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A Comparative Meta-Analysis of Unidisciplinary Psychology and Interdisciplinary Treatment Outcomes Following Acceptance and Commitment Therapy for Adults with Chronic Pain.

While much of the literature provides positive support for psychological interventions for chronic pain, two recent meta-analyses indicate small to moderate benefits only. This inconsistency in findings suggests that there are other treatment-related variables to consider. One possible consideration pertains to treatment format, as psychological models form the basis for both unidisciplinary psychology and integrated interdisciplinary treatments for chronic pain. Therefore, a comparative meta-analysis of unidisciplinary and interdisciplinary treatments was performed to determine whether there were differences in treatment effect size (ES) at post-treatment and follow-ups of up to one year. One specific treatment model, Acceptance and Commitment Therapy (ACT), was investigated as it was felt that this literature was extensive enough to perform the planned analysis, while also being circumscribed enough in size to make it feasible. In total, 29 articles met inclusion criteria, 13 reported outcomes for unidisciplinary ACT and 15 for interdisciplinary ACT. At both post-treatment and follow-up, interdisciplinary ACT had a greater ES for physical disability, psychosocial impact and depression compared to unidisciplinary ACT. No differences in ES were observed for pain intensity, pain-related anxiety, or pain acceptance. Findings remained the same when study heterogeneity was considered. There was a significant difference observed between treatment format and treatment duration – on average, unidisciplinary interventions were of shorter duration than interdisciplinary interventions. Moderation analyses examining the relation between total treatment duration and ES generally indicated a moderate positive relation between treatment length and ES. This relation was strong for psychosocial impact. Perspective: A comparative meta-analysis examined the relative ES of unidisciplinary (i.e., clinical psychology only) and interdisciplinary ACT for chronic pain in 29 studies. The ES for interdisciplinary ACT was larger than unidisciplinary ACT for physical disability, psychosocial impact, and depression. No differences were present for pain intensity, anxiety, and acceptance.

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My body is not working right: a cognitive behavioral model of body image and chronic pain.

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Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis.

Recent studies revealed the existence of unique functional links between mast cells and nociceptors in the skin. Here, we propose that mast cells and nociceptors form a single regulatory unit in both physiology and disease. In this model, MrgprB2/X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters that regulate pain, inflammation, and itch.

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Ephrin-B2 signaling in the spinal cord as a player in post-inflammatory and stress-induced visceral hypersensitivity.

Ephrin-B2/EphB receptor signaling contributes to persistent pain states such as postinflammatory and neuropathic pain. Visceral hypersensitivity (VHS) is a major mechanism underlying abdominal pain in patients with irritable bowel syndrome (IBS) and inflammatory bowel diseases (IBD) in remission, but the underlying pathophysiology remains unclear. Here, we evaluated the spinal ephrin-B2/EphB pathway in VHS in 2 murine models of VHS, that is, postinflammatory TNBS colitis and maternal separation (MS).

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Identification of a sacral, visceral sensory transcriptome in embryonic and adult mice.

Visceral sensory neurons encode distinct sensations from healthy organs and initiate pain states that are resistant to common analgesics. Transcriptome analysis is transforming our understanding of sensory neuron subtypes but has generally focused on somatic sensory neurons or the total population of neurons in which visceral neurons form the minority. Our aim was to define transcripts specifically expressed by sacral visceral sensory neurons, as a step towards understanding the unique biology of these neurons and potentially leading to identification of new analgesic targets for pelvic visceral pain. Our strategy was to identify genes differentially expressed between sacral dorsal root ganglia (DRG) that include somatic neurons and sacral visceral neurons, and adjacent lumbar DRG that comprise exclusively of somatic sensory neurons. This was performed in adult and E18.5 male and female mice. By developing a method to restrict analyses to nociceptive Trpv1 neurons, a larger group of genes were detected as differentially expressed between spinal levels. We identified many novel genes that had not previously been associated with pelvic visceral sensation or nociception. Limited sex differences were detected across the transcriptome of sensory ganglia, but more were revealed in sacral levels and especially in Trpv1 nociceptive neurons. These data will facilitate development of new tools to modify mature and developing sensory neurons and nociceptive pathways. In this study of mouse dorsal root ganglia, we have identified numerous features of sensory neurons that vary between lumbar and sacral spinal levels and that are potentially involved in unique physiology and pathophysiology of visceral sensation and pain. We further identify maturational components of this sacral visceral transcriptome by comparing data from embryonic and adult mice. There are limited sex differences across the transcriptome of embryonic or adult sensory ganglia, but in adults these can be revealed in sacral levels and especially in Trpv1 nociceptive neurons. These data sets will encourage identification of new tools to modify mature or developing sensory neurons and adult nociceptive pathways.

