Chronic Muscle Pain, Biofeedback, and the Neurophysiology of Pain

Biofeedback ◽  
2016 ◽  
Vol 44 (1) ◽  
pp. 19-23
Author(s):  
Gabriel E Sella ◽  
Donald Moss
Keyword(s):  
Chronic Pain ◽  
Muscle Pain ◽  
Muscle Physiology ◽  
Relaxation Model ◽  
Comprehensive Education ◽  
Biofeedback Treatment ◽  
Human Costs ◽  
Poor Outcomes ◽  
Chronic Muscle Pain

This article examines the economic and human costs of muscle pain and the role of biofeedback in treating chronic muscle pain. The article reviews the physiology of the musculature and the myofascial mantle and the contributions of physiological dysfunction to pain. The article critiques the relaxation model as an inadequate foundation for biofeedback treatment of pain and calls for more comprehensive education for biofeedback practitioners in muscle physiology yet emphasizes the promise of surface electromyographic treatment for chronic pain and for opioid abuse, when the muscle biofeedback intervention is well informed by medical and physiological knowledge. Medical factors that commonly contribute to pain are examined, along with a number of preventable sources for poor outcomes for muscle biofeedback treatment.

scholarly journals Assessment of the Potential Role of Muscle Spindle Mechanoreceptor Afferents in Chronic Muscle Pain in the Rat Masseter Muscle

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e11131 ◽  
Author(s):  
James P. Lund ◽  
Somayeh Sadeghi ◽  
Tuija Athanassiadis ◽  
Nadia Caram Salas ◽  
François Auclair ◽  
...  
Keyword(s):  
Muscle Spindle ◽  
Muscle Pain ◽  
Masseter Muscle ◽  
Potential Role ◽  
Chronic Muscle Pain

scholarly journals Regular physical activity prevents development of chronic pain and activation of central neurons

2013 ◽  
Vol 114 (6) ◽  
pp. 725-733 ◽  
Author(s):  
Kathleen A. Sluka ◽  
James M. O'Donnell ◽  
Jessica Danielson ◽  
Lynn A. Rasmussen
Keyword(s):  
Physical Activity ◽  
Chronic Pain ◽  
Nervous System ◽  
Nmda Receptor ◽  
Muscle Pain ◽  
Regular Physical Activity ◽  
Muscle Inflammation ◽  
Exercise Induced ◽  
Running Wheels ◽  
Chronic Muscle Pain

Chronic musculoskeletal pain is a significant health problem and is associated with increases in pain during acute physical activity. Regular physical activity is protective against many chronic diseases; however, it is unknown if it plays a role in development of chronic pain. The current study induced physical activity by placing running wheels in home cages of mice for 5 days or 8 wk and compared these to sedentary mice without running wheels in their home cages. Chronic muscle pain was induced by repeated intramuscular injection of pH 4.0 saline, exercise-enhanced pain was induced by combining a 2-h fatiguing exercise task with a low-dose muscle inflammation (0.03% carrageenan), and acute muscle inflammation was induced by 3% carrageenan. We tested the responses of the paw (response frequency) and muscle (withdrawal threshold) to nociceptive stimuli. Because the rostral ventromedial medulla (RVM) is involved in exercise-induced analgesia and chronic muscle pain, we tested for changes in phosphorylation of the NR1 subunit of the N-methyl-d-aspartate (NMDA) receptor in the RVM. We demonstrate that regular physical activity prevents the development of chronic muscle pain and exercise-induced muscle pain by reducing phosphorylation of the NR1 subunit of the NMDA receptor in the central nervous system. However, regular physical activity has no effect on development of acute pain. Thus physical inactivity is a risk factor for development of chronic pain and may set the nervous system to respond in an exaggerated way to low-intensity muscle insults.

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

What is the role of fear and escape/avoidance in chronic pain? Models, structural analysis and future directions

2012 ◽  
Vol 2 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Gordon JG Asmundson ◽  
Holly A Parkerson ◽  
Mark Petter ◽  
Melanie Noel
Keyword(s):  
Chronic Pain ◽  
Structural Analysis ◽  
Future Directions ◽  
Pain Models

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 The Role of Nutrient Supplementation in the Management of Chronic Pain in Fibromyalgia: A Narrative Review

2021 ◽  
Author(s):  
Hannah Waleed Haddad ◽  
Nikita Reddy Mallepalli ◽  
John Emerson Scheinuk ◽  
Pranav Bhargava ◽  
Elyse M. Cornett ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Narrative Review ◽  
Nutrient Supplementation

scholarly journals Prospects for the Personalized Multimodal Therapy Approach to Pain Management via Action on NO and NOS

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2431
Author(s):  
Natalia A. Shnayder ◽  
Marina M. Petrova ◽  
Tatiana E. Popova ◽  
Tatiana K. Davidova ◽  
Olga P. Bobrova ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Molecular Genetic ◽  
Pain Syndrome ◽  
Medical Problem ◽  
Single Nucleotide Variants ◽  
Genetic Studies ◽  
Pain Syndromes ◽  
Nos Inhibitors ◽  
Peripheral Pain

Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Back pain, neuropathic pain, and posttraumatic pain are the most important pathological processes associated with chronic pain in adults. Standard approaches to the treatment of them do not solve the problem of pain chronicity. This is the reason for the search for new personalized strategies for the prevention and treatment of chronic pain. The nitric oxide (NO) system can play one of the key roles in the development of peripheral pain and its chronicity. The purpose of the study is to review publications devoted to changes in the NO system in patients with peripheral chronical pain syndromes. We have carried out a search for the articles published in e-Library, PubMed, Oxford Press, Clinical Case, Springer, Elsevier, and Google Scholar databases. The search was carried out using keywords and their combinations. The role of NO and NO synthases (NOS) isoforms in peripheral pain development and chronicity was demonstrated primarily from animal models to humans. The most studied is the neuronal NOS (nNOS). The role of inducible NOS (iNOS) and endothelial NOS (eNOS) is still under investigation. Associative genetic studies have shown that single nucleotide variants (SNVs) of NOS1, NOS2, and NOS3 genes encoding nNOS, iNOS, and eNOS may be associated with acute and chronic peripheral pain. Prospects for the use of NOS inhibitors to modulate the effect of drugs used to treat peripheral pain syndrome are discussed. Associative genetic studies of SNVs NOS1, NOS2, and NOS3 genes are important for understanding genetic predictors of peripheral pain chronicity and development of new personalized pharmacotherapy strategies.

Sign in / Sign up

Export Citation Format

Share Document