.00906

[19] Preoperative Peripheral Nerve Blocks in Orthopaedic Trauma Surgery: A Guide to Diagnosis-Based Treatment. Journal of the American Academy of Orthopaedic Surgeons. 2021. DOI: 10.5435/jaaos-d-20-01325

[20] Cutaneous Neuroma Physiology and Its Relationship to Chronic Pain. The Journal of Hand Surgery. 2009. DOI: 10.1016/j.jhsa.2009.04.003

[21] Neuromas of the Hand and Upper Extremity. The Journal of Hand Surgery. 2010. DOI: 10.1016/j.jhsa.2009.12.019

[22] Consensus statement on the anticipation and prevention of acute postoperative pain: multidisciplinary RADAR approach. Current Medical Research and Opinion. 2009. DOI: 10.1185/03007990903281059

[23] Strategies for preventing side effects of systemic opioid in postoperative pediatric patients. Pediatric Anesthesia. 2014. DOI: 10.1111/pan.12420

[24] Poorly controlled postoperative pain: prevalence, consequences, and prevention. Journal of Pain Research. 2017. DOI: 10.2147/jpr.s144066

[25] Advances in perioperative pain management for total knee arthroplasty: a review of multimodal analgesic approaches. Journal of Orthopaedic Surgery and Research. 2024. DOI: 10.1186/s13018-024-05324-4

[26] Behavioral, Psychological, Neurophysiological, and Neuroanatomic Determinants of Pain. Journal of Bone and Joint Surgery. 2020. DOI: 10.2106/jbjs.20.00082

[27] Towards a Comprehensive Theory of Non-Cancer Acute and Chronic Pain Management: The Critical Role of Reactive Oxygen and Nitrogen Species in Pain, and Opioid Dependence, Addiction, Hyperalgesia, and Tolerance. Advances in Redox Research. 2021. DOI: 10.1016/j.arres.2021.100003

[29] Acute pain. The Lancet. 1999. DOI: 10.1016/s0140-6736(99)03313-9

[30] Preoperative Pain Catastrophizing Predicts Pain Outcome after Knee Arthroplasty. Clinical Orthopaedics & Related Research. 2010. DOI: 10.1007/s11999-009-0963-y

[31] Managing Prolonged Pain After Surgery: Examining the Role of Opioids. The Journal of Arthroplasty. 2018. DOI: 10.1016/j.arth.2018.08.005

[32] Chronic non-specific low back pain – sub-groups or a single mechanism?. BMC Musculoskeletal Disorders. 2008. DOI: 10.1186/1471-2474-9-11

[33] Mechanism-specific rehabilitation management of complex regional pain syndrome: Proposed recommendations from evidence synthesis. Journal of Hand Therapy. 2018. DOI: 10.1016/j.jht.2018.01.007

[35] Systematic review of persistent pain and psychological outcomes following traumatic musculoskeletal injury. Journal of Pain Research. 2013. DOI: 10.2147/jpr.s38878

[36] The Use of Cannabinoids in the Treatment of Peripheral Neuropathy and Neuropathic Pain: A Systematic Review. The Journal of Hand Surgery. 2025. DOI: 10.1016/j.jhsa.2024.09.015

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Section 6 -- Term and Termination.

a. This Public License applies for the term of the Copyright and Similar Rights licensed here. However, if You fail to comply with this Public License, then Your rights under this Public License terminate automatically.

b. Where Your right to use the Licensed Material has terminated under Section 6(a), it reinstates:

1. automatically as of the date the violation is cured, provided it is cured within 30 days of Your discovery of the violation; or

2. upon express reinstatement by the Licensor.

For the avoidance of doubt, this Section 6(b) does not affect any right the Licensor may have to seek remedies for Your violations of this Public License.

c. For the avoidance of doubt, the Licensor may also offer the Licensed Material under separate terms or conditions or stop distributing the Licensed Material at any time; however, doing so will not terminate this Public License.

d. Sections 1, 5, 6, 7, and 8 survive termination of this Public License.

Section 7 -- Other Terms and Conditions.

a. The Licensor shall not be bound by any additional or different terms or conditions communicated by You unless expressly agreed.

b. Any arrangements, understandings, or agreements regarding the Licensed Material not stated herein are separate from and independent of the terms and conditions of this Public License.

Section 8 -- Interpretation.

a. For the avoidance of doubt, this Public License does not, and shall not be interpreted to, reduce, limit, restrict, or impose conditions on any use of the Licensed Material that could lawfully be made without permission under this Public License.

b. To the extent possible, if any provision of this Public License is deemed unenforceable, it shall be automatically reformed to the minimum extent necessary to make it enforceable. If the provision cannot be reformed, it shall be severed from this Public License without affecting the enforceability of the remaining terms and conditions.

c. No term or condition of this Public License will be waived and no failure to comply consented to unless expressly agreed to by the Licensor.

d. Nothing in this Public License constitutes or may be interpreted as a limitation upon, or waiver of, any privileges and immunities that apply to the Licensor or You, including from the legal processes of any jurisdiction or authority.

Creative Commons is not a party to its public licenses. Notwithstanding, Creative Commons may elect to apply one of its public licenses to material it publishes and in those instances will be considered the “Licensor.” The text of the Creative Commons public licenses is dedicated to the public domain under the CC0 Public Domain Dedication. Except for the limited purpose of indicating that material is shared under a Creative Commons public license or as otherwise permitted by the Creative Commons policies published at creativecommons.org/policies, Creative Commons does not authorize the use of the trademark "Creative Commons" or any other trademark or logo of Creative Commons without its prior written consent including, without limitation, in connection with any unauthorized modifications to any of its public licenses or any other arrangements, understandings, or agreements concerning use of licensed material. For the avoidance of doubt, this paragraph does not form part of the public licenses.

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