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Attitudes Toward a Pre-authorized Concealed Opioid Taper: A Qualitative Analysis of Patient and Clinician Perspectives.

Standard opioid tapers tend to be associated with increased patient anxiety and higher pain ratings. Pre-authorized concealed opioid reductions may minimize expectations such as fear of increased pain due to the reduction of opioids and, prolong analgesic benefits in experimental settings. We recently observed that patients and clinicians are open to concealed opioid tapering. However, little is known about the "why" behind their attitudes. Based on this lack of data, we analyzed qualitative responses to survey questions on patients' and clinicians' acceptance of a concealed opioid reduction for chronic pain. Seventy-four patients with a history of high dose opioid therapy and 49 clinicians completed a web-based questionnaire with open-ended questions examining responses to two hypothetical clinical trials comparing a concealed opioid reduction pre-authorized by patients vs. standard tapering. We used content analysis based on qualitative descriptive methodology to analyze comments from the patients and clinicians. Five themes were identified: informed consent; anxiety; safety; support; and ignorance is bliss, or not. These themes highlight the overall positive attitudes toward concealed opioid tapers. Our findings reinforce the importance of patient-centered care and are expected to inform the design of clinical trials from both the patient and clinician perspective. This qualitative study presents patients' and clinicians' attitudes toward hypothetical scenarios for a trial of pre-authorized reduction of opioids. The findings indicate positive attitudes and the relevance of engaging patients with effective decision-making processes.

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The Effects of Patient Education on Psychological Status and Clinical Outcomes in Rheumatoid Arthritis: A Systematic Review and Meta-Analysis.

Rheumatoid arthritis (RA) is a common systemic inflammatory autoimmune disease. The disease has a serious impact on mental health and requires more effective non-pharmacological interventions.

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Cutting-Edge Technologies for Inflamed Joints on Chip: How Close Are We?

Osteoarthritis (OA) is a painful and disabling musculoskeletal disorder, with a large impact on the global population, resulting in several limitations on daily activities. In OA, inflammation is frequent and mainly controlled through inflammatory cytokines released by immune cells. These outbalanced inflammatory cytokines cause cartilage extracellular matrix (ECM) degradation and possible growth of neuronal fibers into subchondral bone triggering pain. Even though pain is the major symptom of musculoskeletal diseases, there are still no effective treatments to counteract it and the mechanisms behind these pathologies are not fully understood. Thus, there is an urgent need to establish reliable models for assessing the molecular mechanisms and consequently new therapeutic targets. Models have been established to support this research field by providing reliable tools to replicate the joint tissue . Studies firstly started with simple 2D culture setups, followed by 3D culture focusing mainly on cell-cell interactions to mimic healthy and inflamed cartilage. Cellular approaches were improved by scaffold-based strategies to enhance cell-matrix interactions as well as contribute to developing mechanically more stable models. The progression of the cartilage tissue engineering would then profit from the integration of 3D bioprinting technologies as these provide 3D constructs with versatile structural arrangements of the 3D constructs. The upgrade of the available tools with dynamic conditions was then achieved using bioreactors and fluid systems. Finally, the organ-on-a-chip encloses all the state of the art on cartilage tissue engineering by incorporation of different microenvironments, cells and stimuli and pave the way to potentially simulate crucial biological, chemical, and mechanical features of arthritic joint. In this review, we describe the several available tools ranging from simple cartilage pellets to complex organ-on-a-chip platforms, including 3D tissue-engineered constructs and bioprinting tools. Moreover, we provide a fruitful discussion on the possible upgrades to enhance the systems making them more robust regarding the physiological and pathological modeling of the joint tissue/OA.

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Pain and the Triple Network Model.

Acute pain is a physiological response that causes an unpleasant sensory and emotional experience in the presence of actual or potential tissue injury. Anatomically and symptomatically, chronic pathological pain can be divided into three distinct but interconnected pathways, a lateral "painfulness" pathway, a medial "suffering" pathway and a descending pain inhibitory circuit. Pain (fullness) can exist without suffering and suffering can exist without pain (fullness). The triple network model is offering a generic unifying framework that may be used to understand a variety of neuropsychiatric illnesses. It claims that brain disorders are caused by aberrant interactions within and between three cardinal brain networks: the self-representational default mode network, the behavioral relevance encoding salience network and the goal oriented central executive network. A painful stimulus usually leads to a negative cognitive, emotional, and autonomic response, phenomenologically expressed as pain related suffering, processed by the medial pathway. This anatomically overlaps with the salience network, which encodes behavioral relevance of the painful stimuli and the central sympathetic control network. When pain lasts longer than the healing time and becomes chronic, the pain- associated somatosensory cortex activity may become functionally connected to the self-representational default mode network, i.e., it becomes an intrinsic part of the self-percept. This is most likely an evolutionary adaptation to save energy, by separating pain from sympathetic energy-consuming action. By interacting with the frontoparietal central executive network, this can eventually lead to functional impairment. In conclusion, the three well-known pain pathways can be combined into the triple network model explaining the whole range of pain related co-morbidities. This paves the path for the creation of new customized and personalized treatment methods.

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A Bibliometric Analysis of Research on Ketamine From 2001 to 2020.

Ketamine is an intravenous anesthetic with analgesic effects that has a rapid onset and short duration of action. Many studies have been conducted on the use of ketamine; however, the quantity and quality of such studies have not been reported. Therefore, we aimed to conduct a bibliometric analysis of research on ketamine from 2001 to 2020.

