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Self-report measures are needed to better understand the relationships among sleep, itching, scratching, and chronic itch conditions and their associations with disease severity, quality of life, health, and functioning. Two scales related to sleep and/or scratch were recently developed and assessed in 137 patients with chronic itch and atopic dermatitis or psoriasis. The Scratch Intensity and Impact Scale consisted of two factors (Scratching Intensity and Impact of Scratching on Quality of Life) that accounted for 64.59% of the variance with a total of 13 items, an overall Cronbach's alphas of 0.93, and test-retest reliability of 0.66. The Sleep-Related Itch and Scratch Scale consisted of one factor that accounted for 63.01% of the variance with a total of 16 items, an overall Cronbach's alphas of 0.98, and test-retest reliability of 0.66. Both measures demonstrated significant correlations with each other as well as other itch-related measures and non-significant correlations with scales hypothesized to be unrelated. The final measures demonstrated adequate preliminary psychometric characteristics. It is hoped that these scales will be used for future research and clinical purposes to help fill recognized gaps in understanding about sleep, itch, scratching, atopic dermatitis, and psoriasis.
Learn More >This study aimed to: (1) examine changes in pain, psychosocial functioning, and healthcare utilization among children and adolescents with sickle cell disease (SCD) over a 2-year period; and (2) identify baseline biopsychosocial variables associated with the development and maintenance of chronic SCD pain at follow-up.
Learn More >The purpose of this study was to examine genetic variability and knee pain in persons with osteoarthritis (OA). Seventy-five participants with medial compartment knee OA were recruited from a large Midwestern tertiary care center. Participants exhibited a mean age of 56.3 years; females comprised 61% of the sample. Measures of pain included subjective pain intensity at rest and with movement, cutaneous mechanical sensation and pain testing, heat pain threshold, and pressure pain threshold. Seventy-four participants were genotyped for 25 genetic variants across 15 candidate genes for central or peripheral pain pathways. Analysis suggests a role for four genes (EDNRA, COMT, BDRKB1, and IL1B) in several components of pain in persons with knee OA. The results from this study will help guide the development and evaluation of tailored strategies to decrease pain, improve function, and prevent the development of new chronic pain syndromes in older adults experiencing OA. [Research in Gerontological Nursing, xx(x), xx-xx.].
Learn More >Studies evaluating sensory function of the entire trigeminocervical region in patients with cluster headache (CH), migraine (MH), and tension-type headache (TH) are required. The purpose of the present study was to evaluate and compare sensory function in the trigeminocervical region in patients with CH, MH, and TH and healthy controls (HC).
Learn More >While CNS microglia have been extensively studied, relatively little is known about macrophages populating the peripheral nervous system. Here we performed ontogenic, transcriptomic and spatial characterization of sciatic nerve macrophages (snMacs). Using multiple fate-mapping systems, we show that snMacs do not derive from the early embryonic precursors colonizing the CNS, but originate primarily from late embryonic precursors and become replaced by bone-marrow-derived macrophages over time. Using single-cell transcriptomics, we identified a tissue-specific core signature of snMacs and two spatially separated snMacs: RelmαMgl1 snMacs in the epineurium and RelmαMgl1 snMacs in the endoneurium. Globally, snMacs lack most of the core signature genes of microglia, with only the endoneurial subset expressing a restricted number of these genes. In response to nerve injury, the two resident snMac populations respond differently. Moreover, and unlike in the CNS, monocyte-derived macrophages that develop during injury can engraft efficiently in the pool of resident peripheral nervous system macrophages.
Learn More >We studied the color of lighting chosen as comfortable for reading by individuals with migraine and controls. We explored the effects of the chosen color on visual performance.
