SIG Chronic Pain Report 2022

EAPM- Special Interest Group “Chronic Pain”

Mission Statement

The SIG of chronic pain will contribute in collaboration with the EAPM to increase the knowledge about psychosomatic components of chronic pain in this way:

1. To stimulate multinational and multi-professional exchange between researchers and clinicians that are active on the field of chronic pain. The SIG will encourage this exchange inside the EAMP as well as with other medical and psychological associations. This includes to create connections between EAPM and Pain societies;
2. To disseminate, between EAPM members, the evidences relative to the impact of psychological, psychopathological and neurobiological components on the perception and disability of pain;
3. To organize symposia in the EAPM congresses – and also beyond – focusing on research activities and also on clinical and service developmental aspects;
4. To stimulate the new generation to study chronic pain becoming a bridge for knowledge exchange between specialized centers in pain;
5. To setup joint studies and to write or support articles and books in this field.

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2022: an updated on the proposed new definition of pain, new diagnosis of chronic pain and its assessment 

Antonella Ciaramella MD, F-EAPM 

 

1. 1. Definition of pain

In these recent years the meaning of assessment of pain has been discuss and several criticism to the previous perspective have been done. 

The last definition of pain:  An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (IASP, 1979) was introduced by Merskey (Psychiatrist) in the 1978, however in these recent years this definition has been subject of criticism and questioning for: 

a: it emphasizes self-verbal excluding the pain of people who are unable to communicate it verbally such as infants or elderly or people with impaired cognition or language skills 

1. b. does not exclude wilfully wrong verbal reports such as in malingering.
2. c. it is in a “Cartesian perspective” ignoring the multiplicity of mind-body interaction
3. d. it excluded cognitive and social factors that are integral in the experience of pain
4. Merskey with this definition over-emphasizes the psychological aspects of pain

If initially the criticism was such as to suggest a new definition that completely overturned the previous one: Pain is a mutually recognizable somatic experience that reflects a person’s apprehension of threat to their bodily or existential integrity (Cohen et al., 2018), during the same period, Treede and colleagues (2018) underlines the validity of the old definition especially because the past definition: 

1. a. underlines the subjective experience 
2. Link pain to both neurobiology of emotion and sensory system physiology
3. c. pain is associated with a specific noxious stimulus as threat of tissue damage. 
4. d. includes multidimensional aspects of pain
5. e. it’s short and simple
6. The footnote of last definition included the sentence “The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment”, thus also including the pain of the subjects with language impairment.
   

Judith Turner in the 2018, gathered 14 member of IASP Task force (2018-2020) deciding to work to a revision of definition of pain because the definition “should be retained or changed based on current evidence-based knowledge” 

Pain can range widely in intensity, quality and duration and has diverse pathophysiologic mechanisms and meaning. Therefore defining the concept of pain in a concise and precise manner presents a challenge.  

 

Revised IASP Definition of Pain (2020) (by Raja et al., 2020) 

 

Pain: An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage. 

Notes 

• Pain is always a personal experience that is influenced to varying degrees by

biological, psychological, and social factors. 

• Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
• Through their life experiences, individuals learn the concept of pain.
• A person’s report of an experience as pain should be respected.
• Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.
• Verbal description is only one of several behaviours to express pain; inability to communicate does not negate the possibility that a human or a non-human animal experiences pain.

An insight into pain terminology: 

Nociception	A function of a specific sensory system
		Third-person perspective
		Stimulus related
		Sensory discrimination
Pain	A result of network activity in the brain
		First-person perspective
		Perception-related
		Suffering
Nociceptive pain	Results from an injury or disease affecting somatic structures such as skin, muscle, tendons, bone, and joints.
Neuropathic pain	is defined as pain caused by a lesion or disease affecting the somatosensory system
Nociplastic pain	is pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain

 

For more details click on: https://www.practicalpainmanagement.com/resources/news-and-research/pain-redefined-inside-iasp-updated-definition  

References 

Cohen M, Quintner J, van Rysewyk S. Reconsidering the IASP definition of pain. PAIN Reports 2018. DOI: 10.1097/PR9.0000000000000634. 

