Pain
-
We deployed an online pain sensitivity questionnaire (PSQ) and an at-home version of the cold pressor test (CPT) in a large genotyped cohort. We performed genome-wide association studies on the PSQ score (25,321 participants) and CPT duration (6853). ⋯ Gene-based analysis followed by pathway analysis showed that genome-wide association studies results were enriched for genes expressed in the brain and involved in neuronal development and glutamatergic synapse signaling pathways. Finally, we confirmed that females with red hair were more sensitive to pain and found that genetic variation in the MC1R gene was associated with an increase in self-perceived pain sensitivity as assessed by the PSQ.
-
Adolescent pain is common and continues into adulthood, leading to negative long-term outcomes including substance-related morbidity: an empirical definition of its construct may inform the early detection of persistent pain trajectories. These secondary analyses of a classical twin study assessed whether headaches, back pains, abdominal pain, chest pains, stabbing/throbbing pain, and gastric pain/nausea, measured in 501 pairs across 5 waves between age 12 and 17 years, fit a unitary construct or constitute independent manifestations. We then assessed which symptoms were associated with a steady, "frequent pain" trajectory that is associated with risk for early opioid prescriptions. ⋯ The highest area under the curve was attained by "back pain" at age 14 years (0.835); for multiple cut-off thresholds of symptom frequency, "back pain" showed good sensitivity/false alarm probability trade-offs, predominantly in the 13 to 15 years age range, to predict the "frequent pain" trajectory. These data support a unitary conceptualization and assessment of adolescent pain, which is advantageous for epidemiological, clinical, and translational purposes. Persistent back pain constitutes a sensitive indicator of a steady trajectory of adolescent pain.
-
For the first time, the upcoming International Classification of Diseases and Related Health Problems, Eleventh Revision (ICD-11) will include a comprehensive classification of chronic pain, which is based on the biopsychosocial definition of chronic pain. This presents a great opportunity for pain research and clinical practice. The new classification consists of 7 main diagnostic categories of chronic pain, which are further divided into increasingly specific levels of diagnoses. ⋯ Furthermore, the authors collected questions posted to the ICD-11 browser and contacted early users of the classification to enquire about their most frequent difficulties when applying the new diagnoses. The authors of the present publication prepared answers to these frequently asked questions. This publication intends to act as a guide for the future users of the new ICD-11 chronic pain classification, hence facilitating its implementation.
-
Chronic pain is a major healthcare issue posing a large burden on individuals and society. Converging lines of evidence indicate that chronic pain is associated with substantial changes of brain structure and function. However, it remains unclear which neuronal measures relate to changes of clinical parameters over time and could thus monitor chronic pain and treatment responses. ⋯ Thus, changes in chronic pain might be reflected by global network changes in the theta band. These longitudinal insights further the understanding of the brain mechanisms of chronic pain. Beyond, they might help to identify biomarkers for the monitoring of chronic pain.
-
Defined by dysfunction or degeneration of Aδ and C fibers, small fiber neuropathies (SFNs) entail a relevant health burden. In 50% of cases, the underlying cause cannot be identified or treated. In 100 individuals (70% female individuals; mean age: 44.8 years) with an idiopathic, skin biopsy-confirmed SFN, we characterized the symptomatic spectrum and measured markers of oxidative stress (vitamin C, selenium, and glutathione) and inflammation (transforming growth factor beta, tumor necrosis factor alpha), as well as neurotoxic 1-deoxy-sphingolipids. ⋯ Reduced glutathione was lower in patients with Aδ dysfunction ( P < 0.05). Idiopathic SFNs are heterogeneous. As a new pathomechanism, plasma 1-deoxy-sphingolipids might link the metabolic syndrome with small fiber degeneration.