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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.
There is no consensus regarding the effectiveness of Transcutaneous Electrical Nerve Stimulation (TENS) for chronic musculoskeletal or low back pain. A review of previous trial methodology identified problems with treatment fidelity. Qualitative research with experienced TENS users identified specific contexts for TENS use, leading to individualised outcomes. There is little information available to guide the selection of Patient Reported Outcome Measures (PROMs) appropriate for TENS evaluation.
Drawing on advances in chronic pain metrics, a simplified Graded Chronic Pain Scale Revised (GCPS-R) was developed to differentiate mild, bothersome and high impact chronic pain. GCPS-R was validated among adult enrollees of two health plans (N=2021). In this population, the prevalence of chronic pain (pain present most or every day, prior 3 months) was 40.5%: 15.4% with mild chronic pain (lower pain intensity and interference); 10.1% bothersome chronic pain (moderate to severe pain intensity with lower life activities interference); and 15.0% high impact chronic pain (sustained pain-related activity limitations). Persons with mild chronic pain versus those without chronic pain showed small differences on ten health status indicators (unfavorable health perceptions, activity limitations, receiving long-term opioid therapy), with non-significant differences for 7 of 10 indicators. Persons with bothersome versus mild chronic pain differed significantly on 6 of 10 indicators (e.g., negative pain coping beliefs, psychological distress, unfavorable health perceptions and pain-related interference with overall activities). Persons with high impact chronic pain differed significantly from those with mild chronic pain on all 10 indicators. Persons with high impact chronic pain, relative to those with bothersome chronic pain, were more likely to have substantial activity limitations (significant differences for 4 of 5 disability indicators) and more often received long-term opioid therapy. GCPS-R strongly predicted five activity limitation indicators with area under receiver operating characteristic curve coefficients of 0.76 to 0.89. We conclude that the 5 item GCPS-R and its scoring rules provide a brief, simple and valid method for assessing chronic pain.
The complex mechanisms underlying migraine are not entirely understood. It has been suggested that descending endogenous pain modulation is an important contributing factor, although research is controversial. A frequently used method to quantify the inhibitory pain modulation system is offset analgesia (OA), defined as a disproportionally large decrease in pain perception in response to a small decrease of painful stimulation. The aim of this study is to evaluate the OA response in patients with migraine and healthy controls, measured at the forehead (trigeminal, V1) and forearm (extra-trigeminal). Patients with episodic migraine during the headache free interval (n=26) and age and sex matched headache-free controls (n=26) were included in this cross-sectional study. All participants underwent an individualized OA paradigm consisting of three-stimulus offset trials and three constant temperature trials examined at both, a trigeminal and an extra-trigeminal test site. Items from the quantitative sensory testing protocol were additionally included. In contrast to the extra-trigeminal area, a reduced offset analgesia response was shown in the trigeminal area in patients with migraine compared to healthy controls (p<0.01, MD: 13.7, 95%CI: 3.8; 23.6). Statistically significant differences between the trigeminal area and the extra-trigeminal area were neither observed in healthy controls nor in patients with migraine (p>0.05). Mechanical detection, mechanical pain threshold, warm detection and heat pain threshold showed no significant differences between groups or test sites (p>0.05). In summary, patients with episodic migraine in the headache free interval exhibited somatotopically specific differences in endogenous pain modulation.
Post-traumatic Stress Disorder (PTSD) commonly co-occurs with chronic pain. Although PTSD symptoms are associated with negative health outcomes in patients with chronic pain, PTSD is typically under-detected and under-treated in outpatient pain settings. There is a need for rapid, brief screening tools to identify those at greatest risk for severe PTSD symptoms. To achieve that goal, our aim was to use item response theory (IRT) to identify the most informative PTSD symptoms characterizing severe PTSD in patients with chronic pain.
To study the various pain assessment tools based on their psychometric properties and ease of use.
To describe morphological changes associated with degeneration and regeneration of large fibers in the skin using a model of chronic compression of the median nerve.
Compromised Na/K-ATPase function is associated with the occurrence of spreading depolarization (SD). Mutations in ATP1A2, the gene encoding the α2 isoform of the Na/K-ATPase, were identified in patients with familial hemiplegic migraine type 2 (FHM2), a Mendelian model disease for SD. This suggests a distinct role for the α2 isoform in modulating SD susceptibility and raises questions about underlying mechanisms including the roles of other Na/K-ATPase α isoforms. Here, we investigated the effects of genetic ablation and pharmacological inhibition of α1, α2, and α3 on SD using heterozygous knock-out mice. We found that only α2 heterozygous mice displayed higher SD susceptibility when challenged with prolonged extracellular high potassium concentration ([K]), a pronounced post SD oligemia and higher SD speed in-vivo. By contrast, under physiological [K], α2 heterozygous mice showed similar SD susceptibility compared to wild-type littermates. Deficiency of α3 resulted in increased resistance against electrically induced SD in-vivo, whereas α1 deficiency did not affect SD. The results support important roles of the α2 isoform in SD. Moreover, they suggest that specific experimental conditions can be necessary to reveal an inherent SD phenotype by driving a (meta-) stable system into decompensation, reminiscent of the episodic nature of SDs in various diseases.