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Influence of self-reported physical activity and sleep quality on conditioned pain modulation in the orofacial region.

To evaluate the influence of self-reported physical activity and sleep quality on conditioned pain modulation (CPM) in the orofacial region.

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Predictors and mediators of outcome in cognitive behavioral therapy for chronic pain: the contributions of psychological flexibility.

There is now a consensus in the literature that future improvements in outcomes obtained from cognitive behavioral therapy (CBT) for chronic pain will require research to identify patient and treatment variables that help explain outcomes. The first aim of this study was to assess whether pre-treatment scores on measures of psychological (in)flexibility, acceptance, committed action, cognitive (de)fusion, and values-based action predict outcomes in a multidisciplinary, multicomponent, group-based CBT program for adults with chronic pain. The second aim was to assess whether change scores on these same measures mediate outcomes in the treatment program. Participants were 232 people attending treatment for chronic pain. Of the psychological flexibility measures, only pre-treatment scores on the psychological inflexibility scale predicted outcomes; higher scores on this measure were associated with worse outcomes. However, change scores on each of the psychological flexibility measures separately mediated outcomes. The efficacy of CBT for chronic pain may be improved with a greater focus on methods that increase psychological flexibility.

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The influence of friendship on migraine in young adolescents: A social network analysis.

The current study explored whether the chances of having migraine are influenced by a youth's friendship with a migraineur.

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Brain-behaviour correlates of habitual motivation in chronic back pain.

Chronic pain may sap the motivation for positive events and stimuli. This may lead to a negative behavioural cycle reducing the establishment of appetitive habitual engagement. One potential mechanism for this might be biased learning. In our experiment, chronic back pain patients and healthy controls completed an appetitive Pavlovian-instrumental transfer procedure. We examined participants` behaviour and brain activity and reported pain, depression and anxiety. Patients showed reduced habitual behaviour and increased responses in the hippocampus than controls. This behavioural bias was related to motivational value and reflected in the updating of brain activity in prefrontal-striatal-limbic circuits. Moreover, this was influenced by pain symptom duration, depression and anxiety (explained variance: up to 50.7%). Together, findings identify brain-behaviour pathways for maladaptive habitual learning and motivation in chronic back pain, which helps explaining why chronic pain can be resistant to change, and where clinical characteristics are significant modulators.

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Acute sleep deprivation enhances susceptibility to the migraine substrate cortical spreading depolarization.

Migraine is a common headache disorder, with cortical spreading depolarization (CSD) considered as the underlying electrophysiological event. CSD is a slowly propagating wave of neuronal and glial depolarization. Sleep disorders are well known risk factors for migraine chronification, and changes in wake-sleep pattern such as sleep deprivation are common migraine triggers. The underlying mechanisms are unknown. As a step towards developing an animal model to study this, we test whether sleep deprivation, a modifiable migraine trigger, enhances CSD susceptibility in rodent models.

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Delta opioid receptor activation modulates affective pain and modality-specific pain hypersensitivity associated with chronic neuropathic pain.

Delta opioid receptor (DOR) agonists alleviate nociceptive behaviors in various chronic pain models, including neuropathic pain, while having minimal effect on sensory thresholds in the absence of injury. The mechanisms underlying nerve injury-induced enhancement of DOR function are unclear. We used a peripheral nerve injury (PNI) model of neuropathic pain to assess changes in the function and localization of DORs in mice and rats. Intrathecal administration of DOR agonists reversed mechanical allodynia and thermal hyperalgesia. The dose-dependent thermal antinociceptive effects of DOR agonists were shifted to the left in PNI rats. Administration of DOR agonists produced a conditioned place preference in PNI, but not in sham, animals, whereas the DOR antagonist naltrindole produced a place aversion in PNI, but not in sham, mice, suggesting the engagement of endogenous DOR activity in suppressing pain associated with the injury. GTPγS autoradiography revealed an increase in DOR function in the dorsal spinal cord, ipsilateral to PNI. Immunogold electron microscopy and in vivo fluorescent agonist assays were used to assess changes in the ultrastructural localization of DORs in the spinal dorsal horn. In shams, DORs were primarily localized within intracellular compartments. PNI significantly increased the cell surface expression of DORs within lamina IV-V dendritic profiles. Using neonatal capsaicin treatment, we identified that DOR agonist-induced thermal antinociception was mediated via receptors expressed on primary afferent sensory neurons but did not alter mechanical thresholds. These data reveal that the regulation of DORs following PNI and suggest the importance of endogenous activation of DORs in regulating chronic pain states.

