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Song, Soo Youn, Ye Won Jung, WonKyo Shin, Mia Park, Geon Woo Lee, Soohwa Jeong, Sukjeong An, et al. "Endometriosis-Related Chronic Pelvic Pain." Biomedicines 11, no. 10 (October 23, 2023): 2868. http://dx.doi.org/10.3390/biomedicines11102868.
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Endometriosis, which is the presence of endometrial stroma and glands outside the uterus, is one of the most frequently diagnosed gynecologic diseases in reproductive women. Patients with endometriosis suffer from various pain symptoms such as dysmenorrhea, dyspareunia, and chronic pelvic pain. The pathophysiology for chronic pain in patients with endometriosis has not been fully understood. Altered inflammatory responses have been shown to contribute to pain symptoms. Increased secretion of cytokines, angiogenic factors, and nerve growth factors has been suggested to increase pain. Also, altered distribution of nerve fibers may also contribute to chronic pain. Aside from local contributing factors, sensitization of the nervous system is also important in understanding persistent pain in endometriosis. Peripheral sensitization as well as central sensitization have been identified in patients with endometriosis. These sensitizations of the nervous system can also explain increased incidence of comorbidities related to pain such as irritable bowel disease, bladder pain syndrome, and vulvodynia in patients with endometriosis. In conclusion, there are various possible mechanisms behind pain in patients with endometriosis, and understanding these mechanisms can help clinicians understand the nature of the pain symptoms and decide on treatments for endometriosis-related pain symptoms.
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Aguggia, Marco, M. G. Saracco, M. Cavallini, G. Bussone, and P. Cortelli. "Sensitization and pain." Neurological Sciences 34, S1 (May 2013): 37–40. http://dx.doi.org/10.1007/s10072-013-1382-0.
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Ramalingam, Thangamani, Pooja Desai, Dhruvi Ghoghari, Vidhi Jethva, and Rushvi Shah. "Neurophysiology of pain education knowledge, pain disability, patient satisfaction and central sensitization in chronic musculoskeletal pain." IP Journal of Surgery and Allied Sciences 4, no. 4 (January 15, 2023): 137–41. http://dx.doi.org/10.18231/j.jsas.2022.026.
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Chronic musculoskeletal pains are multifaceted, and Central sensitization is a potential pathophysiological mechanism underlying a group of chronic musculoskeletal pain disorders. Neurophysiology of pain education knowledge and patient satisfaction levels of chronic musculoskeletal pain subjects may contribute to central nervous system sensitization. Hence, the aim of the study was to evaluate the impact of neurophysiology of pain education knowledge and patient satisfaction levels on central sensitization in large population of patient with chronic musculoskeletal pain. The study included 200 chronic musculoskeletal pain subjects that persisted more than 3 months with average age of 43.93±13.62. A cross-sectional study used non probability sampling. Neurophysiology of pain Questionnaire (NPQ) to know the conceptualization of pain, mood rating scale(MRS) to measure patient’s mood fluctuation because of pain, pain disability scale (PDS) for evaluating patients ability to perform certain activity, central sensitization inventory(CSI) to measure nervous system sensitization and patients satisfaction scale(PSS) to understand patient’s satisfaction towards the treatment and health care provider were used. Descriptive and correlation analyses were used for analysis. The correlation analyses showed that patient disability scale negatively correlated with mood scale and positively correlated with the age, duration of the condition, impact of pain on ADL and central sensitization. And there was a positive correlation between patient satisfaction and impact of pain on ADL. The age, mood, duration of the condition and pain disability were the factors behind central sensitization in patients with chronic musculoskeletal pain. And the neuro physiology of pain knowledge had impact on pain disability and patient satisfaction.
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Coderre, Terence J., and Joel Katz. "Peripheral and central hyperexcitability: Differential signs and symptoms in persistent pain." Behavioral and Brain Sciences 20, no. 3 (September 1997): 404–19. http://dx.doi.org/10.1017/s0140525x97251484.
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This target article examines the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain in four key areas: cutaneous hyperalgesia, referred pain, neuropathic pain, and postoperative pain. Each suggests that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. It is instructive to think of central sensitization as comprised of both an initial central sensitization and an ongoing central sensitization driven by inputs from peripheral sources. Each of these factors, initial sensitization, ongoing central sensitization, and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons and thus influences the expression of persistent pain or hyperalgesia. Since each factor, peripheral inputs and central sensitization (initial or ongoing), can contribute to both the initiation and maintenance of persistent pain, therapies should target both peripheral and central sources of pathology.
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Lee, Jaesung, Seohyun Chung, Minkyu Hwang, Yeongkag Kwon, Seung Hyun Han, and Sung Joong Lee. "Estrogen Mediates the Sexual Dimorphism of GT1b-Induced Central Pain Sensitization." Cells 12, no. 5 (March 6, 2023): 808. http://dx.doi.org/10.3390/cells12050808.
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We have previously reported that the intrathecal (i.t.) administration of GT1b, a ganglioside, induces spinal cord microglia activation and central pain sensitization as an endogenous agonist of Toll-like receptor 2 on microglia. In this study, we investigated the sexual dimorphism of GT1b-induced central pain sensitization and the underlying mechanisms. GT1b administration induced central pain sensitization only in male but not in female mice. Spinal tissue transcriptomic comparison between male and female mice after GT1b injection suggested the putative involvement of estrogen (E2)-mediated signaling in the sexual dimorphism of GT1b-induced pain sensitization. Upon ovariectomy-reducing systemic E2, female mice became susceptible to GT1b-induced central pain sensitization, which was completely reversed by systemic E2 supplementation. Meanwhile, orchiectomy of male mice did not affect pain sensitization. As an underlying mechanism, we present evidence that E2 inhibits GT1b-induced inflammasome activation and subsequent IL-1β production. Our findings demonstrate that E2 is responsible for sexual dimorphism in GT1b-induced central pain sensitization.
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De Meulemeester, Kayleigh, Mira Meeus, Robby De Pauw, Barbara Cagnie, Hannah Keppler, and Dorine Lenoir. "Suffering from chronic tinnitus, chronic neck pain, or both: Does it impact the presence of signs and symptoms of central sensitization?" PLOS ONE 18, no. 8 (August 24, 2023): e0290116. http://dx.doi.org/10.1371/journal.pone.0290116.
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Chronic subjective tinnitus is a prevalent symptom, which has many similarities with chronic pain. Central sensitization is considered as a possible underlying mechanism of both symptoms. Central sensitization has already been investigated in chronic pain populations but not in patients with chronic subjective tinnitus. Therefore, the main objective of this cross-sectional study was to compare signs and symptoms, indicative for central sensitization, in tinnitus patients with and without chronic idiopathic neck pain, patients with chronic idiopathic neck pain only, and healthy controls. Also, differences in psychological and lifestyle factors, possibly influencing the association between central sensitization and tinnitus, were examined as well as correlations between signs and symptoms of central sensitization, and tinnitus, pain, psychological and lifestyle factors. Differences in signs and symptoms of central sensitization were examined using the self-report Central Sensitization Inventory and QST protocol (local and distant mechanical and heat hyperalgesia, conditioned pain modulation). Tinnitus, pain, psychological and lifestyle factors were evaluated using self-report questionnaires. Symptoms of central sensitization and local mechanical hyperalgesia were significantly more present in both tinnitus groups, compared to healthy controls, but were most extensive in the group with chronic tinnitus+chronic idiopathic neck pain. Distant mechanical hyperalgesia, indicative for central sensitization, was only observed in the group with both chronic tinnitus+chronic idiopathic neck pain. This group also displayed a significantly higher psychological burden and poorer sleep than patients with chronic tinnitus only and healthy controls. Signs and symptoms of central sensitization were also shown to be associated with tinnitus impact, pain-related disability, psychological burden and sleep disturbances. This study shows preliminary evidence for the presence of central sensitization in patients with chronic tinnitus+chronic idiopathic neck pain. This could be explained by the higher perceived tinnitus impact, psychological burden and sleep problems in this group. Trial registration: This study is registered as NCT05186259 (www.clinicaltrials.gov).
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AKULINUSHKINA, EKATERINA Y., SVETLANA P. YAKUPOVA, EDUARD Z. YAKUPOV, LARISA V. IVANOVA, TATYANA A. BRAGINA, and NIKOLAI I. MAKSIMOV. "CENTRAL SENSITIZATION IN PSORIATIC ARTHRITIS." Bulletin of Contemporary Clinical Medicine 16, no. 5 (October 2023): 16–21. http://dx.doi.org/10.20969/vskm.2023.16(5).16-21.
