scholarly journals Dor articular: inflamatória ou neuropática? / Joint pain: inflammatory or neuropathic pain?

2017 ◽  
Vol 7 (1) ◽  
pp. 9-14
Author(s):  
Juliana Barcellos de Souza
Keyword(s):  
Rheumatoid Arthritis ◽  
Chronic Pain ◽  
Neuropathic Pain ◽  
Joint Pain ◽  
Biopsychosocial Model ◽  
Therapeutic Approaches ◽  
Joint Structure ◽  
Education Of Patients ◽  
Artrite Reumatoide ◽  
Costs Of Treatment

Neste artigo de revisão narrativa atualizam-se alguns conceitos de dor articular. A prevalência da dor articular aumenta com o avanço da idade, assim como os custos no tratamento das limitações e incapacidades. Compreender as diferenças entre dor aguda e dor crônica permite melhor abordagem das dores articulares, onde a primeira representa um sinal de alerta e a segunda é considerada uma patologia em si. As causas da cronificação da dor ainda são incertas, porém, alguns modelos são propostos e discutidos, como a sensibilização central por excesso de informação nociceptiva, seja esta de origem inflamatória, traumática ou outra. Em dores crônicas inflamatórias - como nas Artrites reumatoides – destaca-se a importância de iniciar o tratamento precoce de forma agressiva para inibir o processo inflamatório e as deformidades estruturais. Osteoartrites, embora sejam predominantemente descritas por suas alterações degenerativas nas articulações, têm atualmente reconhecida sua fase inflamatória inicial. A dor articular tende a ser abordada predominantemente sob o ponto de vista biomecânico e inflamatório, contudo, a ausência da abordagem do componente neuropática da dor crônica, nas fases iniciais, é uma das causas de elevados custos e de grandes deformidades articulares.  Finalmente aborda-se a importância do movimento e da educação do paciente com dor articular com base no modelo biopsicossocial de saúde e dor.Palavras-chave: Dor articular; Artrite reumatoide; Osteoartrite; Dor inflamatória e neuropáticaABSTRACTThis article is a joint pain update. Prevalence rates, incapacity, and social and economic burden of joint pain increase with the advancing age. Understanding differences about acute and chronic pain could improve therapeutic approaches. Negligence early treatment of acute joint pain can increase costs of treatment and joint deformities. Rheumatoid arthritis guidelines propose an aggressive initial approach of treatment with the aim to protect joint structure from inflammation and deformity. In addition to inflammatory joint pain, the neuropathic pain was also explained; central sensitization and neuropathic pain associated to joint pain. Finally, the importance of motion and education of patients with chronic pain were addressed following the pain and health biopsychosocial model. Keywords: Joint pain; Rheumatoid arthritis; Osteoarthritis; Inflammatory and neuropathic pain

Neuropathic pain in patients with haemophilia, that is the question

2015 ◽  
Vol 35 (S 01) ◽  
pp. S5-S9 ◽  
Author(s):  
S. Krüger ◽  
T. Hilberg
Keyword(s):  
Rheumatoid Arthritis ◽  
Chronic Pain ◽  
Neuropathic Pain ◽  
Differential Diagnosis ◽  
Pain Management ◽  
Pain Mechanisms ◽  
Number Of Patients ◽  
Paindetect Questionnaire ◽  
Chronic Disorders ◽  
Chronic Pain Conditions

SummaryChronic pain caused by recurrent joint bleedings affects a large number of patients with haemophilia (PwH). The basis of this pain, nociceptive or neuropathic, has not been investigated so far. In other pain-related chronic disorders such as osteoarthritis or rheumatoid arthritis, initial studies showed nociceptive but also neuropathic pain features. 137 PwH and 33 controls (C) completed the painDETECT-questionnaire (pDq), which identifies neuropathic components in a person´s pain profile. Based on the pDq results, a neuropathic pain component is classified as positive, negative or unclear. A positive neuropathic pain component was found in nine PwH, but not in C. In 20 PwH an unclear pDq result was observed. In comparison to C the allocation of pDq results is statistically significant (p≤0.001). Despite various pDq results in PwH and C a similar appraisal pain quality, but on a different level, was determined. Summarising the results, there is a potential risk to misunderstand underlying pain mechanisms in PwH. In chronic pain conditions based on haemophilic arthopathy, a differential diagnosis seems to be unalterable for comprehensive and individualised pain management in PwH.

