The journal of pain : official journal of the American Pain Society
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This study investigated the association between anxiety sensitivity and pain catastrophizing in children, caregivers' anxiety sensitivity and catastrophizing about children's pain and responses to children's pain, pain intensity reported by children, and pain intensity estimated by caregivers. The participants were 102 children scheduled for outpatient surgery and their female caregivers. Before the operation, caregivers' catastrophizing about children's pain, children's pain catastrophizing, and their anxiety sensitivity were assessed, as well as caregivers' responses to children's pain. Pain intensity reported by children and estimated by caregivers was evaluated after the operation and 24 hours afterward. Analyses were performed via path analysis. The results indicated that children and caregivers characterized by higher levels of anxiety sensitivity reported higher levels of pain catastrophizing and catastrophic thinking about children's pain, respectively. Caregivers with higher levels of catastrophic thinking about the children's pain reported higher levels of solicitousness and higher estimations of the children's pain intensity after the operation. Higher levels of children's pain catastrophizing were associated with more frequent responses of discouragement and higher pain intensity reported after the operation. These findings highlight the relevance of catastrophizing about children's pain and children's pain catastrophizing in the experience of postoperative pain in children. ⋯ Path analysis was used to test a hypothetical model of the associations between anxiety sensitivity, catastrophizing, parental responses, and postoperative pain in children. The results highlight the association between children's and parents' pain catastrophizing and discouragement and solicitous responses and the role of anxiety sensitivity as a traitlike factor associated with catastrophizing.
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α1-Adrenoceptor expression on nociceptors may play an important role in sympathetic-sensory coupling in certain neuropathic pain syndromes. The aim of this study was to determine whether α1-adrenoceptor expression was upregulated on surviving peptidergic, nonpeptidergic, and myelinated nerve fiber populations in the skin after chronic constriction injury of the sciatic nerve in rats. Seven days after surgery, α1-adrenoceptor expression was upregulated in the epidermis and on dermal nerve fibers in plantar skin ipsilateral to the injury but not around blood vessels. This α1-adrenoceptor upregulation in the plantar skin was observed on all nerve fiber populations examined. However, α1-adrenoceptor expression was unaltered in the dorsal hind paw skin after the injury. The increased expression of α1-adrenoceptors on cutaneous nociceptors in plantar skin after chronic constriction injury suggests that this may be a site of sensory-sympathetic coupling that increases sensitivity to adrenergic agonists after nerve injury. In addition, activation of upregulated α1-adrenoceptors in the epidermis might cause release of factors that stimulate nociceptive signaling. ⋯ Our findings indicate that peripheral nerve injury provokes upregulation of α1-adrenoceptors on surviving nociceptive afferents and epidermal cells in the skin. This might contribute to sympathetically maintained pain in conditions such as complex regional pain syndrome, painful diabetic neuropathy, and postherpetic neuralgia.
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Estrogen reportedly facilitates visceral nociception at the spinal or supraspinal level. The present study was aimed to investigate whether estrogen modulates visceral pain through the vagal pathway. Ovariectomized rats received estradiol, which was administered subcutaneously (to act through both the vagal and spinal pathways) or intraduodenally (to preferentially act through the vagal pathway). Luminally applied estradiol induced a rapid and significant decrease in the visceromotor response to colorectal distension, with increased c-Fos expression in nodose ganglion neurons. Systemically injected estradiol increased visceromotor response and c-Fos expression in both nodose and dorsal root ganglion (T6-12) neurons. The antinociceptive effect of estrogen was abolished by surgical vagotomy or chemical denervation of vagal afferents. Both luminally and systemically administered estradiol elicited selective 5-hydroxytryptamine secretion from the duodenum. Granisetron, a 5-hydroxytryptamine 3 receptor antagonist, reversed the antinociceptive effect of estrogen. Intestinal mucosal mast cell stabilizers prevented estradiol-induced antinociception and 5-hydroxytryptamine secretion. Ultrastructural analysis revealed that estradiol caused piecemeal degranulation of intestinal mucosal mast cells. The actions of estradiol were inhibited by an estrogen receptor β antagonist and mimicked by an estrogen receptor β agonist. These results suggest that estrogen can trigger vagus-mediated antinociception, which is masked by its spinally mediated pronociception. ⋯ This study is the first to show a vagus-mediated estrogenic antinociception, in which the nongenomic estrogen receptor β-mediated, intestinal mucosal mast cell-derived 5-hydroxytryptamine/5-hydroxytryptamine 3 receptor pathway is involved. This work may provide new insights into the sex hormone modulation of visceral sensitivity related to irritable bowel syndrome and indicate potential therapeutic targets to manage this disease.
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Complex regional pain syndrome (CRPS) is a chronic condition that involves significant hyperalgesia of the affected limb, typically accompanied by localized autonomic abnormalities and frequently by motor dysfunction. Although central brain systems are thought to play a role in the development and maintenance of CRPS, these systems have not been well characterized. In this study, we used structural magnetic resonance imaging to characterize differences in gray matter volume between patients with right upper extremity CRPS and matched controls. Analyses were carried out using a whole brain voxel-based morphometry approach. The CRPS group showed decreased gray matter volume in several pain-affect regions, including the dorsal insula, left orbitofrontal cortex, and several aspects of the cingulate cortex. Greater gray matter volume in CRPS patients was seen in the bilateral dorsal putamen and right hypothalamus. Correlation analyses with self-reported pain were then performed on the CRPS group. Pain duration was associated with decreased gray matter in the left dorsolateral prefrontal cortex. Pain intensity was positively correlated with volume in the left posterior hippocampus and left amygdala, and negatively correlated with the bilateral dorsolateral prefrontal cortex. Our findings demonstrate that CRPS is associated with abnormal brain system morphology, particularly pain-related sensory, affect, motor, and autonomic systems. ⋯ This paper presents structural changes in the brains of patients with CRPS, helping us differentiate CRPS from other chronic pain syndromes and furthering our understanding of this challenging disease.
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Decreased voluntary wheel running has recently been proposed as a preclinical pain measure for inflammatory pain, but whether this reflects pain evoked by use of the affected limbs is unknown. To assess the role of inflammation site as a determinant of this measure, complete Freund's adjuvant (CFA), formalin, or equivolume vehicle was subcutaneously injected into the plantar surface of the hind paws (bilateral) or L1 dorsum dermatome (leaving paws unaffected) of male Sprague Dawley rats. CFA-induced hind paw mechanical allodynia (P < .001) did not correlate with reduced voluntary wheel running. Intraplantar formalin did not attenuate voluntary running, despite eliciting robust licking/writhing/flinching behavior and hind paw mechanical allodynia (P < .001). Subcutaneous L1 dorsum dermatome formalin, but not CFA, induced licking/writhing/flinching behavior (P < .001), but neither induced hind paw mechanical allodynia or attenuated voluntary running. That voluntary running is decreased by hind paw CFA, but not by L1 dorsum CFA, implies that the behavior is a measure of CFA-induced pain evoked by use of the affected limbs rather than supraspinal pain processing that is independent of inflammation site. Furthermore, the results suggest that interpretation of voluntary wheel running data cannot simply be explained by correlation with mechanical allodynia. ⋯ Whether decreased voluntary running is dependent on inflammation site is unknown. We show that intraplantar, but not L1 dorsum, CFA suppressed voluntary running and formalin-induced licking/writhing/flinching behavior but had no effect on voluntary running. These data suggest that suppressed voluntary running by CFA likely reflects pain evoked by use of the affected limbs.