Medicine, Faculty of
Other UBC
Obstetrics and Gynaecology, Department of
DSpace
Journal of Clinical Medicine 13 (24): 7521 (2024)
Women's Health Research Institute (British Columbia)
Gentles, Avonae
Goodwin, Emma
Bedaiwy, Yomna
Marshall, Nisha
Yong, Paul J.
Endometriosis is an inflammatory chronic condition associated with nociceptive, neuropathic, and nociplastic pain. Central sensitization (CS) is the primary nociplastic pain mechanism. However, there are currently no standardized methods for detecting CS or nociplastic pain. This review aims to identify available tools for characterizing CS/nociplastic pain in endometriosis-related chronic pelvic pain. Following the PRISMA-P protocol, MEDLINE, Embase, Scopus, and PsychINFO databases were searched on 23 April 2024, for the terms “endometriosis”, “central sensitization”, “nociplastic pain”, “widespread pain”, and “assessment tools”. Publications were selected if they mentioned tool(s) for detecting nociplastic pain or CS in endometriosis patients. Information was extracted on study demographics, assessment types, and the tools used for detection. Of the 379 citations retrieved, 30 papers met the inclusion criteria. When working to identify CS and nociplastic pain, fourteen studies exclusively used patient-reported questionnaires, six used quantitative sensory testing (QST), two used clinical assessments, and eight used multiple approaches combining patient-reported questionnaires and clinical assessment. This review illustrates the diversity of tools currently used to identify CS and nociplastic pain in endometriosis patients. Further research is needed to evaluate their validity and to standardize methods in order to improve the accuracy of nociplastic pain identification and guide treatment.
Citation: Gentles, A.; Goodwin, E.;Bedaiwy, Y.; Marshall, N.; Yong, P.J.Nociplastic Pain in Endometriosis: AScoping Review. J. Clin. Med. 2024, 13,7521. https://doi.org/10.3390/jcm13247521Academic Editor: CorneliaBachmannReceived: 22 October 2024Revised: 30 November 2024Accepted: 5 December 2024Published: 10 December 2024Copyright: © 2024 by the authors.Licensee MDPI, Basel, Switzerland.This article is an open access articledistributed under the terms andconditions of the Creative CommonsAttribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).ReviewNociplastic Pain in Endometriosis: A Scoping ReviewAvonae Gentles 1,2 , Emma Goodwin 2, Yomna Bedaiwy 2, Nisha Marshall 1 and Paul J. Yong 1,2,3,*1 Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, BC V6H 3N1, Canada;avonae.gentles@cw.bc.ca (A.G.); nisha.marshall@cw.bc.ca (N.M.)2 BC Women’s Center for Pelvic Pain and Endometriosis, Vancouver, BC V6H 3N1, Canada;emma.goodwin@cw.bc.ca (E.G.); yomna04@student.ubc.ca (Y.B.)3 Women’s Health Research Institute, Vancouver, BC V6H 3N1, Canada* Correspondence: paul.yong@vch.ca; Tel.: +1-604-875-2534; Fax: +1-604-875-2569Abstract: Endometriosis is an inflammatory chronic condition associated with nociceptive, neuro-pathic, and nociplastic pain. Central sensitization (CS) is the primary nociplastic pain mechanism.However, there are currently no standardized methods for detecting CS or nociplastic pain. Thisreview aims to identify available tools for characterizing CS/nociplastic pain in endometriosis-related chronic pelvic pain. Following the PRISMA-P protocol, MEDLINE, Embase, Scopus, andPsychINFO databases were searched on 23 April 2024, for the terms “endometriosis”, “central sensiti-zation”, “nociplastic pain”, “widespread pain”, and “assessment tools”. Publications were selected ifthey mentioned tool(s) for detecting nociplastic pain or CS in endometriosis patients. Informationwas extracted on study demographics, assessment types, and the tools used for detection. Of the379 citations retrieved, 30 papers met the inclusion criteria. When working to identify CS and noci-plastic pain, fourteen studies exclusively used patient-reported questionnaires, six used quantitativesensory testing (QST), two used clinical assessments, and eight used multiple approaches combiningpatient-reported questionnaires and clinical assessment. This review illustrates the diversity of toolscurrently used to identify CS and nociplastic pain in endometriosis patients. Further research isneeded to evaluate their validity and to standardize methods in order to improve the accuracy ofnociplastic pain identification and guide treatment.Keywords: endometriosis; nociplastic pain; central sensitization; peripheral sensitization; pain phenotyping1. IntroductionThe goal of this scoping review is to assess the state of the literature regarding no-ciplastic pain in endometriosis. In 2021, the International Association for the Study ofPain (IASP) updated their definitions and clinical criteria for musculoskeletal pain [1].One of the aims of this update was to provide more precise definitions of 3 pain types:nociceptive, neuropathic, and nociplastic pain [2]. According to the IASP, nociceptivepain refers to “pain that arises from actual or threatened damage to non-neural tissue andis due to the activation of nociceptors” [1]. This differs from neuropathic pain, which isdescribed as “pain caused by a lesion or disease of the somatosensory nervous system” [1,2].Nociplastic pain is a descriptive term used to characterize the pain phenotype that couldnot be exclusively defined as nociceptive or neuropathic [3]. In the 2021 definition, theIASP defines nociplastic pain as “[p]ain that arises from altered nociception despite noclear evidence of actual or threatened tissue damage causing the activation of peripheralnociceptors or evidence for disease or lesion of the somatosensory system causing thepain” [1,2]. Clinically, nociplastic pain is defined by four patient-reported requirements:(1) A pain duration of at least 3 months;(2) A regional pain distribution (i.e., not discrete);(3) Pain that is not entirely explained by nociceptive or neuropathic mechanisms;(4) Signs of pain hypersensitivity [2].J. Clin. Med. 2024, 13, 7521. https://doi.org/10.3390/jcm13247521 https://www.mdpi.com/journal/jcmJ. Clin. Med. 2024, 13, 7521 2 of 17If a patient meets all four of these criteria, they are considered to have “possible nociplasticpain” [1,2]. However, if a patient meets these criteria, has a history of hypersensitivity in theregion of pain, and one or more of the following