scholarly journals Neuropathic pain in rheumatoid arthritis

2020 ◽  
Vol 12 (5) ◽  
pp. 60-65
Author(s):  
E. S. Filatova ◽  
A. M. Lila ◽  
V. A. Parfenov
Keyword(s):  
Quality Of Life ◽  
Rheumatoid Arthritis ◽  
Chronic Pain ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Pain Syndrome ◽  
Chronic Pain Syndrome ◽  
Paindetect Questionnaire ◽  
Somatosensory Nervous System

Objective: to identify the signs of neuropathic pain (NP) in patients with rheumatoid arthritis (RA) on the basis of the PainDETECT questionnaire and neurological examination.Patients and methods. A total of 208 RA patients (39 men and 169 women; mean age, 47.7 years) with chronic pain syndrome were examined. The patients underwent rheumatological and neurological examinations; NP was diagnosed using the PainDETECT questionnaire; inflammation severity (DAS28 index), pain intensity (VAS), affective disorders (HADS), and quality of life (EQ-5D) were assessed.Results and discussion. 172 (82.7%) patients had moderate and high disease activity according to the DAS28. The signs of possible and highly probable NP according to the PainDETECT questionnaire were detected in 29.8 and 26.9% of patients, respectively; they were significantly more likely to be detected in patients with more severe pain syndrome, clinically significant anxiety, and worse quality of life, but were unassociated with RA activity according to the DAS28. Somatosensory nervous system injury (polyneuropathy, tunnel syndromes, and cervical myelopathy) was found in 77.6% of patients with possible NP and in 80.4% with highly probable NP. In other patients, NP might be caused by central sensitization. Conclusion. In patients with a RA exacerbation, chronic pain syndrome is caused not only by an active inflammatory process in the joint area and adjacent tissues, but also by somatosensory nervous system injury and central sensitization.

scholarly journals The Safety and Effect of Local Botulinumtoxin A Injections for Long-Term Management of Chronic Pain in Post-Herpetic Neuralgia: Literature Review and Cases Report Treated with Incobotulinumtoxin A

2021 ◽  
Vol 11 (8) ◽  
pp. 758
Author(s):  
Songjin Ri ◽  
Anatol Kivi ◽  
Jörg Wissel
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Adverse Events ◽  
Case Reports ◽  
Pain Reduction ◽  
Post Herpetic Neuralgia ◽  
Botulinumtoxin A ◽  
Incobotulinumtoxin A ◽  
Term Management

There are few reports on the safety and effectiveness of long-term botulinumtoxin A (BoNT A) therapy in severe chronic pain of post-herpetic neuralgia (PHN). The literature was searched with the term “neuropathic pain” and “botulinum” on PubMed (up to 29 February 2020). Pain was assessed with the Visual Analogue Scale (VAS) before and after BoNT A therapy. A total of 10 clinical trials and six case reports including 251 patients with PHN were presented. They showed that BoNT A therapy had significant pain reduction (up to 30–50%) and improvement in quality of life. The effect duration seems to be correlated with BoNT A doses injected per injection site. Intervals between BoNT A injections were 10–14 weeks. No adverse events were reported in cases and clinical studies, even in the two pregnant women, whose babies were healthy. The repeated (≥6 times) intra/subcutaneous injections of incobotulinumtoxin A (Xeomin®, Merz Pharmaceuticals, Germany) over the two years of our three cases showed marked pain reduction and no adverse events. Adjunctive local BoNT A injection is a promising option for severe PHN, as a safe and effective therapy in long-term management for chronic neuropathic pain. Its effect size and -duration seem to be depended on the dose of BoNT A injected per each point.

