Pain
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To develop a machine learning model to investigate the discriminative power of whole-brain gray-matter (GM) images derived from primary dysmenorrhea (PDM) women and healthy controls (HCs) during the pain-free phase and further evaluate the predictive ability of contributing features in predicting the variance in menstrual pain intensity. Sixty patients with PDM and 54 matched female HCs were recruited from the local university. All participants underwent the head and pelvic magnetic resonance imaging scans to calculate GM volume and myometrium-apparent diffusion coefficient (ADC) during their periovulatory phase. ⋯ In the regression analysis, demographical indicators and myometrium ADC accounted for a total of 29.37% of the variance in pain intensity. After regressing out these factors, GM features explained 60.33% of the remaining variance. Our results suggested that GM volume can be used to discriminate patients with PDM and HCs during the pain-free phase, and neuroimaging features can further predict the variance in the intensity of menstrual pain, which may provide a potential imaging marker for the assessment of menstrual pain intervention.
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Facial expressions of pain are not undefined grimaces, but they convey specific information about the internal state of the individual in pain. With this systematic review, we aim to answer the question of which facial movements are displayed most consistently during pain. We searched for studies that used the Facial Action Coding System to analyze facial activity during pain in adults, and that report on distinct facial responses (action units [AUs]). ⋯ This subset was found independently of the cognitive status of the individuals and was stable across clinical and experimental pain with only one variation, namely that eye closure (AU43) occurred more frequently during clinical pain. This subset of pain-related facial responses seems to encode the essential information about pain available in the face. However, given that these pain-related AUs are most often not displayed all at once, but are differently combined, health care professionals should use a more individualized approach, determining which pain-related facial responses an individual combines and aggregates to express pain, instead of erroneously searching for a uniform expression of pain.
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A large body of evidence indicates that nitric oxide (NO)/cGMP signaling essentially contributes to the processing of chronic pain. In general, NO-induced cGMP formation is catalyzed by 2 isoforms of guanylyl cyclase, NO-sensitive guanylyl cyclase 1 (NO-GC1) and 2 (NO-GC2). However, the specific functions of the 2 isoforms in pain processing remain elusive. ⋯ By contrast, mice lacking NO-GC2 exhibited increased hypersensitivity in models of inflammatory pain, but their neuropathic pain behavior was unaltered. Cre-mediated deletion of NO-GC1 or NO-GC2 in spinal dorsal horn neurons recapitulated the behavioral phenotypes observed in the global knockout. Together, these results indicate that cGMP produced by NO-GC1 or NO-GC2 in spinal dorsal horn neurons exert distinct, and partly opposing, functions in chronic pain processing.
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Obesity has been found to increase the risk of musculoskeletal pain (MSP) in other settings, but to our knowledge, the influence of increased body mass index on pain outcomes after common trauma exposures such as motor vehicle collision (MVC) has not been assessed. In addition, obesity results in biomechanical changes, as well as physiologic changes including reduced hypothalamic pituitary adrenal axis negative feedback inhibition, but mechanisms by which obesity may result in worse post-traumatic outcomes remain poorly understood. ⋯ After adjusting for an array of sociodemographic factors, obesity (particularly morbid obesity) was an independent risk factor for worse MSP after MVC (eg, RR 1.41 [95% CI 1.11, 1.80] for moderate or severe MSP 6 months after MVC among morbidly obese vs normal weight MVC survivors). Interestingly, substantial effect modification was observed between obesity risk and a genetic variant known to reduce hypothalamic pituitary adrenal axis negative feedback inhibition (FKBP5 rs9380526). (eg, 41% vs 16% increased risk of moderate or severe MSP at 6 months among obese individuals with and without the risk allele.) Further studies are needed to elucidate mechanisms underlying chronic pain development in obese trauma survivors and to develop interventions that will reduce chronic pain severity among this common, at-risk group.
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Integration of nociceptive information is essential to produce adapted responses, to promote body integrity and survival. However, how the brain integrates nociceptive inputs from different body areas remains unknown. The aim of this study was to examine the cortical integration of bilateral nociceptive inputs evoked by laser heat stimuli. ⋯ By contrast, pain was not significantly different in any condition (P > 0.05). These findings show that although more nociceptive inputs reach the brain with multiple nociceptive stimuli, their sensory representation is decreased while pain perception remains unchanged. These interactions between cerebral processing of nociceptive information from different body regions could support coordinated behavioral responses when pain origins from multiple sources.