Merskey H. Diagnosis of the patient with chronic pain. J Human Stress. 1978 Jun;4(2):3-7. doi: 10.1080/0097840X.1978.9934979. PMID: 659854. 

Raja SN, Carr DB, Cohen M, Finnerup NB, Flor H, Gibson S, Keefe FJ, Mogil JS, Ringkamp M, Sluka KA, Song XJ, Stevens B, Sullivan MD, Tutelman PR, Ushida T, Vader K. The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain. 2020 Sep 1;161(9):1976-1982. doi: 10.1097/j.pain.0000000000001939. PMID: 32694387; PMCID: PMC7680716. 

Treede RD. The International Association for the Study of Pain definition of pain: as valid in 2018 as in 1979, but in need of regularly updated footnotes. Pain Rep. 2018 Mar 5;3(2):e643. doi: 10.1097/PR9.0000000000000643. PMID: 29756089; PMCID: PMC5902252. 

 

2. Diagnosis of Chronic Pain

 

The previous multiaxial classification of chronic pain developed by a task force of the International Association for the Study of Pain (IASP, 2015),  was a systematic classification of chronic pain distinguished Axis I (region), II (Systems), III temporal characteristics, IV (Intensity), V (Aetiology). In the International classification of Disease (ICD) the chronic pain diagnosis are not represented systematically and the last IASP classification did not emphasize the relevance of pathophysiology and etiology, the latter relegated to the V axis. 

The ICD-11 development process requires the generation of content models for each diagnostic entity, which contain definitions, diagnostic criteria, and synonyms and the well know scientific information about each entities according to the model of WHO 2011. The ICD 11 classification distinguishes chronic primary and chronic secondary pain syndromes, integrates existing pain diagnoses including headaches, and provides precise definitions and further characteristic features of the respective diagnoses according to the content model of the WHO for ICD-11. This model includes the severity of pain, its temporal course, and evidence for psychological and social factors. These pain diagnoses have been implemented in the 11th version of ICD that was released by WHO in June 2018. 

The goal was to create a classification system that is applicable in clinical settings for specialized pain management and in primary care. 

The ICD-11 development process requires the generation of content models for each diagnostic entity, which contain definitions, diagnostic criteria, and synonyms as well as state of the art scientific information about the respective entity as reported in the contend model of WHO 2011.  

 

Definition of Chronic Pain  

 

Chronic pain was defined previously as pain that persists past normal healing time and hence lacks the acute warning function of physiological nociception. The difficulty to apply this definition in some conditions as migraine headache, the temporal criterion was chosen: chronic pain is pain that lasts or recurs for longer than 3 months (Treede et al., 2015). 

 

Chronic primary pain syndromes (figure 1) 

 

Chronic primary pain is defined as pain in one or more anatomical regions that persists or recurs for longer than 3 months and is associated with significant emotional distress or functional disability (interference with activities of daily life and participation in social roles) and that cannot be better accounted for by another pain conditions (Nicholas et al., 2019). Some entities belonging to several field called “multiple parenting”: Multiple parenting allows that one definition (the child) may be accessed from more than one higher level category (parent), but the child will have the same unique definition under both parent codes.   

The nociplastic pain has been suggested as a pathogenetic mechanism of primary pain of almost of the syndromes (Kosec et al., 2016).  

 

Chronic secondary syndromes (figure 1) 

 

Chronic secondary pain syndromes are linked to other diseases as the underlying cause, for which pain may initially be regarded as a symptom. The ICD 11 underline the relevance of pain in subject with pain associated to a disease and need special care. The new coding will facilitate the treatment of pain recognizing the early or in the course of disease.  