scholarly journals AB0648 REACTIVE ARTHRITIS IN SYPHILIS MIMICKING RHEUMATOID ARTHRITIS: A CASE REPORT

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1357.1-1357
Author(s):  
S. M. Lao ◽  
J. Patel
Keyword(s):  
Rheumatoid Arthritis ◽  
Reactive Arthritis ◽  
Joint Pain ◽  
Inflammatory Markers ◽  
Morning Stiffness ◽  
Treponema Pallidum ◽  
Case Series ◽  
Penicillin G ◽  
Joint Involvement ◽  
Igg Antibody

Background:Reactive arthritis is a form of spondyloarthritis with aseptic joint involvement occurring after a gastrointestinal or urogenital infection. Most commonly associated with Chlamydia trachomatis, Salmonella, Shigella, Campylobacter, and Yersinia. Syphilis is an infection caused by the spirochete Treponema pallidum and is not usually associated with reactive arthritis. Syphilis is a great imitator of other diseases due to its broad presentation including painless chancre, constitutional symptoms, adenopathy, rash, synovitis, neurological and ocular findings.Objectives:To discuss a patient who presented with symptoms of rheumatoid arthritis (RA) but was later diagnosed with syphilis.Methods:31 year old male, former tobacco smoker, referred to Rheumatology for sudden onset joint pains, elevated anti-cyclic citrullinated peptide (anti-CCP), and elevated inflammatory markers. He reported pain in bilateral wrists, fingers, and right elbow for 6 weeks. Associated with 45 minutes of morning stiffness and new onset lower back pain without stiffness. He denied trauma, fever, chills, skin rash, dysuria, or diarrhea. Initiated trial naproxen 500mg twice a day only to have minimal relief. Patient is sexually active with men and was recently diagnosed with oropharyngeal gonorrhea treated with azithromycin 4 months prior. All other STI screening including syphilis, gonorrhea, HIV were negative at that time. Patient is on emtricitabine and tenofovir disoproxil fumarate for HIV pre-exposure prophylaxis. He denied family history of immune mediated conditions. Exam was significant for mild synovitis of both wrists and bilateral 2nd metacarpophalangeal joints. Initial labs revealed weakly positive anti-CCP 21 (normal <20), sedimentation rate 64 (normal ESR 0-15 mm/hr), C-reactive protein 24 (normal CRP 0-10 mg/L), and negative RF, ANA, HLA B27. During a short trial of prednisone taper, there was temporary improvement in symptoms, however synovitis recurred upon completion. Hydroxychloroquine (HCQ) 200mg twice a day was started for possible RA and he was referred to Ophthalmology for baseline retinopathy screening. Incidentally, he developed right sided blurry vision 2 weeks after initiation of HCQ. He was diagnosed with panuveitis of the right eye with inflammation of the optic nerve head and prednisone 40mg daily was initiated for presumed ocular manifestation of RA. However, further workup of panuveitis revealed reactive Treponema pallidum antibody and RPR quantity 1:32. Prednisone was immediately discontinued and he was referred to the emergency department for possible neurosyphilis.Results:Lumbar puncture showed cerebral spinal fluid with 260 red blood cells, 1 white blood cell, 27mg/dL protein, 60mg/dL glucose, non reactive VDRL, reactive pallidum IgG antibody, and negative cultures. Meningitis and encephalitis panels were negative. Patient completed a 14 day course of IV penicillin G with complete remission of joint pain, visual symptoms, and normalization of anti-CCP, ESR, and CRP.Conclusion:This case highlights how syphilis may mimic signs and symptoms of RA including symmetrical small joint pain, morning stiffness, elevated inflammatory markers, and positive anti-CCP. Anti-CCP is >96% specific for RA but was a false positive in this patient. There have only been few reported cases noting positive anti-CCP with reactive arthritis. This is a rare case of reactive arthritis secondary to syphilis with resolution of symptoms upon treating the syphilis.References:[1]Carter JD. Treating reactive arthritis: insights for the clinician. Ther Adv Musculoskelet Dis. 2010 Feb;2(1):45-54.[2]Cohen SE, Klausner JD, Engelman J, Philip S. Syphilis in the modern era: an update for physicians. Infect Dis Clin North Am. 2013 Dec;27(4):705-22.[3]Singh Sangha M, Wright ML, Ciurtin C. Strongly positive anti-CCP antibodies in patients with sacroiliitis or reactive arthritis post-E. coli infection: A mini case-series based review. Int J Rheum Dis. 2018 Jan;21(1):315-321.Disclosure of Interests:None declared.