comorbidities—increased sensitivity to sound,light, and/or odors, sleep disturbance, fatigue, or cognitive problems—they are considered tohave “probable nociplastic pain” [2].Notably, there is a lack of clinical criteria for definite nociplastic pain. This uncertaintyin the definition of nociplastic pain has resulted in variability in its clinical interpretationand identification. Patients with conditions such as fibromyalgia, irritable bowel syndrome,and bladder pain syndrome are often characterized as having nociplastic pain. Thiscan be attributed to heightened pain perception, which results in symptoms of chronicabdominopelvic pain and widespread musculoskeletal pain [3–5]. Chronic pain conditionstend to be highly heterogenous, with some patients experiencing more than one of thesethree types of pain [6]. To add further complexity, nociceptive inputs from peripheraltissues and neuropathic pain can also influence the development and persistence of centralnervous system (CNS) sensitization [7,8].Central nervous system sensitization (central sensitization or CS) describes the “am-plification of neural signaling within the CNS that elicits pain hypersensitivity” and is theprimary underlying mechanism in nociplastic pain [3,9]. CS can develop from differentunderlying causes. In some cases, peripheral damage can lead to the sensitization of theCNS in a way that persists over time but can be resolved with interventions that treat theperipheral cause. In other cases, CS is driven by a central component that is independent ofperipheral damage, and thus does not respond to treatments that target this damage [7].The peripheral sensitization of local nociceptors, which describes increased responsivenessat the primary site of pain (called primary hyperalgesia), can also occur, and this maylead to the development of, or exist alongside, CS [10,11]. However, while peripheralsensitization is a local pathology, one indicator of CS is an increased sensitivity to stimulioutside of the area where the primary injury or damage occurred (secondary hyperalge-sia) [7,11]. Other clinical manifestations of CS include regional allodynia, defined as paindue to a normally non-painful stimulus [1,12]. CS has also been linked to psychologicalfactors such as anxiety, panic attacks, and depression [13]. While some conditions, such asfibromyalgia, have been studied in relation to CS and treatment outcomes, others are stilllacking research [7].Endometriosis is an inflammatory chronic pain condition characterized by the growthof endometrial-like lesions outside of the uterus [14]. These lesions are predominantlyfound in the abdominopelvic organs and peritoneal cavity [15,16]. These endometrial-liketissues are hormonally regulated (estrogen-dependent), with a component of local inflam-mation contributing to nociceptive pain [15]. Increasing evidence also supports the roleof multifactorial contributors to pain such as abdominal wall pain, pelvic floor myalgia,and higher scores on the pain catastrophizing scale in individuals with endometriosis [17].Endometriosis-related pain can take several forms, including dysmenorrhea (painful men-struation), dyschezia (painful bowel movements), dysuria (painful urination), dyspareunia(painful sexual activity), and cyclical and noncyclic pelvic pain [18]. Endometriosis isknown to be heterogenous, and patients often report a variety of outcomes for the sametreatment [19]. Nociplastic pain may provide an explanation for some of this heterogeneity.However, there are currently no known standardized methods for characterizing nociplas-tic pain in endometriosis-specific populations. This gap presents a limitation in treatingendometriosis-related chronic pelvic pain. As such, this review intends to elucidate the cur-rent tools that are being used to identify nociplastic pain in endometriosis pain populationsand assess the quality of evidence in support of their use.Historically, endometriosis-related pain was considered a result of local inflammationand irritation from lesions or nodules and was thus conceptualized as predominantlynociceptive [20]. Recent studies suggest nociceptive, neuropathic, and nociplastic mecha-nisms could all be associated with endometriosis-related pain [18]. Endometriosis-relatedneuropathic pain results from damage to the nerves surrounding endometriosis lesionsJ. Clin. Med. 2024, 13, 7521 3 of 17or nodules [19]. CS and nociplastic pain are clinically relevant, as studies show thatendometriosis patients with more symptoms of CS are more likely to experience worsepelvic pain symptoms, independent of endometriosis type or previous surgery [21]. Infact, endometriosis patients with clinical indicators or comorbidities commonly associ-ated with CS have a worse quality of life and higher pain scores for chronic pelvic pain,deep dyspareunia, dyschezia, and back pain following surgical treatment for endometrio-sis [10,22,23]. Thus, the ability to clinically assess for nociplastic pain characteristics andthe presence of CS is imperative. Moreover, the improved classification of nociplastic painand CS in clinical settings could enable the implementation of more personalized paintreatments, targeting specific pain phenotypes and their multifactorial influences in peoplewith endometriosis-related pain [7].We conducted a scoping review to determine the scope of available tools and resourcesfor characterizing CS in endometriosis patients and assess their quality.2. Scoping Review: Identifying Nociplastic Pain in Endometriosis2.1. RationaleIdentifying patients with endometriosis who present with symptoms of CS, andconsequently, nociplastic pain, is paramount to improving their quality of life and painoutcomes. While there are various questionnaires and assessments clinically used to detectnociceptive and neuropathic pain in endometriosis populations, there are currently nostandardized methods of detecting nociplastic pain. This discrepancy may stem fromthe relative novelty of the nociplastic pain phenotype in the research community [9].Nociplastic pain and CS exemplify neuroplasticity, occurring at cellular and functionallevels, and often present unclear clinical features [2,8,24]. Combined with the subjectivenature of pain and the frequently heterogeneous clinical presentations that overlap withpsychological factors such as anxiety and depression, capturing instances of