Saturday, January 30, 2021

Grey matter brain alterations in temporomandibular disorder tested in a population cohort and three clinical samples

Using voxel based morphometry (VBM) two samples with chronic temperomandibular pain were compared to controls investigating the brains grey matter volume (GMV). Only the clinical sample showed a decease in anterior cingulate GMV. Contradicting results on GMV loss in temperomandibular pain might be based on small samples in prior studies.

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Friday, January 29, 2021

Imprecise visual feedback about hand location increases a classically conditioned pain expectancy effect

Chronic musculoskeletal pain is a major health problem with a one-year prevalence of 25% to 36% in the general population35. Costs related to persistent pain in the United States of America are between $560 and $635 billion annually18. Many persistent pain states are not associated with ongoing tissue pathology, an originally perplexing observation that is now explained by functional changes in the nociceptive system and brain79-81. Broadly speaking, these functional changes may be considered learning; stimulus-response profiles change such that stimuli that are not normally painful come to evoke pain, a situation termed allodynia, and normally painful stimuli come to evoke more pain, a situation termed hyperalgesia79.

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Effect of topical analgesia on desensitization following 8% topical capsaicin application

The transient receptor potential V1 (TRPV1) is a non-selective cation channel activated by heat and capsaicin, the pungent ingredient contained in hot chili peppers.35 TRPV1 is expressed in the majority of polymodal nociceptors (thinly myelinated Aδ and unmyelinated C-fibers)3,7,50 involved in the transduction of nociceptive and pruritic signals and in the pathophysiology of neuropathic pain.1 Initially, the activation of TRPV1 by capsaicin induces an influx of Ca2+ and Na+ ions resulting in depolarization and thereby generating an action potential.

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Effectiveness of a structured group intervention based on pain neuroscience education for patients with fibromyalgia in primary care: a multicenter randomized open‐label controlled trial

Abstract

Background

There has been increased interest in pain neuroscience education (PNE) as a therapeutic approach for the management of fibromyalgia (FM).

Methods

A multicenter randomized, open‐label, controlled trial was conducted to assess the effectiveness of a structured group intervention based on PNE in patients with FM. A total of 139 patients were included in the study and randomized to the intervention group (7 group sessions of education in neurobiology of pain) or to the control group (treatment as usual only). The primary outcome was the improvement of functional status and pain measured with the Fibromyalgia Impact Questionnaire (FIQ), and secondary outcomes were the reduction of the impact of pain and other symptoms (catastrophizing, anxiety, and depression) and number of patients reaching no worse than moderate functional impairment (FIQ score < 39). Differences between groups were calculated by linear mixed‐effects (intention‐to‐treat approach) and mediational models through path analyses.

Results

At 1 year, improvements in FIQ scores were higher in the intervention group with moderate or high effect size, and decreases of ≥ 20% in 69.1% of patients (20.9 % in the control group) and of ≥ 50% in 39.7% (4.5% in the control group). Also, 52.9% of patients had a FIQ < 39 points (13.4% in the control group).

Conclusions

In this sample of patients with FM, the improvement in quality of life and control of symptoms obtained by adding a PNE intervention showed promising results, equaling or surpassing previously reported outcomes.



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Non-steroidal anti-inflammatory drugs (NSAIDs) for musculoskeletal pain

What you need to knowOral non-steroidal anti-inflammatory drugs (NSAIDs) can reduce musculoskeletal pain but increase the risk of gastrointestinal (perforation, ulcers, bleeding), cardiovascular...


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Thursday, January 28, 2021

[Clinical Picture] Widespread soft tissue calcification in systemic sclerosis, polymyositis, and polyarthritis

A 55-year-old woman was admitted to our department with gradual onset of pain in her hands, hips, and knees, which had progressively limited her mobility over the past 6 years. She also reported feeling tired and feverish.

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Wednesday, January 27, 2021

Inhibition of ferroptosis‐like cell death attenuates neuropathic pain reactions induced by peripheral nerve injury in rats

Abstract

Background

Relationships between iron dependent ferroptosis and nerve system diseases have been recently revealed. However, the role of ferroptosis in neuropathic pain (NeP) remains to be elucidated. Thus, we aimed to investigate whether ferroptosis in spinal cord contributes to NeP induced by a chronic constriction injury (CCI) of the sciatic nerve.

Method

Forty Sprague Dawley rats received CCI or sham surgery, and were randomly assigned to the following four groups: sham group; CCI+LIP group; CCI+Veh group; and CCI group. Liproxstatin‐1 or corn oil were separately injected intraperitoneally for three consecutive days after surgery in the CCI+LIP or CCI+Veh group. The mechanical and thermal hypersensitivities were tested after surgery. Biochemical and morphological changes related to ferroptosis in the spinal cord were also assessed. These included iron content, glutathione peroxidase 4 (GPX4) and anti‐acyl‐CoA synthetase long‐chain family member 4 (ACSL4) expression, lipid peroxidation assays, as well as mitochondrial morphology.

Result

CCI‐induced NeP was followed by iron accumulation, increased lipid peroxidation, and dysregulation of ACSL4 and GPX4. Moreover, transmission electron microscopy confirmed the presence of aberrant morphological changes on mitochondrial, such as mitochondria shrinkage and membrane rupture. Furthermore, the administration of liproxstatin‐1 on CCI rats attenuated hypersensitivities, lowered the iron level, decreased spinal lipid peroxidation, restored the dysregulations in GPX4 and ACSL4 levels, and protected against CCI induced morphological changes in mitochondria.

Conclusion

Our findings indicated the involvement of ferroptosis in CCI induced NeP, and point to ferroptosis inhibitors such as liproxstatin‐1 as potential therapies for hypersensitivity induced by peripheral nerve injury.



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