Pain
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Many patients experience pain after surgery. Psychological factors such as emotion and cognition are shown to be associated with the development of acute and chronic postsurgical pain (CPSP). Therefore, the question arises whether targeting these psychological factors can reduce negative postsurgical outcomes. ⋯ In addition, interventions delivered after surgery and interventions delivered by a psychologist tended to be more effective than interventions delivered before surgery and interventions delivered by another healthcare provider. Furthermore, the current review points to the need for more research to determine which specific type of intervention may be most beneficial for surgical patients. Finally, the current review identified that research in this domain has concerns regarding bias in missing outcome data due to withdrawal and drop out.
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The aim of this review or meta-analysis is to synthesize the prevalence of post-coronavirus disease (COVID) pain symptoms of musculoskeletal origin in hospitalized or nonhospitalized patients recovered from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. MEDLINE, CINAHL, PubMed, EMBASE, and Web of Science databases, as well as medRxiv and bioRxiv preprint servers were searched up to May 1, 2021. Studies or preprints reporting data on post-COVID pain symptoms such as myalgias, arthralgias, or chest pain after SARS-CoV-2 infection and collected by personal, telephonic, or electronical interview were included. ⋯ The overall prevalence of post-COVID myalgia, joint pain, and chest pain ranged from 5.65% to 18.15%, 4.6% to 12.1%, and 7.8% to 23.6%, respectively, at different follow-up periods during the first year postinfection. Time trend analysis showed a decrease prevalence of musculoskeletal post-COVID pain from the symptom's onset to 30 days after, an increase 60 days after, but with a second decrease ≥180 days after. This meta-analysis has shown that almost 10% of individuals infected by SARS-CoV-2 will suffer from musculoskeletal post-COVID pain symptomatology at some time during the first year after the infection.
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Nav1.7 is a promising drug target for the treatment of pain. However, there is a mismatch between the analgesia produced by Nav1.7 loss-of-function and the peripherally restricted Nav1.7 inhibitors, which may reflect a lack of understanding of the function of Nav1.7 in the transmission of nociceptive information. In the periphery, the role of Nav1.7 in transduction at nociceptive peripheral terminals has been comprehensively examined, but its role in axonal propagation in these neurons is less clearly defined. ⋯ Next, we applied PF-05198007 (300 nM-1 µM) to the sciatic nerve between stimulating and recording sites to selectively block axonal Nav1.7 channels. One hundred to three hundred nanomolar PF-05198007 blocked propagation in 63% of C-fiber sensory neurons, whereas similar concentrations produced minimal block (5%) in rapidly conducting A-fiber neurons. We conclude that Nav1.7 is essential for axonal propagation in around two-thirds of nociceptive cutaneous C-fiber neurons and a lower proportion (≤45%) of nociceptive neurons innervating muscle.
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Meta Analysis
Nerve pathology and neuropathic pain after whiplash injury: a systematic review and meta-analysis.
There is no clear understanding of the mechanisms causing persistent pain in patients with whiplash-associated disorder (WAD). The aim of this systematic review was to assess the evidence for nerve pathology and neuropathic pain in patients with WAD. EMBASE, PubMed, CINAHL (EBSCO), and MEDLINE were searched from inception to September 1, 2020. ⋯ Similar sensory dysfunction and nerve mechanosensitivity was seen in WAD grade II, which contradicts its traditional definition of absent nerve involvement. Our findings strongly suggest a subset of patients with WAD demonstrate signs of peripheral nerve pathology and neuropathic pain. Although there was heterogeneity among some studies, typical WAD classifications may need to be reconsidered and include detailed clinical assessments for nerve integrity.
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We conducted a complier average causal effect (CACE) analyses for 2 pragmatic randomised controlled trials. We aimed to assess the effectiveness of telephone-based lifestyle weight loss interventions compared with usual care among compliers. Participants from 2 trials with low back pain (n = 160) and knee osteoarthritis (n = 120) with a body mass index ≥27 kg/m2 were included. ⋯ Complier average causal effect estimates showed potentially clinically meaningful effects, but with low certainty because of wide confidence intervals, for pain intensity (-1.4; 95% confidence interval, -3.1, 0.4) and small but also uncertain effects for disability (-2.1; 95% confidence interval, -8.6, 4.5) among compliers in the low back pain trial intervention compared with control but not in the knee osteoarthritis trial. Our findings showed that compliers of a telephone-based weight loss intervention in the low back pain trial generally had improved outcomes; however, there were inconsistent effects in compliers from the knee osteoarthritis trial. Complier average causal effect estimates were larger than intention-to-treat results but must be considered with caution.