scholarly journals TOLERANCE TIME OF EXPERIMENTAL THERMAL PAIN (COLD INDUCED) IN VOLUNTEERS

1998 ◽  
Vol 54 (4) ◽  
pp. 315-318
Author(s):  
VN VAID ◽  
NS WILKHOO ◽  
AK JAIN
Keyword(s):  
2020 ◽  
Author(s):  
EAR Losin ◽  
CW Woo ◽  
NA Medina ◽  
JR Andrews-Hanna ◽  
Hedwig Eisenbarth ◽  
...  

© 2020, The Author(s), under exclusive licence to Springer Nature Limited. Understanding ethnic differences in pain is important for addressing disparities in pain care. A common belief is that African Americans are hyposensitive to pain compared to Whites, but African Americans show increased pain sensitivity in clinical and laboratory settings. The neurobiological mechanisms underlying these differences are unknown. We studied an ethnicity- and gender-balanced sample of African Americans, Hispanics and non-Hispanic Whites using functional magnetic resonance imaging during thermal pain. Higher pain report in African Americans was mediated by discrimination and increased frontostriatal circuit activations associated with pain rating, discrimination, experimenter trust and extranociceptive aspects of pain elsewhere. In contrast, the neurologic pain signature, a neuromarker sensitive and specific to nociceptive pain, mediated painful heat effects on pain report largely similarly in African American and other groups. Findings identify a brain basis for higher pain in African Americans related to interpersonal context and extranociceptive central pain mechanisms and suggest that nociceptive pain processing may be similar across ethnicities.


Author(s):  
I. V. Cheretaev ◽  
D. R. Khusainov ◽  
E. N. Chuyan ◽  
M. Yu. Ravaeva ◽  
A. N. Gusev ◽  
...  

The purpose of the review is to summarize current literature data and the results of our own research on the analgesic and anti-inflammatory effects of acetylsalicylic acid, as well as the physiological mechanisms underlying them. This acid is the most studied reference representative of salicylates, which is convenient to consider the physiological effects characteristic in general for this group of chemical and medicinal products. Acetylsalicylic acid has analgesic properties against thermal pain and pain caused by electrical stimuli, as well as a pronounced anti-inflammatory effect. The realization of these properties depends on the peculiarities of aspirin metabolism in the body, ion and synaptic mechanisms for controlling the functional state of the cell, neurotransmitter systems of the сentral nervous system, and mechanisms of peripheral and сentral analgesia. Analgesic properties of acetylsalicylic acid founded not only in normal, but also in ultra-small doses. Various physical and especially chemical factors significantly change their effects. This increases the interest in studying the analgesic activity of salicylates and their physiological mechanisms, since such studies can serve as a basis for creating new non-steroidal anti-inflammatory drugs with low toxicity and high safety for patients, and improve the strategy of their practical use. Currently, the most detailed study of the physiological mechanism of analgesic and anti-inflammatory action of aspirin and its main metabolite – salicylic acid. However, it should be note that despite the abundance of existing data obtained in scientific studies of the effects of aspirin and its practical use, there are a number of unexplained aspects of the action of this drug, the mechanism of which has not yet been deciphered. The continuing interest in the effects and mechanisms of action of this drug and in connection with the expansion of its use evidenced by a consistently high number of scientific publications on aspirin in the most famous foreign and domestic publications. At the same time, the number of publications about aspirin is an order of magnitude higher than about any other drug known to humanity.


2011 ◽  
Vol 15 (4) ◽  
pp. 376-383 ◽  
Author(s):  
Alban Y. Neziril ◽  
Pasquale Scaramozzinol ◽  
Ole K. Andersenl ◽  
Anthony H. Dickensonl ◽  
Lars Arendt-Nielsenl ◽  
...  

Symmetry ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1042
Author(s):  
Oscar J. Pellicer-Valero ◽  
José D. Martín-Guerrero ◽  
César Fernández-de-las-Peñas ◽  
Ana I. De-la-Llave-Rincón ◽  
Jorge Rodríguez-Jiménez ◽  
...  