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Introduction. Chronic pain consists of nociceptive, neuropathic and nociplastic components. Nociplastic pain based on central sensitization. Patients with central sensitization may experience severe pain even with no any signs of clinical and laboratory inflammation, and describe it in descriptors of neuropathic pain. The prevalence and influence of central sensitization in clinical and laboratory activity, the development of mood disorders in patients with psoriatic arthritis are not explored well. Aim. To assess the prevalence of central sensitization in patients with psoriatic arthritis, to compare the parameters of patients with and without central sensitization. Materials and methods. We examined 107 patients with psoriatic arthritis: number of tender and swollen joints, severity of pain, patient global assessment, and C-reactive protein were determined. Activity of disease was assessed with Disease activity in psoriatic arthritis, Ankylosing Spondylitis Disease Activity Score. Central sensitization was determined with Central Sensitization Inventory, presence of anxiety and depression - with Hospital Anxiety and Depression Scale. Descriptors of neuropathic pain were determined with Pain Detect Questionnaire. Statistical processing was carried out with Statistics 26.0. Differences were considered significant at p-value < 0.05. Results and discussion. Central sensitization was found in 46 (43%) patients – they had patient global assessment (p=0.004) and severity of pain (p=0.002) in higher values. The C-reactive protein (p=0.423), Disease activity in psoriatic arthritis (p=0.083) did not differ between groups, but the Ankylosing Spondylitis Disease Activity Score (p=0.002) was higher in patients with central sensitization. High prevalence of anxiety (25.2%) and depression (40.2%) was found; more often in patients with central sensitization (p=0.001 and p=0.004). Most of patients described the tactile allodynia, «electric shocks», and burning. Conclusion. Significant contribution of central sensitization to the persistence of pain in patients with psoriatic arthritis was found. The frequency of clinically significant anxiety and depression in patients with psoriatic arthritis was shown, as well as their higher prevalence among patients with central sensitization. Patients with psoriatic arthritis often described pain like neuropathic pain, which can indicate both local damage to the nervous system and the formation of pain sensitization without direct damage to peripheral nerve structures.
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Previtali, Davide, Gianluigi Capone, Paolo Marchettini, Christian Candrian, Stefano Zaffagnini, and Giuseppe Filardo. "High Prevalence of Pain Sensitization in Knee Osteoarthritis: A Meta-Analysis with Meta-Regression." CARTILAGE 13, no. 1 (January 2022): 194760352210876. http://dx.doi.org/10.1177/19476035221087698.
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Objective The aim of this meta-analysis was to study the evidence on pain sensitization in knee osteoarthritis (OA), providing a quantitative synthesis of its prevalence and impact. Factors associated with pain sensitization were also investigated. Methods Meta-analysis; PubMed (MEDLINE), Cochrane Central Register (CENTRAL), and Web of Science were searched on February 2021. Level I to level IV studies evaluating the presence of pain sensitization in patients with symptomatic knee OA, documented through a validated method (questionnaires or quantitative sensory testing), were included. The primary outcome was the prevalence of pain sensitization. Factors influencing the prevalence were also evaluated, as well as differences in terms of pain thresholds between knee OA patients and healthy controls. Results Fifty-three articles including 7,117 patients were included. The meta-analysis of proportion documented a prevalence of pain sensitization of 20% (95% confidence interval [CI] = 16%-26%) with a significant heterogeneity of results ( I2 = 89%, P < 0.001). The diagnostic tool used was the main factor influencing the documented prevalence of pain sensitization ( P = 0.01). Knee OA patients presented higher pain sensitivity compared with healthy controls, both in terms of local pressure pain threshold (standardized mean difference [SMD] = −1.00, 95% CI = −1.67 to −0.32, P = 0.007) and distant pressure pain threshold (SMD = −0.54, 95% CI = −0.76 to −0.31, P < 0.001). Conclusions Knee OA pain presents features that are consistent with a significant degree of pain sensitization. There is a high heterogeneity in the reported results, mainly based on the diagnostic tool used. The identification of the best methods to detect pain sensitization is warranted to correctly evaluate and manage symptoms of patients affected by knee OA. Registration: PROSPERO CRD42019123347.
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Nijs, Jo. "Applying Modern Pain Neuroscience in Clinical Practice: Criteria for the Classification of Central Sensitization Pain." Pain Physician 5;17, no. 5;9 (September 14, 2014): 447–57. http://dx.doi.org/10.36076/ppj.2014/17/447.
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Background: The awareness is growing that central sensitization is of prime importance for the assessment and management of chronic pain, but its classification is challenging clinically since no gold standard method of assessment exists. Objectives: Designing the first set of classification criteria for the classification of central sensitization pain. Methods: A body of evidence from original research papers was used by 18 pain experts from 7 different countries to design the first classification criteria for central sensitization pain. Results: It is proposed that the classification of central sensitization pain entails 2 major steps: the exclusion of neuropathic pain and the differential classification of nociceptive versus central sensitization pain. For the former, the International Association for the Study of Pain diagnostic criteria are available for diagnosing or excluding neuropathic pain. For the latter, clinicians are advised to screen their patients for 3 major classification criteria, and use them to complete the classification algorithm for each individual patient with chronic pain. The first and obligatory criterion entails disproportionate pain, implying that the severity of pain and related reported or perceived disability are disproportionate to the nature and extent of injury or pathology (i.e., tissue damage or structural impairments). The 2 remaining criteria are 1) the presence of diffuse pain distribution, allodynia, and hyperalgesia; and 2) hypersensitivity of senses unrelated to the musculoskeletal system (defined as a score of at least 40 on the Central Sensitization Inventory). Limitations: Although based on direct and indirect research findings, the classification algorithm requires experimental testing in future studies. Conclusion: Clinicians can use the proposed classification algorithm for differentiating neuropathic, nociceptive, and central sensitization pain. Key words: Chronic pain, diagnosis, hypersensitivity, classification, neuropathic pain
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Wakaizumi, Kenta. "Brain imaging study for central sensitization." PAIN RESEARCH 36, no. 3 (September 30, 2021): 180–85. http://dx.doi.org/10.11154/pain.36.180.
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Ursin, Holger. "Sensitization: A mechanism for somatization and subjective health complaints?" Behavioral and Brain Sciences 20, no. 3 (September 1997): 469. http://dx.doi.org/10.1017/s0140525x97551491.
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The brain seems to be able to generate and uphold sensitization by itself, based on previous experience, or genetic disposition. This seems to be particularly important for muscle pain. There seem to be positive feedback loops where pain produces more pain, and more sensitization. Musculoskeletal pain is the most common pain state. It amounts to almost 50% of all long term sickness absence. But other subjective complaints are also common, and may depend on sensitization. Sensitization has been introduced as an explanation for subjective complaints from the gastrointestinal tract and the brain, like fatigue, tiredness, dizziness, and vertigo. [coderre & katz]
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Gungor, Zeynep, and Senem Sas. "Evaluation of central sensitization and presence of neuropathic pain in patients with rheumatoid arthritis and its relationship with quality of life." Medicine Science | International Medical Journal 13, no. 3 (2024): 699. http://dx.doi.org/10.5455/medscience.2024.07.072.
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Central sensitization and neuropathic pain may develop in rheumatological diseases. This study aimed to investigate the presence of central sensitization and neuropathic pain in patients with rheumatoid arthritis (RA). We used the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) questionnaire to evaluate neuropathic pain (NP) in patients with RA. The presence of central sensitization in patients was evaluated using the central sensitization inventory (CSI). Demographic and clinical data were obtained from patients and interviews. Beck Depression Scale (BDS) was used to evaluate the mood of the patients, and the Short Form-36 (SF-36) quality of life scale was used to evaluate the quality of life. A total of 104 patients participated in our study, and 33 (31.7%) of them were found to be NP. CSI scores indicated central sensitization in 41 (39.4%) of the patients. A positive significant relationship was detected between LANSS and Visual Analog Scale (VAS), BDI, and Disease Activity Score 28 (DAS28). Central sensitization (CS) and neuropathic pain (NP) significantly contribute to functional disability in RA patients. Central sensitization and neuropathic pain significantly contribute to functional disability in patients experiencing neuropathic pain, with CS having a detrimental impact on their quality of life. Thus, it is imperative to consider neuropathic pain and CS during disease monitoring and follow-up.
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Hendriks, Erwin, Lennard Voogt, Dorine Lenoir, Iris Coppieters, and Kelly Ickmans. "Convergent Validity of the Central Sensitization Inventory in Chronic Whiplash-Associated Disorders; Associations with Quantitative Sensory Testing, Pain Intensity, Fatigue, and Psychosocial Factors." Pain Medicine 21, no. 12 (September 16, 2020): 3401–12. http://dx.doi.org/10.1093/pm/pnaa276.
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Abstract Objective Central sensitization is present in different pain conditions, including chronic whiplash-associated disorders. In the absence of a gold standard method of assessment to determine the presence of central sensitization, quantitative sensory testing is currently understood as an optimal proxy. Laboratory sensory testing is, however, not feasible in clinical practice, and the Central Sensitization Inventory was developed as an alternative. The aim of the current study was to evaluate the convergent validity of the Central Sensitization Inventory in chronic whiplash-associated patients by determining the association between the Central Sensitization Inventory and quantitative sensory testing, pain intensity, fatigue, and psychosocial factors. Methods A total of 125 chronic whiplash-associated patients completed multiple questionnaires and were subjected to pressure pain thresholds and temporal summation. Results . The Central Sensitization Inventory showed a strong association with constructs of general psychopathology, anxiety, distress, depression, and somatization in chronic whiplash-associated disorders. Moderate correlations were found with fatigue and intrusive and avoidant phenomena after a variety of traumatic events. No significant association was found between the Central Sensitization Inventory and pressure pain thresholds and temporal summation, nor between the Central Sensitization Inventory and other pain measurements. Conclusions Overall, we found that the Central Sensitization Inventory is better in identifying the psychosocial factors related to central sensitization in chronic whiplash-associated disorders than the central nervous system adaptations. Thus, the convergent validity of the Central Sensitization Inventory appears to be only partially present in chronic whiplash-associated disorders.