CS in a clinicalsetting is challenging [25,26]. Fortunately, there are an increasing number of methodsfor detecting and quantifying the degree of CS that may act as a proxy for nociplasticpain in chronic pain populations. For example, the Central Sensitization Inventory (CSI)has been validated and used to assess CS in endometriosis populations [27]. It providesan estimate of the impact of CS symptoms on a scale from 0 to 100. The CSI is able todistinguish between patients with chronic overlapping pain conditions (COPCs) and thosewith chronic pain conditions without a central pain component, as well as between patientswith COPCs and healthy controls [28,29]. Additionally, in an endometriosis population, a40-point cutoff has shown clinical significance [27], which the CSI correlating with worsepain outcomes following endometriosis surgery [23]. However, the CSI is only a proxyand may primarily be associated with psychological factors such as stress, depression, andanxiety [26]. Nonetheless, having a standardized and widely accepted clinical tool that canefficiently and effectively identify these patients is essential for treating endometriosis andmanaging pain.Quantitative sensory testing (QST) is a semi-objective test that is frequently used todetect modulations in somatosensory processing in people with CS through a battery ofsensory and pain threshold tests [30]. Another method includes using functional magneticresonance imaging (fMRI) to detect changes in gray matter in areas of the brain related topain sensation [31]. However, both these methods are resource-extensive and not feasiblefor use in clinical settings. Furthermore, ongoing research is needed to further validatethese methods as an indicator of CS in endometriosis populations. As a result, there may bea subset of people living with endometriosis who also experience CS and nociplastic painthat remains unrecognized and untreated. In fact, within 5 years of standard endometriosistreatment, over 40% of patients will experience persistent or recurrent pain [32]. Thisscoping review investigates the range of questionnaires, tools, and clinical assessmentsbeing used to detect CS or nociplastic pain in populations with endometriosis-relatedpain. This review will provide an overview of current tools and methods of assessmentbeing used to detect CS and nociplastic pain in an endometriosis pain population, alongJ. Clin. Med. 2024, 13, 7521 4 of 17with supporting evidence. The findings from this review will inform future researchseeking to determines the optimal clinical approach for identifying CS and nociplastic painin endometriosis.2.2. MethodsThis scoping review adhered to the Preferred Reporting Items for Systematic Reviewsand Meta-analysis extension for Scoping Review (PRISMA-ScR) (Table S2 in SupplementaryMaterials) [33]. Additionally, the protocol was created using the Preferred Reporting Itemsfor Systematic Reviews and Meta-analysis Protocols (PRISMA-P) and was revised by theresearch team. The final protocol was registered on the Open Science Framework (OSF)(https://www.cos.io/ accessed on 12 April 2024) on 12 April 2024 and can be found at(https://doi.org/10.17605/OSF.IO/S358T) [34,35].With the aid of a health science librarian, we conducted a systematic search of MED-LINE, Embase, Scopus, and PsychINFO on 23 April 2024. We used the following keyterms: “endometriosis”, “central sensitization”, “nociplastic pain”, “widespread pain”,and “assessment tools”. The final search strategy used for MEDLINE can be found inTable S1 in the Supplementary Materials. Given the novelty of nociplastic pain in IASP’scharacterization of pain, we did not apply any time limits. The final search was uploadedto Veritas Health Innovation (Melbourne, Australia) Covidence systematic review software(www.covidence.org accessed on 23 April 2024), an online platform that facilitates the pro-duction of systematic and other literature reviews [36]. We excluded published abstracts,editorial letters, preclinical studies, and studies that were not written in English.Abstract and full-text text screening were conducted in duplicate by two independentreviewers (AG and NM) according to eligibility criteria outlined in the review protocol. Allpublications that explicitly mentioned the use of a tool to detect nociplastic pain or centralsensitization in people with endometriosis-related pain were included. All discrepancies wereresolved by a third party (EG) or discussion. Before screening, AG, NM, and EG reviewedfive publications together to ensure a clear understanding of the eligibility criteria. The datacollection form was jointly created by members of the team in order to determine variablesthat were meaningful for extraction. Data extraction was conducted by AG and NM, who usedinformation on study demographics (i.e., country of origin, author, study type), assessment type(i.e., patient-reported, clinician-reported, etc.), the tool used for detecting nociplastic pain orcentral sensitization, and the study’s reasoning or psychometric properties if they were available.We conducted a narrative synthesis of all included studies, which were groupedaccording to assessment type and the tool used. When we encountered a systematic review,we noted the type of assessment used to identify central sensitization or nociplastic pain ineach study.2.3. ResultsA total of 379 citations were retrieved from the databases. After removing 148 du-plicates, 231 citations underwent title and abstract screening. Of these, 67 proceeded tofull-text screening and were assessed for eligibility. All told, 37 studies were excluded forthe following reasons: 1 was a letter to the editor, 11 were published abstracts, 3 did nothave the full text available, 1 did not have an endometriosis population, 9 did not mentionan assessment tool or questionnaire, and 12 did not focus on central sensitization (CS),nociplastic pain, or widespread pain. In total, 30 papers were included in the final reviewand underwent data extraction. The PRISMA flow diagram for study inclusion is shown inFigure 1. Of the 30 papers, 21 (70%) were primary research articles including cross-sectional(n = 12), cohort (n = 7), case–control (n = 1), and cross-over (n = 1) studies, where themethod used to identify sample endometriosis participants with CS or nociplastic painwas clearly stated. The remaining 9 papers