Risperidone in analgesia induced by paracetamol and meloxicam in experimental pain

AbstractMusic-induced analgesia (MIA) is a phenomenon that describes a situation in which listening to music influences pain perception. The heterogeneity of music used in MIA studies leads to a problem of a specific effect for an unspecified stimulus. To address this, we use a previously established model of musical preferences that categorizes the multidimensional sonic space of music into three basic dimensions: arousal, valence and depth. Participants entered an experimental pain stimulation while listening to compilations of short musical excerpts characteristic of each of the three attribute dimensions. The results showed an effect on the part of music attribute preferences on average pain, maximal pain, and pain tolerance after controlling for musical attributes and order effects. This suggests that individual preferences for music attributes play a significant role in MIA and that, in clinical contexts, music should not be chosen arbitrarily but according to individual preferences.

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Trait perceived injustice is associated with pain outcomes in healthy participants undergoing an experimental pain induction procedure: scale development and validation

Journal of Pain ◽

10.1016/j.jpain.2017.12.112 ◽

2018 ◽

Vol 19 (3) ◽

pp. S40

Author(s):

E. Yakobov ◽

C. Suso-Ribera ◽

T. Vrincenau ◽

M. Sullivan

Keyword(s):

Scale Development ◽

Experimental Pain ◽

Perceived Injustice ◽

Induction Procedure ◽

Scale Development And Validation ◽

Pain Outcomes ◽

Development And Validation ◽

Healthy Participants

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The association between selected genetic variants and individual differences in experimental pain

Scandinavian Journal of Pain ◽

10.1515/sjpain-2020-0091 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Marie Udnesseter Lie ◽

Bendik Winsvold ◽

Johannes Gjerstad ◽

Dagfinn Matre ◽

Linda M. Pedersen ◽

...

Keyword(s):

Individual Differences ◽

Genetic Variants ◽

Pain Threshold ◽

Experimental Pain ◽

Pain Tolerance ◽

Heat Pain ◽

Low Back ◽

Secondary Hyperalgesia ◽

Heat Pain Threshold ◽

Pain Patients

AbstractObjectivesThe underlying mechanisms for individual differences in experimental pain are not fully understood, but genetic susceptibility is hypothesized to explain some of these differences. In the present study we focus on three genetic variants important for modulating experimental pain related to serotonin (SLC6A4 5-HTTLPR/rs25531 A>G), catecholamine (COMT rs4680 Val158Met) and opioid (OPRM1 rs1799971 A118G) signaling. We aimed to investigate associations between each of the selected genetic variants and individual differences in experimental pain.MethodsIn total 356 subjects (232 low back pain patients and 124 healthy volunteers) were genotyped and assessed with tests of heat pain threshold, pressure pain thresholds, heat pain tolerance, conditioned pain modulation (CPM), offset analgesia, temporal summation and secondary hyperalgesia. Low back pain patients and healthy volunteers did not differ in regards to experimental test results or allelic frequencies, and were therefore analyzed as one group. The associations were tested using analysis of variance and the Kruskal-Wallis test.ResultsNo significant associations were observed between the genetic variants (SLC6A4 5-HTTLPR/rs25531 A>G, COMT rs4680 Val158Met and OPRM1 rs1799971 A118G) and individual differences in experimental pain (heat pain threshold, pressure pain threshold, heat pain tolerance, CPM, offset analgesia, temporal summation and secondary hyperalgesia).ConclusionsThe selected pain-associated genetic variants were not associated with individual differences in experimental pain. Genetic variants well known for playing central roles in pain perception failed to explain individual differences in experimental pain in 356 subjects. The finding is an important contribution to the literature, which often consists of studies with lower sample size and one or few experimental pain assessments.

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Acute experimentally-induced pain replicates the distribution but not the quality or behaviour of clinical appendicular musculoskeletal pain. A systematic review

Scandinavian Journal of Pain ◽

10.1515/sjpain-2020-0076 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Brendon Ford ◽

Mark Halaki ◽

Joanna Diong ◽

Karen A Ginn

Keyword(s):

Systematic Review ◽

Musculoskeletal Pain ◽

Full Text ◽

Experimental Pain ◽

Common Mechanism ◽

Mcgill Pain Questionnaire ◽

Pain Response ◽

Provocation Testing ◽

Experimentally Induced

AbstractObjectivesExperimental pain is a commonly used method to draw conclusions about the motor response to clinical musculoskeletal pain. A systematic review was performed to determine if current models of acute experimental pain validly replicate the clinical experience of appendicular musculoskeletal pain with respect to the distribution and quality of pain and the pain response to provocation testing.MethodsA structured search of Medline, Scopus and Embase databases was conducted from database inception to August 2020 using the following key terms: “experimental muscle pain” OR “experimental pain” OR “pain induced” OR “induced pain” OR “muscle hyperalgesia“ OR (“Pain model” AND “muscle”). Studies in English were included if investigators induced experimental musculoskeletal pain into a limb (including the sacroiliac joint) in humans, and if they measured and reported the distribution of pain, quality of pain or response to a provocation manoeuvre performed passively or actively. Studies were excluded if they involved prolonged or delayed experimental pain, if temporomandibular, orofacial, lumbar, thoracic or cervical spine pain were investigated, if a full text of the study was not available or if they were systematic reviews. Two investigators independently screened each title and abstract and each full text paper to determine inclusion in the review. Disagreements were resolved by consensus with a third investigator.ResultsData from 57 experimental pain studies were included in this review. Forty-six of these studies reported pain distribution, 41 reported pain quality and six detailed the pain response to provocation testing. Hypertonic saline injection was the most common mechanism used to induce pain with 43 studies employing this method. The next most common methods were capsaicin injection (5 studies) and electrical stimulation, injection of acidic solution and ischaemia with three studies each. The distribution of experimental pain was similar to the area of pain reported in clinical appendicular musculoskeletal conditions. The quality of appendicular musculoskeletal pain was not replicated with the affective component of the McGill Pain Questionnaire consistently lower than that typically reported by musculoskeletal pain patients. The response to provocation testing was rarely investigated following experimental pain induction. Based on the limited available data, the increase in pain experienced in clinical populations during provocative maneuvers was not consistently replicated.ConclusionsCurrent acute experimental pain models replicate the distribution but not the quality of chronic clinical appendicular musculoskeletal pain. Limited evidence also indicates that experimentally induced acute pain does not consistently increase with tests known to provoke pain in patients with appendicular musculoskeletal pain. The results of this review question the validity of conclusions drawn from acute experimental pain studies regarding changes in muscle behaviour in response to pain in the clinical setting.

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