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Fernández-de-las-Peñas, César, Carlos Guijarro, Juan Torres-Macho, Oscar J. Pellicer-Valero, Ana Franco-Moreno, Jo Nijs, and María Velasco-Arribas. "Serological Biomarkers at Hospital Admission and Hospitalization Treatments Are Not Related to Sensitization-Associated Symptoms in Patients with Post-COVID Pain." Pathogens 12, no. 10 (October 12, 2023): 1235. http://dx.doi.org/10.3390/pathogens12101235.
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Current evidence suggests that a group of patients who had survived coronavirus disease, 2019 (COVID-19) and developed post-COVID pain can exhibit altered nociceptive processing. The role of serological biomarkers and hospitalization treatments in post-COVID pain is unclear. This study aimed to investigate the association of serological biomarkers and treatments received during hospitalization with sensitization-associated symptoms in COVID-19 survivors with post-COVID pain. One hundred and eighty-three (n = 183) patients who had been hospitalized due to COVID-19 in one urban hospital of Madrid (Spain) during the first wave of the pandemic were assessed in a face-to-face interview 9.4 (SD 3.4) months after hospitalization. Levels of 19 serological biomarkers, hospitalization data, and treatments during hospitalization were obtained from hospital records. Sensitization-associated symptoms (Central Sensitization Inventory, CSI), sleep quality (Pittsburgh Sleep Quality Index, PSQI), pain catastrophism (Pain Catastrophizing Scale), and anxiety/depressive level (Hospital Anxiety and Depression Scale, HADS) were assessed. The prevalence of post-COVID pain was 40.9% (n = 75). Twenty-nine (38.6%) patients had sensitization-associated symptoms. Overall, no differences in hospitalization data and serological biomarkers were identified according to the presence of sensitization-associated symptoms. The analysis revealed that patients with sensitization-associated symptoms exhibited higher lymphocyte count and lower urea levels than those without sensitization-associated symptoms, but differences were small. Pain catastrophism and depressive levels, but not fatigue, dyspnea, brain fog, anxiety levels, or poor sleep, were higher in individuals with sensitization-associated symptoms. In conclusion, this study revealed that sensitization-associated post-COVID pain symptoms are not associated with serological biomarkers at hospital admission and hospitalization treatments received.
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Cordaro, Marika, Rosalba Siracusa, Ramona D’Amico, Tiziana Genovese, Gianluca Franco, Ylenia Marino, Davide Di Paola, et al. "Role of Etanercept and Infliximab on Nociceptive Changes Induced by the Experimental Model of Fibromyalgia." International Journal of Molecular Sciences 23, no. 11 (May 30, 2022): 6139. http://dx.doi.org/10.3390/ijms23116139.
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Background: Fibromyalgia is a clinical condition that affects 1% to 5% of the population. No proper therapy has been currently found. It has been described that inflammation plays a central role in the nerve sensitizations that characterize the pathology. Methods: This paper aimed to evaluate the efficacy of etanercept and infliximab in the management of pain sensitization. Fibromyalgia was induced by three injections once a day of reserpine at the dose of 1 mg/kg. Etanercept (3 mg/kg) and infliximab (10 mg/kg) were administered the day after the last reserpine injection and then 5 days after that. Behavioral analyses were conducted once a week, and molecular investigations were performed at the end of the experiment. Results: Our data confirmed the major effect of infliximab administration as compared to etanercept: infliximab administration strongly reduced pain sensitization in thermal hyperalgesia and mechanical allodynia. From the molecular point of view, infliximab reduced the activation of microglia and astrocytes and the expression of the purinergic P2X7 receptor ubiquitously expressed on glia and neurons. Downstream of the P2X7 receptor, infliximab also reduced p38-MAPK overexpression induced by the reserpine administration. Conclusion: Etanercept and infliximab treatment caused a significant reduction in pain. In particular, rats that received infliximab showed less pain sensitization. Moreover, infliximab reduced the activation of microglia and astrocytes, reducing the expression of the purinergic receptor P2X7 and p38-MAPK pathway.
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Gold, Michael S., and Gerald F. Gebhart. "Nociceptor sensitization in pain pathogenesis." Nature Medicine 16, no. 11 (October 14, 2010): 1248–57. http://dx.doi.org/10.1038/nm.2235.
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Dickenson, A. H. "6 CENTRAL SENSITIZATION - WIDESPREAD PAIN." European Journal of Pain 10, S1 (September 2006): S2b—S3. http://dx.doi.org/10.1016/s1090-3801(06)60009-8.
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You, Dokyoung Sophia, and Mary W. Meagher. "Childhood Adversity and Pain Sensitization." Psychosomatic Medicine 78, no. 9 (2016): 1084–93. http://dx.doi.org/10.1097/psy.0000000000000399.
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Walsh, David A. "Editorial: Synovitis and Pain Sensitization." Arthritis & Rheumatology 68, no. 3 (February 24, 2016): 561–62. http://dx.doi.org/10.1002/art.39487.
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Rubal, Cristina, Augusto Pereira, Laura Calles Sastre, Belén Almoguera Pérez-Cejuela, Sofía Herrero Gámiz, Pilar Chaves, and Tirso Pérez Medina. "Managing Vulvodynia with Central Sensitization: Challenges and Strategies." Journal of Clinical Medicine 12, no. 11 (June 5, 2023): 3851. http://dx.doi.org/10.3390/jcm12113851.
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Background: Vulvodynia is defined as a chronic idiopathic vulvar pain condition. This study aimed to investigate the effect of central sensitization on the prognosis of neuromodulator treatment for vulvodynia. Method: A total of 105 patients with vulvodynia who underwent pelvic mapping pain exploration were included and scored according to the Convergence PP Criteria for pelvic pain and central sensitization. The patients were treated according to chronic pelvic pain guidelines, and their response to treatment was evaluated. Results: A total of 35 out 105 patients (33%) with vulvodynia had central sensitization, which was associated with comorbidities, dyspareunia, pain with micturition, and pain with defecation. Dyspareunia and pain with defecation were independent prognostic factors for central sensitization. Patients with central sensitization experienced more pain during intercourse, urination, or defecation, had more comorbidities, and responded worse to treatment. They required more treatment, with a longer response time (over 2 months). Patients with localized vulvodynia were treated with physiotherapy and lidocaine, while patients with generalized vulvodynia were treated with neuromodulators. Amitriptyline was effective in treating patients with generalized spontaneous vulvodynia and dyspareunia. Conclusions: Overall, this study highlights the importance of considering central sensitization in the diagnosis and treatment of vulvodynia and the need for individualized treatment based on the patient’s symptoms and underlying mechanisms. Vulvodynia patients with central sensitization had more pain during intercourse, urination, or defecation, and responded worse to treatment, requiring more time and medication.
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van den Broeke, Emanuel N. "Central sensitization and pain hypersensitivity: Some critical considerations." F1000Research 7 (August 21, 2018): 1325. http://dx.doi.org/10.12688/f1000research.15956.1.
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Since its discovery, central sensitization has gained enormous popularity. It is widely used to explain pain hypersensitivity in a wide range of clinical pain conditions. However, at present there is no general consensus on the definition of central sensitization. Moreover, the use of the term central sensitization in the clinical domain has been criticized. The aim of this paper is to foster the discussion on the definition of central sensitization and its use.
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van den Broeke, Emanuel N. "Central sensitization and pain hypersensitivity: Some critical considerations." F1000Research 7 (August 31, 2018): 1325. http://dx.doi.org/10.12688/f1000research.15956.2.
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Since its discovery, central sensitization has gained enormous popularity. It is widely used to explain pain hypersensitivity in a wide range of clinical pain conditions. However, at present there is no general consensus on the definition of central sensitization. Moreover, the use of the term central sensitization in the clinical domain has been criticized. The aim of this paper is to foster the discussion on the definition of central sensitization and its use.
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Dirks, Jesper, Karin L. Petersen, Michael C. Rowbotham, and Jørgen B. Dahl. "Gabapentin Suppresses Cutaneous Hyperalgesia following Heat-Capsaicin Sensitization." Anesthesiology 97, no. 1 (July 1, 2002): 102–7. http://dx.doi.org/10.1097/00000542-200207000-00015.