were reviews that explicitly stated a tool orassessment method used to identify CS, nociplastic pain, or widespread pain.J. Clin. Med. 2024, 13, 7521 5 of 17J. Clin. Med. 2024, 13, x FOR PEER REVIEW 5 of 18 was clearly stated. The remaining 9 papers were reviews that explicitly stated a tool or assessment method used to identify CS, nociplastic pain, or widespread pain. Figure 1. PRISMA flow diagram. Most studies were from the United States (n = 8), Italy (n = 6), and Canada (n = 4). The remaining countries, each with fewer than 4 studies, were Australia, Brazil, China, Den-mark, France, New Zealand, Spain, Sweden, and the United Kingdom. All studies refer-enced an adult population experiencing endometriosis-related chronic pelvic pain. A complete list of included papers and their general demographics is shown in Table 1. Ap-proximately, half (14/30) of the studies reported the exclusive use of patient-reported questionnaires to identify CS and nociplastic pain. Conversely, 6 papers exclusively refer-enced the use of semi-objective assessments like QST to identify CS and nociplastic pain, with the pressure pain threshold (PPT) consistently used across all studies. Only 2 studies exclusively mentioned clinical assessments as a method of detecting CS: one focused on identifying abdominopelvic trigger points, while the other used the convergence pelvic and perineal (PP) criteria. Lastly, 27% (8/30) of the papers used mixed methods of identi-fication. This involved the collective use of patient-reported questionnaires, including the PainDETECT questionnaire, the McGill questionnaire, the brief pain inventory, and the Figure 1. PRISMA flow diagram.Most studies were from the United States (n = 8), Italy (n = 6), and Canada (n = 4).The remaining countries, each with fewer than 4 studies, were Australia, Brazil, China,Denmark, France, New Zealand, Spain, Sweden, and the United Kingdom. All studiesreferenced an adult population experiencing endometriosis-related chronic pelvic pain.A complete list of included papers and their general demographics is shown in Table 1.Approximately, half (14/30) of the studies reported the excl sive se of patient-reportequestionnaires to i e tif a ci lastic ai . ersel , 6 a ers e cl si el refer-e ce t e se of se i- jecti t li t i tif i l ti i ,ith the pressure pain threshold (PPT) consistently used acros all studies. nly 2 st iesexcl si l i li t f etecti : o e foc se oni e tif i i t i i il t t r use the convergence pelvica ri l 30) of the papers used mixed methods of identification. This involved the collective use of patient-reported questionnaires, includingthe PainDETECT questionnaire, the McGill questionnaire, the brief pain i ventory, andthe visual analogue scale (VAS), along with QST modalities and clinical assessments. Asummary of the assessments identified in all 30 papers is shown in Table 2.J. Clin. Med. 2024, 13, 7521 6 of 17Table 1. Study characteristics.Authors, Year. Country Study Type Assessment Type Methods for CS/Nociplastic Detection1 Bajaj et al.,2003 [37] Denmark Case–control MixedVAS and McGill pain questionnaire +body mapPressure pain threshold (PPT)Tactile threshold2 Laursen et al.,2005 [38] Denmark Cross-sectional Semi-objective Pressure pain threshold (PPT)3 He et al.,2010 [39] China Prospective cohort MixedElectrical pain threshold (EPT)Ischemic pain tests (IPTs)Short-form McGill pain questionnaire4 Napadowet al., 2012 [40] United States Cross-over Semi-objectivePressure pain threshold (PPT)Wind-up ratio (WUR)Diffuse noxious inhibitorycontrol (DNIC)5 Giamberardinoet al., 2014 [41] Italy Narrative review Semi-objectiveSomatic pain thresholdsElectrical pain threshold (EPT)Ischemic pain tests (IPTs)6 Aredo et al.2017 [42] United States Narrative review Clinical examinationDigital exam of myofascial triggerpoints in abdominopelvic areacoupled withneuromusculoskeletal exam7 Costantiniet al., 2017 [43] Italy Prospective cohort Semi-objectivePressure pain threshold (PPT)Electrical pain thresholds (EPT)8 Grundstromet al., 2019 [44] Sweden Cross-sectional Semi-objectiveHeat pain threshold (HPT)Cold pain threshold (CPT)Pressure pain threshold (PPT)9 Orr et al.,2020 [45] Canada Cross-sectional MixedCentral sensitization inventory (CSI)+ Digital exam for bladder/pelvicfloor tenderness10 As-Sanie et al.,2021 [46] United States Prospective cohortPatient-reportedquestionnaire Fibromyalgia survey score (FSS)11 Evans et al.,2021 [47] Australia Cross-sectionalPatient-reportedquestionnaire Fibromyalgia survey score (FSS)12 Phan et al.,2021 [48] United States Cross-sectional MixedBrief pain inventory (BPI)Pressure pain threshold (PPT)Digital exam of myofascial triggerpoints in abdominopelvic areacoupled withneuromusculoskeletal exam13 Shafrir et al.,2021 [49] United States Cross-sectional Semi-objective Pressure pain threshold (PPT)14 De Arrudaet al., 2022 [50] Brazil Cross-sectionalPatient-reportedquestionnaire Central sensitization inventory (CSI)15 Green et al.,2022 [51] United States Narrative reviewPatient-reportedquestionnaire Central sensitization inventory (CSI)16 Orr et al.,2022 [27] Canada Prospective cohort MixedCentral sensitization inventory (CSI)Central sensitivity syndromes andother pelvic pain relatedcomorbidities (CSSs)17 Ryan et al.,2022 [52] New Zealand Cross-sectionalPatient-reportedquestionnaire Central sensitization inventory (CSI)18 Simpson et al.,2022 [53] Australia Systematic review MixedIschemic pain test (IPT)Electrical pain test (EPT)McGill pain questionnaire + VASWind-up ratio (WUR)Mechanical pain threshold (MPT)Digital exam of myofascial triggerpoints in abdominopelvic areaCentral sensitivity syndromes andother pelvic pain relatedcomorbidities (CSSs)J. Clin. Med. 2024, 13, 7521 7 of 17Table 1. Cont.Authors, Year. Country Study Type Assessment Type Methods for CS/Nociplastic Detection19 Till et al.,2022 [54] United States Narrative reviewPatient-reportedquestionnaire Fibromyalgia survey score (FSS)20 Cardaillacet al., 2023 [55] France Prospective cohort Clinical examinationConvergence PP criteria(10 clinical criteria)21 Cetera et al.,2023 [56] Italy Narrative reviewPatient-reportedquestionnaireCentral sensitization inventory (CSI)Fibromyalgia survey score (FSS)22 Cetera et al.,2023 [57] Italy Literature reviewPatient-reportedquestionnaire Central sensitization inventory (CSI)23 Coxon et al.,2023 [18] United Kingdom