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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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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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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Review Meta Analysis
Structural brain anomalies and chronic pain: a quantitative meta-analysis of gray matter volume.
The diversity of chronic pain syndromes and the methods employed to study them make integrating experimental findings challenging. This study performed coordinate-based meta-analyses using voxel-based morphometry imaging results to examine gray matter volume (GMV) differences between chronic pain patients and healthy controls. There were 12 clusters where GMV was decreased in patients compared with controls, including many regions thought to be part of the "pain matrix" of regions involved in pain perception, but also including many other regions that are not commonly regarded as pain-processing areas. The right hippocampus and parahippocampal gyrus were the only regions noted to have increased GMV in patients. Functional characterizations were implemented using the BrainMap database to determine which behavioral domains were significantly represented in these regions. The most common behavioral domains associated with these regions were cognitive, affective, and perceptual domains. Because many of these regions are not classically connected with pain and because there was such significance in functionality outside of perception, it is proposed that many of these regions are related to the constellation of comorbidities of chronic pain, such as fatigue and cognitive and emotional impairments. Further research into the mechanisms of GMV changes could provide a perspective on these findings. ⋯ Quantitative meta-analyses revealed structural differences between brains of individuals with chronic pain and healthy controls. These differences may be related to comorbidities of chronic pain.
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Patients and physicians report that discussions about pain are frequently frustrating and unproductive. However, the relationship between discussions about pain and patient-physician communication is poorly understood. We analyzed 133 video-recorded visits and patient self-report data collected at a clinic providing primary care to a low-income, black patient population. We used "thin slice" methods to rate two or three 30-second video segments from each visit on variables related to patient and physician affect (ie, displayed emotion) and patient-physician rapport. Discussions about pain were associated with a .32 increase in patient unease (P < .001) and a .21 increase in patient positive engagement (P = .004; standardized coefficients) compared to discussions about other topics during the same visit. Discussions about pain were not significantly associated with patient-physician rapport, physician unease, or physician positive engagement. Patient pain severity was significantly associated with greater physician and patient unease (P = .01), but not with other variables. Findings suggest that primary care patients, but not their physicians, display significantly greater emotional intensity during discussions about pain compared to discussions about other topics. ⋯ This study used direct observation of video-recorded primary care visits to show that discussions about pain are associated with heightened displays of both positive and negative patient emotions. These displays of emotion could potentially influence pain-related outcomes.