 

 

Figure 1: Structure of the IASP Classification of Chronic Pain (from Treed et al., 2019) 

 

References 

Kosek E, Cohen M, Baron R, Gebhart GF, Mico JA, Rice ASC, Rief W, Sluka AK. Do we need a third mechanistic descriptor for chronic pain states? PAIN 2016;157:1382–6. 

Nicholas M, Vlaeyen JWS, Rief W, Barke A, Aziz Q, Benoliel R, Cohen M, Evers S, Giamberardino MA, Go ̈bel A, Korwisi B, Perrot S, Svensson P, Wang SJ, Treede RD. The IASP Taskforce for the Classification of Chronic pain. The IASP classification of chronic pain for ICD-11: chronic primary pain. PAIN 2019;160:28–37. 

Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, Cohen M, Evers S, Finnerup NB, First MB, Giamberardino MA, Kaasa S, Kosek E, Lavand’homme P, Nicholas M, Perrot S, Scholz J, Schug S, Smith BH, Svensson P, Vlaeyen JW, Wang SJ. A classification of chronic pain for ICD-11. PAIN 2015;156:1003–7. 

Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, Cohen M, Evers S, Finnerup NB, First MB, Giamberardino MA, Kaasa S, Korwisi B, Kosek E, Lavand’homme P, Nicholas M, Perrot S, Scholz J, Schug S, Smith BH, Svensson P, Vlaeyen JWS, Wang SJ. Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11). Pain. 2019 Jan;160(1):19-27. doi: 10.1097/j.pain.0000000000001384. PMID: 30586067. 

World Health Organization. ICD-11 alpha. Content model reference guide. Geneva: WHO, 2011. 

3. IMMPACT recommendations: Patients phenotyping

 

The inter-individual large variability in the response to analgesic treatments and the evidence-based research to identify the algorithm for an optimal treatment (called also “precision medicine” or personalized pain treatment), led various researchers to search for new benchmarks for the therapeutic approach. The need for a change of perspective was summarized by: 

1. Numerous high quality randomized controlled trial (RCT) for drugs in several chronic pain syndromes produced negative results although the preclinical and previous clinical studies were encouraging.
2. b. multiple pain mechanism and outcome patients characteristics leading to marked variation in the treatment effect among patients. 
3. c. long term analgesic treatment involves risks of overdose (opioids), drug abuse or misuse or organ damage

The variability of phenotypic presentation of different pain syndromes indicating that mechanistic etiologies and subsequent successful treatment are likely to be based at the level of the individual rather than at the level of the disease. 

A consortium called Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT), convened a meeting to developed recommendations for the domain and specific measures to apply the patients phenotyping for chronic pain clinical trials (phase 2 and 3).  This perspective is relevant to investigate several factors to recognise which phenotypic characteristics can predict the placebo response. For example, some researches identify that the higher level of intensity of pain at baseline is correlated with active agents than placebo in the trial clinic (Dworkin et al., 2012). However, this is not true for neuropathic pain because the more intense pain at baseline is selectively associated with greater improvement of active treatment vs placebo (Dworkin et al., 2013)   

There are some “moderators” (phenotypic characteristics is differently associated with outcome in different study treatment arms) that enhancing the assay sensitivity of analgesic trials (Edward et al., 2016).  

Some patient’s characteristics have been identified. 

Phenotypic Domains 

 

1. Psychosocial factors

Mood disorders 

Depression  

Anxiety 

Stress 

High level of negative affect 

Pain specific distress 

These factors reduced benefit from a variety of potentially pain-reducing treatments (Edwards et al. 2011). 

The HADS (Hospital Anxiety depression scale) self report assessment for depression and anxiety has been suggested the better questionnaire because not include items for somatic distress symptoms (Arnold et al., 2007; Ciaramella & Poli, 2001). 

 

2. 2. Pain variability and pain qualities

 

The use of methods that capture in the real-time the outcome measures in analgesic trials as patients differ widely in the degree of temporal variability in their ratings of pain intensity. For example the Fibromyalgia have a stable rating of intensity of pain during one study (Dworkin et al., 2012), suggesting a placebo response in them with high variability.   