Identification of subgroups of patients with chronic pain provides meaningful insights into the characteristics of a specific population, helping to identify individuals at risk of chronification and to determine appropriate therapeutic strategies. This paper proposes the use of spectral clustering (SC) to distinguish subgroups (clusters) of individuals with carpal tunnel syndrome (CTS), making use of the obtained patient profiling to argue about potential management implications. SC is a powerful algorithm that builds a similarity graph among the data points (the patients), and tries to find the subsets of points that are strongly connected among themselves, but weakly connected to others. It was chosen due to its advantages with respect to other simpler clustering techniques, such as k-means, and the fact that it has been successfully applied to similar problems. Clinical (age, duration of symptoms, pain intensity, function, and symptom severity), psycho-physical (pressure pain thresholds—PPTs—over the three main nerve trunks of the upper extremity, cervical spine, carpal tunnel, and tibialis anterior), psychological (depressive levels), and motor (pinch tip grip force) variables were collected in 208 women with clinical/electromyographic diagnosis of CTS, whose symptoms usually started unilaterally but eventually evolved into bilateral symmetry. SC was used to identify clusters of patients without any previous assumptions, yielding three clusters. Patients in cluster 1 exhibited worse clinical features, higher widespread pressure pain hyperalgesia, higher depressive levels, and lower pinch tip grip force than the other two. Patients in cluster 2 showed higher generalized thermal pain hyperalgesia than the other two. Cluster 0 showed less hypersensitivity to pressure and thermal pain, less severe clinical features, and more normal motor output (tip grip force). The presence of subgroups of individuals with different altered nociceptive processing (one group being more sensitive to pressure pain and another group more sensitive to thermal pain) could lead to different therapeutic programs.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Lin Xiao ◽  
Dongping Gong ◽  
Loufeng Liang ◽  
Anwei Liang ◽  
Huaxin Liang ◽  
...  

Abstract Background Intervertebral disc degeneration (IDD) is a major cause of lower back pain. This study aimed at exploring the effects of histone deacetylase 4 (HDAC4) and its upstream and downstream signaling molecules on IDD development. Methods A murine IDD model was established by inducing a needle puncture injury to the vertebrate, whereupon we isolated and transfected of nucleus pulposus (NP) cells. Disc height index (DHI) of the mice was determined by X-ray tomography, while the pain experienced by the IDD mice was evaluated by mechanical and thermal sensitivity tests. Next, the interaction between GSK3β and HDAC4 as well as that between HDAC4 and KLF5 acetylation was assessed by co-immunoprecipitation, while the promoter region binding was assessed identified by chromatin immunoprecipitation. By staining methods with TUNEL, Safranin O fast green, and hematoxylin and eosin, the NP cell apoptosis, degradation of extracellular matrix, and morphology of intervertebral disc tissues were measured. Furthermore, mRNA and protein expressions of GSK3β, HDAC4, KLF5, and ASK1, as well as the extent of HDAC4 phosphorylation, were determined by RT-qPCR and Western blotting. Results GSK3β was identified to be downregulated in the intervertebral disc tissues obtained from IDD mice, while HDAC4, KLF5, and ASK1 were upregulated. HDAC4 silencing alleviated IDD symptoms. It was also found that GSK3β promoted the phosphorylation of HDAC4 to increase its degradation, while HDAC4 promoted ASK1 expression through upregulating the expression of KLF5. In IDD mice, GSK3β overexpression resulted in increased DHI, inhibition of NP cell apoptosis, alleviation of disc degeneration, and promoted mechanical and thermal pain thresholds. However, HDAC4 overexpression reversed these effects by promoting ASK1 expression. Conclusion Based on the key findings of the current study, we conclude that GSK3β can promote degradation of HDAC4, which lead to an overall downregulation of the downstream KLF5/ASK1 axis, thereby alleviating the development of IDD.