Narrative review MixedDFNS 13 QST ModalitiesPainDETECT Questionnaire24 Orr et al.,2023 [23] Canada Prospective cohortPatient-reportedquestionnaire Central sensitization inventory (CSI)25Quintas-Marques et al.,2023 [58]Spain Cross-sectional Patient-reportedquestionnaire Central sensitization inventory (CSI)26 Raimondoet al., 2023 [13] Italy Cross-sectionalPatient-reportedquestionnaire Central sensitization inventory (CSI)27 Till et al.,2023 [21] United States Cross-sectionalPatient-reportedquestionnaire Fibromyalgia survey score (FSS)28 Cetera et al.,2023 [59] Italy Systematic reviewPatient-reportedquestionnaireCentral sensitization inventory (CSI)Fibromyalgia survey score (FSS)29 Coxon et al.,2023 [4] United Kingdom Cross-sectional MixedDFNS 13 QST ModalitiesPainDETECT Questionnaire30 Liu et al.,2024 [60] Canada Prospective cohortPatient-reportedquestionnaire Central sensitization inventory (CSI)Table 2. Summary of assessments/tools for nociplastic pain in endometriosis.ClinicalPatient-Reported Outcomes and Physical Examination• Central sensitization inventory (CSI);• Fibromyalgia survey score (FSS);• PainDETECT;• Brief pain inventory (BPI);• McGill pain questionnaire;• Visual analog scale (VAS);• Central sensitivity syndromes (CSS) or Chronic overlapping pain conditions (COPC);• Digital exam of myofascial trigger points (e.g., abdominal);• Digital exam for (bladder +) pelvic floor tenderness;• Convergence PP criteria.ResearchSensory Testing• Quantitative sensory resting (QST) 1;• Diffuse noxious inhibitory control (DNIC);• Electrical pain threshold (EPT);• Ischemic pain tests (IPTs).1 DFNS QST protocol [30].2.4. Discussion2.4.1. Patient-Reported QuestionnairesGiven the complex pathophysiology of nociplastic pain and the mechanisms underly-ing CS development, detection through subjective assessments, such as questionnaires, ischallenging. However, with increasing amounts of research identifying conditions withshared symptomatology, such as in chronic overlapping pain conditions (COPCs), ques-tionnaire tools designed to differentiate based on CS-related symptoms are becoming moreprevalent in clinical practice [61].Most studies in this review exclusively used independent patient-reported question-naires as proxies of centralized pain. The American College of Rheumatology (ACR) 2011J. Clin. Med. 2024, 13, 7521 8 of 17fibromyalgia survey score (FSS) was referenced as the sole indicator of CS [21,46,47,54], orwas used alongside the CSI [56,59]. The fibromyalgia questionnaire assesses widespreadpain using a 19-point body map and a 12-point symptom severity scale to give a total scoreout of 31. A score of ≥13/31 indicates fibromyalgia; however, recent studies suggest usingthe score as a continuous measure to assess the degree of CS present [46]. As-Sanie et al.(2021) [46] found a 27% increase in the odds of post-hysterectomy persistent pelvic painwith every 1-point increase in the pre-operative FSS. Endometriosis and fibromyalgia areboth on the National Institutes of Health Pain Consortium list of COPCs. These conditionsfrequently co-occur and are postulated to share CS as their underlying mechanism of per-sistent pain [46,61]. Therefore, using the FSS as an indicator of CS—and by extension, thenociplastic pain phenotype—is promising in clinical settings involving both endometriosisand fibromyalgia. However, there are limited studies focusing exclusively on the use of theFSS in an endometriosis population.The CSI was another questionnaire that was frequently used to identify CS in clinicalsettings [13,23,27,45,50–52,56–60]. This questionnaire has 25 items and focuses on thepsychophysiological symptoms of daily living that indicate CS, such as sensitivity to lightand restlessness, as well as more localized pain in areas such as the pelvis [62]. It scorespatients from 0 to 100, with higher scores indicating a greater degree of CS [62]. Unlikethe FSS, the CSI has a validated cut-off point (≥40/100) that indicates CS symptoms inan endometriosis pain population [27]. Orr et al. (2022, 2023) [23,27] demonstrated thatendometriosis patients who scored above the 40-point cut-off on the CSI also have poorerpatient-reported pain outcomes, indicating its potential use as a screening tool for painoutcomes. Similarly, using the CSI, Raimondo et al. (2023) [13] found that individualswith CS also had higher rates of first-line hormonal treatment failure compared to thosewithout CS. Furthermore, in people with endometriosis, the CSI score was significantlyassociated with a number of COPCs, which in this paper were part of a wider category oftermed central sensitization syndromes and pelvic pain-related comorbidities [23]. Thesesyndromes/comorbidities have been shown to be independent predictors of quality of lifefollowing endometriosis surgery [22].However, there has been speculation as to whether the CSI measures symptoms relatedto CS or simply the presence of a hypervigilant psychological state related to stress [59]. Thistheory is further supported by the strong association between CSI scores and psychologicalmarkers, like pain catastrophizing, depression, and anxiety [26]. Alternatively, the CSI hasalso shown significant correlations with QST measures like the pressure pain threshold(PPT) (r = −0.25 [95% CI: −0.28 to −0.21]) in chronic pain populations [63]. Therefore,there is a need for more research that explicitly looks at the relationship between the CSIand semi-objective assessments of somatosensory changes, like QST, in an endometriosispopulation.Some studies noted the use of the PainDETECT questionnaire, a 7-item self-reportedform asking patients to rate the quality, severity, and characteristics of their pain in orderto assign a total score from −1 to 38 [64,65]. This questionnaire was initially developedin association with the German Research Network on Neuropathic Pain (DFNS) (Munich,Germany) to aid clinicians in detecting neuropathic-like pain in chronic lower back painpatients. It was found to have sensitivity and specificity values of 84%, with a cut-offpoint of ≥19/31 indicating a likely “neuropathic-like” component [64,66]. Since then, it hasbeen used in other chronic-pain related studies including a cross-sectional study looking atwomen with endometriosis-associated pain, where the PainDETECT cut-off scores are usedto group participants into those with nociceptive (≤12), mixed nociceptive and neuropathicpain (13–18), and neuropathic-like (≥19) pain; 40% were classified as neuropathic, 35% asmixed, and 25% as nociceptive [67]. They also showed that women classified as having“neuropathic-like” pain also reported more psychological distress (i.e., anxiety, depression,etc.) and higher pain intensity scores [67]. Moreover, there have been strong correlationsbetween PainDETECT scores and FSSs (rho = 0.441, p < 0.001) [67]. Since fibromyalgia isconsidered a nociplastic pain condition, the strong association between the PainDETECTJ. Clin. Med. 2024, 13, 7521 9 of 17and FSS indicates that the PainDETECT questionnaire may have the ability to capture thosewith nociplastic pain. Within the same study, the Pain Sensitivity Questionnaire (PSQ)was also correlated with the FSS but was not found to have clinical significance despitepreviously showing positive correlations with experimental pain intensity rating in peoplewith chronic pain [68] and endometriosis [69]. Whether the PSQ has clinical applications asa CS proxy in endometriosis populations is still to be determined.Additionally, in a sample of women with endometriosis, bladder pain syndrome, andpelvic pain, Coxon et al. (2023) correlated the seven sensory-based questions from thePainDETECT questionnaire to QST modalities that measured the same stimulus–responserelationship. The heat pain threshold (HPT) correlated significantly with the question “iscold or heat (bath water) in this area occasionally painful?” (r = 0.32, p = 0.032), the pressurepain threshold (PPT) correlated significantly with the question “does slight pressure in thisarea, e.g., with a finger, trigger pain?” (r =0.47, p < 0.001), and mechanical pain sensitivity(MPS) correlated significantly with the question “is light touching (clothing, a blanket) inthis area painful?” (r = 0.38, p = 0.009) [4]. They also found that women in the endometriosisgroup described “painful attacks” as their most common sensory symptom [4].Given its association with HPT, PPT, and MPS, as well as its moderate associationwith the FSS, the PainDETECT questionnaire may be a promising tool for classifyingCS and the presence of nociplastic pain in endometriosis populations with mixed painphenotypes. However, there are limited studies exclusively examining the neuropathic-likepain subgroup, which may include a subset with concurrent nociplastic pain and CS, usingPainDETECT [67]. Therefore, additional investigation in an endometriosis pain populationis needed to determine if the PainDETECT can distinguish those in the neuropathic paingroup who exclusively have neuropathic pain from those with nociplastic pain features.Lastly, Phan et al. (2021) [48] used a cut-off >9/75 painful sites on the brief paininventory (BPI) body map as an identifier of widespread pain. The BPI was created by thePain Research Group of the World Health Organization (WHO) Collaborating Centre forSymptom Evaluation in Cancer Care to assess pain intensity and daily interference withlife in cancer patients [70]. Phan et al. (2021) [48] only noted the use of the BPI body map incollaboration with the PPT and myofascial trigger points. Its short form has been used inendometriosis-associated pain assessments and has indicated minimal clinically importantdifferences (MCIDs) after treatment [71]. However, like the visual analogue scale (VAS)and Numerical Scale Rating (NRS), which have also shown MCID in endometriosis painpopulations [71], there are limited studies specifically looking at the BPI map or score, andany association with CS and nociplastic pain.It is important to note that the presence of CS in and of itself indicates altered CNSprocessing, and therefore, outside of their use as patient-reported outcome measures,simple NRS and VAS questionnaires asking patients to rate their general pain may not bereliable indicators of CS [9]. However, some studies have used a VAS in association withother questionnaires such as the McGill pain questionnaire to help identify widespreadhyperalgesia [37].2.4.2. Semi-Objective AssessmentsQuantitative Sensory Testing (QST) is an objective measure of altered somatosensationand CS. Standardized by the German Research Network on Neuropathic Pain (DFNS) in2006, QST assesses sensory loss or gain and identifies patterns of large- and small-nerve fiberdysfunction through 13 different modalities [72]. Although the DFNS recommends usingthe full QST protocol, most studies in this review did not. Only Coxon et al. (2023) [4] usedall 13 DFNS modalities, along with the PainDETECT questionnaire, in their “TranslationalResearch in Pelvic Pain” study. The DFNS modalities include 1) thermal tests such as heatand cold detection and pain thresholds (HPT, HDT, CPT, CDT), thermal sensory limen(TSL), and paradoxical heat sensation (PHS), and 2) mechanical tests such as mechanicaldetection threshold (MDT), mechanical pain threshold (MPT), stimulus–response functionincluding mechanical pain sensitivity (MPS) and dynamic mechanical allodynia (DMA), theJ. Clin. Med. 2024, 13, 7521 10 of 17wind-up ratio (WUR), vibrational detection threshold (VDT), and pressure pain threshold(PPT) [4,30].Furthermore, when all 13 modalities are assessed together, the scores from eachmodality can be entered into a non-deterministic clustering algorithm and used to grouppatients into different sensory profiles: (1) sensory loss; (2) mechanism hyperalgesia;(3) thermal hyperalgesia; or (4) healthy [73]. A key feature of distinguishing CS fromperipheral sensitization with QST is the use of a primary site, usually the site of localpain for detecting peripheral sensitization, and the use of a heterotopic site away from theprimary noxious stimulus for CS [30]. Additionally, the assessment of sensory changesmust be compared using reference values for the body site, age, and sex to ensure propercomparisons can be made [30,72]. The assessment of whether reported QST was properlystandardized using reference data was outside the scope of this review; however, thismay be a further research interest for studies investigating the validity of QST results inendometriosis populations.However, other methods of pain stimulation and assessment were used in the papersreviewed, such as the electrical pain threshold test (EPT), which involved the application ofelectrical pulses using the PainMatcher (Cefar Medical