 

3. Neuropathic pain symptom reporting instruments

Several questionnaires (LANSS; DN4; pain DETECT questionnaire) have been suggested to assess neuropathic pain but for diagnostic purposes, self-report screening instruments should not replace a comprehensive clinical examination (Haanpaa et al., 2011). 

4. Sleep and Fatigue

Longitudinal studies have been showed a reciprocal relationship between pain and insomnia (Finan et al., 2013). The treatment outcome is influenced by this reciprocal influence. For example the phenotypic measure for a better outcome of Pregabalin treatment is the disrupted sleep at baseline (Vinik et al., 2014). Fatigue co-occur with sleep for symptoms cluster in the persistent pain conditions but not published data have been reported that demonstrates fatigue as the phenotypic measure (Vincent et al., 2014). 

5. Quantitative sensory testing (QST) and sensory profiling

QST refers to a set of psychophysical methods used to quantify somatosensory function. It is a psychophysical method and it can consider as a “trans-etiological” making information about sensory deficit and pain sensory mechanisms being a fruitful target for specific therapeutic approaches. For example the cold hyperalgesia is a potent predictor of placebo response among patients with unilateral lateral epicondylalgia (Coombes et al., 2015). 

6. Conditioned pain modulation [CPM] and other indices of pain modulation

Applying Diffuse Noxious Inhibitory Control (DNIC) paradigms to humans, Yarnitsky and colleagues postulated that patients showing decrements in CPM should benefit more from serotonin-noradrenaline re-uptake inhibitors (SNRIs), which augment descending inhibition by spinal monoamine reuptake inhibition, than patients whose CPM appears to be functioning effectively (Yarnitsky et al., 2012). 

7. Response to pharmacologic challenge

Using predicted pharmacological test can help to predict the outcome of treatments. For example: Cohen and colleagues has suggested that response to an IV ketamine infusion is a significant predictor of intermediate-term relief with subsequent dextromethorphan treatment in patients with neuropathic pain (Cohen et al., 2006). 

References 

Arnold LM, Crofford LJ, Martin SA, Young JP, Sharma U. The effect of anxiety and depression on improvements in pain in a randomized, controlled trial of pregabalin for treatment of fibromyalgia. Pain Med. 2007; 8(8):633–638. [PubMed: 18028041] 

Ciaramella A, Poli P. Assessment of depression among cancer patients: the role of pain, cancer type and treatment. Psychooncology. 2001 Mar-Apr;10(2):156-65. doi: 10.1002/pon.505. PMID: 11268142. 

Cohen SP, Verdolin MH, Chang AS, Kurihara C, Morlando BJ, Mao J. The intravenous ketamine test predicts subsequent response to an oral dextromethorphan treatment regimen in fibromyalgia patients. J Pain. 2006; 7(6):391–398. [PubMed: 16750795] 

Coombes BK, Bisset L, Vicenzino B. Cold hyperalgesia associated with poorer prognosis in lateral epicondylalgia: a 1-year prognostic study of physical and psychological factors. Clin J Pain. 2015; 31(1):30–35. [PubMed: 24480912] 

Dworkin RH, Turk DC, Peirce-Sandner S, Burke LB, Farrar JT, Gilron I, Jensen MP, Katz NP, Raja SN, Rappaport BA, Rowbotham MC, Backonja MM, Baron R, Bellamy N, Bhagwagar Z, Costello A, Cowan P, Fang WC, Hertz S, Jay GW, Junor R, Kerns RD, Kerwin R, Kopecky EA, Lissin D, Malamut R, Markman JD, McDermott MP, Munera C, Porter L, Rauschkolb C, Rice AS, Sampaio C, Skljarevski V, Sommerville K, Stacey BR, Steigerwald I, Tobias J, Trentacosti AM, Wasan AD, Wells GA, Williams J, Witter J, Ziegler D. Considerations for improving assay sensitivity in chronic pain clinical trials: IMMPACT recommendations. Pain. 2012; 153(6):1148–1158. [PubMed: 22494920] 

