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Chronic pain is often associated with changes in brain structure and function, and also cognitive deficits. It has been noted that these chronic pain-related alterations may resemble changes found in healthy aging, and thus may represent accelerated or pre-mature aging of the brain. Here we test the hypothesis that patients with chronic non-cancer pain demonstrate accelerated brain aging compared to healthy control subjects. The predicted brain age of 59 patients with chronic pain (mean chronological age ± standard deviation: 53.0 ± 9.0 years; 43 women) and 60 pain-free healthy controls (52.6 ± 9.0 years; 44 women) was determined using the software brainageR. This software segments the individual T1-weighted structural MR images into gray and white matter and compares gray and white matter images to a large (n = 2001) training set of structural images, using machine learning. Finally, brain age delta, which is the predicted brain age minus chronological age, was calculated and compared across groups. This study provided no evidence for the hypothesis that chronic pain is associated with accelerated brain aging (Welch's t-test, p = 0.74, Cohen's d = 0.061). A Bayesian independent samples t-test indicated moderate evidence in favor of the null hypothesis (BF01 = 4.875, i.e. group means were equal). Our results provide indirect support for recent models of pain related-changes of brain structure, brain function, and cognitive functions. These models postulate network-specific maladaptive plasticity, rather than wide-spread or global neural degeneration.
Learn More >Despite rising morbidity and mortality from the opioid epidemic and other addictions, people who inject drugs (PWID) remain understudied regarding pain outcomes. Data among PWID regarding chronic pain and drug use, including non-medical use of opioids, is largely unknown. We examined the prevalence of chronic pain and drug use for pain in this population.
Learn More >Potential protective effects of nonpharmacological treatments (NPT) against long-term pain-related adverse outcomes have not been examined.
Learn More >TRESK background K channel is expressed in sensory neurons and acts as a brake to reduce neuronal activation. Deletion of the channel enhances the excitability of nociceptors Skin nociceptive C-fibers show an enhanced activation by cold and mechanical stimulation in TRESK KO animals. Channel deletion selectively enhances mechanical and cold sensitivity in mice, without altering sensitivity to heat. These results indicate that the channel regulates the excitability of specific neuronal subpopulations involved in mechanosensitivity and cold-sensing.
Learn More >This issue of the Clinical Journal of Pain includes a series of review articles from the international symposium "Approach to physical activity in pain: translation from theory to the lab, from the clinic to the patient" which was held as an Official Satellite Symposium of the 17 World Congress on Pain, 2018 in Boston, USA and organized by the Mind and Pain in Motion Research Group (Chair: MIH) and colleagues from the field of clinical rehabilitation in Austria (EF, GE). The symposium brought together world's leading researchers from multiple disciplines to further advance our understanding of the complex interaction of cognitive, behavioral and neuromuscular mechanisms that may play a role for the development and maintenance of chronic musculoskeletal pain. Following up on a previous Satellite Meeting 2012 in Nottwil, Switzerland and the first Mind and Pain in Motion Symposium, held 2016 at Ruhr University of Bochum, Germany, the 2018 meeting in Boston presented (1) new theoretical approaches in psychobiological pain research, (2) current experimental research in endogenous pain modulation, initiated by exercise behavior, stress and pain cognitions (3) latest findings on the phenomena of physical overactvity, endurance-related pain response pattern, neuromuscular activity and possible interrelations, and (4) clinical approaches to a more individualized, patient-oriented management in the field of musculoskeletal pain disorders.
Learn More >Psychologically informed practice (PIP) is advocated for physiotherapists to help people with chronic pain. There is little research observing how PIP is delivered in clinical practice. This study describes behaviours and techniques used by experienced physiotherapists working with groups of people with chronic pain.
