scholarly journals Modulating pain thresholds through classical conditioning

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6486 ◽  
Author(s):  
Juliane Traxler ◽  
Victoria J. Madden ◽  
G. Lorimer Moseley ◽  
Johan W.S. Vlaeyen

Background Classical conditioning has frequently been shown to be capable of evoking fear of pain and avoidance behavior in the context of chronic pain. However, whether pain itself can be conditioned has rarely been investigated and remains a matter of debate. Therefore, the present study investigated whether pain threshold ratings can be modified by the presence of conditioned non-nociceptive sensory stimuli in healthy participant. Methods In 51 healthy volunteers, pain threshold to electrocutaneous stimuli was determined prior to participation in a simultaneous conditioning paradigm. Participants underwent an acquisition phase in which one non-painful vibrotactile stimulus (CS+) was repeatedly paired with a painful electrocutaneous stimulus, whereas a second vibrotactile stimulus of the same quality and intensity (CS−) was paired with a non-painful electrocutaneous stimulus. Stimulation was provided on the lower back with close proximity between the conditioned stimulus and the unconditioned stimulus. In the test phase, electrocutaneous stimuli at the individually-set threshold intensity were simultaneously delivered together with either a CS+ or CS−. Pain intensity ratings were obtained after each trial; expectancy ratings were obtained after each block. The primary outcome was the percentage of test stimuli that were rated as painful. Results Test stimuli were more likely to be rated as painful when they were paired with the CS+ than when they were paired with the CS−. This effect was not influenced by contingency awareness, nor by expectancies or mood states. Discussion The findings support the notion that the judgement of an event being painful or non-painful can be influenced by classical conditioning and corroborate the possible role of associative learning in the development and maintenance of chronic pain.


2021 ◽  
Vol 11 (2) ◽  
pp. 79-85
Author(s):  
V.I. Romanenko

The article is devoted to the problem of effective ma­nagement of chronic pain. A review of the known mechanisms of development and maintenance of chronic pain and possible me­thods of influence is given. One of the reasons for the lack of chro­nic pain treatment effectiveness in some patients is the use of treatment regimens with drugs acting exclusively on the targets loca­ted in the nerve structures. Today an important role of micro­glia and mast cells in the development and maintenance of chronic pain conditions is well acknowledged. A new class of drugs from the group of acylethanolamides is described. One of the representatives of this group is palmitoylethanolamide. This drug may mo­dulate the activity of microglia and mast cells, thus increasing the pain threshold and the effectiveness of therapy. The use of palmitoylethanolamide in patients with chronic pain can increase the effectiveness of therapy.



2021 ◽  
Author(s):  
Laila Katharina Franke ◽  
Stephan F Miedl ◽  
Sarah K. Danböck ◽  
Michael Liedlgruber ◽  
Markus Grill ◽  
...  

Psychological trauma is typically accompanied by physical pain, and posttraumatic stress disorder (PTSD) often co-occurs with chronic pain. Clinical reports suggest that pain in the aftermath of trauma may be part of a re-experiencing symptomatology. Previously, we demonstrated that classical conditioning can underlie visual re-experiencing since intrusions appear to occur as conditioned responses (CRs) to trauma-related cues. Possibly, classical conditioning also plays a role in re-experiencing of pain. However, this hypothesis has so far remained untested. Sixty-five participants underwent classical conditioning, where painful electrical stimulation and highly aversive film-clips served as unconditioned stimuli (USs) in a 2 (pain/no pain) x 2 (aversive/neutral film) design. Conditioned stimuli (CSs) were neutral pictures depicting contextual details from the films. One day later, participants were re-exposed to CSs during a memory-triggering-task (MTT). Pain-CRs were assessed by self-report and an fMRI-based marker of nociceptive pain, the neurologic pain signature (NPS).During conditioning, pain-signaling CSs elicited more self-reported pain and NPS responses than no-pain-signaling CSs. Self-reported pain-CRs but not NPS CRs recurred 24h later when participants were re-exposed to CSs during MTT. Both during acquisition and MTT, the aversive affective film-context blurred the difference in participants´ pain-reports to pain-signaling and no-pain-signaling CSs.Our data support the hypothesis that pain can emerge as a classically conditioned response. Pain as a CR to pain-signaling cues could represent an instance of pain re-experiencing in PTSD. Possibly, this mechanism may perpetuate pain beyond tissue healing and thereby explain the comorbidity between chronic pain and PTSD.



2007 ◽  
Author(s):  
Jeffrey I. Gold ◽  
Trina Haselrig ◽  
D. Colette Nicolaou ◽  
Katharine A. Belmont


Author(s):  
Sascha R. A. Alles ◽  
Anne-Marie Malfait ◽  
Richard J. Miller

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.



2019 ◽  
Vol 712 ◽  
pp. 134483
Author(s):  
Morayo G. Adebiyi ◽  
Jeanne Manalo ◽  
Rodney E. Kellems ◽  
Yang Xia


2012 ◽  
Vol 2 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Gordon JG Asmundson ◽  
Holly A Parkerson ◽  
Mark Petter ◽  
Melanie Noel


2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 278-279
Author(s):  
M Defaye ◽  
N Abdullah ◽  
M Iftinca ◽  
C Altier

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



2021 ◽  
Author(s):  
Hannah Waleed Haddad ◽  
Nikita Reddy Mallepalli ◽  
John Emerson Scheinuk ◽  
Pranav Bhargava ◽  
Elyse M. Cornett ◽  
...  


Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2431
Author(s):  
Natalia A. Shnayder ◽  
Marina M. Petrova ◽  
Tatiana E. Popova ◽  
Tatiana K. Davidova ◽  
Olga P. Bobrova ◽  
...  

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