AB, Lund, Sweden), and ischemicpain tests (IPTs), which measure the pain response following a reduction in blood flow to alimb [39,74]. Although there may be similarities between these tests and the 13 DFNS tests,it is important to note that they measure different mechanisms of pain. For instance, the PPT,which was the most commonly referenced semi-objective assessment, can detect CS in deeptissue as a result of pressure application, while the ischemic pain test measures the painthreshold as a result of reduced blood flow and lactic acid build-up in the muscles [4,39,72].While there is sufficient evidence supporting the connection between PPT and CS in womenwith endometriosis, studies tying ischemic pain to CS in women with endometriosis arelimited [4,69,75,76].Despite the standardization of the QST methodology by the DFNS, many studiesdescribe alternative ways to record and measure modalities. For example, some usea pressure cuff [40] instead of an algometer [37,38,43,48,49,69] for PPT determination.Another example is using the 1st, 5th, and 10th mechanical stimulus ratings to determinemoderately painful stimuli for WUR as an alternative to the DFNS recommendation of256 mN [40,72]. Therefore, it appears that even in an endometriosis pain sensitivity researchsetting, there is no standard method or equipment used to conduct QST or any of theassociated modalities, as many deviate from the DFNS recommendations. This makes itdifficult to compare results across studies and to reproduce findings.2.4.3. Clinician AssessmentsVarious physician-led clinical assessments were used to detect the presence ofendometriosis-related sensitization. For instance, Aredo et al. (2017) [42] and Phan et al.(2021) [48] noted the use of a digital exam to identify active myofascial trigger points in thepelvic region as possible indicators of abdominopelvic tenderness and allodynia, whichare proxies of sensitization. Somatosensory signaling from visceral and somatic organssometimes converges on the same sensory neuron within the CNS [77] (pp. 175–177). Thisprocess is known as viscerosomatic convergence and provides an explanation for the painexperienced by some women with endometriosis [19,77]. However, this viscerosomaticneural interaction also explains how chronic visceral pain signals can sensitize afferentneurons in the spinal cord, resulting in symptoms of widespread hyperalgesia and allody-nia [8,78]. Additionally, prolonged viscerosomatic convergence from pain signaling canlead to hypertrophy in skeletal muscles in the referred area, which can present itself asviscerosomatic reflexes like myofascial trigger points [79]. Aredo et al. (2017) [42] proposedexamining the number and location of abdominopelvic myofascial trigger points, as wellas the intensity rating of the pain elicited, as indicators of CS. Furthermore, some studieshave linked the presence of active myofascial trigger points to sustained nociception anddecreased pain thresholds following the removal of the initial noxious stimulus [8,79].J. Clin. Med. 2024, 13, 7521 11 of 17Following the examination, Aredo et al. (2017) [42] also conducted a semi-objectiveneuromusculoskeletal pain assessment of dermatome allodynia and hyperalgesia usinga pinch-and-roll technique and a Wartenburg pinwheel, respectively. They also assessedmyotome myofascial trigger points in regional and general muscles. However, althoughmyofascial trigger points are frequently found in endometriosis patients and in those withother COPCs like irritable bowel syndrome, bladder pain syndrome, and vulvodynia, thereis limited evidence supporting the belief that all endometriosis patients with these triggerpoints also have CS [12,80,81].Alternatively, Cardaillac et al. (2023) used the convergence pelvic and perineal (PP)pain criteria, which were developed by an international panel of specialists to help facilitateCS detection in people with chronic pelvic pain [55,82]. The convergence PP criteria promptclinicians to assess pelvic sensitivity and pain diffusion in the lower urinary and digestivetract, the genito-sexual tract, the mucocutaneous area, and the muscular system using achecklist of 10 items [82]. This clinical method has shown excellent specificity (87%) andsensitivity (95%), with a score ≥5/10 in people with pelvic perineal pain when comparedto expert diagnosis, and has been used to identify sensitivity in various chronic pelvic painpopulations [83].3. Application to Endometriosis Clinical CareIn endometriosis, nociceptive pain arises from the endometriosis lesions themselves,which can be locally invasive, due in part to somatic driver mutations [84], and/or beassociated with peripheral (local) neuroproliferation in the microenvironment. This isassociated with the expression of inflammatory and neurotrophic factors by endometriosis-related and other cell types [84–90]. Although this suggests that there may be a correlationbetween these peripheral factors and pain symptoms, more sufficiently powered studiesto investigate their influence on nociceptive pain are needed. As endometriosis is also anestrogen-dependent disease, nociceptive pain in endometriosis could be treated by hor-monal suppression of the endometrial-like lesions themselves as well as the hypothalamic–pituitary–ovarian axis. In addition, the surgical excision of these endometrial-like lesionswould be expected to improve nociceptive pain. Deeply invasive endometrial-like lesionsthat infiltrate peripheral nerves (e.g., sciatic) may also contribute to neuropathic painin patients, which can be treated by hormonal suppression or surgical excision of theendometrial-like lesions themselves.Unlike neuropathic and nociceptive pain, CS and nociplastic pain persist despiteunclear evidence regarding tissue damage in the somatosensory system [9]. Consequently,other measures such as those reviewed in this article are needed to identify nociplasticpain in endometriosis patients. Furthermore, treating the central contributors of pain inendometriosis largely depends on identifying the mechanism of sensitization development:is it ‘bottom-up,’ where peripheral influences and nociception drive CNS neuroplasticity,ultimately resulting in nociplastic pain, or is it ‘top-down,’ where pain amplification inthe CNS exists independently of peripheral influences [91]? Nonetheless, endometriosispatients with a significant