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To use clustering analysis of patient symptoms to discover common patient subtypes in females and males with interstitial cystitis/bladder pain syndrome (IC/BPS) or chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).
Learn More >The host evolves redundant mechanisms to preserve physiological processing and homeostasis. These functions range from sensing internal and external threats, creating a memory of the insult and generating reflexes which aim to resolve inflammation. Impairment in such functioning leads to chronic inflammatory diseases. By interacting through a common language of ligands and receptors, the immune and sensory nervous systems work in concert to accomplish such protective functions. While this bidirectional communication helps to protect from danger, it can contribute to disease pathophysiology. Thus, the somatosensory nervous system is anatomically positioned within primary and secondary lymphoid tissues and mucosa to modulate immunity directly. Upstream of this interplay, neurons detect danger which prompts the release of neuropeptides initiating i) defensive reflexes (ranging from withdrawal response to coughing); and ii) chemotaxis, adhesion and local infiltration of immune cells. The resulting outcome of such neuro-immune interplay is still ill-defined, but consensual findings start to emerge and support neuropeptides as blockers of T 1-mediated immunity but also as drivers of T 2 immune responses. However, the modalities detected by nociceptors revealed broader than mechanical pressure and temperature sensing and include signals as various as cytokines and pathogens to immunoglobulins and even microRNAs. Along these lines, we aggregated various dorsal root ganglion sensory neurons expression profiling datasets supporting such wide-ranging sensing capabilities and to help identify novel danger detection modalities of these cells. Thus, revealing unexpected aspects of nociceptor neurons biology might prompt the identification of novel drivers of immunity, means to resolve inflammation and strategies to safeguard homeostasis. This article is protected by copyright. All rights reserved.
Learn More >Supportive touch has remarkable benefits in childbirth and during painful medical procedures. But does social touch influence pain neurophysiology, ie, the brain processes linked to nociception and primary pain experience? What other brain processes beyond primary pain systems mediate their analgesic effects? In this study, women (N = 30) experienced thermal pain while holding their romantic partner's hand or an inert device. Social touch reduced pain and attenuated functional magnetic resonance imaging activity in the Neurologic Pain Signature (NPS)-a multivariate brain pattern sensitive and specific to somatic pain-and increased connectivity between the NPS and both somatosensory and "default mode" regions. Brain correlates of touch-induced analgesia included reduced pain-related activation in (1) regions targeted by primary nociceptive afferents (eg, posterior insula, and anterior cingulate cortex); and (b) regions associated with affective value (orbitofrontal cortex), meaning (ventromedial prefrontal cortex [PFC]), and attentional regulation (dorsolateral PFC). Activation reductions during handholding (vs holding a rubber device) significantly mediated reductions in pain intensity and unpleasantness; greater pain reductions during handholding correlated with greater increases in emotional comfort, which correlated with higher perceived relationship quality and (a trend toward) greater perceived closeness with the romantic partner. The strongest mediators of analgesia were activity reductions in a brain circuit traditionally associated with stress and defensive behavior in mammals, including ventromedial and dorsomedial PFC, rostral anterior cingulate cortex, amygdala/hippocampus, hypothalamus, and periaqueductal gray matter. Social touch affects core brain processes that contribute to pain and pain-related affective distress in females, and should be considered alongside other treatments in medical and caregiving contexts.
Learn More >Recent studies have indicated that inflammatory pathways and hypothalamic-pituitary-adrenal (HPA) axis function may be responsible for the interaction between pain and depression.