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Background The anticonvulsant gabapentin, proven effective for neuropathic pain in two large, placebo-controlled clinical trials, is widely used for treatment of chronic pain. Preclinical studies have demonstrated analgesic and antiallodynic effects in models involving neuronal sensitization and nerve injury, without affecting acute pain transmission. The aim of the present study was to link data from animal models and clinical trials for chronic pain by investigating the effect of gabapentin on acute nociception and experimentally induced cutaneous hyperalgesia in healthy volunteers. Methods The human experimental hyperalgesia model, the heat-capsaicin sensitization model, was induced in 25 healthy male volunteers. Subjects received oral gabapentin (1,200 mg) or placebo after heat-capsaicin sensitization was established on the forearm. The primary outcome measures were the sizes of the areas of secondary hyperalgesia to von Frey hair and brush stimulation on the forearm. Secondary outcome measures were as follows: (1) size of secondary hyperalgesia area in response to brief thermal sensitization procedure on the thigh; (2) heat pain detection thresholds in normal and sensitized skin; and (3) painfulness of 1 min of 45 degrees C stimulation in normal skin. Results Oral gabapentin profoundly suppressed established cutaneous sensitization on the forearm and prevented development of cutaneous sensitization on the thigh. Thermal nociception in normal skin was unchanged. Side effects were modest. Conclusion The results link preclinical findings with results from clinical trials of neuropathic pain. The results further suggest that gabapentin may prove effective in acute pain disorders involving neuronal sensitization, such as postoperative pain and acute herpetic pain, and could prove effective in prevention of chronic pain.
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Tedeschi, Roberto, Federica Giorgi, Daniela Platano, and Lisa Berti. "Classifying Low Back Pain Through Pain Mechanisms: A Scoping Review for Physiotherapy Practice." Journal of Clinical Medicine 14, no. 2 (January 10, 2025): 412. https://doi.org/10.3390/jcm14020412.
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Background: Low back pain (LBP) is a leading cause of disability worldwide, often driven by distinct pain mechanisms: nociceptive, neuropathic, and central sensitization. Accurate classification of these mechanisms is critical for guiding effective, targeted treatments. Methods: A scoping review was conducted following the Joanna Briggs Institute methodology and reported according to PRISMA-ScR guidelines. A comprehensive literature search was performed in MEDLINE, Cochrane CENTRAL, Scopus, PEDro, and Web of Science. Eligible studies included adults with LBP and focused on clinical criteria for classifying pain mechanisms. Data on study methods, population characteristics, and outcomes were extracted and synthesized. Results: Nine studies met the inclusion criteria. Nociceptive pain was characterized by localized symptoms proportional to mechanical triggers, with no neurological signs. Neuropathic pain was associated with burning sensations, dysaesthesia, and a positive neurodynamic straight leg raise (SLR) test. Central sensitization featured widespread pain, hyperalgesia, and disproportionate symptoms. Tools such as painDETECT, DN4, and the Central Sensitisation Inventory (CSI) were validated for neuropathic and central sensitization pain. Central sensitization and neuropathic pain were linked to greater disability and psychological distress compared to nociceptive pain. Conclusions: This review aims to provide a historical perspective on pain mechanism classifications and to explore how previous frameworks have influenced current diagnostic concepts in physiotherapy practice. By synthesizing key clinical criteria used to differentiate between nociceptive, neuropathic, and central sensitization pain, this review proposes a practical framework to improve the accuracy of pain classification in clinical settings.
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Nijs, Jo. "Low Back Pain: Guidelines for the Clinical Classification of Predominant Neuropathic, Nociceptive, or Central Sensitization Pain." May 2015 3;18, no. 3;5 (May 14, 2015): E333—E346. http://dx.doi.org/10.36076/ppj.2015/18/e333.
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Background: Low back pain (LBP) is a heterogeneous disorder including patients with dominant nociceptive (e.g., myofascial low back pain), neuropathic (e.g., lumbar radiculopathy), and central sensitization pain. In order to select an effective and preferably also efficient treatment in daily clinical practice, LBP patients should be classified clinically as either predominantly nociceptive, neuropathic, or central sensitization pain. Objective: To explain how clinicians can differentiate between nociceptive, neuropathic, and central sensitization pain in patients with LBP. Study Design: Narrative review and expert opinion. Setting: Universities, university hospitals and private practices. Methods: Recently, a clinical method for the classification of central sensitization pain versus neuropathic and nociceptive pain was developed. It is based on a body of evidence of original research papers and expert opinion of 18 pain experts from 7 different countries. Here we apply this classification algorithm to the LBP population. Results: The first step implies examining the presence of neuropathic low back pain. Next, the differential diagnosis between predominant nociceptive and central sensitization pain is done using a clinical algorithm. Limitations: The classification criteria are substantiated by several original research findings including a Delphi survey, a study of a large group of LBP patients, and validation studies of the Central Sensitization Inventory. Nevertheless, these criteria require validation in clinical settings. Conclusion: The pain classification system for LBP should be an addition to available classification systems and diagnostic procedures for LBP, as it is focussed on pain mechanisms solely. Key words: Chronic pain, neuroscience, diagnosis, clinical reasoning, examination, assessment
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Kwon, Ohyun. "Pathophysiology of neuropathic pain." Journal of the Korean Medical Association 64, no. 7 (July 10, 2021): 468–76. http://dx.doi.org/10.5124/jkma.2021.64.7.468.
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Background: Neuropathic pain is notoriously difficult to manage properly, not only because of its varied nature and the absence of objective diagnostic tools but also because of extensive reciprocal neuronal interactive pathogenic mechanism from the molecular level to patient’s own psychophysical characteristics. This paper briefly reviews the pathophysiology of neuropathic pain to the level of clinicians’ interest and its potential in clinical practiceCurrent Concepts: Recent research progress now allows us to obtain a bird view of neuropathic pain pathophysiology: peripheral and central sensitization. For peripheral sensitization, a local inflammatory milieu of the injured nerve primarily drives sequential phenotypic changes, which are critical and shared by both neuropathic and inflammatory pain. Central sensitization is led either by the hyperexcitability of the second-order afferent neuron itself or loss of physiological inhibitory control of the transmission of pain signal to the higher nervous system. Peripheral and central sensitization work synergistically but can also introduce neuropathic pain alone.Discussion and Conclusion: The cause of neuropathic pain is diverse, and understanding of its pathophysiology is still insufficient to realize a mechanism-based approach to clinical phenotypes or therapeutic applications. In dealing with chronic neuropathic pain, it is highly desirable to assess key aspects of a patient’s pain based on a plausible mechanism and select the best management method accordingly.
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Groef, An De. "Unraveling Self-Reported Signs of Central Sensitization in Breast Cancer Survivors with Upper Limb Pain: Prevalence Rate and Contributing Factors." January 2018 1, no. 21;1 (May 15, 2018): E247—E256. http://dx.doi.org/10.36076/ppj.2018.3.e247.
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Background: Hypersensitivity of the central nervous system to environmental and chemical stimuli is a clinical feature of central sensitization mechanisms that can be assessed with the central sensitization inventory (CSI). Objective: The aim was to determine prevalence rate of this feature and explore the treatment-, patient-, pain-, and psychosocial-related variables associated with the degree of self-reported signs of central sensitization, assessed with the CSI (0-100), in breast cancer survivors at long-term. Study Design: Cross-sectional study. Setting: University Hospitals, Leuven, Belgium. Methods: One hundred and forty-six women with persistent pain, more than one year after breast cancer surgery, were included. The following factors were analyzed by bivariable and multivariable analysis: 1) treatment-related variables (type of surgery, levels of lymph node dissected, radiotherapy, chemotherapy, hormone therapy, and trastuzumab); 2) patient’s related variables (age and body mass index); 3) pain-related variables (pain intensity, pain quality, primary hyperalgesia, and index of widespread pain); and 4) psychosocial variables (the degree of pain catastrophizing and vigilance and awareness to pain). The dependent variable was degree of central sensitization measured with the CSI. Additionally, a stepwise regression was performed. Results: Fifty-five (38%) patients reported signs of central sensitization measured with the CSI (i.e., > 40/100). From multivariable analysis, it appears that more severe pain quality and higher levels of pain catastrophizing contribute to a higher degree of central sensitization. The stepwise regression revealed that up to 24% of variance of the CSI can be explained by these factors. Limitations: A selection bias may be present since patients were all recruited from a larger cohort participating in clinical trials on the effectiveness of physical therapy after breast cancer treatment. Conclusion: Signs of central sensitization cannot be neglected in breast cancer survivors at long term. More severe pain quality and pain catastrophizing contribute to higher levels of central sensitization in this population. Key words
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Jardim, Marina Leonardi, Alex Moreira Mélo, Melissa de Oliveira Melchior, and Laís Valencise Magri. "CATASTROPHIZING, CENTRAL SENSITIZATION AND CHRONIC PAIN-RELATED TMD: HOW IS THIS ASSOCIATION?" Revista Gestão e Conhecimento 16, no. 1 (September 13, 2022): 565–78. http://dx.doi.org/10.55908/rgcv16n1-033.