Learn More >Itch is a highly prevalent and multi-dimensional symptom. We aimed to analyze the association between itch and mental health in dermatological patients. This multi-center study is observational cross-sectional conducted in dermatological clinics across 13 European countries. A total of 3530 patients and 1094 healthy controls were included. Patients were examined clinically. Outcome measures were itch (presence, chronicity and intensity), the Hospital Anxiety and Depression Scale, EQ5D-VAS, sociodemographics, suicidal ideation, stress (negative life events and economic difficulties). Ethical approval was obtained. Results showed significant association between the presence of itch in patients and clinical depression, suicidal ideation and economic difficulties (odds ratios respectively OR 1.53 (95% CI 1.15 to 2.02), OR 1.27 (95% CI 1.01 to 1.60), OR 1.24 (95% CI 1.10 to 1.50). The mean score of reported generic health status assessed by the EQ5D-VAS was 65.9 (SD=20.1) in patients with itch, compared to 74.7 (SD= 18.0) in patients without itch, p value < .001 and 74.9 (SD= 15.7) in controls with itch compared to 82.9 (SD= 15.6) in controls without itch, p value <.001. Itch contributes substantially to the psychological disease burden in dermatological patients and the management of patients should include access to multidisciplinary care.
Learn More >The serine hydrolase monoacylglycerol lipase (MAGL) is the rate-limiting enzyme responsible for the degradation of the endocannabinoid 2-arachidonoylglycerol (2-AG) into arachidonic acid and glycerol. Inhibition of 2-AG degradation leads to elevation of 2-AG, the most abundant endogenous agonist of the cannabinoid receptors CB1 and CB2. Activation of these receptors have demonstrated beneficial effects on mood, appetite, pain and inflammation. Therefore, MAGL inhibitors have the potential to produce therapeutic effects in a vast array of complex human diseases. The present report describes the pharmacologic characterization of JNJ-42226314, [1-(4-fluorophenyl)indol-5-yl]-[3-[4-(thiazole-2-carbonyl)piperazin-1-yl]azetidin-1-yl]methanone, a reversible and highly selective MAGL inhibitor. JNJ-42226314 inhibits MAGL in a competitive mode with respect to the 2-AG substrate. In rodent brain, the compound time- and dose-dependently bound to MAGL, indirectly led to CB1 occupancy by raising 2-AG levels and raised norepinephrine levels in cortex. In vivo, the compound exhibited antinociceptive efficacy in both the rat complete Freund's adjuvant (CFA)-induced radiant heat hypersensitivity and chronic constriction injury (CCI)-induced cold hypersensitivity models of inflammatory and neuropathic pain, respectively. Although 30 mg/kg induced hippocampal synaptic depression, altered sleep onset and decreased EEG gamma power, 3 mg/kg still provided approximately 80% enzyme occupancy, significantly increased 2-AG and norepinephrine levels and produced neuropathic antinociception without synaptic depression or decreased gamma power. Thus, it is anticipated that the profile exhibited by this compound will allow for precise modulation of 2-AG levels in vivo, supporting potential therapeutic application in several CNS disorders. SIGNIFICANCE STATEMENT: Potentiation of endocannabinoid signaling activity via inhibition of the serine hydrolase monoacylglycerol lipase (MAGL) is an appealing strategy in the development of treatments for several disorders, including ones related to mood, pain and inflammation. JNJ-42226314 is presented in this report to be a novel, potent, selective and reversible non-covalent MAGL inhibitor that demonstrates dose-dependent enhancement of the major endocannabinoid 2-arachidonoylglycerol as well as efficacy in models of neuropathic and inflammatory pain.
Learn More >This paper addresses the problem of long-term opioid use by chronic pain patients. The study involved a secondary analysis of unanalysed data from a published study of two versions of CBT-based interdisciplinary treatment for chronic pain. In this paper we examined whether the use of opioids by 140 chronic pain patients could be ceased sustainably over 12-months following participation in the comprehensive interdisciplinary pain management program aimed at enhancing pain self-management. On admission to the treatment there were no significant differences between those patients taking or not taking opioids on usual pain, pain interference in daily activities, pain-related disability, depression severity, as well as in pain cognitions. Following the treatment the use of opioids was significantly reduced, both in numbers taking any and in mean doses, and these gains were maintained over the 12-month follow-up. Finally, cessation of opioids during treatment was associated with more substantial and consistent improvements in usual pain, depression severity, pain interference, pain-related disability, and pain cognitions, relative to those who reduced their opioids but did not cease them. These findings support the idea of using training in pain self-management strategies as a viable alternative to long-term opioid use by patients with chronic pain.
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