Learn More >Morphine-induced alterations in sphingolipid metabolism in the spinal cord and increased formation of the bioactive sphingolipid metabolite sphingosine-1-phosphate (S1P) have been implicated in the development of morphine-induced hyperalgesia (OIH; increased pain sensitivity) and antinociceptive tolerance. These adverse effects hamper opioid use for treating chronic pain and contribute to dependence and abuse. S1P produces distinct effects through five G protein-coupled receptors (S1PR1-5) and several intracellular targets. How S1P exerts its effects in response to morphine remains unknown. Here, we report that S1P contributes to the development of OIH and tolerance through S1P1 receptor subtype 1 (S1PR1) signaling in uninjured male and female rodents that can be blocked by targeting S1PR1 with S1PR1 antagonists or RNA silencing. In mouse neuropathic pain models, S1PR1 antagonists blocked the development of tolerance to the anti-allodynic effects of morphine without altering morphine pharmacokinetics and prevented prolonged morphine-induced neuropathic pain. Targeting S1PR1 reduced morphine-induced neuroinflammatory events in the dorsal horn of the spinal cord: increased glial marker expression, mitogen-activated protein kinase p38 and nuclear factor κB activation and increased inflammatory cytokine expression, such as interleukin-1β, a cytokine central in the modulation of opioid-induced neural plasticity. Our results identify S1PR1 as a critical path for S1P signaling in response to sustained morphine and reveal downstream neuroinflammatory pathways impacted by S1PR1 activation. Our data support investigating S1PR1 antagonists as a clinical approach to mitigate opioid-induced adverse effects and repurposing the functional S1PR1 antagonist FTY720, which is FDA-approved for multiple sclerosis, as an opioid adjunct.
Learn More >Skeletal metastases are frequently accompanied by chronic pain that is mechanoceptive in nature. Mechanistically, cancer-induced bone pain (CIBP) is mediated by peripheral sensory neurones innervating the cancerous site, the cell bodies of which are housed in the dorsal root ganglia (DRG). How these somatosensory neurons encode sensory information in CIBP remains only partly explained. Using a validated rat model, we first confirmed cortical bone destruction in CIBP but not sham-operated rats (day 14 post-surgery, designated 'late' stage bone cancer). This occurred with behavioural mechanical hypersensitivity (Kruskal-Wallis H for independent samples; CIBP vs. Sham-operated, day 14; p < 0.0001). Next, hypothesising that the proportion and phenotype of primary afferents would be altered in the disease state, DRG in vivo imaging of genetically-encoded calcium indicators and Markov Cluster Analysis were employed to analyse 1748 late-stage CIBP (n=10), and 757 sham-operated (n=9), neurons. Distinct clusters of responses to peripheral stimuli were revealed. In CIBP rats, upon knee compression of the leg ipsilateral to the tumour: (1) three times as many sensory afferents responded (RM-ANOVA: p < 0.0001 (vs. sham)); (2) there were significantly more small neurons responding (Kruskal-Wallis for independent samples (vs. sham): p < 0.0001) and (3) approximately 13% of traced tibial cavity afferents responded (no difference observed between CIBP and sham-operated animals). We conclude that an increased sensory afferent response is present in CIBP rats and this is likely to reflect afferent recruitment from outside of the bone rather than increased intraosseous afferent activity.
Learn More >The neuropeptide oxytocin (OT) has been shown to play a modulatory role in nociception. However, analgesic effects of OT in chronic pain conditions remain elusive and the neural underpinnings have not yet been investigated in humans. Here, we conducted an exploratory, randomized, placebo-controlled, cross-over study to examine effects of intranasal OT in male patients suffering from chronic low back pain (CBP) versus healthy controls (HC). N = 22 participants with CBP and 22 HCs were scanned using functional magnetic resonance imaging (fMRI) while they continuously rated either spontaneously occurring back pain or acute thermal pain stimuli applied to the lower back. During heat pain processing we found that OT versus PL attenuated pain intensity ratings and increased BOLD responses in the caudate nucleus of the striatum in CBP versus HCs. Spontaneously experienced pain in contrast to heat pain was associated with activation changes in the medial frontal cortex (MFC) and the anterior cingulate cortex (ACC) as reported in previous studies. However, we did not observe OT effects on spontaneously experienced pain in CBP patients. Overall, our preliminary data may suggest that the striatum is a key structure underlying the pain-modulating effects of OT in patients with chronic pain and adds to the growing evidence linking the neuropeptide to pain modulation in humans. Further studies on neuronal OT effects in larger samples of chronic back pain patients are needed to understand probable mechanisms of OT effects in chronic pain.
Learn More >Chronic headaches are poorly diagnosed and managed and can be exacerbated by medication overuse. There is insufficient evidence on the non-pharmacological approaches to helping people living with chronic headaches.
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