Learn More >Previous research has shown that self-compassion is associated with improved functioning and health outcomes among multiple chronic illnesses. However, the role of self-compassion in chronic pain-related functioning is understudied. The present study sought to understand the association between self-compassion and important measures of functioning within a sample of patients with chronic pain. Treatment-seeking individuals (N= 343 with chronic pain) that were mostly White (97.9%) and female (71%) completed a battery of assessments that included the Self-Compassion Scale (SCS), as well as measures of pain-related fear, depression, disability, pain acceptance, success in valued activity, and use of pain coping strategies. Cross-sectional multiple regression analyses that controlled for age, sex, pain intensity, and pain duration, revealed that self-compassion accounted for a significant and unique amount of variance in all measures of functioning (r range: .07 – .32, all p < .001). Beta weights indicated that higher self-compassion was associated with lower pain-related fear, depression, and disability, as well as greater pain acceptance, success in valued activities, and utilization of pain coping strategies. These findings suggest that self-compassion may be a relevant adaptive process in those with chronic pain. Targeted interventions to improve self-compassion in those with chronic pain may be useful. SIGNIFICANCE: Self-compassion is associated with better functioning across multiple general and pain-specific outcomes, with the strongest associations among measures related to psychological functioning and valued living. These findings indicate that self-compassion may be an adaptive process that could minimize the negative impact of chronic pain on important areas of life. This article is protected by copyright. All rights reserved.
Learn More >Self-regulatory (SR) ability is an important resource for managing pain, but chronic pain patients experience chronic self-regulatory fatigue even when they are not in pain. Pressure pain thresholds (PPT) and pain inhibition are two mechanisms that differentiate people with and without chronic pain. It was hypothesized that trait SR ability would be associated with higher PPT and better pain inhibition and that PPT and pain inhibition would be lower following high versus low SR fatigue. Three studies tested these hypotheses. Study 1 had 240 pain-free undergraduates complete measures of trait SR ability and PPT; 122 also provided data on pain inhibition. Study 2 had 38 of Study 1's participants return for two additional sessions in which they underwent PPT testing under conditions of high or low SR fatigue (within-person, counterbalanced). Study 3 repeated these procedures with pain inhibition as the outcome (n = 39). Results revealed that individual differences in SR ability were not associated with PPT or pain inhibition (all ps > 0.05). Within people, neither PPT (F(1, 36) = 1.57, p = 0.22) nor pain inhibition (F(1, 37) = 1.79, p = 0.19) were significantly different under conditions of low versus high SR fatigue. Results do not support the hypotheses that PPT or pain inhibition associate with individual differences in trait SR ability or transient changes in state SR fatigue in the absence of pain. Instead, the SR deficits in chronic pain patients may arise from the experience of chronic pain.
Learn More >To systematically review the available literature on the diagnostic accuracy of questionnaires and measurement instruments for headaches associated with musculoskeletal symptoms.
Learn More >Chronic pain remains a major public health issue that affects the lives of many worldwide, including patients with chronic pain. Comorbidities like depression have been associated with decreased quality of sleep, decreased enjoyment of life activities, increased anxiety, and decreased efficacy in treatments among patients with chronic pain. Despite these associations, the trends and demographic characteristics of patients with chronic pain with depression is yet to be investigated.
Learn More >To characterize unmet treatment needs in a sample of Migraine in America Symptoms and Treatment (MAST) Study participants using oral, acute prescription migraine medications.
Learn More >Dysfunction of inhibitory circuits in the rostral anterior cingulate cortex underlies the affective (aversive), but not the sensory-discriminative features (hypersensitivity) of the pain experience. To restore inhibitory controls, we transplanted inhibitory interneuron progenitor cells into the rostral anterior cingulate cortex in a chemotherapy-induced neuropathic pain model. The transplants integrated, exerted a GABA-A mediated inhibition of host pyramidal cells and blocked gabapentin preference (i.e. relieved ongoing pain) in a conditioned place preference paradigm. Surprisingly, pain aversiveness persisted when the transplants populated both the rostral and posterior anterior cingulate cortex. We conclude that selective and long lasting inhibition of the rostral anterior cingulate cortex, in the mouse, has a profound pain relieving effect against nerve injury-induced neuropathic pain. However, the interplay between the rostral and posterior anterior cingulate cortices must be considered when examining circuits that influence ongoing pain and pain aversiveness.
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