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Previous studies reported the presence of widespread pressure pain sensitivity in patients with tension-type headache. However, most of the studies assessed pressure pain sensitivity over muscle tissue. Our aim was to investigate the difference in pressure pain sensitivity over musculoskeletal and nerve symptomatic and distant areas between women with frequent episodic tension-type headache (FETTH) and healthy subjects.
Learn More >Low back pain (LBP) is highly prevalent in the general population and is responsible for increased health-care costs, pain, impairment of activity, and if chronic, is associated with a range of comorbidities.
Learn More >Chronic pain disorders have been associated separately with neuropsychiatric conditions such as depression and alcohol abuse. However, in individuals who suffer from non-cancer chronic pain disorders, it is not clear if the burden of depressive disorders is similar for those with and without a history of alcohol abuse. Using data from the Collaborative Psychiatric Epidemiology Surveys (CPES), we found depressive disorders to have a high burden in men and women with a history of alcohol abuse, independently of the presence or absence of chronic pain. We also found that, although the incidence of persistent depressive disorder was comparable in men and women with a history of alcohol abuse, and significantly higher than in control men and women, the incidence of a major depressive episode was higher in women with a history of alcohol abuse independently of the presence or absence of chronic pain. The age of onset of depressive disorders, independently of pain status, was younger for individuals with a history of alcohol abuse. The findings of this study have important implications for the clinical management of individuals who suffer from chronic pain comorbidly with depression and/or alcohol abuse.
Learn More >Establish the impact of pain severity on the cost-effectiveness of generic duloxetine for knee osteoarthritis (OA) in the United States.
Learn More >Emotional and cognitive impairments are common comorbidities of chronic neuropathic pain that significantly impact the quality of life of patients. While the nociceptive components of the peripheral nerve chronic constriction injury (CCI) animal model have been extensively analyzed, data related to the development of mood and cognitive disorders, and especially its impact on female rats remains fragmented. We systematically reviewed the literature analyzing the methods used to induce and evaluate the development of emotional- and cognitive-like impairments and sex-specific differences in the CCI model.
Learn More >Despite classic analgesic or effective treatments in rheumatic diseases, such as synthetic DMARDs in RA, patients remain in pain and often turn to non-prescribed pharmacological alternatives, such as cannabis self-therapeutic use. However, this medical use of cannabis has not been thoroughly studied.
Learn More >Sex differences in the quality and prevalence of chronic pain are manifold, with females generally presenting higher incidence and severity. Uncovering chronic pain-related sex differences informs neural mechanisms and may lead to novel treatment routes. In a multi-center morphological study (total n=374), we investigated whether the shape of subcortical regions would reflect sex differences in back pain. Given the hormone-dependent functions of the hippocampus, and its role in the transition to chronic pain, this region constituted our primary candidate. We found that the anterior part of the left hippocampus (alHP) presented outer deformation in females with chronic back pain (CBP), identified in CBP in the USA (n=77 females vs. n=78 males) and validated in a Chinese dataset (n=29 females vs. n=58 males with CBP, in contrast to n=53 female and n=43 male healthy controls). Next, we examined this region in subacute back pain (SBP) who persisted with back pain a year later (SBPp; n=18 females vs. n=18 males), and in a subgroup with persistent back pain for 3-years. Weeks after onset of back pain there was no deformation within alHP, but at 1-year and 3-years females exhibited a trend for outer deformation. The alHP partly overlapped with the subiculum and entorhinal cortex, whose functional connectivity, in healthy subjects, was associated with emotional and episodic memory related terms (Neurosynth, reverse inference). These findings suggest that in females alHP undergoes anatomical changes with pain persistence, highlighting sexually-dimorphic involvement of emotional and episodic memory-related circuitry with chronic pain.
Learn More >Experimental data have suggested that in neuropathic pain, tricyclic antidepressants may work solely through a β2-agonist action. The aim of this study was to test if the β2-agonist terbutaline relieves painful polyneuropathy. The study was a randomized, double-blind, placebo- and active-controlled, 3-way, cross-over trial among patients with painful polyneuropathy. The treatment periods were of 5 weeks' duration and were preceded by 1 week for washout and 1 week for baseline observations. The patients received terbutaline (5 to 15 mg), imipramine (30 to 150 mg), or placebo in random order. Drug doses depended on age and metabolizer status. Change in total pain recorded from ratings in diaries (NRS 0-10) was the primary outcome and change in rating of specific pain symptoms (NRS 0-10), patient global impression of change and sleep disturbance were secondary outcomes. Forty-seven patients were randomized. Median score for total pain changed from NRS 6.4 to 6.1 from baseline to week 5 on terbutaline with an average effect during the treatment period as compared to placebo of 0.13 (95% CI -0.12;0.38, p = 0.32). Median score for total pain on imipramine changed from NRS 6.6 to 4.8 with an average effect as compared to placebo of -1.17 (95% CI -1.42; -0.92, p < 0.001). Secondary outcomes were also unaltered by terbutaline but improved by imipramine. The β2-agonist terbutaline has no effect in painful polyneuropathy. β2 -agonism seems not to be an important mechanism of action of TCAs in neuropathic pain.
Learn More >Cranial hypersensitivity is a prominent symptom of migraine, exhibited as migraine headache exacerbated with physical activity, and cutaneous facial allodynia and hyperalgesia. The underlying mechanism is believed to be, in part, activation and sensitization of dural-responsive trigeminocervical neurons. Validated preclinical models that exhibit this phenotype have great utility for understanding putative mechanisms, and as a tool to screen therapeutics. We have previously shown that nitroglycerin triggers cranial allodynia in association with migraine-like headache, and this translates to neuronal cranial hypersensitivity in rats. Further, responses in both humans and rats are aborted by triptan administration, similar to responses in spontaneous migraine. Here, our objective was to study the nitroglycerin model examining the effects on therapeutic targets with newly approved treatments, specifically gepants and ditans, for the acute treatment of migraine. Using electrophysiological methods, we determined changes to ongoing firing and somatosensory-evoked cranial sensitivity, in response to nitroglycerin, followed by treatment with a CGRP receptor antagonist, gepant (olcegepant), a 5-HT1F receptor agonist, ditan (LY344864) and an NK1 receptor antagonist (GR205171). Nitroglycerin induced activation of migraine-like central trigeminocervical neurons, and intracranial and extracranial neuronal hypersensitivity. These responses were aborted by olcegepant and LY344864. However, GR205171, which failed in clinical trial for both abortive and preventive treatment of migraine, had no effect. These data support the nitroglycerin model as a valid approach to study cranial hypersensitivity and putative mechanisms involved in migraine, and as a screen to dissect potentially efficacious migraine therapeutic targets.
Learn More >The spinal dorsal horn is a major site for the induction and maintenance of mechanical allodynia, but the circuitry that underlies this clinically important form of pain remains unclear. The studies presented here provide strong evidence that the neural circuits conveying mechanical allodynia in the dorsal horn differ by the nature of the injury. Calretinin (CR) neurons in lamina II inner convey mechanical allodynia induced by inflammatory injuries, while protein kinase C gamma (PKCγ) neurons at the lamina II/III border convey mechanical allodynia induced by neuropathic injuries. Cholecystokinin (CCK) neurons located deeper within the dorsal horn (laminae III-IV) are important for both types of injuries. Interestingly, the Maf subset of CCK neurons is composed of transient vesicular glutamate transporter 3 (tVGLUT3) neurons, which convey primarily dynamic allodynia. Identification of an etiology-based circuitry for mechanical allodynia in the dorsal horn has important implications for the mechanistic and clinical understanding of this condition.
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