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Neurological symptoms and disorders following electrical injury: A register-based matched cohort study.

Electric shocks may have neurological consequences for the victims. Although the literature on the neurological consequences of electric shocks is limited by retrospective designs, case studies and studies of selected patient groups, previous research provides some evidence of a link between electric shocks, and diseases and symptoms of the central nervous system (CNS)(e.g. epilepsy, migraine and vertigo) and the peripheral nervous system (PNS)(e.g. loss of sensation, neuropathy and muscle weakness). This study aims to employ a register-based, matched cohort study, to investigate whether individuals demonstrate a greater risk of neurological diseases and symptoms of the CNS or PNS in the years following an electrical injury.

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Painful Truth: The Need to Re-Center Chronic Pain on the Functional Role of Pain.

Pain is undesirable, whether it is a symptom of mild or severe illness or instead indicates disorder in the nervous system's ability to perceive and process sensory information. Nonetheless, pain is part of the body's ability to defend itself and promote its own survival-this is its fundamental evolutionary function. This normal expression of pain is not limited to what is considered useful because it alerts us to the initiation of illness. It also applies to pain that continues when illness or noxious stimuli persist. However, the parameters of what is here termed functional pain are not fully understood and are seldom explicitly the focus of research. This paper posits that failure to appreciate the functional role of pain in research has had significant unintended consequences and may be contributing to inconsistent research findings. To that end, the paper describes the misclassification issue at the core of chronic pain research-whether a given pain reflects functional or pathological processes-and discusses research areas where reconsidering the functional role of pain may lead to advancements.

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fNIRS brain measures of ongoing nociception during surgical incisions under anesthesia.

: Functional near-infrared spectroscopy (fNIRS) has evaluated pain in awake and anesthetized states. : We evaluated fNIRS signals under general anesthesia in patients undergoing knee surgery for anterior cruciate ligament repair. : Patients were split into groups: those with regional nerve block (NB) and those without (non-NB). Continuous fNIRS measures came from three regions: the primary somatosensory cortex (S1), known to be involved in evaluation of nociception, the lateral prefrontal cortex (BA9), and the polar frontal cortex (BA10), both involved in higher cortical functions (such as cognition and emotion). : Our results show three significant differences in fNIRS signals to incision procedures between groups: (1) NB compared with non-NB was associated with a greater net positive hemodynamic response to pain procedures in S1; (2) dynamic correlation between the prefrontal cortex (PreFC) and S1 within 1 min of painful procedures are anticorrelated in NB while positively correlated in non-NB; and (3) hemodynamic measures of activation were similar at two separate time points during surgery (i.e., first and last incisions) in PreFC and S1 but showed significant differences in their overlap. Comparing pain levels immediately after surgery and during discharge from postoperative care revealed no significant differences in the pain levels between NB and non-NB. : Our data suggest multiple pain events that occur during surgery using devised algorithms could potentially give a measure of "pain load." This may allow for evaluation of central sensitization (i.e., a heightened state of the nervous system where noxious and non-noxious stimuli is perceived as painful) to postoperative pain levels and the resulting analgesic consumption. This evaluation could potentially predict postsurgical chronic neuropathic pain.

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Safety of Interlaminar Cervical Epidural Injections: Experience With 12,168 Procedures in a Single Pain Clinic.

Cervical epidural steroid injections have long been utilized to treat intraspinal inflammation causing cervicalgia and/or cervical radiculopathy, and much has been written about safety and efficacy. There are published opinions, without evidence basis, that these injections should not be performed above C7-T1 for fear of dural puncture, spinal cord injury, and other complications that might occur more frequently at higher spinal levels. However, many experienced interventional pain physicians believe that epidural injections targeted to the level of spinal inflammation may be more effective. Although medication injected at the lowest cervical level C7-T1 may ascend to higher spinal levels, it often does not since inflammation and swelling at the cervical level of pathology may increase epidural pressure causing the injectate to move caudally down the path of least resistance.

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Placebo and hypnosis in the clinical setting: Contextual factors in hypnotic analgesia.

The assumption that hypnotic analgesia produces placebo effects is controversial. The cognitive dimension that can distinguish hypnosis from placebo analgesia has been suggested as hypnotic susceptibility. The aim of this study is to investigate the role of the relationship between patient and therapist, assumed to produce the placebo effect, in the clinical context of hypnotic treatment for pain. Seventy subjects were given hypnosis administered by the therapist in person (Group A) and 37 practiced self-hypnosis (Group B) for 8 weeks. The Somatosensory Amplification Scale (SSAS), Stanford hypnotic susceptibility scale type A, Cold pressor test (CPT) and SCL-90 were administered at baseline, and Italian Pain Questionnaire (IPQ) dimensions were used as outcome measures. The SSAS did appear to reflect the efficacy of hypnotic analgesia in all pain variables explored, but only in Group B. An improvement in pain intensity and all IPQ dimensions were found at 8 weeks. In particular, an improvement in the affective dimension of pain, with a medium-high effect size (η2 = .774), was recorded after hypnotic analgesia, with the outcome being better in Group A than in Group B ( = .001). This outcome was independent of hypnotic susceptibility in both groups. Considering our hypothesis that, given the administration of the same suggestions, the therapist could promote the placebo response, contributing to the improvement in the affective dimension of pain outcome, which exhibited a response to the hypnotic treatment independently of hypnotic susceptibility.

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