Pain
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Endogenous pain inhibition is less efficient in chronic pain patients. Diffuse noxious inhibitory control (DNIC), a form of endogenous pain inhibition, is compromised in women and older people, making them more vulnerable to chronic pain. However, the underlying mechanisms remain unclear. ⋯ The reduced efficiency of DNIC in young females seemed to be driven by widespread brain connectivity. Old males showed increased connectivity between PAG, raphe nuclei, pontine reticular nucleus, and hippocampus, which may not be dependent on connections to ACC, whereas old females showed increased connectivity between ACC, PAG, and more limbic regions. These findings suggest that distinct brain circuitries including the limbic system may contribute to higher susceptibility to pain modulatory deficits in the elderly population, and sex may be a risk factor for developing age-related chronic pain.
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The role of immune mediators, including proinflammatory cytokines in chemotherapy-induced peripheral neuropathy (CIPN), remains unclear. Here, we studied the contribution of interleukin-20 (IL-20) to the development of paclitaxel-induced peripheral neuropathy. Increased serum levels of IL-20 in cancer patients with chemotherapy were accompanied by increased CIPN risk. ⋯ Importantly, IL-20 suppression did not alter paclitaxel efficacy on cancer treatment both in vitro and in vivo. Together, targeting IL-20 ameliorates paclitaxel-induced peripheral neuropathy by suppressing neuroinflammation and restoring Ca homeostasis. Therefore, the anti-IL-20 monoclonal antibody is a promising therapeutic for the prevention and treatment of paclitaxel-induced neuropathy.
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Randomized Controlled Trial
A randomized placebo-controlled trial of desipramine, cognitive behavioral therapy, and active placebo therapy for low back pain.
This clinical trial evaluated the independent and combined effects of a tricyclic antidepressant (desipramine) and cognitive behavioral therapy (CBT) for chronic back pain relative to an active placebo treatment. Participants (n = 142) were patients experiencing daily chronic back pain at an intensity of ≥4/10 who were randomized to a single-center, double-blind, 12-week, 4-arm, parallel groups controlled clinical trial of (1) low concentration desipramine titrated to reach a serum concentration level of 15 to 65 ng/mL; (2) CBT and active placebo medication (benztropine mesylate, 0.125 mg); (3) low concentration desipramine and CBT; and (4) active benztropine placebo medication. Participants completed the Differential Description Scale and Roland Morris Disability Questionnaires before and after treatment as validated measures of outcomes in back pain intensity and disability, respectively. ⋯ However, intent-to-treat analyses at post-treatment showed no significant differences between any condition, with small effect sizes ranging from 0.06 to 0.27. The results from this clinical trial did not support the hypothesis that desipramine, CBT, or their combination would be statistically superior to an active medicine placebo for reducing chronic back pain intensity or disability. Key limitations included recruiting 71% of the planned sample size and use of multiple inclusion/exclusion criteria that may limit generalizability to broader populations of patients with chronic back pain.
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Data on all outpatient opioid prescriptions (N = 71,647) to youth below age 21 (N = 42,020) from 2005 to 2016 were extracted from electronic medical records within a university hospital system in New Mexico (NM) as were demographic details and markers of morbidity/mortality. Relative risk was calculated for markers of morbidity/mortality based on sociodemographic characteristics. The sample was primarily male (55.0%), Hispanic/Latinx (50.1%), English-speaking (88.9%), and publicly insured (50.1%). ⋯ Significantly increased risk of adverse outcomes was observed in patients receiving multiple opioid prescriptions, and in patients who were older, of minority race, received their first prescription in an outpatient clinic, and publicly insured or uninsured. Results add to the growing literature concerning opioid prescription rates over time. They also provide important information on potential additive risks of adverse outcomes when pediatric patients receive multiple opioid prescriptions.
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Theoretical models and evidence increasingly identify chronic pain as a family issue. To date, much of this work has focused on risk conferred by parental chronic pain status despite evidence suggesting parent mental illness and non-pain-related chronic illness may also contribute to poorer chronic pain outcomes in children. This study is the first to test interpersonal fear avoidance processes as possible mechanisms through which parent health (mental and physical) influences pediatric chronic pain functioning. ⋯ The model demonstrated excellent fit to the data (χ[5] = 5.04, ns; χ/df = 1.01; comparative fit index = 1.00, root mean square error of approximation = 0.004 [90% confidence interval = 0.000 to 0.066]). Exploratory multiple-group comparison structural equation model revealed moderation of specific model paths based on child age group (8- to 12-year-olds vs 13- to 18-year-olds) and parent pain status (present vs absent). This study integrates family models of pain with the interpersonal fear avoidance model to extend our mechanistic understanding of parental physical and mental health contributors to pediatric chronic pain.