2020 ◽  
pp. 1-7
Author(s):  
Raymond R. Romano ◽  
Michael A. Carter ◽  
Mary S. Dietrich ◽  
Ronald L. Cowan ◽  
Stephen P. Bruehl ◽  
...  

Background: This study evaluated whether the apolipoprotein ɛ4 (APOE4) allele, a genetic marker associated with increased risk of developing late-onset Alzheimer’s disease (AD), was associated with differences in evoked pain responsiveness in cognitively healthy subjects. Objective: The aim was to determine whether individuals at increased risk of late-onset AD based on APOE allele genotype differ phenotypically in their response to experimentally-induced painful stimuli compared to those who do not have at least one copy of the ɛ4 allele. Methods: Forty-nine cognitively healthy subjects aged 30–89 years old with the APOE4 allele (n = 12) and without (n = 37) were assessed for group differences in pain thresholds and affective (unpleasantness) responses to experimentally-induced thermal pain stimuli. Results: Statistically significant main effects of APOE4 status were observed for both the temperature at which three different pain intensity percepts were reached (p = 0.040) and the level of unpleasantness associated with each (p = 0.014). APOE4 positive participants displayed lower overall pain sensitivity than those who were APOE4 negative and also greater overall levels of pain unpleasantness regardless of intensity level. Conclusion: Cognitively healthy APOE4 carriers at increased risk of late-onset AD demonstrated reduced thermal pain sensitivity but greater unpleasantness to thermal pain stimuli relative to individuals at lower risk of late-onset AD. These results suggest that altered evoked pain perception could potentially be used as a phenotypic biomarker of late-onset AD risk prior to disease onset. Additional studies of this issue may be warranted.


Pain ◽  
1996 ◽  
Vol 64 (1) ◽  
pp. 143-152 ◽  
Author(s):  
M. C. Chakour ◽  
S. J. Gibson ◽  
M. Bradbeer ◽  
R. D. Helme

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Rebecca Tronarp ◽  
André Nyberg ◽  
Mattias Hedlund ◽  
Charlotte K. Häger ◽  
Suzanne McDonough ◽  
...  

Aim.Establishing the effects of low intensity cycling (LC), moderate intensity cycling (MC), and standing at a simulated office workstation on pain modulation, work performance, and metabolic expenditure.Methods.36 healthy adults (21 females), mean age 26.8 (SD 7.6) years, partook in this randomized3×3crossover trial with 75 minutes of LC on 20% of maximum aerobic power (MAP) output, 30 minutes of MC on 50% of MAP, and standing 30 minutes with 48-hour wash-out periods. Outcome measures were pain modulation (pressure pain threshold (PPT) and thermal pain threshold)), work performance (transcription, mouse pointing, and cognitive performance), and metabolic expenditure.Results.PPTs increased in all conditions. PPT trapezius showed the highest increase after LC, 39.3 kilopascals (kPa) (15.6; 78.6), compared to MC, 17.0 kPa (2.8; 49.9), and standing, 16.8 kPa (−5.6; 39.4),p=0.015. Transcription was reduced during LC and MC. Mouse pointing precision was best during standing and worst and slowest during MC. Cognitive performance did not differ between conditions. Metabolic expenditure rates were 1.4 (1.3; 1.7), 3.3 (2.3; 3.7), and 7.5 (5.8; 8.7) kcal/minute during standing, LC, and MC, respectively(p<0.001).Conclusions.LC seems to be the preferred option; it raised PPTs, more than doubled metabolic expenditure, whilst minimally influencing work performance.


2009 ◽  
Vol 40 (2) ◽  
pp. 257-263 ◽  
Author(s):  
G. Pavlaković ◽  
K. Züchner ◽  
A. Zapf ◽  
C.G. Bachmann ◽  
B.M. Graf ◽  
...  

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