The journal of pain : official journal of the American Pain Society
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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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Randomized Controlled Trial
Spinal manipulative therapy-specific changes in pain sensitivity in individuals with low back pain (NCT01168999).
Spinal manipulative therapy (SMT) is effective for some individuals experiencing low back pain; however, the mechanisms are not established regarding the role of placebo. SMT is associated with changes in pain sensitivity, suggesting related altered central nervous system response or processing of afferent nociceptive input. Placebo is also associated with changes in pain sensitivity, and the efficacy of SMT for changes in pain sensitivity beyond placebo has not been adequately considered. We randomly assigned 110 participants with low back pain to receive SMT, placebo SMT, placebo SMT with the instructional set "The manual therapy technique you will receive has been shown to significantly reduce low back pain in some people," or no intervention. Participants receiving the SMT and placebo SMT received their assigned intervention 6 times over 2 weeks. Pain sensitivity was assessed prior to and immediately following the assigned intervention during the first session. Clinical outcomes were assessed at baseline and following 2 weeks of participation in the study. Immediate attenuation of suprathreshold heat response was greatest following SMT (P = .05, partial η(2) = .07). Group-dependent differences were not observed for changes in pain intensity and disability at 2 weeks. Participant satisfaction was greatest following the enhanced placebo SMT. This study was registered at www.clinicaltrials.gov under the identifier NCT01168999. ⋯ The results of this study indicate attenuation of pain sensitivity is greater in response to SMT than the expectation of receiving an SMT. These findings suggest a potential mechanism of SMT related to lessening of central sensitization and may indicate a preclinical effect beyond the expectations of receiving SMT.
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Randomized Controlled Trial
Latent myofascial trigger points are associated with an increased intramuscular electromyographic activity during synergistic muscle activation.
The aim of this study was to evaluate intramuscular muscle activity from a latent myofascial trigger point (MTP) in a synergistic muscle during isometric muscle contraction. Intramuscular activity was recorded with an intramuscular electromyographic (EMG) needle inserted into a latent MTP or a non-MTP in the upper trapezius at rest and during isometric shoulder abduction at 90° performed at 25% of maximum voluntary contraction in 15 healthy subjects. Surface EMG activities were recorded from the middle deltoid muscle and the upper, middle, and lower parts of the trapezius muscle. Maximal pain intensity and referred pain induced by EMG needle insertion and maximal pain intensity during contraction were recorded on a visual analog scale. The results showed that higher visual analog scale scores were observed following needle insertion and during muscle contraction for latent MTPs than non-MTPs (P < .01). The intramuscular EMG activity in the upper trapezius muscle was significantly higher at rest and during shoulder abduction at latent MTPs compared with non-MTPs (P < .001). This study provides evidence that latent MTPs are associated with increased intramuscular, but not surface, EMG amplitude of synergist activation. The increased amplitude of synergistic muscle activation may result in incoherent muscle activation pattern of synergists inducing spatial development of new MTPs and the progress to active MTPs. ⋯ This article presents evidence of increased intramuscular, but not surface, muscle activity of latent MTPs during synergistic muscle activation. This incoherent muscle activation pattern may overload muscle fibers in synergists during muscle contraction and may contribute to spatial pain propagation.
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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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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.