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Let it be: Mindful-acceptance down-regulates pain and negative emotion.

Mindfulness training ameliorates clinical and self-report measures of depression and chronic pain, but its use as an emotion regulation strategy – in individuals who do not meditate – remains understudied. As such, whether it (a) down-regulates early affective brain processes and (b) depends on cognitive control systems remains unclear. We exposed meditation-naïve participants to two kinds of stimuli: negative vs. neutral images and painful vs. warm temperatures. On alternating blocks, we asked participants to either react naturally or exercise mindful-acceptance. Emotion regulation using mindful-acceptance was associated with reductions in reported pain and negative affect, reduced amygdala responses to negative images, and reduced heat-evoked responses in medial and lateral pain systems. Critically, mindful-acceptance significantly reduced activity in a distributed, a-priori neurologic signature that is sensitive and specific to experimentally-induced pain. In addition, these changes occurred in the absence of detectable increases in prefrontal control systems. The findings support the idea that momentary mindful-acceptance regulates emotional intensity by changing initial appraisals of the affective significance of stimuli, which has consequences for clinical treatment of pain and emotion.

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Epithelial-Neuronal Communication in the Colon: Implications for Visceral Pain.

Visceral hypersensitivity and pain result, at least in part, from increased excitability of primary afferents that innervate the colon. In addition to intrinsic changes in these neurons, emerging evidence indicates that changes in lining epithelial cells may also contribute to increased excitability. Here we review recent studies on how colon epithelial cells communicate directly with colon afferents. Specifically, anatomical studies revealed specialized synaptic connections between epithelial cells and nerve fibers and studies using optogenetic activation of the epithelium showed initiation of pain-like responses. We review the possible mechanisms of epithelial-neuronal communication and provide an overview of the possible neurotransmitters and receptors involved. Understanding the biology of this interface and how it changes in pathological conditions may provide new treatments for visceral pain conditions.

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Brain networks and endogenous pain inhibition are modulated by age and sex in healthy rats.

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. Here, we used a capsaicin-induced DNIC test and resting state functional MRI to investigate the impact of aging and sex on endogenous pain inhibition and associated brain circuitries in healthy rats. We found that DNIC was less efficient in young females compared to young males. DNIC response was lost in old rats of both sexes, but the brain networks engaged during DNIC differed in a sex-dependent manner. Young males had the most efficient analgesia with the strongest connectivity between anterior cingulate cortex (ACC) and periaqueductal gray (PAG). The reduced efficiency of DNIC in young females appeared to be driven by a 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, while 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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Diabetic neuropathy: what does the future hold?

Frustratingly, disease-modifying treatments for diabetic neuropathy remain elusive. Glycaemic control has a robust effect on preventing neuropathy in individuals with type 1 but not in those with type 2 diabetes, which constitute the vast majority of patients. Encouragingly, recent evidence points to new metabolic risk factors and mechanisms, and thus also at novel disease-modifying strategies, which are desperately needed. Obesity has emerged as the second most important metabolic risk factor for neuropathy (diabetes being the first) from consensus findings of seven observational studies in populations across the world. Moreover, dyslipidaemia and altered sphingolipid metabolism are emergent novel mechanisms of nerve injury that may lead to new targeted therapies. Clinical history and examination remain critical components of an accurate diagnosis of neuropathy. However, skin biopsies and corneal confocal microscopy are promising newer tests that have been used as outcome measures in research studies but have not yet demonstrated clear clinical utility. Given the emergence of obesity as a neuropathy risk factor, exercise and weight loss are potential interventions to treat and/or prevent neuropathy, although evidence supporting exercise currently outweighs data supporting weight loss. Furthermore, a consensus has emerged advocating tricyclic antidepressants, serotonin-noradrenaline (norepinephrine) reuptake inhibitors and gabapentinoids for treating neuropathic pain. Out-of-pocket costs should be considered when prescribing these medications since their efficacy and tolerability are similar. Finally, the downsides of opioid treatment for chronic, non-cancer pain are becoming increasingly evident. Despite these data, current clinical practice frequently initiates and continues opioid prescriptions for patients with neuropathic pain before prescribing guideline-recommended treatments.

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Attenuation of fear-conditioned analgesia in rats by monoacylglycerol lipase inhibition in the anterior cingulate cortex: potential role for CB receptors.

Improved understanding of brain mechanisms regulating endogenous analgesia is important from a fundamental physiological perspective and for identification of novel therapeutic strategies for pain. The endocannabinoid system plays a key role in stress-induced analgesia, including fear-conditioned analgesia (FCA), a potent form of endogenous analgesia. Here we studied the role of the endocannabinoid 2-arachidonoyl glycerol (2-AG) within the anterior cingulate cortex (ACC; a brain region implicated in the affective component of pain) in FCA in rats.

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