nociplastic pain component may not respond to hormonal orsurgical treatments alone, and an interdisciplinary approach that addresses multiple paincontributors, whether local, central or psychosocial, may be more appropriate for painmanagement [92,93]. In a randomized controlled trial comparing an interdisciplinary paintreatment plan to standard peripheral pain treatments in women with chronic pelvic pain,75% of patients in the multidisciplinary pain program reported improvements in theiroverall pain after one year, compared to 41% in the standard treatment group (p < 0.01) [94].Additionally, interdisciplinary care models have historically shown significant effects interms of improving patient-reported pain outcomes in people with chronic lower back pain,a known COPC, compared to standard monotherapies [95–98].Many of these interdisciplinary approaches encompass pain neuroscience education,which includes pain beliefs and pain catastrophizing, validates pain despite the absence ofpositive test results, and explains the influences of psychological and social aspects on painJ. Clin. Med. 2024, 13, 7521 12 of 17perception. It has been attributed to reduced pain and disability, and improved function andmovement [99,100]. Health behavior changes, such as the adoption of diets that target co-morbidities, such as irritable bowel syndrome and painful bladder syndrome [17,101,102],and the consumption of whole foods [103,104] have also been found to be effective inreducing pain. Psychological treatments such as cognitive behavioral therapy (CBT), mind-fulness, meditation, and acceptance and commitment therapy can lead to improved mood,function, self-efficacy, and reduced pain and catastrophizing in people with rheumatoidarthritis [105]. CBT can also be effective in treating the adverse effects of chronic pain,such as insomnia and sexual dysfunction [106]. Additionally, site specific manual phys-iotherapy has been proven to significantly improve dysmenorrhea and dyspareunia inwomen with endometriosis [107]. It has also shown a significant effect on global responseassessment, pain intensity, quality of life, fear avoidance, and disability in women withCPP [108–111]. There may also be a role for myofascial trigger point injections, treatmentstargeted to functional bladder and bowel pain, and medications that modulate the nervoussystem [112].4. LimitationsThis scoping review was limited by the novelty of the nociplastic pain phenotypewithin the research and clinical communities. The IASP only recently published definitionsand guidelines for ‘possible’ and ‘probable’ nociplastic pain clinical identification [2].Clinical terminology is still evolving as clinicians and researchers work to better identifynociplastic pain and CS [6,9]. As a result, we may have missed some studies related toendometriosis pain that investigated nociplastic pain using different terms. Additionally,although recent evidence supports the use of biomarker identification in endometriosispathology [113], we did not capture biomarker measures of nociplastic pain in this review.Another limitation was the inclusion criteria, which allowed the use of all study types,including review articles. The inclusion of review articles may have hindered comparisonsacross the different articles. Furthermore, we utilized a narrative analysis to identify toolsand methods of assessments. While this allows for a comprehensive qualitative synthesisand interpretation of the available literature, it also inherently introduces a degree ofselection and interpretation bias, modulated by reviewer expertise. Additionally, manystudies were of mixed pelvic pain groups, that included endometriosis patients, whichprevented further analysis of population characteristics across studies.5. ConclusionsThis review provided a glimpse into the breadth of assessments used to identifyevidence of CS and the presence of the nociplastic pain phenotype in individuals withendometriosis-related pain. Multiple tools were used, including patient-reported question-naires such as the CSI, FSS, and PainDETECT, as well as clinician assessments of triggerpoints in the abdominopelvic area and QST. However, the ability of these tools to accuratelyidentify CS and nociplastic pain within an endometriosis population is still under investiga-tion. More primary research is needed to elucidate the mechanisms of CS in endometriosisand provide a core set of validated clinically and feasible methods of identifying both CSand nociplastic pain in endometriosis.Supplementary Materials: The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/jcm13247521/s1, Table S1: Ovid MEDLINE (R) ALL <1946 to 22 April 2024>;Table S2: Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for ScopingReviews (PRISMA-ScR) Checklist.Author Contributions: Conceptualization, A.G. and P.J.Y.; methodology, A.G. and P.J.Y.; formalanalysis, A.G., N.M., and E.G.; investigation, A.G., and N.M.; writing—original draft preparation,A.G., E.G., Y.B., N.M. and P.J.Y.; writing—review and editing, A.G., E.G., Y.B., N.M. and P.J.Y.;visualization, A.G.; supervision, P.J.Y. All authors have read and agreed to the published version ofthe manuscript.J. Clin. Med. 2024, 13, 7521 13 of 17Funding: This research was funded by the Canadian Institutes for Health Research (PJT-156084). P.J.Y.is supported by the Canada Research Chairs program.Institutional Review Board Statement: Not applicable.Data Availability Statement: Data sharing is not applicable to this article.Conflicts of Interest: The authors declare no conflicts of interest.References1. IASP. Terminology|International Association for the Study of Pain; International Association for the Study of Pain|IASP: Washington,DC, USA, 1994.2. Nijs, J.; Lahousse, A.; Kapreli, E.; Bilika, P.; Saraçog˘lu, I˙.; Malfliet, A.; Coppieters, I.; De Baets, L.; Leysen, L.; Roose, E.; et al.Nociplastic Pain Criteria or Recognition of Central Sensitization? Pain Phenotyping in the Past, Present and Future. J. Clin. Med.2021, 10, 3203. [CrossRef] [PubMed]3. Kosek, E.; Cohen, M.; Baron, R.; Gebhart, G.F.; Mico, J.-A.; Rice, A.S.C.; Rief, W.; Sluka, A.K. 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endometriosis
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pain phenotyping
Nociplastic Pain in Endometriosis: A Scoping Review
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