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Persistent pain extending beyond 6 months after breast cancer surgery when adjuvant therapies have ended is a recognised phenomenon. The evolution of postsurgery pain is therefore of interest for future patient management in terms of possible prognoses for distinct groups of patients to enable better patient information.
The presence of calcitonin gene-related peptide and its receptors in multiple brain areas and peripheral tissues previously implicated in migraine initiation and its many associated symptoms raises the possibility that humanized monoclonal anti-calcitonin gene-related peptide antibodies (CGRP-mAbs) can prevent migraine by modulating neuronal behavior inside and outside the brain. Critical to our ability to conduct a fair discussion over the mechanisms of action of CGRP-mAbs in migraine prevention is data generation that determines which of the many possible peripheral and central sites are accessible to these antibodies – a question raised frequently due to their large size.
Mirror image sensory dysfunction (MISD) after breast surgery has not yet been studied. This prospective observational study aimed to determine the incidence of MISD, persistent postoperative pain (PPP) and mirror image pain (MIP) during 6 months after total unilateral mastectomy.Visual analogue scale (VAS), Neuropathic Pain Symptom Inventory (NPSI), Pain Catastrophizing Scale (PCS), Hospital Anxiety and Depression Scale (HADS), Life orientation test (LOT) and Quantitative Sensory Testing (QST) (in ipsi and contralateral breast, axilla and thigh) were recorded. VAS > 3 at 1, 3, and 6 postoperative months was considered PPP. Contralateral changes of QST at any time was considered indicative of MISD and spontaneous contralateral VAS ≥ 1 as MIP.Sixty-four patients were included. PPP at 1, 3 and 6 months was 18.8%, 56.2%, and 21.3%, respectively Ten patients presented MIP. MISD was detected in 79.7% patients in contralateral breast and 62.5% in contralateral axilla. Furthermore, changes in QST were present in 39.1% of patients in thigh. Electronic Von Frey (EVF) changes in both contralateral breast and axilla, and in thigh significantly diminished at all postoperative times. Changes of postoperative EVF ≥ 20% in contralateral breast were associated to higher VAS values. NPSI scores were significantly higher at all postoperative times. At 1 month, PCS, depression HADS subscale and LOT scores were significantly worse than all the other periods.MISD incidence was almost 80%, and 15.6% of patients showed spontaneous contralateral VAS ≥ 1. At 6 months 21.3% of patients manifested PPP. The worst alteration of factors related to PPP occurred at 1 postoperative month. Most consistent QST was EVF.
Although migraine is the second most disabling condition worldwide, there is poor awareness of it.
The aim of this study was to better understand the role that physical, cognitive and social factors play in pain interference with activities of daily living among individuals with cancer and chronic pain.
Studies point to an increased hereditary risk of cluster headache. HCRTR2 gene rs2653349 and ADH4 gene rs1800759 polymorphisms have been associated with cluster headache susceptibility. Also, GNB3 rs5443 polymorphism, associated with increased signal transduction via GPCRs, seems to influence triptan treatment response. DNA from 114 cluster headache patients and 570 non-related controls, representing a general Southeastern European Caucasian (SEC) population, was extracted from buccal swabs and genotyped using real-time PCR. Gene distribution for the rs2653349 was GG = 79.8%, GA = 18.4%, and AA = 1.8% for patients and GG = 79.1%, GA = 19.1%, and AA = 1.8% for controls. The frequency of the mutated A allele was 11.0% for patients and 11.3% for controls. The frequencies for rs5443 were CC = 44.7%, CT = 44.7%, and TT = 10.5% for patients and CC = 43.9%, CT = 42.6%, and TT = 13.5% for controls. The frequency of the mutated T allele was 32.9% for patients and 34.8% for controls. A 2.7-fold more frequent appearance of the mutated T allele was observed in patients with better triptan treatment response, although not statistically significant. For rs1800759, the frequencies were CC = 36.0%, CA = 43.0%, and AA = 21.0% for patients and CC = 34.0%, CA = 50.2%, and AA = 15.8% for controls. The frequency of the mutated A allele was 42.5% and 40.9% for patients and controls, respectively. The mutated T allele of GNB3 rs5443 polymorphism was more prevalent in patients with better triptan treatment response, indicating a possible trend of association between this polymorphism and triptan treatment response in SEC population. According to our observation, no association of HCRTR2 rs2653349 and ADH4 rs1800759 polymorphisms and cluster headache in SEC population could be documented.
Opioids have been increasingly prescribed for chronic non-cancer pain (CNCP). An association between long-term opioid treatment (L-TOT) of CNCP patients and suppression of both the innate and the adaptive immune system has been proposed. This systematic review aims at investigating the effects of L-TOT on the immune system in CNCP patients.
Observational studies have implicated migraine as a risk factor for coronary artery disease (CAD) and atrial fibrillation (AF), however it is unclear whether migraine is causal in this relationship. We investigated potential causality between genetically instrumented liability to migraine and cardiovascular disease outcomes using two-sample Mendelian randomization.
To examine the effect of a case manager-assisted rehabilitation programme as an add-on to usual physical rehabilitation in patients undergoing lumbar spinal fusion.
Local microvascular dysfunction and consequent tissue ischemia/hypoxia contribute to the symptoms of complex regional pain syndrome (CRPS) and peripheral neuropathic pain. As nitric oxide (NO) is a key regulator of microvascular blood flow, compounds that increase it are potentially therapeutic for these pain conditions. This led us to hypothesize that the topical administration of drugs that modulate local tissue NO levels can alleviate the pain of CRPS and peripheral neuropathic pain. We investigated the anti-allodynic effect of a combination of two NO-modulating drugs: meldonium and N-acetylcysteine (NAC). An equimolar topical formulation of the two drugs was tested on chronic post-ischemic pain (CPIP), a rat model of CRPS, chronic constriction injury (CCI) of the sciatic nerve and chemotherapy-induced painful neuropathy (CIPN), rat models of peripheral neuropathic pain. Topical meldonium-NAC produced significant anti-allodynia in CPIP, CCI and CIPN rats. Moreover, repeated application of topical meldonium-NAC produced an increase in the duration of anti-allodynia in the CPIP and CCI rats. While pre-treatment with an NO synthase inhibitor attenuated the anti-allodynic effects of meldonium-NAC, 30-min hyperbaric oxygen treatment combined with a non-effective dose of meldonium-NAC produced significant anti-allodynic effects in CPIP rats. Both experiments implicated NO in the drug combination's anti-allodynic effects. To ascertain the role played by changes in local tissue NO, we performed a quantification of plantar muscle NO in CPIP rats after hind paw topical treatment with meldonium-NAC and revealed significantly increased plantar muscle NO levels in drug-treated rats. The drug combination also reversed the reduction in tissue oxygenation normally observed in CPIP hind paws. In addition to introducing a novel topical treatment for mechanical allodynia in CRPS and peripheral neuropathic pain, this work showcases the analgesic potential of locally targeting microvascular dysfunction and tissue ischemia/hypoxia in these conditions, with emphasis on the role of NO.