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INTRODUCTION: most of the individuals who present catastrophizing and central sensitization also present chronic pain, as temporomandibular disorders (TMD). AIM: to analyze whether there is an association between the variables of pain intensity, central sensitization, and catastrophizing in women with chronic pain-related TMD. METHODS: an observational descriptive cross-sectional study was conducted, comprising a sample of 50 women diagnosed with chronic pain-related TMD according to the DC/TMD – Brazilian Portuguese version. The following questionnaires/protocols were applied: Pain Catastrophizing Scale (PCS), Central Sensitization Inventory (BP-CSI)), pain intensity (Visual Analogue Scale, VAS). For the analysis of the PCS and CSI scores, the 75th percentile was used to determine the cutoff points, and Multiple Linear Regression Tests (p < 0.05) was applied. RESULTS: The sample showed overall higher cutoff values for catastrophization (32.3), rumination (12.4), magnification (5.7), helplessness (13.9), and central sensitization (52.2). Statistical association was found between the time of pain-related TMD (in months), number of painful points, and total catastrophizing score (F = 0.72; p = 0.004). This association was not found to central sensitization. That is, higher pain-related TMD time and/or higher number of painful points, also higher the catastrophizing. CONCLUSION: women with chronic painful TMD tend to have high levels of catastrophizing and central sensitization. There is a positive and proportional association between the duration of pain and/or the number of pailful points and catastrophizing in women with chronic pain-related TMD.
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Pervaiz, Rameesha, Somia Faisal, Nabeela Safdar, Fiza Saleem, and Hafiz Muhammad Asim. "Severity of central sensitization in patients with chronic low back pain." Foundation University Journal of Rehabilitation Sciences 3, no. 2 (July 31, 2023): 77–84. http://dx.doi.org/10.33897/fujrs.v3i2.321.
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Background: Low back pain develops into Chronic Low Back Pain (CLBP) due to the contribution of various psychosocial factors in approximately 10-20% of all patients. CLBP is classified into three groups namely neuropathic, nociceptive and central sensitization (CS). CS results in pain due to hyper-responsive nociceptive neurons and recruitment of sub-threshold or normal stimuli. Objective: To determine the frequency of central sensitization in patients with chronic low back pain Methods: A descriptive cross-sectional observational study was conducted on 388 patients with CLBP, aged between 18 to 44 years, using non-probability convenient sampling. Patients were recruited from Ghurki Trust and Teaching Hospital, whereas, adults with a history of spinal surgery within the last 12 months, use of NSAIDs/analgesics, and coexisting neurological, respiratory, cardiac, or rheumatic disorder were excluded. The participants were requested to fill the Central Sensitization Inventory (CSI) questionnaire which has a test-retest reliability of 0.817. Results: Out of 388 participants, 22.7% (n=88) of the participants demonstrated subclinical central sensitization. Mild central sensitization was reported by 33.0% (n=128) participants, 20.6% (n=80) demonstrated moderate central sensitization scores on the CSI. Whereas, severe central sensitization was found in 13.4% (n=52) participants and 10.3% (n=40) of the participants reported extreme central sensitization category based on their scores on the CSI. Conclusion: Mild central sensitization was reported frequently among patients with chronic low back pain.
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Orr, Natasha L., Alice J. Huang, Yang Doris Liu, Heather Noga, Mohamed A. Bedaiwy, Christina Williams, Catherine Allaire, and Paul J. Yong. "Association of Central Sensitization Inventory Scores With Pain Outcomes After Endometriosis Surgery." JAMA Network Open 6, no. 2 (February 27, 2023): e230780. http://dx.doi.org/10.1001/jamanetworkopen.2023.0780.
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ImportanceA subset of people who undergo surgery for endometriosis have persistent pain, suggesting that other factors besides the endometriosis, such as central sensitization, may play a role in this pain. The Central Sensitization Inventory, a validated self-reported questionnaire of central sensitization symptoms, may identify individuals with endometriosis who have more pain after surgery due to pain sensitization.ObjectiveTo examine whether greater baseline Central Sensitization Inventory scores are associated with postsurgical pain outcomes.Design, Setting, and ParticipantsThis prospective, longitudinal cohort study performed at a tertiary center for endometriosis and pelvic pain in British Columbia, Canada, included all patients aged 18 to 50 years with diagnosed or suspected endometriosis and a baseline visit between January 1, 2018, and December 31, 2019, who underwent surgery after the baseline visit. Individuals who were menopausal, had a prior hysterectomy, or were missing data for outcomes or measures were excluded. Data analysis was performed from July 2021 to June 2022.Main Outcomes and MeasuresThe primary outcome was chronic pelvic pain at follow-up measured on a scale of 0 to 10, with 0 to 3 indicating no pain or mild pain, 4 to 6 indicating moderate pain, and 7 to 10 indicating severe pain. Secondary outcomes were deep dyspareunia, dysmenorrhea, dyschezia, and back pain at follow-up. The main variable of interest was baseline Central Sensitization Inventory score (measured from 0 to 100, consisting of 25 self-reported questions rated from 0 to 4 [never, rarely, sometimes, often, and always, respectively]).ResultsA total of 239 patients (mean [SD] age, 34 [7] years; 189 [79.1%] White [11 (5.8%) identified as White mixed with another ethnicity], 1 [0.4%] Black or African American, 29 [12.1%] Asian, 2 [0.8%] Native Hawaiian or Pacific Islander, 16 [6.7%] other, and 2 [0.8%] mixed race or ethnicity) with follow-up data at more than 4 months after surgery were included in this study (71.0% follow-up rate). The mean (SD) baseline Central Sensitization Inventory score was 43.8 (18.2), and the mean (SD) follow-up was 16.1 (6.1) months. Higher baseline Central Sensitization Inventory scores were significantly associated with higher chronic pelvic pain (odds ratio [OR], 1.02; 95% CI, 1.00-1.03; P = .02), deep dyspareunia (OR, 1.03; 95% CI, 1.01-1.04; P = .004), dyschezia (OR, 1.03; 95% CI, 1.01-1.04; P &lt; .001), and back pain (OR, 1.02; 95% CI, 1.00-1.03; P = .02) at follow-up, when controlling for baseline pain scores. The Central Sensitization Inventory scores themselves decreased slightly from baseline to follow-up (mean [SD] score, 43.8 [18.2] vs 41.7 [18.9]; P = .05); however, individuals with high baseline Central Sensitization Inventory scores still had high scores at follow-up.Conclusions and RelevanceIn this cohort study of 239 patients with endometriosis, higher Central Sensitization Inventory scores at baseline were associated with worse pain outcomes after endometriosis surgery, when controlling for baseline pain scores. The Central Sensitization Inventory could be used to counsel patients with endometriosis on their expected outcomes after surgery.
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Goudman, Lisa, Ann De Smedt, Stijn Roggeman, César Fernández-de-las-Peñas, Samar M. Hatem, Marc Schiltz, Maxime Billot, Manuel Roulaud, Philippe Rigoard, and Maarten Moens. "Association between Experimental Pain Measurements and the Central Sensitization Inventory in Patients at Least 3 Months after COVID-19 Infection: A Cross-Sectional Pilot Study." Journal of Clinical Medicine 12, no. 2 (January 13, 2023): 661. http://dx.doi.org/10.3390/jcm12020661.
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Fatigue, pain, headache, brain fog, anosmia, ageusia, mood symptoms, and sleep disorders are symptoms commonly experienced by people with post-COVID-19 condition. These symptoms could be considered as manifestations of central sensitization. The aim of this study is to evaluate whether there are indicators of central sensitization by using experimental pain measurements and to determine their association with patient-reported outcome measures (PROMs). A cross-sectional study including 42 patients after COVID-19 infection was conducted. The central sensitization inventory (CSI) was administered as a PROM to evaluate central-sensitization-associated symptoms. Pressure pain thresholds (PPT), temporal summation, and descending nociceptive pain inhibition (CPM) were assessed as experimental pain measurements. The median score on the CSI was 46.5 (Q1–Q3: 33–54). The presence of central-sensitization-associated symptoms was seen in 64.3% of patients based on the CSI (≥40/100 points). A deficient CPM was seen in 12% and 14% of patients when measured at the trapezius and rectus femoris, respectively. A negative correlation between pressure sensitivity on the rectus femoris and the CSI score (r = −0.36, 95%CI −0.13 to −0.65, p = 0.007) was observed. Central-sensitization-associated symptoms were present in up to 64.3% of patients post-COVID-19 infection, based on a PROM, i.e., the CSI. A more objective evaluation of nociceptive processing through experimental pain measurements was less suggestive of indicators of central sensitization. Only a small negative correlation between pressure sensitivity and the CSI was observed, thereby pointing towards the discrepancy between the CSI and experimental pain measurements and presumably the complementary need for both to evaluate potential indicators of central sensitization in this population.
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Hirata, Koichi, Daisuke Danno, Shoji Kikui, Keisuke Suzuki, and Takao Takeshima. "Central sensitization and chronic pain: study for migraine." PAIN RESEARCH 35, no. 2 (June 30, 2020): 73–79. http://dx.doi.org/10.11154/pain.35.73.
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Ketenci, Ayşegül, Mert Zure, Fatma Merih Akpınar, Yelda Soluk Özdemir, Özlem Balbaloğlu, Mazlum Serdar Akaltun, Ender Erden, et al. "Pain types and risk factors in post-COVID-19." Turkish Journal of Physical Medicine and Rehabilitation 70, no. 1 (February 1, 2024): 30–38. https://doi.org/10.5606/tftrd.2024.13828.