Dworkin RH, Turk DC, Peirce-Sandner S, He H, McDermott MP, Farrar JT, Katz NP, Lin AH, Rappaport BA, Rowbotham MC. Assay sensitivity and study features in neuropathic pain trials: an ACTTION meta-analysis. Neurology. 2013; 81(1):67–75. [PubMed: 23700332] 

Edwards RR, Cahalan C, Mensing G, Smith M, Haythornthwaite JA. Pain, catastrophizing, and depression in the rheumatic diseases. Nat Rev Rheumatol. 2011; 7(4):216–224. [PubMed: 21283147] 

Edwards RR, Dworkin RH, Turk DC, Angst MS, Dionne R, Freeman R, Hansson P, Haroutounian S, Arendt-Nielsen L, Attal N, Baron R, Brell J, Bujanover S, Burke LB, Carr D, Chappell AS, Cowan P, Etropolski M, Fillingim RB, Gewandter JS, Katz NP, Kopecky EA, Markman JD, Nomikos G, Porter L, Rappaport BA, Rice ASC, Scavone JM, Scholz J, Simon LS, Smith SM, Tobias J, Tockarshewsky T, Veasley C, Versavel M, Wasan AD, Wen W, Yarnitsky D. Patient phenotyping in clinical trials of chronic pain treatments: IMMPACT recommendations. Pain. 2016 Sep;157(9):1851-1871. doi: 10.1097/j.pain.0000000000000602. PMID: 27152687; PMCID: PMC5965275. 

Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013; 14(12):1539–1552. [PubMed: 24290442] 

Haanpaa M, Attal N, Backonja M, Baron R, Bennett M, Bouhassira D, Cruccu G, Hansson P, Haythornthwaite JA, Iannetti GD, Jensen TS, Kauppila T, Nurmikko TJ, Rice AS, Rowbotham M, Serra J, Sommer C, Smith BH, Treede RD. NeuPSIG guidelines on neuropathic pain assessment. Pain. 2011; 152(1):14–27. [PubMed: 20851519] 

Vincent A, Hoskin TL, Whipple MO, Clauw DJ, Barton DL, Benzo RP, Williams DA. OMERACT-based fibromyalgia symptom subgroups: an exploratory cluster analysis. Arthritis Res Ther. 2014; 16(5):463. [PubMed: 25318839] 

Vinik A, Emir B, Parsons B, Cheung R. Prediction of pregabalin-mediated pain response by severity of sleep disturbance in patients with painful diabetic neuropathy and post-herpetic neuralgia. Pain Med. 2014; 15(4):661–670. [PubMed: 24330406] 

Yarnitsky D, Granot M, Nahman-Averbuch H, Khamaisi M, Granovsky Y. Conditioned pain modulation predicts duloxetine efficacy in painful diabetic neuropathy. Pain. 2012; 153(6):1193– 1198. [PubMed: 22480803] 

 

Antonella Ciaramella  

Lab. Psychosomatic medicine 

GIFT Institute of Integrative Medicine Pisa, Italy 

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Reply by Antonella Ciaramella about the Psychological Aetiology of pain, diagnosis proposed for the IASP classification, as suggested during the 2022 EAPM SIG Chronic pain zoom meeting in Vienna.  

Since the time of Freud the conversion of pain, the negative emotions converted into the body pain (Breuer and Freud, 1957), the psychological pain entity has been debated. This nosological entity was subsequently revised by Engel (1959) and Blumer and Heilbron (1981) intruduced the concept of pain prone subjects as a variant of depressive illness. 

Subsequent proposals have been made in this regard and recently the classification of ICD-11 includes the psychological aspects as integrative part of primary pain (Treede et al., 2019).  