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Measurement properties of Patient-Reported Outcome Measures used to assess the sleep quality in adults with high prevalence chronic pain conditions: a systematic review.

To provide a comprehensive overview of the measurement properties of patient-reported outcome measures (PROMs) used to assess sleep quality in adult patients with prevalent pain-related conditions.

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The dynamic relationship between pain, depression and cognitive function in a sample of newly diagnosed arthritic adults: a cross-lagged panel model.

Pain and depression are common in the population and co-morbid with each other. Both are predictive of one another and are also associated with cognitive function; people who are in greater pain and more depressed respectively perform less well on tests of cognitive function. It has been argued that pain might cause deterioration in cognitive function, whereas better cognitive function earlier in life might be a protective factor against the emergence of disease. When looking at the dynamic relationship between these in chronic diseases, studying samples that already have advanced disease progression often confounds this relationship.

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Exendin-4 attenuates pain-induced cognitive impairment by alleviating hippocampal neuroinflammation in a rat model of spinal nerve ligation.

Glucagon-like peptide-1 receptor has anti-apoptotic, anti-inflammatory, and neuroprotective effects. It is now recognized that the occurrence and development of chronic pain are strongly associated with anti-inflammatory responses; however, it is not clear whether glucagon-like peptide-1 receptor regulates chronic pain via anti-inflammatory mechanisms. We explored the effects of glucagon-like peptide-1 receptor on nociception, cognition, and neuroinflammation in chronic pain. A rat model of chronic pain was established using left L5 spinal nerve ligation. The glucagon-like peptide-1 receptor agonist exendin-4 was intrathecally injected into rats from 10 to 21 days after spinal nerve ligation. Electrophysiological examinations showed that, after treatment with exendin-4, paw withdrawal frequency of the left limb was significantly reduced, and pain was relieved. In addition, in the Morris water maze test, escape latency increased and the time to reach the platform decreased following exendin-4 treatment. Immunohistochemical staining and western blot assays revealed an increase in the numbers of activated microglia and astrocytes in the dentate gyrus of rat hippocampus, as well as an increase in the expression of tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6. All of these effects could be reversed by exendin-4 treatment. These findings suggest that exendin-4 can alleviate pain-induced neuroinflammatory responses and promote the recovery of cognitive function via the glucagon-like peptide-1 receptor pathway. All experimental procedures and protocols were approved by the Experimental Animal Ethics Committee of Renmin Hospital of Wuhan University of China (approval No. WDRM 20171214) on September 22, 2017.

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Is there a relationship between cannabis use problems, emotion dysregulation, and mental health problems among adults with chronic pain?

Cannabis is often used to manage pain among persons who suffer from chronic pain. Yet, despite much literature suggesting cannabis use problems are associated with mental health problems, little work has examined mechanisms of this relationship among a chronic pain population. Chronic pain is also associated with emotion dysregulation. Individuals with chronic pain who experience cannabis use problems may have less capacity to regulate negative emotions, which could relate to greater anxiety, depression, and suicidal ideation. Thus, the current study explored whether emotion dysregulation explained, in part, the relation between cannabis use problems and anxiety, depression, and suicidal ideation among adults with chronic pain. Participants were 431 opioid-using adults with current moderate to severe chronic pain, 176 were current cannabis users, of which 30.20% reported cannabis use problems. Results indicated a significant indirect relationship between cannabis use problems and anxiety [95% CI (.03, .05)], depression [95% CI (.03, .06)], and suicidal ideation [95% CI (.01, .01)] via emotion dysregulation. Tests of specificity suggested potential for a bi-directional effect for suicidal ideation (.001). Initial findings suggest that emotion dysregulation may be an important mechanism in the relationship between cannabis use problems and mental health among adults with chronic pain.

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