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Objectives: This study aims to accurately evaluate pain lasting longer than three months and falls under the category of chronic pain and to determine the risk factors to follow up and treat properly and to develop appropriate diagnostic and treatment algorithms. Patients and methods: Between March 2021 and December 2021, a total of 437 patients (162 males, 275 females; mean age: 44±14.6 years; range, 12 to 82 years) who were referred to the participating centers due to pain complaints and were diagnosed with post-COVID-19 condition according to the criteria defined by the World Health Organization (WHO) were included in the study. The patients were divided into three groups as nociceptive pain, neuropathic pain, and central sensitization, based on the physician's clinical evaluation and the Self-Report Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS) and Central Sensitization Inventory scores. Results: The most common diagnosis was nociceptive pain followed by central sensitization. Patients with nociceptive pain had less pain. It was found that not exercising regularly, having a chronic disease and being a woman were risk factors for central sensitization, having thyroid disease before COVID-19, and defining the current pain as very severe were risk factors for neuropathic pain. Conclusion: In the evaluation of post-COVID-19 pain, neuropathic pain and central sensitization should be also considered in addition to nociceptive pain and the severity of pain, systemic diseases and physical activity should be questioned.
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Skorupska, Elżbieta. "CENTRAL SENSITIZATION OF PAIN IN PHYSIOTHERAPY." Issues of Rehabilitation, Orthopaedics, Neurophysiology and Sport Promotion – IRONS 32, no. 32 (September 2020): 35–39. http://dx.doi.org/10.19271/irons-000120-2020-32.
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Nowadays, there are three main pain descriptors: nociceptive pain, neuropathic pain, and nociplastic pain. The last one is the newest expression defining pain as ‘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’ (International Association for the Study of Pain). The implementation of modern pain neuroscience in practice is said to be the most important for musculoskeletal physical therapists around the world. One of the examples of the nociplastic pain mechanism can be myofascial trigger points that are connected with central sensitization (one of the subtypes of nociplastic pain). Central sensitization (CS) is defined as an amplification of neural signaling within the central nervous system that elicits pain hypersensitivity and ongoing neuronal excitation which outlasts the initial nociceptor input. Features typical of that state are abnormally low peripheral thresholds for pain from pressure, temperature, electrical, and other stimuli and it has been proposed that trigger points may function as peripheral mediators of CS.
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Toyama, Midori, Chiho Kudo, Chikako Mukai, Mika Inoue, Aiko Oyamaguchi, Hiroshi Hanamoto, Mitsutaka Sugimura, and Hitoshi Niwa. "Trigeminal nervous system sensitization by infraorbital nerve injury enhances responses in a migraine model." Cephalalgia 37, no. 14 (November 12, 2016): 1317–28. http://dx.doi.org/10.1177/0333102416678387.
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Background Although the peripheral and central sensitizations of trigeminal nervous system may be one of the important factors of migraine, the precise mechanism is not fully understood. In this study, we examined the influence of the sensitization of the second division of the trigeminal nerve (V2) by chronic constriction injury (CCI) of the infraorbital nerve (ION) on migraine headache, using the capsaicin-induced migraine model. Methods Male Sprague-Dawley rats were assigned to four groups: (a) sham surgery and topical-dural vehicle application (Sham + Vehicle) group, (b) CCI-ION and topical-dural vehicle application (CCI-ION + Vehicle) group, (c) sham surgery and topical-dural capsaicin application (Sham + Capsaicin) group, (d) CCI-ION and topical-dural capsaicin application (CCI-ION + Capsaicin) group. Behavioral testing and immunohistochemical staining were performed. Results In the behavioral test, the Sham + Capsaicin group showed significantly longer duration of immobilization and shorter duration of exploration compared with the Sham + Vehicle group, which is similar to clinical features of migraine patients. Moreover, CCI-ION enhanced these effects in the CCI-ION + Capsaicin group. Immunohistochemical staining for phospho-extracellular signal-related kinase (pERK) in the trigeminal ganglion (TG) containing first and second divisions of the trigeminal nerve and the trigeminocervical complex (TCC) revealed that pERK expression was significantly increased in the CCI-ION + Capsaicin group compared with the other groups. However, comparing between effects of the peripheral and central sensitizations (in the TG and TCC), from our results, peripheral sensitization would play a much less or not significant role. Conclusions These data demonstrate that the sensitization of V2 could influence the activation and the sensitization of the first division of the trigeminal nerve in the TCC, subsequently exacerbating pain sensation and pain-related behaviors. We have shown for the first time that the existence of the central sensitization of V2 can be an exacerbating factor for migraine related nociceptive thresholds/activation.
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Liew, Bernard X. W., Juan Antonio Valera-Calero, Umut Varol, Jo Nijs, Lars Arendt-Nielsen, Gustavo Plaza-Manzano, and César Fernández-de-las-Peñas. "Distress and Sensitization as Main Mediators of Severity in Women with Fibromyalgia: A Structural Equation Model." Biomedicines 10, no. 5 (May 20, 2022): 1188. http://dx.doi.org/10.3390/biomedicines10051188.
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We aimed to explore a path model identified using a structural equation model (SEM) which best explains the multivariate contributions of sensitization, sensitivity, and emotional variables to clinical severity in women with FMS. Pain features, the Central Sensitization Inventory (CSI), painDETECT, S-LANSS, the Hospital Anxiety and Depression Scale (HADS), the Pittsburgh Sleep Quality Index (PSQI), the Pain Catastrophizing Scale (PCS), the Pain Vigilance and Awareness Questionnaire (PVAQ), the 11-item Tampa Scale for Kinesiophobia (TSK-11), and pressure pain thresholds (PPTs) were collected from 113 women with FMS. Four latent variables were created: severity (clinical pain features), sensitivity (PPTs), sensitization (S-LANSS, CSI, painDETECT), and distress (HADS-A, HADS-D, PCS, PVAQ, TSK-11). Data fit for the measurement model were considered excellent (RMSEA = 0.043, CFI = 0.966, SRMR = 0.067, and NNFI = 0.960). Distress had a significant relationship with the mediators of sleep (β = 0.452, p = 0.031) and sensitization (β = 0.618, p = 0.001). The only mediator with a significant effect (β = 1.113, p < 0.001) on severity was sensitization. A significant indirect effect of sensitization (β = 0.687, p = 0.001) that explained the relationship between distress and severity was also identified. The proposed model suggests that distress and sensitization, together with poor sleep, have a complex mediating effect on severity in women with FMS. The identified path model can be leveraged in clinical trials investigating treatment approaches for FMS.
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Barcelon, Ellane, Seohyun Chung, Jaesung Lee, and Sung Joong Lee. "Sexual Dimorphism in the Mechanism of Pain Central Sensitization." Cells 12, no. 16 (August 9, 2023): 2028. http://dx.doi.org/10.3390/cells12162028.
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It has long been recognized that men and women have different degrees of susceptibility to chronic pain. Greater recognition of the sexual dimorphism in chronic pain has resulted in increasing numbers of both clinical and preclinical studies that have identified factors and mechanisms underlying sex differences in pain sensitization. Here, we review sexually dimorphic pain phenotypes in various research animal models and factors involved in the sex difference in pain phenotypes. We further discuss putative mechanisms for the sexual dimorphism in pain sensitization, which involves sex hormones, spinal cord microglia, and peripheral immune cells. Elucidating the sexually dimorphic mechanism of pain sensitization may provide important clinical implications and aid the development of sex-specific therapeutic strategies to treat chronic pain.
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Balasch-Bernat, Mercè, Lirios Dueñas, Marta Aguilar-Rodríguez, Deborah Falla, Alessandro Schneebeli, Marta Navarro-Bosch, Enrique Lluch, and Marco Barbero. "The Spatial Extent of Pain Is Associated with Pain Intensity, Catastrophizing and Some Measures of Central Sensitization in People with Frozen Shoulder." Journal of Clinical Medicine 11, no. 1 (December 28, 2021): 154. http://dx.doi.org/10.3390/jcm11010154.
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The aim of this cross-sectional study was to explore the spatial extent of pain and its association with clinical symptoms, psychological features, and pain sensitization in people with frozen shoulder (FS). Forty-eight individuals with FS completed pain drawings (PDs) and reported their clinical symptoms including pain intensity (Visual Analogue Scale) and shoulder disability (Shoulder Pain and Disability Index). Moreover, pain sensitization measurements (pressure pain thresholds, temporal summation, conditioned pain modulation, and Central Sensitization Inventory (CSI)) were assessed. Psychological features were assessed by Pain Catastrophizing Scale (PCS) and Pain Vigilance and Awareness Questionnaire. Pain frequency maps were generated, Margolis rating scale was used for pain location, and Spearman correlation coefficients were computed. The mean (SD) pain extent was 12.5% (6.7%) and the most common painful area was the anterolateral shoulder region (100%). Women presented a more widespread pain distribution compared with men. Significant positive associations were obtained between pain extent and current pain intensity (rs = 0.421, p < 0.01), PCS (rs = 0.307, p < 0.05) and CSI (rs = 0.358, p < 0.05). The anterolateral region of the shoulder was the most common painful area in people with FS. Women with FS presented more extended areas of pain; and a more widespread distribution of pain was correlated with higher levels of pain, pain catastrophizing and pain sensitization.
