The journal of pain : official journal of the American Pain Society
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Persistent pain following breast cancer surgery is a significant clinical problem. Although immune mechanisms may play a role in the development and maintenance of persistent pain, few studies have evaluated for associations between persistent breast pain following breast cancer surgery and variations in cytokine genes. In this study, associations between previously identified extreme persistent breast pain phenotypes (ie, no pain vs severe pain) and single nucleotide polymorphisms (SNPs) spanning 15 cytokine genes were evaluated. In unadjusted analyses, the frequency of 13 SNPs and 3 haplotypes in 7 genes differed significantly between the no pain and severe pain classes. After adjustment for preoperative breast pain and the severity of average postoperative pain, 1 SNP (ie, interleukin [IL] 1 receptor 2 rs11674595) and 1 haplotype (ie, IL10 haplotype A8) were associated with pain group membership. These findings suggest a role for cytokine gene polymorphisms in the development of persistent breast pain following breast cancer surgery. ⋯ This study evaluated for associations between cytokine gene variations and the severity of persistent breast pain in women following breast cancer surgery. Variations in 2 cytokine genes were associated with severe breast pain. The results suggest that cytokines play a role in the development of persistent postsurgical pain.
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Postherpetic neuralgia (PHN) is one of the most severe sequelae of herpes zoster events. Several risk factors have been reported for PHN, including old age, severe skin rash, and intense pain. This study therefore aims to evaluate the usefulness of the Self-completed Leeds Assessment of Neuropathic Symptoms and Signs pain scale (S-LANSS) in conjunction with previously reported risk factors for predicting PHN. A group of herpes zoster patients (N = 305) were included in the cohort study. Subjects were asked for their demographic information, clinical symptoms and signs, intensity of pain by visual analog scale (VAS), and S-LANSS. They were followed up in clinical visits or via telephone for 12 months. Nineteen patients (6.2%) suffered from PHN in this study. Using logistic regression, 3 risk factors for PHN were identified: age ≥70 years, high VAS scores, and high S-LANSS scores. Prediction of PHN using VAS (≥8) and S-LANSS (≥15) criteria achieved a sensitivity of 78.9% and specificity of 78.0%. Prediction of PHN in elderly patients (≥70 years), using the criteria of VAS (≥6) and S-LANSS (≥15) as well, achieved 100% sensitivity and 57.1% specificity. S-LANSS could be a useful prediction tool for PHN, particularly if combined with previously well-known risk factors and VAS. ⋯ Among acute herpes zoster patients, subjects with characteristics of neuropathic pain showed high frequency of PHN. The tools for screening neuropathic pain like S-LANSS could be helpful for predicting PHN and enabling early intervention of pain management.
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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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Neurobiological evidence points to altered central nervous system processing of nociceptive stimuli in fibromyalgia. Enzymes like catechol-O-methyl-transferase (COMT) are involved in the elimination of catecholamines playing a possible role in central sensitization and pain. We used quantitative sensory testing to evidence central sensitization in fibromyalgia patients and test whether COMTVal158Met polymorphism, associated with a reduction in enzyme activity, plays a role in sensitized patients. Pain evaluation and quantitative sensory testing were performed including the spinal nociceptive flexion reflex, a physiologic correlate for the evaluation of central nociceptive pathways. Quality of life and distress questionnaires were used. A total of 137 fibromyalgia patients were assessed and compared to 99 matched controls. Central sensitization (nociceptive flexion reflex <27 mA) was present in 95/134 (71%) patients. Among them, COMT p.Val158Met polymorphism displayed a significant linear "genotype effect" (P = .033), with the Met/Met (mean = 17.8 ± 4.8 mA) and Val/Val (mean = 21.4 ± 4.6 mA) subgroups at the opposite ends of the nociceptive flexion reflex threshold (Met/Met vs Val/Val P = .015) and the Val/Met subgroup (mean = 19 ± 4.9 mA) in between (Val/Met vs Val/Val P = .041). Spontaneous moderate to severe pain was more likely to be associated with COMT Met/Met genotype. Patients showed important emotional distress compared to controls. In sensitized patients, the COMT Met/Met subgroup showed systematically-though not significantly-worse scores for all psychological variables. ⋯ The association between COMT p.Val158Met polymorphism and central sensitization in fibromyalgia is essential as it refers to the severity of central sensitization and may be a risk factor for treatment outcome.
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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.