The Role of Central Sensitization in Chronic Pain of Rheumatic Diseases

2014 ◽  
Vol 34 (2) ◽  
pp. 81 ◽  
Author(s):  
Hye-Soon Lee
Keyword(s):  
Chronic Pain ◽  
Rheumatic Diseases ◽  
Central Sensitization

scholarly journals A38 TRPV1 VISCERAL AFFERENTS CONTROL CENTRAL SENSITIZATION IN IBD

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 278-279
Author(s):  
M Defaye ◽  
N Abdullah ◽  
M Iftinca ◽  
C Altier
Keyword(s):  
Chronic Pain ◽  
Central Sensitization ◽  
Microglial Activation ◽  
Visceral Pain ◽  
Purinergic Signaling ◽  
Designer Drugs ◽  
Visceral Afferents ◽  
Peripheral Sensitization ◽  
Specific Expression

Abstract Background Long-lasting changes in neural pain circuits precipitate the transition from acute to chronic pain in patients living with inflammatory bowel diseases (IBDs). While significant improvement in IBD therapy has been made to reduce inflammation, a large subset of patients continues to suffer throughout quiescent phases of the disease, suggesting a high level of plasticity in nociceptive circuits during acute phases. The establishment of chronic visceral pain results from neuroplasticity in nociceptors first, then along the entire neural axis, wherein microglia, the resident immune cells of the central nervous system, are critically involved. Our lab has shown that spinal microglia were key in controlling chronic pain state in IBD. Using the Dextran Sodium Sulfate (DSS) model of colitis, we found that microglial G-CSF was able to sensitize colonic nociceptors that express the pain receptor TRPV1. While TRPV1+ nociceptors have been implicated in peripheral sensitization, their contribution to central sensitization via microglia remains unknown. Aims To investigate the role of TRPV1+ visceral afferents in microglial activation and chronic visceral pain. Methods We generated DREADD (Designer Receptors Exclusively Activated by Designer Drugs) mice in which TRPV1 sensory neurons can be inhibited (TRPV1-hM4Di) or activated (TRPV1-hM3Dq) in a time and tissue specific manner using the inert ligand Clozapine-N-Oxide (CNO). To test the inhibition of TRPV1 neurons in DSS-induced colitis, TRPV1-hM4Di mice were treated with DSS 2.5% or water for 7 days and received vehicle or CNO i.p. injection twice daily. To activate TRPV1 visceral afferents, TRPV1-hM3Dq mice received vehicle or CNO daily for 7 days, by oral gavage. After 7 days of treatment, visceral pain was evaluated by colorectal distension and spinal cords tissues were harvested to measure microglial activation. Results Our data validated the nociceptor specific expression and function of the DREADD in TRPV1-Cre mice. Inhibition of TRPV1 visceral afferents in DSS TRPV1-hM4Di mice was able to prevent the colitis-induced microglial activation and thus reduce visceral hypersensitivity. In contrast, activation of TRPV1 visceral afferents in TRPV1-hM3Dq mice was sufficient to drive microglial activation in the absence of colitis. Analysis of the proalgesic mediators derived from activated TRPV1-hM3Dq neurons identified ATP as a key factor of microglial activation. Conclusions Overall, these data provide novel insights into the mechanistic understanding of the gut/brain axis in chronic visceral pain and suggest a role of purinergic signaling that could be harnessed for testing effective therapeutic approaches to relieve pain in IBD patients. Funding Agencies CCCACHRI (Alberta Children’s Hospital Research Institute) and CSM (Cumming School of Medicine) postdoctoral fellowship

scholarly journals AB0165 CENTRAL SENSITIZATION IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1109.2-1109
Author(s):  
E. Filatova ◽  
E. Pogozheva ◽  
V. Amirdzhanova ◽  
A. Karateev ◽  
A. Lila
Keyword(s):  
Quality Of Life ◽  
Rheumatoid Arthritis ◽  
Chronic Pain ◽  
Disease Activity ◽  
Rheumatic Diseases ◽  
Central Sensitization ◽  
Nociceptive Pain ◽  
The Central Nervous System ◽  
Clinically Significant

Background:Central Sensitization (CS) is a proposed physiological phenomenon in which dysregulation in the central nervous system causes neuronal dysregulation and hyperexcitability, resulting in hypersensitivity to both noxious and non-noxious stimuli. The term Central Sensitivity Syndrome (CSS) describes a group of medically indistinct (or nonspecific) disorders, such as fibromyalgia (FM) (1, 2).The prevalence of FM has been estimated at 2-7% in general population, but 10-30% patients with several rheumatic diseases fulfill the FM criteria, which suggests that they have not only nociceptive pain, but signs of CS or nocyplastic pain. (3)Objectives:to identify the signs of central sensitization (CS) in patients with rheumatoid arthritis (RA) with the central sensitization inventory (CSI).Methods:We examined 43 RA patients (mean age 45.5 [29.0; 53.0] years) with chronic pain. The patients underwent rheumatological examinations; CS was diagnosed using the CSI(4).; inflammation severity (DAS28 index), pain intensity (VAS), affective disorders (HADS), and quality of life (EQ-5D) were assessed.Results:We recruited 36 women and 7 men, mostly with moderate and high disease activity according to the DAS28 index.Using the CSI subclinical CS was found in 9 patients (20.9%), mild in 7 (16.3%), moderate in 8 (18.6%), severe in 16 (37.2%), and extremely severe sensitization in 3 (6.7%). Thus, 62.5% of patients with RA had had clinically significant CS (CS>40 points according to the CSI questionnaire).Patients with the presence of CS were characterized by more severe anxiety (10.0 [7.0; 11.0] vs 5.0 [3.0; 6.0], p=0.001) and lower quality of life (0.52 [-0.02; 0.52] vs 0.52 [0.52; 0.69], p= 0.02).The CSI tests not only pain but also other diseases associated with CS. Comorbid disorders associated with CS were found in patients with RA: 34.9% had cognitive impairment, 39.5% had signs of depression.Conclusion:Central sensitization was detected in 62.5% of patients with RA using the CSI questionnaire. CS is associated with anxiety and depression and negatively affects the patients’ quality of life. Chronic pain in RA can be of a mixed nature: nociceptive and neoplastic, which must be taken into account in the selection of personalized therapy.References:[1]Wolfe F. Fibromyalgianess. Arthritis Rheum. 2009; 61: 715-6.[2]Martins Rocha T, Pimenta S, Bernardo A, et al. Determinants of non-nociceptive pain in Rheumatoid Arthritis. Acta Reumatol Port. 2018 Oct-Dec;43(4):291-303.[3]Halioglu S, Carlioglu A., Akdeniz D., Karaaslan Y., Kosar A. Fibromyalgia in patients user rheumatic patients with several rheumatic diseases: prevalence and relationship with disease activity. Reumatol. Int. 2014 Sep; 34(90:1275-80 doi:10.1007/s00296-014-2972.Disclosure of Interests:None declared

