and MeSH terms for “pain” and “manikin” to identify original studies in English that used a digital pain manikin for collecting information from adults with any condition. We extracted and descriptively synthesised data on the characteristics of studies and digital pain manikins and mapped them to a stage of the translational pathway (ie, design, testing, metric validation, and diffusion). We screened 6,189 articles, of which we included 104. Articles reported on 31 unique digital pain manikins. Most studies were conducted in Europe (n = 60; 58%), recruited people with pain/painful conditions (n = 69; 66%) from clinical settings (n = 67; 64%). Of the 31 manikins, the majority were two-dimensional (n = 21; 68%) with a front and back body view (n = 18; 58%) and allowed users to draw their pain on any area of the manikin (n = 23; 74%). Most manikins were still in the development and testing stages (n = 23; 74%). Only eight (26%) had progressed fully through the translational pathway, taki

r fluctuations in sensory cortex activity are associated with pain sensitivity. Objectives: To examine (1) the trajectory of changes in sensory cortex activity over a period of six months from the onset of acute LBP; (2) the assoication between sesnory cortex activity and pain pain sensitivity. Methods: In a prospective cohort study (N = 120), sensory evoked potentials (SEPs) were recorded using electroencephalography within 6 weeks of LBP onset (baseline) and at 3- and 6-month follow-up. Pain sensitivity was assessed using quantitative sensory testing (QST). Results: At baseline, individuals who developed chronic pain at 6-month follow-up exhibited less nonnoxious sensory processing (smaller area of N80, N150, and P260 SEP components) compared with those who recovered. In individuals who recovered, SEP measures did not change over time. In individuals who developed chronic pain, N80 and N150 SEP area increased between baseline and 3 months, while P260 SEP area increased between baseli

nisms, we performed a placebo-controlled, double-blind crossover study with 51 participants (21 patients with migraine without aura and 30 healthy controls). Methods: Participants received a low-dose citalopram- or placebo challenge on 2 separate days. Prechallenge and postchallenge assessment of cortisol concentrations and transcriptomic changes using RNA-seq was performed from whole blood samples. Analysis of an accidental attack following the citalopram challenge was also conducted. Results: Neuroendocrine challenge elicited elevated cortisol concentrations at 30 (P-value = 0.1355) and 70 minutes (P-value = 0.07292) postchallenge in patients with migraine compared with controls. Gene expression analysis showed 10 differentially expressed genes (2 down- and 8 upregulated, P-value ≤ 0.005) and 10 dysregulated gene sets (P-value ≤ 0.005). Among them, dysregulated IKBKGP1 and NKRF genes and upregulated protein synthesis and translation, carbohydrate metabolism, and, attack-related, glyc

rsen pain symptoms over time. Understanding patterns of sleep medication use is necessary for increasing appropriate treatments for sleep problems among patients with pain. Objectives: To understand the prevalence and clinical characteristics associated with sleep medication use among veterans with chronic pain. Methods: We conducted a retrospective secondary data analysis of Veterans Health Administration medical records and identified patients with a chronic pain diagnosis receiving care from October 2018 through September 2021. Using multivariate logistic regression, we examined associations between patient and clinical characteristics and sleep medication use. Results: Among all identified patients with chronic pain (N = 1,706,241), 38% carried a sleep disorder diagnosis and 19% were prescribed sleep medications. Sleep medications were prescribed in 42% of patients with insomnia and 14% of patients without active sleep problems. Insomnia, mental health comorbidities, and current or