Pain
-
The purpose of this study was to examine the dyadic and individual level effects of parent and child pain catastrophizing on child health-related quality of life (HRQOL) in pediatric sickle cell disease. Questionnaires assessing child pain frequency, child and parent pain catastrophizing, and child HRQOL were completed by youth and their primary caregiver. A Common Fate Model was estimated to test the dyadic level relationship between parent and child pain catastrophizing and child HRQOL. ⋯ Individual level effects were net of same-rater bias, which was significant for both parents and children. Both the unique and the overlapping aspects of parent and child pain catastrophizing are significant contributors to associations with child HRQOL, such that higher levels of pain catastrophizing are associated with worse child HRQOL. Findings suggest the need for multipronged intervention targeting factors common to parent-child dyads and factors unique to parents and children, respectively.
-
To elucidate the physiological, cellular, and molecular mechanisms responsible for initiating and sustaining ocular neuropathic pain, we created a blue-light-exposure model in C57BL/6 mice. Mice were exposed to 12 h of blue or white light followed by 12 h of darkness. Before blue light exposure, baseline tear secretion, stability, and ocular hyperalgesia were assessed by measuring hyper- or hypo-osmotic solution-induced eye wiping, wind-induced eye closing, and cold-induced eye blinking. ⋯ TRPV1 and substance P expression was increased, whereas CGRP expression deceased at the mRNA level in isolated corneal projecting neurons. Hence, our blue-light exposure B6 mouse model for assessing tearing and ocular hyperalgesia is useful for studying ocular pain and its underlying mechanisms. Blue-light-induced alterations in tearing and ocular hyperalgesia may be related to the elevated expression of TRPV1, SP, and/or the suppressed expression of CGRP at the ocular surface.
-
Meta Analysis
Stress biomarkers in individuals with fibromyalgia syndrome: a systematic review with meta-analysis.
Evidence suggests an involvement of hypothalamic-pituitary-adrenal (HPA) axis dysregulation in the development and maintenance of fibromyalgia syndrome (FMS). However, studies on the stress response via the HPA-axis in individuals with FMS show conflicting results. To better understand the relationship between FMS and HPA-axis dysregulation, we (1) systematically summarized the current level of evidence on HPA biomarkers in individuals with FMS compared with individuals without and (2) evaluated whether FMS is associated with a specific pattern of HPA dysregulation. ⋯ However, heterogeneity of data was high with significant evidence for publication bias. Overall, the data are compatible with association of FMS with adrenocortical hypofunction in the presence of increased sympathetic tone. However, the data are partially contradictory, so it must be assumed that the data are highly dependent on the respective study designs, patient samples, and analytical methods and do not necessarily demonstrate an abnormal HPA-axis function in FMS.