scholarly journals Neural Mechanisms of Temporomandibular Joint and Masticatory Muscle Pain: A Possible Role for Peripheral Glutamate Receptor Mechanisms

2005 ◽  
Vol 10 (3) ◽  
pp. 145-152 ◽  
Author(s):  
David K Lam ◽  
Barry J Sessle ◽  
Brian E Cairns ◽  
James W Hu

The purpose of the present review is to correlate recent knowledge of the role of peripheral ionotropic glutamate receptors in the temporomandibular joint and muscle pain from animal and human experimental pain models with findings in patients. Chronic pain is common, and many people suffer from chronic pain conditions involving deep craniofacial tissues such as temporomandibular disorders or fibromyalgia. Animal and human studies have indicated that the activation of peripheral ionotropic glutamate receptors in deep craniofacial tissues may contribute to muscle and temporomandibular joint pain and that sex differences in the activation of glutamate receptors may be involved in the female predominance in temporomandibular disorders and fibromyalgia. A peripheral mechanism involving autocrine and/or paracrine regulation of nociceptive neuronal excitability via injury or inflammation-induced release of glutamate into peripheral tissues that may contribute to the development of craniofacial pain is proposed.

2018 ◽  
Author(s):  
Axel Davies Vittersø ◽  
Monika Halicka ◽  
Gavin Buckingham ◽  
Michael J Proulx ◽  
Mark Wilson ◽  
...  

Representations of the body and peripersonal space can be distorted for people with some chronic pain conditions. Experimental pain induction can give rise to similar, but transient distortions in healthy individuals. However, spatial and bodily representations are dynamic, and constantly update as we interact with objects in our environment. It is unclear whether induced pain disrupts the mechanisms involved in updating these representations. In the present study, we sought to investigate the effect of induced pain on the updating of peripersonal space and body representations during and following tool-use. We compared performance under three conditions (pain, active placebo, neutral) on a visuotactile crossmodal congruency task and a tactile distance judgement task to measure updating of peripersonal space and body representations, respectively. We induced pain by applying 1% capsaicin cream to the arm, and for placebo we used a gel that induced non-painful warming. Consistent with previous findings, the difference in crossmodal interference from visual distractors in the same compared to opposite visual field to the tactile target was less when tools were crossed than uncrossed. This suggests an extension of peripersonal space to incorporate the tips of the tools. Also consistent with previous findings, estimates of the felt distance between two points (tactile distance judgements) decreased after active tool-use. In contrast to our predictions, however, we found no evidence that pain interfered with performance on either task when compared to the control conditions. This suggests that the updating of peripersonal space and body representations is not disrupted by induced pain. Therefore, acute pain does not account for the distorted representations of the body and peripersonal space that can endure in people with chronic pain conditions.


2018 ◽  
Vol 18 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Kristian Kjær Petersen ◽  
Hjalte Holm Andersen ◽  
Masato Tsukamoto ◽  
Lincoln Tracy ◽  
Julian Koenig ◽  
...  

AbstractBackground and aimsThe autonomic nervous system (ANS) is capable of modulating pain. Aberrations in heart rate variability (HRV), reflective of ANS activity, are associated with experimental pain sensitivity, chronic pain, and more recently, pain modulatory mechanisms but the underlying mechanisms are still unclear. HRV is lowered during experimental pain as well as in chronic pain conditions and HRV can be increased by propranolol, which is a non-selective β-blocker. Sensitization of central pain pathways have been observed in several chronic pain conditions and human mechanistic pain biomarkers for these central pain pathways include temporal summation of pain (TSP) and conditioned pain modulation (CPM). The current study aimed to investigate the effect of the β-blocker propranolol, and subsequently assessing the response to standardized, quantitative, mechanistic pain biomarkers.MethodsIn this placebo-controlled, double-blinded, randomized crossover study, 25 healthy male volunteers (mean age 25.6 years) were randomized to receive 40 mg propranolol and 40 mg placebo. Heart rate, blood pressure, and HRV were assessed before and during experimental pain tests. Cuff pressure pain stimulation was used for assessment of pain detection (cPDTs) and pain tolerance (cPTTs) thresholds, TSP, and CPM. Offset analgesia (OA) was assessed using heat stimulation.ResultsPropranolol significantly reduced heart rate (p<0.001), blood pressure (p<0.02) and increased HRV (p<0.01) compared with placebo. No significant differences were found comparing cPDT (p>0.70), cPTT (p>0.93), TSP (p>0.70), OA-effect (p>0.87) or CPM (p>0.65) between propranolol and placebo.ConclusionsThe current study demonstrated that propranolol increased HRV, but did not affect pressure pain sensitivity or any pain facilitatory or modulatory outcomes.ImplicationsAnalgesic effects of propranolol have been reported in clinical pain populations and the results from the current study could indicate that increased HRV from propranolol is not associated with peripheral and central pain pathways in healthy male subjects.