scholarly journals Chronic pain and central sensitization in immuno-inflammatory rheumatic diseases: pathogenesis, clinical manifestations, the possibility of using targeted disease modifying antirheumatic drugs

2019 ◽  
Vol 57 (2) ◽  
pp. 197-209 ◽  
Author(s):  
A. E. Karateev ◽  
E. L. Nasonov
Keyword(s):  
Chronic Pain ◽  
Rheumatic Diseases ◽  
Central Sensitization ◽  
Effective Means ◽  
Clinical Manifestations ◽  
Inflammatory Rheumatic Diseases ◽  
Disease Modifying Antirheumatic Drugs ◽  
Antirheumatic Drugs ◽  
Nociceptive Neurons ◽  
Disease Modifying

Chronic pain is one of the main manifestations of immuno-inflammatory rheumatic diseases (IIRD), such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA), which determines the severity of suffering, reduced quality of life and disability of patients. Unfortunately, the use of synthetic and biological disease modifying antirheumatic drugs, as well as non-steroidal anti-inflammatory drugs does not always provide sufficient control of pain in IIRD, even when it is possible to achieve a significant reduction in inflammatory activity. The reason for this is the complex mechanism of chronic pain. It includes not onlystimulation of pain receptors caused by damage of the elements of the musculoskeletal system, but also a change in the perception of pain associated with the phenomenon of central sensitization (CS). CS is characterized by a significant and persistent increase in the sensitivity of nociceptive neurons to pain and nonpain stimuli. One of the main theories of the CS development consider this phenomenon as an inflammatory reaction of the neuronenvironmentthe activation of astrocytes and microglial cells, local hyperproduction of cytokines, inflammatory mediators and neurotrophic factors. Factors contributing to the development of CS in IIRD are obesity, depression and anxiety, damage of the somatosensory system, insufficient relief of pain in the onset of the disease. Clinical manifestations of CS in IIRD is hyperalgesia, allodinia, «expanded pain» and secondary fibromyalgia. An important role in the development of chronic pain and CS plays the intracellular inflammatory pathway JAK-STAT. Therefore, JAK inhibitors, such as tofacitinib, used in RA and PsA, can also be considered as an effective means of controlling chronic pain in these diseases.

Role of Ethnicity on Pain Perception, Fatigue, and Quality of Life in a Pediatric Chronic Pain Population

2007 ◽  
Author(s):  
Jeffrey I. Gold ◽  
Trina Haselrig ◽  
D. Colette Nicolaou ◽  
Katharine A. Belmont
Keyword(s):  
Quality Of Life ◽  
Chronic Pain ◽  
Pain Perception ◽  
Pediatric Chronic Pain

Chemo- and Optogenetic Strategies for the Elucidation of Pain Pathways

2019 ◽  
pp. 816-832 ◽  
Author(s):  
Sascha R. A. Alles ◽  
Anne-Marie Malfait ◽  
Richard J. Miller
Keyword(s):  
Chronic Pain ◽  
Pain Response ◽  
Conscious Perception ◽  
Novel Therapies ◽  
The Past ◽  
Nociceptive Pathways ◽  
Pain Pathways ◽  
Technical Advances ◽  
The Brain

Pain is not a simple phenomenon and, beyond its conscious perception, involves circuitry that allows the brain to provide an affective context for nociception, which can influence mood and memory. In the past decade, neurobiological techniques have been developed that allow investigators to elucidate the importance of particular groups of neurons in different aspects of the pain response, something that may have important translational implications for the development of novel therapies. Chemo- and optogenetics represent two of the most important technical advances of recent times for gaining understanding of physiological circuitry underlying complex behaviors. The use of these techniques for teasing out the role of neurons and glia in nociceptive pathways is a rapidly growing area of research. The major findings of studies focused on understanding circuitry involved in different aspects of nociception and pain are highlighted in this article. In addition, attention is drawn to the possibility of modification of chemo- and optogenetic techniques for use as potential therapies for treatment of chronic pain disorders in human patients.

Differential role of adenosine signaling cascade in acute and chronic pain

2019 ◽  
Vol 712 ◽  
pp. 134483
Author(s):  
Morayo G. Adebiyi ◽  
Jeanne Manalo ◽  
Rodney E. Kellems ◽  
Yang Xia
Keyword(s):  
Chronic Pain ◽  
Signaling Cascade ◽  
Adenosine Signaling
Sign in / Sign up

Export Citation Format

Share Document