The journal of pain : official journal of the American Pain Society
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We evaluated the responsiveness of the Patient Reported Outcome Information System Pain Interference item bank in patients with musculoskeletal pain by testing predefined hypotheses about the relationship between the change scores on the item bank, change scores on legacy instruments and Global Ratings of Change (GRoC), and we estimated Minimal Important Change (MIC). Patients answered the full Dutch-Flemish V1.1 item bank. From the responses we derived scores for the standard 8-item short form (SF8a) and a CAT-score was simulated. ⋯ Almost all predefined hypotheses were met (94%). The PROMIS-PI item bank correlated well with several legacy instruments which supports generic use of the item bank. MIC for PROMIS-PI was estimated to be 3.2 T-score points.
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Recent research suggests that recovery sleep (RS) has the potential to restore pain sensitivity and modulation after hyperalgesia due to preceding sleep deprivation. However, it has not yet been systematically examined whether the restoration of these pain parameters is driven by sleep characteristics of RS. Thus, the present study assessed changes in experimental pain during RS after total sleep deprivation (TSD) to test whether RS parameters predicted the restoration of the pain system. ⋯ Thus, results indicate moderate effects of sleep manipulations on pain sensitivity, but not on pain modulation. PERSPECTIVE: This article highlights the potential of recovery sleep to let pain thresholds return to normal following their decrease after a night of total sleep deprivation. In contrast, endogenous pain modulation (temporal pain summation, conditioned pain modulation) was not affected by sleep deprivation and recovery sleep.
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Chronic pain is frequently comorbid with depression. However, the mechanisms underlying chronic pain-induced depression remain unclear. Here, we found that DNA methyltransferase 1 (DNMT1) was upregulated in the central amygdala (CeA) of spared nerve injury (SNI)-induced chronic pain-depression rats, and knockdown of DNMT1 could improve the depression-like behaviors in SNI rats. ⋯ These data provide novel insight into understanding the pathogenesis of chronic pain-induced depression and identify a potential therapeutic target. PERSPECTIVE: LncRNA XR_351665 in CeA functions as a ceRNA to block the inhibitory effect of miR-152-3p on DNMT1 and contributes to the development of chronic pain-induced depression. These data suggest that manipulation of XR_351665/miR-152-3p/DNMT1 axis may be a potential method to attenuate chronic pain-induced depression.
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Dysregulation of circular RNAs (circRNAs) has been reported to be functionally associated with chronic pain, but it is unknown whether and how circRNAs participate in visceral hypersensitivity. The expression of circKcnk9 was increased in spinal neurons of irritable bowel syndrome (IBS)-like rats. ShcircKcnk9 attenuated visceral hypersensitivity and inhibited c-Fos expression in IBS-like rats, whereas overexpression of spinal circKcnk9 induced visceral hypersensitivity and increased c-Fos expression in control rats. ⋯ Finally, the signal transducer and activator of transcription 3 (STAT3), validated as a target of miR-124-3p, could play a critical role in visceral hypersensitivity by regulating NSF/GluR2. PERSPECTIVE: Spinal circKcnk9 functions as a miR-124-3p sponge to promote visceral hypersensitivity by regulating the STAT3/NSF/GluR2 pathway. This pathway might provide a novel epigenetic mechanism of visceral hypersensitivity and a potential circRNA therapeutic target for IBS.
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Tension type headache (TTH) is a prevalent but poorly understood pain disease. Current understanding supports the presence of multiple associations underlying its pathogenesis. Our aim was to compare competing multivariate pathway models that explains the complexity of TTH. ⋯ Our data-driven model could be leveraged in clinical trials investigating treatment approaches in TTH. PERSPECTIVE: A theoretical model proposes a relationship where psycho-physical and psychological factors result in clinical manifestations of headache and ultimately affect disability. A data-driven model proposes a more complex relationship where poor sleep, psychological factors, and number of years with pain takes more relevance at influencing disability.