Author(s):  
Bethea A. Kleykamp ◽  
McKenzie C. Ferguson ◽  
Ewan McNicol ◽  
Ida Bixho ◽  
Lesley M. Arnold ◽  
...  

Ból ◽  
2020 ◽  
Vol 21 (3) ◽  
pp. 1-15
Author(s):  
Carina Fernandes ◽  
Marina Pidal-Miranda ◽  
Noelia Samartin-Veiga ◽  
María T. Carrillo-de-la-Peña

Conditioned pain modulation (CPM) is a promising psychophysical biomarker of central pain mechanisms because it significantly discriminates patients with chronic pain from healthy controls. Nevertheless, it is unclear in what extent CPM assessed experimentally is correlated with clinical manifestations of pain. To assess the concurrent validity of CPM, we performed a systematic review of the literature reporting correlations between CPM responses and pain intensity, disability, duration, and area in patients with different chronic pain conditions. We included 32 studies that altogether encompassed data from 1958 patients and provided 62 correlations. The majority of the results (69%) reported nonsignificant correlations between CPM efficiency and clinical manifestations of pain, whereas the remaining results showed a correlation between CPM reduction and worse clinical symptoms of pain. The modality of stimulation, the type of pain, and the stimulation site appear to be critical variables that influenced the pattern of results. Given that most of the studies were conducted with highly heterogeneous methodologies and unclear risk of bias, the findings highlight the need for future studies using standardized measures of clinical and experimental pain before considering CPM as a valid biomarker of pain. We discuss some guidelines to overcome the constraints in this promising line of research.


2017 ◽  
Vol 15 (1) ◽  
pp. 104-105 ◽  
Author(s):  
Harald Breivik ◽  
Stephen Butler

AbstractIn this issue of the Scandinavian Journal of Pain Kari Sørensen and Bjørg Christiansen publish their report on in depth interviews of young patients suffering from CRPS or from severe muscle pain [1]. These patients were recovering from their chronic pain conditions after treatment by a multidisciplinary rehabilitation team.


Pain ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 1266-1278 ◽  
Author(s):  
Eric Bair ◽  
Sheila Gaynor ◽  
Gary D. Slade ◽  
Richard Ohrbach ◽  
Roger B. Fillingim ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1226
Author(s):  
Maria Carla Gerra ◽  
Cristina Dallabona ◽  
Lars Arendt-Nielsen

Prescription opioids are used for some chronic pain conditions. However, generally, long-term therapy has unwanted side effects which may trigger addiction, overdose, and eventually cause deaths. Opioid addiction and chronic pain conditions have both been associated with evidence of genetic and epigenetic alterations. Despite intense research interest, many questions about the contribution of epigenetic changes to this typology of addiction vulnerability and development remain unanswered. The aim of this review was to summarize the epigenetic modifications detected in specific tissues or brain areas and associated with opioid prescription and misuse in patients who have initiated prescribed opioid management for chronic non-cancer pain. The review considers the effects of opioid exposure on the epigenome in central and peripheral tissues in animal models and human subjects and highlights the mechanisms in which opioid epigenetics may be involved. This will improve our current understanding, provide the basis for targeted, personalized pain management, and thus balance opioid risks and benefits in managing chronic pain.


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