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Jarrell, John, Magali Robert, Maria Adele Giamberardino, Selphee Tang, and Kirk Stephenson. "Pain, psychosocial tests, pain sensitization and laparoscopic pelvic surgery." Scandinavian Journal of Pain 18, no. 1 (January 26, 2018): 49–57. http://dx.doi.org/10.1515/sjpain-2017-0127.
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Abstract Background and aims: Individuals with non-acute pain are challenged with variable pain responses following surgery as well as psychological challenges, particularly depression and catastrophizing. The purpose of this study was to compare pre- and postoperative psychosocial tests and the associated presence of sensitization on a cohort of women undergoing elective laparoscopic surgery for non-acute pain defined as pain sufficient for surgical investigation without persistent of chronic pain. Methods: The study was a secondary analysis of a previous report (Am J Obstet Gynecol 2014 Oct;211(4):360–8.). The study was a prospective cohort trial of 77 women; 61 with non-acute pain and 16 women for a tubal ligation. The women had the following tests: Pain Disability Index, Pain Catastrophizing Scale, CES-D (Center for Epidemiologic Studies Depression Scale) depression scale and the McGill Pain Scale (short form) as well as their average pain score and the presence of pain sensitization. All test scores were correlated together and comparisons were done using paired t-test. Results: There were reductions in pain and psychosocial test scores that were significantly correlated. Pre-operative sensitization indicated greater changes in psychosocial tests. Conclusions: There was a close association of tests of psychosocial status with average pain among women having surgery on visceral tissues. Incorporation of these tests in the pre- and postoperative evaluation of women having laparoscopic surgery appears to provide a means to a broader understanding of the woman’s pain experience.
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Lorenzo-Gallego, Laura, Beatriz Arranz-Martín, Helena Romay-Barrero, Virginia Prieto-Gómez, Enrique Lluch, and María Torres-Lacomba. "Changes in Pain Sensitivity in Treatment for Breast Cancer: A 12-Month Follow-Up Case Series." International Journal of Environmental Research and Public Health 19, no. 7 (March 29, 2022): 4055. http://dx.doi.org/10.3390/ijerph19074055.
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This study aimed to investigate changes in the pain sensory profile of women with breast cancer. Five women with unilateral breast cancer were enrolled. Participants were assessed with direct (quantitative sensory testing, QST) and indirect measures of pain sensitization (self-reported central sensitization inventory, CSI) at baseline (before surgery), 1 week after surgery, and at 1, 6, 9, and 12 months post-surgery. In the event of pain occurrence, the Leeds Assessment of Neuropathic Symptoms and Signs was also used. Nociceptive pain was the predominant pain mechanism in the postoperative period, while an increase in sensitization predominated one year after breast cancer surgery, especially in those participants who had received more treatment procedures. The participants who received more therapies for breast cancer experienced persistent pain and a higher level of sensitization. An assessment protocol including direct measurements (QST) and indirect measurement (self-reported CSI) allows for detecting changes in pain sensitivity, which can be useful for characterizing and/or predicting pain before, during, and up to one year following surgical interventions for breast cancer.
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Pedersini, Paolo, Massimiliano Gobbo, Mark D. Bishop, Lars Arendt-Nielsen, and Jorge H. Villafañe. "Functional and Structural Neuroplastic Changes Related to Sensitization Proxies in Patients with Osteoarthritis: A Systematic Review." Pain Medicine 23, no. 3 (October 11, 2021): 488–98. http://dx.doi.org/10.1093/pm/pnab301.
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Abstract Objective Several reports in literature have identified sensitization as a possible basis for the enhanced pain reactions associated with osteoarthritis (OA). The aim of this current systematic review is to summarize functional and structural brain changes associated with surrogate sensitization parameters assessed in patients with OA-related pain. Design Systematic review. Subjects Patients with OA related pain. Methods A literature search was conducted systematically in MEDLINE, CINAHL, EMBASE databases for human studies up to December 2019. Articles were included if they assessed brain imaging and sensitization parameters (quantitative sensory testing and questionnaires) in adults with OA-related pain. Methodological quality was assessed using the Methodological Index for Non-Randomized Studies (MINORS) score. Results Five studies reporting on 138 patients were included in this review. The MINORS scale yielded mean scores of 8.5/16 and 12.3/24, for the cohort and case-control studies respectively. Four low-quality studies suggest a greater pain matrix activation associated with clinical measures of sensitization in patients with OA, while another study underlined the presence of structural changes (reduced gray matter volume) in the cortical areas involved in the nociceptive processing possible also related to sensitization. Conclusions This review shows conflicting evidence for structural and functional neuroplastic brain changes related to sensitization proxies in patients with OA.
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Matre, Dagfinn, and Stein Knardahl. "‘Central sensitization’ in chronic neck/shoulder pain." Scandinavian Journal of Pain 3, no. 4 (October 1, 2012): 230–35. http://dx.doi.org/10.1016/j.sjpain.2012.04.003.
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AbstractBackground and purpose‘Central sensitization’ (CS) may play a major role in maintaining several chronic pain conditions. CS has been proposed to play a significant role in a range of musculoskeletal pain conditions, such as trapezius myalgia, fibromyalgia, temporomandibular disorders, and low back pain. Whether CS varies over time within an individual is not known. This study evaluated (1) whether there is an intraindividual association between clinical pain and signs of CS, and (2) whether there is an inter-individual association between clinical pain and signs of CS.MethodsTwenty-seven sedentary workers (19 women, 8 men) with varying neck/shoulder pain participated in a pre-test and in two test sessions. On one of the test sessions the subjects had weak (or no) clinical pain (weak-pain day). On the other test session the subjects had stronger clinical pain (strong-pain day). As an indicator of ‘central sensitization’, we assessed the area of secondary pinprick hyperalgesia (tested by 84.4 g/mm2 Von Frey hairs) in response to a first-degree burn to the volar fore-arm (contact heat, 46°C, 5 min). While in the lab, the subjects’ current clinical pain intensity (0–10 cm VAS) and distribution was assessed (PINTlab and PDISTlab ). The subjects also rated their pain intensity and distribution retrospectively from the past 30 days (PINT30d and PDIST30d ).ResultsPINTlab was lower on the weak-pain day (1.7 ± 1.5 cm) than on the strong-pain day (4.3 ± 1.6 cm). This was also the case for the other clinical pain measures (PDISTlab, PINT30 d and PDIST30 d ) and indicated that the participants were successfully recruited at days that differed in clinical pain severity. Despite a significant intra-individual difference in clinical pain between days, the area of secondary hyperalgesia did not differ between weak-and strong-pain days (50.3 ± 13.5 cm2 vs. 51.2 ± 12.6 cm2 ). Testing the inter-individual association between clinical pain and secondary hyperalgesia, we found a positive correlation between PINTlab and secondary hyperalgesia on the weak-pain day (rho = 0.6), but not on the strong-pain day (rho = 0.1). Given the stable secondary hyperalgesia across weak-and strong-pain days, this implies that subjects with a small secondary hyperalgesic area exhibited a relatively large variation in clinical pain between days, whereas subjects with a large secondary hyperalgesic area exhibited relatively small variation in clinical pain.ConclusionsWhen subjects are observed across days, ‘central sensitization’, measured as the area of secondary hyperalgesia after a first-degree burn, does not seem to be important for clinical pain intensity per se, but may be important for clinical pain variation. Subjects with indication of low ‘central sensitization’ seem to exhibit larger variation in pain between “good” and “bad” days than subjects with indication of high ‘central sensitization’. The study indicates that ‘central sensitization’ does not explain intra-individual variations in clinical pain.ImplicationsThis study raises the question of the role of ‘central sensitization’ in clinical musculoskeletal pain disorders. Furthermore, a precise definition of the ‘central sensitization’ concept is called for.
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van den Broeke, Emanuel N., Diana M. Torta, and Omer Van den Bergh. "Central Sensitization: Explanation or Phenomenon?" Clinical Psychological Science 6, no. 6 (July 2, 2018): 761–64. http://dx.doi.org/10.1177/2167702618781804.
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Central sensitization (CS) is a popular concept that is frequently used to explain pain hypersensitivity in a large number of pain conditions. However, the concept of CS is now also increasingly used to explain nonpain symptoms. In the present commentary, we argue that CS, as defined by the International Association for the Study of Pain, refers to changes in nociceptive neurons only and therefore cannot be applied to enhanced responses to stimuli other than nociceptive and/or pain. Moreover, the evidence for CS in widespread pain (other than secondary hyperalgesia) and many other conditions is scarce to absent. As a consequence, CS is a descriptive label for the explanandum rather than an explanation and, as such, suffers the risk of being a circular explanation. Finally, cognitive and emotional factors should also be considered as potential mechanisms for the wide range of phenomena that are currently interpreted as evidence for CS.
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Richebé, Philippe, Xavier Capdevila, and Cyril Rivat. "Persistent Postsurgical Pain." Anesthesiology 129, no. 3 (September 1, 2018): 590–607. http://dx.doi.org/10.1097/aln.0000000000002238.