The Neuromatrix introduced by Melzack (2001), emphasizes the inseparable and indistinguishable mind-body aspects of pain. Relevant is what they wrote Melzack and Katz (2013): “Pain is a personal, subjective experience influenced by cultural learning, the meaning of the situation, attention, and other psychological variables”; and still: “the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress”.  

In conclusion, it is impossible to separate the physical component from the psychic one whatever the aetiology. 

 

References 

Breuer, J., & Freud, S. (1957). Studies on hysteria. Basic Books. 

Blumer D, Heilbronn M. The pain-prone disorder: a clinical and psychological profile. Psychosomatics. 1981 May;22(5):395-7, 401-2. doi: 10.1016/S0033-3182(81)73509-6. PMID: 7280171. 

Engel GL. Psychogenic pain and pain-prone patient. Am J Med. 1959 Jun;26(6):899-918. doi: 10.1016/0002-9343(59)90212-8. PMID: 13649716. 

Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, Cohen M, Evers S, Finnerup NB, First MB, Giamberardino MA, Kaasa S, Korwisi B, Kosek E, Lavand’homme P, Nicholas M, Perrot S, Scholz J, Schug S, Smith BH, Svensson P, Vlaeyen JWS, Wang SJ. Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11). Pain. 2019 Jan;160(1):19-27. doi: 10.1097/j.pain.0000000000001384. PMID: 30586067. 

Melzack R. Pain and the neuromatrix in the brain. J Dent Educ. 2001 Dec;65(12):1378-82. PMID: 11780656. 

Melzack R, Katz J. Pain. Wiley Interdiscip Rev Cogn Sci. 2013 Jan;4(1):1-15. doi: 10.1002/wcs.1201. Epub 2012 Oct 4. PMID: 26304172. 

 

 

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Short minutes of the Chronic Pain SIG group meeting, Friday 10th 8-9 am, on site at the EAPM conference in Vienna, and on Zoom. 

 

The meeting was hold by Antonella Ciaramella(  AC)  President of the Chronic Pain SIG group on Zoom and animated by Anne-Françoise Allaz (AFA) on the site. 

About 15 persons participated in the meeting on site. We started with a presentation of each person – which took some time for technical reasons (sound problems). 

 

1. Antonella Ciaramella (AC) presented the new ICD-11 definition of pain and the new categorization of acute and chronic pain.   

Antonella Ciaramella then raised the question of the space left for pain with “psychological aetiology” in this classification. 

In the following discussion:  

• the introduction of pain as an entity in the classification of diseases was greeted. 
• The comprehensive and global system of classification is a seen as useful and opening a new paradigm for pain. 

• Most participants expressed the view that there was enough room for the psychological aspects and were satisfied about their integration in the classification. 

1. At the end of the meeting, very rapidly the impact evaluation was presented by AC. with two cases as an example.
   There was really not enough time to react to this proposal which should be discussed in depth at a later occasion.  

1. Many people marked an interest in the SIG group and accepted to give their mail-addresses. Many thanks to Ina Knoop who collected the addresses and typed them. 

 

1. Propositions (not formally discussed at the meeting, made here by Anne-F Allaz) 

• As already discussed a Zoom meeting of the SIG group should be called at the beginning of september 2022 to prepare a Symposium and a SIG group meeting for the next EAPM conference 2023 (Wroclaw, Poland ). I have been asking personally the President of next years’ meeting to widen the possibility of presenting SIG group symposia… Let’s hope! 
• The new ICD-11 Pain classification could be introduced in our chronic pain page on the EAPM website 
• The Impact evaluation however has not yet been sufficiently discussed and should  be analysed with the group before being posted on our page.  (I must say that I find it problematic and look forward to a discussion). 
• Our activities should be announced to the persons in the e-mail list. 

 

 

Cordially, 

Anne-Françoise Allaz 

Geneva Tuesday June 14th.