scholarly journals AB0713 EVALUATION OF THE EFFECTIVENESS OF LASER THERAPY IN THE TREATMENT OF RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1388.1-1388
Author(s):  
N. Zhuravleva ◽  
L. Karzakova ◽  
S. Kudryashov ◽  
E. Petrova
Keyword(s):  
Rheumatoid Arthritis ◽  
Laser Therapy ◽  
Medical Therapy ◽  
Joint Pain ◽  
Morning Stiffness ◽  
Activity Index ◽  
Clinical Indicators ◽  
On Demand ◽  
Number Of Patients ◽  
Basic Medical

Background:Despite the fact that the introduction of biological disease-modifying antirheumatic medicines (bDMARDs) and the early start of treatment for rheumatoid arthritis (RA) can effectively stop the inflammatory process in RA, a fairly large number of patients continue to experience joint pain [1]. It is assumed that in some cases, joint pain in patients with RA is not associated with the inflammation, so it requires consideration of the possibility of using alternative strategies for the treatment of RA.Objectives:The aim of the research is to study the effectiveness of laser therapy in the treatment of RA.Methods:114 patients with RA aged from 32 to 53 years have been monitored for 6 months. There were 82 women (71.9 %) and 32 men (28.1%) among them. The patients were randomly divided into 2 groups. The first group of patients (57 people) received basic medical therapy with methotrexate 15 mg intramuscularly once a week and nonsteroidal anti-inflammatory medicines (NSAIDs) on demand. The dose of methotrexate was selected taking into account the disease activity index DAS 28. The second group of patients (57 people) received basic medical therapy with methotrexate 15 mg intramuscularly once a week and NSAIDs on demand. In addition, the cutaneous low-intensity laser irradiation of the joints was added along the projection of the joint gap in a pulse mode with a wavelength of 0.89 microns. The pulse frequency is 80-1500 Hz, the pulse power is 5 W, the exposure time in the field is 1-2 minutes and the total radiation time per session is no more than 10 minutes [2]. The course of treatment consisted of 10 procedures (the device “Milta F-8 RD”, Russia, Moscow). The course of laser therapy was repeated after 4 weeks. To assess clinical indicators, patients were examined using the SF-36 questionnaire before treatment and 6 months after the start of treatment.Results:The survey after 6 months revealed the significant decrease in the severity of pain on the VAS from the initial average indicator 4.5±0.2 to 3.69±0.2 points (p<0.01) and morning stiffness from 60±5 to 40.8±4 minutes (p<0.01). In the first group, the dynamics of clinical indicators were not statistically significant: the intensity of pain decreased from 4.6±0.2 to 4.2±0.3 points (p>0.05) and the duration of morning stiffness reduced from 62±7 to 58.6±6 minutes (p>0.05). In the second group the decrease in the need for NSAIDs was observed in 21 patients, while in the first group the same was observed only in 10 patients (px2 = 0.020).Conclusion:Laser therapy in the treatment of patients with RA enabled to decrease the frequency of the need for NSAIDs and reduce morning stiffness. We recommend using laser therapy in patients with RA at the second radiological stage as an addition to basic therapy.References:[1]Altawil R et al. Arthritis Care Res (Hoboken). 2016; 68(8): 1061-1068.[2]Burger M et al. Physiother Theory Pract. 2017; 33(3): 184-197.Disclosure of Interests:None declared

scholarly journals Buprenorphine: Far Beyond the “Ceiling”

