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Chronic pain outcomes are traditionally defined in terms of ability and . A definition of adaptive functioning in the context of chronic pain beyond the mere absence of negative outcomes, is the ability to (i.e., experience emotional, psychological and social ; Keyes, 2002). We explored in two chronic pain samples the prevalence and sociodemographic, physical and psychological correlates of flourishing, and complemented this exploration with a similar examination of to help contextualize findings. Sample 1 ( = 1498) was a nationally representative sample. Subgroups included people with regular joint pain (1), regular joint pain and rheumatoid arthritis (2) and without chronic pain (3). Using chi-square tests we calculated the prevalence of both mental health outcomes and examined if people with or without chronic pain were more/less likely to flourish/at risk for psychopathology. Sample 2 ( = 238) concerned baseline data of a Randomized Controlled Trial on the effectiveness of Acceptance and Commitment Therapy for chronic pain (Trompetter et al., 2015b). We performed logistic regression analysis to identify flourishers/those at risk for depression. The Mental Health Continuum-Short Form was used to measure flourishing. The prevalence of flourishing was 34% (recurrent joint pain) and 38% (recurrent joint pain and arthritis) in sample 1, and 23% in sample 2. Compared to those without chronic pain, people with chronic pain were as likely to flourish, but more likely to be at risk for psychopathology. In sample 2, both flourishing and being at risk for depression were related foremost to correlates. While engaged living was the most important correlate of flourishing, pain catastrophizing and psychological inflexibility were most important correlates of being at risk for depression. In conclusion, people with chronic pain to flourish. Findings suggest that positive and negative chronic pain outcomes function on two different continua, with potentially unique protective and risk factors. The Psychological Flexibility model provides pathways to explain both poor and optimal functioning in the presence of chronic pain. A better understanding of people with chronic pain who are able to flourish can be a fruitful endeavor to improve chronic pain models and interventions.
Learn More >Neurofibromatosis type 1 (NF1) is a neurogenetic disorder affecting 1 in 3000 people worldwide, where individuals are prone to develop benign and malignant tumors. In addition, many people with NF1 complain of pain that limits their daily functioning. Due to the complexity of the disorder, there are few options for treating pain symptoms besides surgery and medications. Moreover, the spectrum of pain symptomatology and treatment, as well as the mechanisms underlying NF1-associated pain, has been understudied.
Learn More >Persistent idiopathic facial pain (PIFP) is a subtype of painful cranial neuropathies and other facial pains. The involvement of neuropathic mechanisms in PIFP, however, remains controversial. Using the Douleur Neuropathique 4 (DN4) questionnaire, the present study examined neuropathic characteristics in patients with PIFP.
Learn More >Oral cancer patients report severe function-induced pain; severity is greater in females. We hypothesize that a neutrophil-mediated endogenous analgesic mechanism is responsible for sex differences in nociception secondary to oral squamous cell carcinoma (SCC). Neutrophils isolated from the cancer-induced inflammatory microenvironment contain β-endorphin protein and are identified by the Ly6G immune marker. We previously demonstrated that male mice with carcinogen-induced oral SCC exhibit less nociceptive behavior and a higher concentration of neutrophils in the cancer microenvironment compared to female mice with oral SCC. Oral cancer cells secrete granulocyte colony stimulating factor (G-CSF), a growth factor that recruits neutrophils from bone marrow to the cancer microenvironment. We found that recombinant G-CSF (rG-CSF, 5 μg/mouse, intraperitoneal) significantly increased circulating Ly6G neutrophils in the blood of male and female mice within 24 h of administration. In an oral cancer supernatant mouse model, rG-CSF treatment increased cancer-recruited Ly6G neutrophil infiltration and abolished orofacial nociceptive behavior evoked in response to oral cancer supernatant in both male and female mice. Local naloxone treatment restored the cancer mediator-induced nociceptive behavior. We infer that rG-CSF-induced Ly6G neutrophils drive an endogenous analgesic mechanism. We then evaluated the efficacy of chronic rG-CSF administration to attenuate oral cancer-induced nociception using a tongue xenograft cancer model with the HSC-3 human oral cancer cell line. Saline-treated male mice with HSC-3 tumors exhibited less oral cancer-induced nociceptive behavior and had more β-endorphin protein in the cancer microenvironment than saline-treated female mice with HSC-3 tumors. Chronic rG-CSF treatment (2.5 μg/mouse, every 72 h) increased the HSC-3 recruited Ly6G neutrophils, increased β-endorphin protein content in the tongue and attenuated nociceptive behavior in female mice with HSC-3 tumors. From these data, we conclude that neutrophil-mediated endogenous opioids warrant further investigation as a potential strategy for oral cancer pain treatment.