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Abstract The development of chronic pain is considered a major complication after surgery. Basic science research in animal models helps us understand the transition from acute to chronic pain by identifying the numerous molecular and cellular changes that occur in the peripheral and central nervous systems. It is now well recognized that inflammation and nerve injury lead to long-term synaptic plasticity that amplifies and also maintains pain signaling, a phenomenon referred to as pain sensitization. In the context of surgery in humans, pain sensitization is both responsible for an increase in postoperative pain via the expression of wound hyperalgesia and considered a critical factor for the development of persistent postsurgical pain. Using specific drugs that block the processes of pain sensitization reduces postoperative pain and prevents the development of persistent postoperative pain. This narrative review of the literature describes clinical investigations evaluating different preventative pharmacologic strategies that are routinely used by anesthesiologists in their daily clinical practices for preventing persistent postoperative pain. Nevertheless, further efforts are needed in both basic and clinical science research to identify preclinical models and novel therapeutics targets. There remains a need for more patient numbers in clinical research, for more reliable data, and for the development of the safest and the most effective strategies to limit the incidence of persistent postoperative pain.
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Janssen, Joel, Elias Abou-Assaly, Nivez Rasic, Melanie Noel, and Jillian Vinall Miller. "Trauma and pain sensitization in youth with chronic pain." PAIN Reports 7, no. 2 (March 2022): e992. http://dx.doi.org/10.1097/pr9.0000000000000992.
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Kraev, Krasimir, Mariela Geneva-Popova, Bozhidar Hristov, Petar Uchikov, Stanislava Popova, Maria Kraeva, Yordanka Basheva-Kraeva, et al. "Exploring the Novel Dimension of Immune Interactions in Pain: JAK Inhibitors’ Pleiotropic Potential." Life 13, no. 10 (September 29, 2023): 1994. http://dx.doi.org/10.3390/life13101994.
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This review explores the link between immune interactions and chronic pain, offering new perspectives on treatment. It focuses on Janus kinase (JAK) inhibitors’ potential in pain management. Immune cells’ communication with neurons shapes neuroinflammatory responses, and JAK inhibitors’ effects on pain pathways are discussed, including cytokine suppression and microglial modulation. This review integrates studies from rheumatoid arthritis (RA) pain and central sensitization to highlight connections between immune interactions and pain. Studies on RA joint pain reveal the shift from cytokines to sensitization. Neurobiological investigations into central sensitization uncover shared pathways in chronic pain. Clinical evidence supports JAK inhibitors’ efficacy on pain-related outcomes and their effects on neurons and immune cells. Challenges and future directions are outlined, including interdisciplinary collaboration and dosing optimization. Overall, this review highlights JAK inhibitors’ potential to target immune-mediated pain pathways, underscoring the need for more research on immune–pain connections.
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San-Antolín, Marta, David Rodríguez-Sanz, Ricardo Becerro-de-Bengoa-Vallejo, Marta Elena Losa-Iglesias, Israel Casado-Hernández, Daniel López-López, and César Calvo-Lobo. "Central Sensitization and Catastrophism Symptoms Are Associated with Chronic Myofascial Pain in the Gastrocnemius of Athletes." Pain Medicine 21, no. 8 (November 13, 2019): 1616–25. http://dx.doi.org/10.1093/pm/pnz296.
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Abstract Objective To compare central sensitization symptoms, presence of central sensitivity syndrome (CSS), catastrophism, rumination, magnification, and helplessness symptoms between athletes with gastrocnemius myofascial pain and healthy athletes. Furthermore, to predict central sensitization symptoms based on sociodemographic and descriptive data, catastrophism features, and presence of gastrocnemius myofascial pain in athletes. Design Case–control study. Setting Outpatient clinic. Subjects Fifty matched paired athletes were recruited and divided into patients with chronic (more than three months) gastrocnemius myofascial pain (N = 25) and healthy subjects (N = 25). Methods Central sensitization symptoms and CSS presence (≥40 points) were determined by the Central Sensitization Questionnaire (CSQ). Catastrophism symptoms and rumination, magnification, and helplessness domains were measured by the Pain Catastrophizing Scale (PCS). Statistical significance was set at P < 0.01 for a 99% confidence interval. Results Statistically significant differences (P ≤ 0.001) with a large effect size (d = 1.05–1.19) were shown for higher CSQ scores and PCS total and domain scores in athletes with gastrocnemius myofascial pain vs healthy athletes. Nevertheless, CSS presence (CSQ ≥ 40 points) did not show statistically significant differences (P = 0.050) between groups. A linear regression model (R2 = 0.560, P < 0.01) predicted higher CSQ scores based on PCS total score (R2 = 0.390), female sex (R2 = 0.095), and myofascial pain presence (R2 = 0.075). Conclusions Greater symptoms of central sensitization, catastrophism, rumination, magnification, and helplessness were shown in athletes with gastrocnemius myofascial pain compared with healthy athletes. Nevertheless, there was not a statistically significant presence of CSS comparing both groups. Greater central sensitization symptoms were predicted by catastrophism symptoms, female sex, and presence of gastrocnemius myofascial pain in athletes.
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Özge Kılıçaslan, Hamide, Aysun Genç, and Safiye Tuncer. "Central sensitization in osteoarthritic knee pain: A cross-sectional study." Turkish Journal of Physical Medicine and Rehabilitation 1, no. 1 (December 14, 2022): 89–96. http://dx.doi.org/10.5606/tftrd.2023.10470.
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Objectives: The aim of this study was to investigate central sensitization and associated factors in knee osteoarthritis (OA) patients and compare them with rheumatoid arthritis (RA) patients and healthy controls. Patients and methods: This cross-sectional study was conducted with 125 participants (7 males, 118 females; mean age: 57.2±8.2 years; range, 45 to 75 years) between January 2017 and December 2018. Sixty-two patients with symptomatic knee OA, 32 RA patients with knee pain, and 31 healthy controls constituted the participants. Central sensitization was investigated with the Central Sensitization Inventory (CSI) and pressure pain threshold (PPT) measurements. Pain, functional status, and psychosocial features were assessed with self-reported questionnaires. Results: The OA and RA groups had significantly lower PPT values at local, peripheral, and remote regions compared to the healthy controls. Pressure hyperalgesia was shown at the knee with a 43.5% prevalence, 27.4% at the leg, and 8.1% at the forearm of OA patients. Pressure hyperalgesia was present at the knee, leg, and forearm in 37.5%, 25%, and 9.4% of RA patients, respectively. Pressure pain threshold values, CSI scores, frequency of pressure hyperalgesia, and frequency of central sensitization according to the CSI were not statistically different between the OA and RA groups. Psychosocial features and structural damage were not correlated with PPT values in the OA group. Conclusion: The severity of chronic pain and functional status may be the clinical clues to recognizing patients with central sensitization since local joint damage does not play a direct role in the etiopathogenesis of central sensitization in OA patients and severe pain persisting in the chronic process is associated with central sensitization regardless of the pathogenesis.
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Fernández-de-las-Peñas, César, Stella Fuensalida-Novo, Ricardo Ortega-Santiago, Juan A. Valera-Calero, Corrado Cescon, Marco Derboni, Vincenzo Giuffrida, and Marco Barbero. "Pain Extent Is Not Associated with Sensory-Associated Symptoms, Cognitive or Psychological Variables in COVID-19 Survivors Suffering from Post-COVID Pain." Journal of Clinical Medicine 11, no. 15 (August 8, 2022): 4633. http://dx.doi.org/10.3390/jcm11154633.
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We aimed to investigate the relationship between pain extent, as a sign of sensitization, and sensory-related, cognitive and psychological variables in hospitalized COVID-19 survivors with post-COVID pain. One hundred and forty-six (67 males, 79 females) previously hospitalized COVID-19 survivors with post-COVID pain completed demographic (age, sex, height, weight), sensory-related (Central Sensitization Inventory, Self-Report Leeds Assessment of Neuropathic Symptoms), cognitive (Pain Catastrophizing Scale, Tampa Scale for Kinesiophobia) and psychological (Hospital Anxiety and Depression Scale, Pittsburgh Sleep Quality Index) variables. Pain extent and frequency maps were calculated from pain drawings using customized software. After conducting a correlation analysis to determine the relationships between variables, a stepwise linear regression model was performed to identify pain extent predictors, if available. Pain extent was significantly and weakly associated with pain intensity (r = −0.201, p = 0.014): the larger the pain extent, the lower the pain intensity. No other significant association was observed between pain extent and sensory-related, cognitive, or psychological variables in individuals with post-COVID pain. Females had higher pain intensity, more sensitization-associated symptoms, higher anxiety, lower sleep quality, and higher kinesiophobia levels than males. Sex differences correlation analyses revealed that pain extent was associated with pain intensity in males, but not in females. Pain extent was not associated with any of the measured variables and was also not related to the presence of sensitization-associated symptoms in our sample of COVID-19 survivors with long-term post-COVID pain.
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Neogi, T. "SP0067 Sensitization and Pain in OA." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 17.4–17. http://dx.doi.org/10.1136/annrheumdis-2016-eular.6336.
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