The journal of pain : official journal of the American Pain Society
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Facial expression provides information for an accurate estimation of others' pain. Nevertheless, little is known about psychophysiological responses to pain faces in chronic pain. Event-related potentials and brain oscillations, corrugator activity, and heart rate were recorded in 20 fibromyalgia patients and 20 pain-free controls when viewing pain, anger, happy, and neutral faces. Pain and anger faces elicited greater unpleasantness and arousal than happy and neutral faces, and pain faces evoked greater corrugator response than the rest of faces in all participants. Fibromyalgia patients displayed greater cardiac deceleration to all facial expressions than pain-free controls, and enhanced N100 amplitudes to pain and anger faces in comparison with neutral faces. Pain-free controls were characterized by enhanced N100 amplitudes to happy faces as compared to patients, and by more positive event-related potential amplitudes to happy than to other faces in the time window of 200 to 300 ms. Fibromyalgia patients showed greater theta power in response to pain and anger faces, as well as more reduced alpha power than pain-free controls to all faces. These findings suggest that information processing in fibromyalgia might be characterized by enhanced defensive reactions and increased mobilization of attention resources to pain and anger faces, and by reduced allocation of attention to happy faces. ⋯ Our findings suggest that brain and cardiac activity elicited by viewing facial expressions of pain and anger in others is altered in fibromyalgia patients. This cognitive bias toward negative emotions could be used in clinical settings as a psychobiological marker during the assessment and treatment of fibromyalgia.
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This study investigated observational learning of pain-related fear and subsequent extinction after first-hand exposure to the feared stimulus. Moreover, the specific contingencies that are learned when observing others in pain were explored. A differential fear-conditioning paradigm was used, showing video models displaying either a painful (CS+ color; aversively conditioned stimulus) or a neutral (CS- color; neutrally conditioned stimulus) facial expression in the presence of a colored warm water task (WWT; observation phase). In 1 condition (open WWT cover), the model's hand was immersed in the colored liquid, while in the other condition (closed WWT cover), no contact was displayed between the model and the liquid. During exposure, participants subsequently immersed their own hand into each WWT with equal temperatures. Results revealed successful acquisition of pain-related fear. Participants with higher levels of pain catastrophizing, intolerance of uncertainty, trait fear of pain, or dispositional empathy were more prone to develop pain-related fear. Pain-related fear extinguished quickly after direct exposure to both WWTs. Contingencies between the color of the WWT and either the painful facial expressions or the assumed properties of the colored liquid were learned in both conditions. Clinical implications and limitations of the current study are discussed, providing avenues for future research in observational learning of pain-related fear. ⋯ Pain-related fear promotes the development as well as the continuation of chronic pain. A better understanding of the acquisition and extinction of this fear may help to improve pain treatment programs. Furthermore, we intended to identify individuals who are more prone to develop pain-related fear.
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Hyperbaric oxygen (HBO) therapy is reported to attenuate pain in both clinical pain conditions and animal pain models, but the underlying mechanism remains to be investigated. Here, we show that 7 daily 60-minute HBO (100% oxygen, 2 atmosphere absolute) treatments effectively and persistently inhibited heat hyperalgesia, mechanical allodynia, and paw edema induced by peripheral injection of complete Freund's adjuvant (CFA). Five daily 60-minute HBO treatments also produced a prolonged reversal effect of the ongoing inflammatory pain. Furthermore, such an HBO treatment reduced CFA-induced activation of glial cells, phosphorylation of mitogen-activated protein kinases, and production of a variety of proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-1 beta [IL-1β], and interleukin-6 [IL-6]) and chemokines (monocyte chemoattractant protein-1 [MCP-1], keratinocyte-derived chemokine [KC], and IFN-gamma-inducible protein 10 [IP-10]) in the spinal cord. HBO treatment also decreased lipopolysaccharide-induced mRNA expression of these cytokines and chemokines in primary cultures of astrocytes and microglia. In addition, the mRNA expressions of IL-1β, IL-6, MCP-1, KC, and IP-10 in the inflamed paw skin were decreased by HBO. Taken together, these data suggest that HBO treatment is an effective therapy for inflammatory pain in animals. The inhibition of the neuroinflammation that is mediated by glial cells and inflammatory mediators may, at least in part, contribute to the antinociceptive effect of HBO therapy. ⋯ Our results suggest that repetitive HBO treatment attenuates CFA-induced pain and reduces glial activation and inflammatory mediators' production. These findings provide evidence of the antinociception effect of HBO on inflammatory pain and characterize some of the underlying mechanisms.
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Chronic pain is extremely difficult to manage, in part due to lack of progress in reversing the underlying pathophysiology. Since translation of messenger ribonucleic acids (mRNAs) in the peripheral terminal of the nociceptor plays a role in the transition from acute to chronic pain, we tested the hypothesis that transient inhibition of translation in the peripheral terminal of the nociceptor could reverse hyperalgesic priming, a model of transition from acute to chronic pain. We report that injection of translation inhibitors rapamycin and cordycepin, which inhibit translation by different mechanisms, at the peripheral terminal of the primed nociceptor produces reversal of priming in the rat that outlasted the duration of action of these drugs to prevent the development of priming. These data support the suggestion that interruption of translation in the nociceptor can reverse a preclinical model of at least 1 form of chronic pain. ⋯ This study provides evidence that ongoing protein translation in the sensory neuron terminals is involved in pain chronification, and local treatment that transiently interrupts this translation may be a useful therapy to chronic pain.
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This study investigated putative mechanisms of impaired spinal opioid antinociception such as a downregulation of mu-opioid receptor (MOR) number, coupling, and efficacy in rats with advanced (12 weeks) streptozotocin (STZ)-induced diabetes. Intravenous injection of STZ (45 mg/kg) in Wistar rats led to selective degeneration of insulin-producing pancreatic ß-cells, elevated blood glucose, and mechanical hyperalgesia. In these animals, dose-dependent and naloxone-reversible intrathecal fentanyl antinociception was significantly impaired and associated with a loss in MOR immunoreactivity of calcitonin gene-related peptide-immunoreactive (CGRP-IR) sensory nerve terminals, membrane-bound MOR binding sites, and MOR-stimulated G protein coupling within the dorsal horn of the spinal cord. Intrathecal delivery of nerve growth factor (NGF) in diabetic animals normalized spinal MOR number and G protein coupling and rescued spinal fentanyl-induced antinociception. These findings identify for the first time a loss in functional MOR on central terminals of sensory neurons as a contributing factor for the impaired spinal opioid responsiveness during advanced STZ-induced diabetes that can be reversed by NGF. Moreover, they support growing evidence of a distinct regulation of opioid responsiveness during various painful states of disease (eg, arthritis, cancer, neuropathy) and may give novel therapeutic incentives. ⋯ In diabetic neuropathy a loss in sensory neuron mu-opioid receptor number and coupling contributes to impaired spinal opioid antinociception that can be reversed by NGF. These findings support growing evidence of a distinct regulation of opioid responsiveness during various painful diseases and may give novel therapeutic incentives.