Learn More >To investigate the required sample size for and feasibility of a full-scale randomized controlled trial examining the impact of the "dose" effect of acupuncture in treating sciatica.
Learn More >Chronic low back pain is very common and often treated with epidural steroid injections (ESIs). As ESI referrals had been rapidly increasing at our Veterans' Administration hospital, we were concerned that they were supplanting more comprehensive care. The objective was to determine how referral patterns and multidisciplinary care might change with the implementation of evidence-based guidelines.
Learn More >Circulating immune cells, which are recruited to the site of injury/disease, secrete various inflammatory mediators that are critical to nociception and pain. The role of tissue-resident immune cells, however, remains poorly characterized. One of the first cells to be activated in peripheral tissues following injury are γδT cells, which serve important roles in infection, disease, and wound healing. Using a mouse line lacking these cells, we sought to identify their contribution to inflammatory pain. Three distinct models of peripheral inflammatory pain were used: intraplantar injection of formalin (spontaneous inflammatory pain), incisional wound (acute inflammatory pain), and intraplantar injection of complete Freund's adjuvant (chronic inflammatory pain). Our results show that absence of γδT cells does not alter baseline sensitivity, nor does it result in changes to mechanical or thermal hypersensitivity after tissue injury. Myeloid cell recruitment did show differential changes between models of acute and chronic inflammatory pain. These results were consistent in both male and female mice, suggesting that there are no sex differences in these outcomes. This comprehensive characterization suggests that γδT cells do not contribute to basal sensitivity or the development and maintenance of inflammatory pain.
Learn More >Many leaders in the field of chronic pain treatment consider interdisciplinary pain management programs to be the most effective treatments available for chronic pain. As programs are instituted and expanded to address demands for nonpharmacological chronic pain interventions, we need to better understand how patients experience program impacts, as well as the challenges and supports patients encounter in trying to maintain and build on intervention gains.
Learn More >Analgesics and sedative hypnotics in clinical use often give rise to significant side effects, particularly respiratory depression. For emergency use, specific antagonists are currently administered to counteract respiratory depression. However, antagonists are often short-lasting and eliminate drug generated analgesia. To resolve this issue, novel positive AMPA modulators, LCX001, was tested to alleviate respiratory depression triggered by different drugs. The acetic acid writhing and hot-plate test were conducted to evaluate analgesic effect of LCX001. Binding assay, whole-cell recording, live cell imaging, and Ca imaging were used to clarify mechanism and impact of LCX001 on respiratory protection. Results showed that LCX001 effectively rescued and prevented opioid (fentanyl and TH-030418), propofol, and pentobarbital-induced respiratory depression by strengthening respiratory frequency and minute ventilation. The acetic acid writhing test and hot-plate test revealed potent anti-nociceptive efficacy of LCX001, in contrast to other typical ampakines that did not affect analgesia. Furthermore, LCX001 potentiated [H]AMPA and L-glutamate binding affinity to AMPA receptors, and facilitated glutamate-evoked inward currents in HEK293 cells stably expressing GluA2(R). LCX001 had a typical positive modulatory impact on AMPAR-mediated function. Importantly, application of LCX001 generated a significant increase in GluA2(R) surface expression, and restrained opioid-induced abnormal intracellular Ca load, which might participate in breathing modulation. Our study improves therapeutic interventions for the treatment of drug induced respiratory depression, and increases understanding of potential mechanism of AMPA receptor modulators.
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