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 816
Author(s):  
Rosmara Infantino ◽  
Consalvo Mattia ◽  
Pamela Locarini ◽  
Antonio Luigi Pastore ◽  
Sabatino Maione ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Chronic Pain ◽  
Neuropathic Pain ◽  
Drug Abuse ◽  
Side Effects ◽  
National Health System ◽  
Analgesic Drugs ◽  
Third Line ◽  
Dynamic Profile

Chronic pain, including neuropathic pain, represents an untreated disease with important repercussions on the quality of life and huge costs on the national health system. It is well known that opioids are the most powerful analgesic drugs, but they represent the second or third line in neuropathic pain, that remain difficult to manage. Moreover, these drugs show several side effects that limit their use. In addition, opioids possess addictive properties that are associated with misuse and drug abuse. Among available opioids compounds, buprenorphine has been suggested advantageous for a series of clinical reasons, including the effectiveness in neuropathic pain. Some properties are partly explained by its unique pharmacological characteristics. However, questions on the dynamic profile remain to be answered. Pharmacokinetics optimization strategies, and additional potentialities, are still to be explored. In this paper, we attempt to conceptualize the potential undiscovered dynamic profile of buprenorphine.

scholarly journals Role of the immune system in neuropathic pain

2019 ◽  
Vol 20 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Marzia Malcangio
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Immune System ◽  
Peripheral Nerve ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Immune Cells ◽  
Peripheral Nerve Injury

AbstractBackgroundAcute pain is a warning mechanism that exists to prevent tissue damage, however pain can outlast its protective purpose and persist beyond injury, becoming chronic. Chronic Pain is maladaptive and needs addressing as available medicines are only partially effective and cause severe side effects. There are profound differences between acute and chronic pain. Dramatic changes occur in both peripheral and central pathways resulting in the pain system being sensitised, thereby leading to exaggerated responses to noxious stimuli (hyperalgesia) and responses to non-noxious stimuli (allodynia).Critical role for immune system cells in chronic painPreclinical models of neuropathic pain provide evidence for a critical mechanistic role for immune cells in the chronicity of pain. Importantly, human imaging studies are consistent with preclinical findings, with glial activation evident in the brain of patients experiencing chronic pain. Indeed, immune cells are no longer considered to be passive bystanders in the nervous system; a consensus is emerging that, through their communication with neurons, they can both propagate and maintain disease states, including neuropathic pain. The focus of this review is on the plastic changes that occur under neuropathic pain conditions at the site of nerve injury, the dorsal root ganglia (DRG) and the dorsal horn of the spinal cord. At these sites both endothelial damage and increased neuronal activity result in recruitment of monocytes/macrophages (peripherally) and activation of microglia (centrally), which release mediators that lead to sensitisation of neurons thereby enabling positive feedback that sustains chronic pain.Immune system reactions to peripheral nerve injuriesAt the site of peripheral nerve injury following chemotherapy treatment for cancer for example, the occurrence of endothelial activation results in recruitment of CX3C chemokine receptor 1 (CX3CR1)-expressing monocytes/macrophages, which sensitise nociceptive neurons through the release of reactive oxygen species (ROS) that activate transient receptor potential ankyrin 1 (TRPA1) channels to evoke a pain response. In the DRG, neuro-immune cross talk following peripheral nerve injury is accomplished through the release of extracellular vesicles by neurons, which are engulfed by nearby macrophages. These vesicles deliver several determinants including microRNAs (miRs), with the potential to afford long-term alterations in macrophages that impact pain mechanisms. On one hand the delivery of neuron-derived miR-21 to macrophages for example, polarises these cells towards a pro-inflammatory/pro-nociceptive phenotype; on the other hand, silencing miR-21 expression in sensory neurons prevents both development of neuropathic allodynia and recruitment of macrophages in the DRG.Immune system mechanisms in the central nervous systemIn the dorsal horn of the spinal cord, growing evidence over the last two decades has delineated signalling pathways that mediate neuron-microglia communication such as P2X4/BDNF/GABAA, P2X7/Cathepsin S/Fractalkine/CX3CR1, and CSF-1/CSF-1R/DAP12 pathway-dependent mechanisms.Conclusions and implicationsDefinition of the modalities by which neuron and immune cells communicate at different locations of the pain pathway under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction and provides opportunities for novel approaches for the treatment of chronic pain.

