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To investigate the specific effect of insomnia on neuropsychological functioning in patients with very complex chronic pain.
Learn More >Nocebo hyperalgesia is an increase in pain through the expectation of such an increase as a consequence of a sham treatment. Nocebo hyperalgesia can be induced by observation of a model demonstrating increased pain via verbal pain ratings. The aim of the present study was to investigate whether observing natural pain behavior, such as facial pain expressions, can also induce nocebo responses.
Learn More >Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by cutaneous lesions and intense pruritus. The warm temperature-activated Ca2+-permeable TRPV3 channel is abundantly expressed in the keratinocytes, and gain-of-function mutations of TRPV3 cause skin lesions and pruritus in rodents and humans, suggesting an involvement of TRPV3 in the pathogenesis of AD. Here we report that pharmacological and genetic inhibition of TRPV3 attenuates skin lesions and dermatitis in mice. In mouse AD-like model induced by topical application of chemical DNFB, we found that TRPV3 proteins together with inflammatory factors TNF-α and IL-6 were upregulated in the skin detected by Western blot and immunostaining assay. Pharmacological activation of TRPV3 by channel agonist skin sensitizer carvacrol resulted in development of AD in WT mice, but not TRPV3 knockout mice. Furthermore, inhibition of TRPV3 by natural osthole reversed the severity of inflammatory dorsal skin and ear edema in dose-dependent manner, and also decreased the expression of inflammatory factors TNF-α and IL-6. Taken together, our findings demonstrate the involvement of overactive TRPV3 in the progressive pathology of AD in mice, and topical inhibition of TRPV3 channel function may represent an effective prevention and therapy for AD or inflammatory skin diseases. SIGNIFICANCE STATEMENT: Overactive TRPV3 channel is critically involved in the pathogenesis of atopic dermatitis. Inhibition of TRPV3 channel function by topical natural osthole may represent an effective therapy for management of atopic dermatitis aimed at preventing or alleviating skin lesions and severe itching.
Learn More >Tolerance to the antinociceptive effect of mu-opioid receptor (MOPr) agonists, such as morphine and fentanyl, greatly limits their effectiveness for long-term use to treat pain. Clinical studies have shown that combination therapy and opioid rotation can be used to enhance opioid-induced antinociception once tolerance has developed. The mechanism and brain regions involved in these processes are unknown. The purpose of this study was to evaluate the contribution of the ventrolateral periaqueductal gray (vlPAG) to antinociceptive tolerance and cross-tolerance between administration and co-administration of morphine and fentanyl. Tolerance was induced by pretreating rats with morphine or fentanyl or low-dose combination of morphine and fentanyl into the vlPAG followed by assessment of cross-tolerance to the other opioid. In addition, tolerance to the combined treatment was assessed. Cross-tolerance did not develop between repeated vlPAG microinjections of morphine and fentanyl. Likewise, there was no evidence of cross-tolerance from morphine or fentanyl to co-administration of morphine and fentanyl. Co-administration did not cause cross-tolerance to fentanyl. Cross-tolerance was only evident to morphine or morphine and fentanyl combined in rats pretreated with co-administration of low-doses of morphine and fentanyl. In conclusion, cross-tolerance does not develop between morphine and fentanyl within the vlPAG. This finding is consistent with the functionally selective signaling that has been reported for antinociception and tolerance following morphine and fentanyl binding to the MOPr. This research supports the notion that combination therapy and opioid rotation may be useful clinical practices to reduce opioid tolerance and other side effects. Perspective: This preclinical study shows that there is a reduction in cross tolerance between morphine and fentanyl within the periaqueductal gray which is key brain region in opioid antinociception and tolerance.
Learn More >Much of the opioid epidemic arose from abuse of prescription opioid drugs. This study sought to determine if the combination of a cannabinoid with an opioid could produce additive or synergistic effects on pain, allowing reduction in the opioid dose needed for maximal analgesia.
Learn More >In this issue you will find a paper by Vibe Fersum et al., entitled "Cognitive Functional Therapy in Patients with Non Specific Chronic Low Back Pain: A Randomized Controlled Trial 3-year Follow Up" (Vibe Fersum 2019). This article is protected by copyright. All rights reserved.
Learn More >Musculoskeletal pain is associated with altered motor control that despite short-term benefit, is hypothesised to have long-term consequences, contributing to the development of chronic pain. However, data on how motor control is altered when pain is sustained beyond a transient event are scarce. Here, we investigated motor adaptation, and its relationship to corticomotor excitability, in the transition to sustained muscle pain. Twenty-eight healthy individuals were injected with nerve growth factor (NGF) into the right extensor carpi radialis brevis (ECRB) muscle on Days 0 and 2. Motor adaptation and corticomotor excitability were assessed on Day -2, prior to injection on Days 0 and 2, and again on Days 4 and 14. Motor adaptation was quantified during a radial-ulnar movement as kinematic variability of wrist flexion-extension and pronation-supination, and as electromyographic (EMG) variability of ECRB activity. Pain, muscle soreness, and functional limitation were assessed from Days 0-14. Pain, muscle soreness and functional limitation were evident at Days 2 and 4 (p<0.001). EMG variability reduced at Days 4 and 14 (p<0.04), with no change in kinematic variability (p=0.9). However, data revealed variation in EMG and kinematic variability between individuals: some displayed increased motor variability while others a decrease. Individuals who displayed an increase in EMG variability following four days of pain also displayed an increase in corticomotor excitability (r=0.43, p=0.034). These findings suggest individual adaptation of the motor system in the transition to sustained pain that could have implications for clinical musculoskeletal pain disorders.
Learn More >To identify migraineurs and headache-free individuals with an online questionnaire and automated analysis algorithm.
Learn More >Chronic widespread pain (CWP) is common and associated with loss of functioning and health. Subjects with chronic non-widespread pain (CnWP) are at increased risk of developing CWP, but few studies have described the nature of the development over time.We followed a random sample of 3105 participants from the population-based HUNT-3 study with five annual measurements of pain over four years. While 29% reported CWP on at least one occasion, only 7% reported it consistently on four or fsive occasions. The average annual cumulative incidence was 5% and the recovery rate was 38%. In mutual adjusted analysis, the risk of developing CWP from one year to the next was higher in subjects with chronic pain (RR=2.4; 95% CI: 1.8-3.4), two or more pain regions (RR= 3.3; 95% CI: 2.5-4.4), moderate pain or more (RR=1.8; 95% CI: 1.5-2.6) and with comorbid chronic disease (RR=1.6; 95% CI: 1.3-1.9). Developing CWP was associated with a modest concurrent change in self-reported mental and physical health. The risk of developing CWP between the fourth and fifth occasions was 80% lower for subjects without a history of CWP, compared to those with. For subjects without previous CWP, the development was associated with previously reported CnWP, but not with the number of occasions with CnWP, in analyses adjusted for sex, age and pain severity.A substantial proportion of the new cases of CWP originates from subjects floating below and above the definition for CWP over time, and thus, do not seem to involve major transitions in health.
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