scholarly journals Pain anticipatory phenomena in patients with central poststroke pain: a magnetoencephalography study

2016 ◽  
Vol 116 (3) ◽  
pp. 1387-1395 ◽  
Author(s):  
Raghavan Gopalakrishnan ◽  
Richard C. Burgess ◽  
Scott F. Lempka ◽  
John T. Gale ◽  
Darlene P. Floden ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Visual Cues ◽  
Neural Substrates ◽  
Cognitive Networks ◽  
Therapeutic Approaches ◽  
Pain Experience ◽  
Time Frequency ◽  
Cognitive Components ◽  
Chronic Effects ◽  
Integrated Approaches

Central poststroke pain (CPSP) is characterized by hemianesthesia associated with unrelenting chronic pain. The final pain experience stems from interactions between sensory, affective, and cognitive components of chronic pain. Hence, managing CPSP will require integrated approaches aimed not only at the sensory but also the affective-cognitive spheres. A better understanding of the brain's processing of pain anticipation is critical for the development of novel therapeutic approaches that target affective-cognitive networks and alleviate pain-related disability. We used magnetoencephalography (MEG) to characterize the neural substrates of pain anticipation in patients suffering from intractable CPSP. Simple visual cues evoked anticipation while patients awaited impending painful (PS), nonpainful (NPS), or no stimulus (NOS) to their nonaffected and affected extremities. MEG responses were studied at gradiometer level using event-related fields analysis and time-frequency oscillatory analysis upon source localization. On the nonaffected side, significantly greater responses were recorded during PS. PS (vs. NPS and NOS) exhibited significant parietal and frontal cortical activations in the beta and gamma bands, respectively, whereas NPS (vs. NOS) displayed greater activation in the orbitofrontal cortex. On the affected extremity, PS (vs. NPS) did not show significantly greater responses. These data suggest that anticipatory phenomena can modulate neural activity when painful stimuli are applied to the nonaffected extremity but not the affected extremity in CPSP patients. This dichotomy may stem from the chronic effects of pain on neural networks leading to habituation or saturation. Future clinically effective therapies will likely be associated with partial normalization of the neurophysiological correlates of pain anticipation.

scholarly journals Sickle cell pain: a critical reappraisal

Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3647-3656 ◽  
Author(s):  
Samir K. Ballas ◽  
Kalpna Gupta ◽  
Patricia Adams-Graves
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Sickle Cell ◽  
Multiorgan Failure ◽  
Organ Damage ◽  
Acute Chest Syndrome ◽  
Prodromal Phase ◽  
Pain Syndromes ◽  
Painful Episode ◽  
Chronic Pain Syndromes

AbstractSickle cell pain includes 3 types: acute recurrent painful crises, chronic pain syndromes, and neuropathic pain. The acute painful crisis is the hallmark of the disease and the most common cause of hospitalization and treatment in the emergency department. It evolves through 4 phases: prodromal, initial, established, and resolving. Each acute painful episode is associated with inflammation that worsens with recurrent episodes, often culminating in serious complications and organ damage, such as acute chest syndrome, multiorgan failure, and sudden death. Three pathophysiologic events operate in unison during the prodromal phase of the crisis: vaso-occlusion, inflammation, and nociception. Aborting the acute painful episode at the prodromal phase could potentially prevent or minimize tissue damage. Our hypothesis is that managing these events with hydration, anti-inflammatory drugs, aggressive analgesia, and possibly vasodilators could abort the crisis and prevent or minimize further damage. Chronic pain syndromes are associated with or accompany avascular necrosis and leg ulcers. Neuropathic pain is not well studied in patients with sickle cell disease but has been modeled in the transgenic sickle mouse. Management of sickle cell pain should be based on its own pathophysiologic mechanisms rather than borrowing guidelines from other nonsickle pain syndromes.

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