Pain
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Patient education has a critical role in the management of pain. There is considerable heterogeneity in patient education for females with persistent pelvic pain (PPP), and it remains unclear what is considered best clinical practice. Therefore, this systematic review identified and summarised recommendations for patient education in the management of benign gynaecological and urological conditions associated with PPP, as endorsed by international guidelines. ⋯ Recommendations for education content were variable, however most frequently covered treatment strategies and pelvic pain diagnoses. For education delivery, the most frequent recommendations were for support groups and written/printed materials. Further research into tailored education interventions is needed for females with PPP.
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Pain neuroscience education (PNE) has shown promising results in the management of patients with chronic spinal pain (CSP). However, no previous review has determined the optimal dose of PNE added to an exercise programme to achieve clinically relevant improvements. The aim was to determine the dose-response association between PNE added to an exercise programme and improvements in pain intensity and disability in patients with CSP. ⋯ In addition, a dose of 200 and 150 minutes of PNE added to an exercise programme was estimated to exceed the minimum clinically important difference described in the literature for pain intensity (-2.61 points, 95% CI = -3.12 to -2.10) and disability (-6.84 points, 95% CI = -7.98 to -5.70), respectively. The pooled effect of the isolated exercise was small. These findings may be useful in optimising the most appropriate PNE dose to achieve clinically relevant improvements in patients with CSP.
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It is not known why some patients develop persistent pain after nerve trauma while others do not. Among multiple risk factors for the development of persistent posttrauma and postsurgical pain, a neuropathic mechanism due to iatrogenic nerve lesion has been proposed as the major cause of these conditions. Because there is some evidence that the human leukocyte antigen (HLA) system plays a role in persistent postsurgical pain, this study aimed to identify the genetic risk factors, specifically among HLA loci, associated with chronic neuropathic pain after traumatic nerve injuries and surgery in the upper extremities. ⋯ We found that the HLA haplotype A*02:01-B*15:01-C*03:04-DRB1*04:01-DQB1*03:02 was associated with an increased risk of developing persistent neuropathic pain in the upper extremity (OR = 9.31 [95% CI 1.28-406.45], P < 0.05). No significant associations were found on an allele level when correcting for multiple testing. Further studies are needed to investigate whether this association is on a haplotypic level or if certain alleles may be causing the association.
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Neuropathic corneal pain (NCP) is a new and ill-defined disease characterized by pain, discomfort, aching, burning sensation, irritation, dryness, and grittiness. However, the mechanism underlying NCP remain unclear. Here, we reported a novel rat model of primary NCP induced by long ciliary nerve (LCN) ligation. ⋯ At a molecular level, upregulated mRNA levels of ion channels Piezo2, TRPM8, and TRPV1, as well as inflammatory factors TNF-α, IL-1β, and IL-6, were also detected in the TG after LCN ligation. Meanwhile, consecutive oral gabapentin attenuated LCN ligation-induced corneal hyperalgesia and increased levels of ion channels and inflammation factors in TG. This study provides a reliable primary NCP model induced by LCN ligation in rats using a simple, minimally invasive surgery technique, which may help shed light on the underlying cellular and molecular bases of NCP and aid in developing a new treatment for the disease.
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Abnormal encoding of somatosensory modalities (ie, mechanical, cold, and heat) are a critical part of pathological pain states. Detailed phenotyping of patients' responses to these modalities have raised hopes that analgesic treatments could one day be tailored to a patient's phenotype. Such precise treatment would require a profound understanding of the underlying mechanisms of specific pain phenotypes at molecular, cellular, and circuitry levels. ⋯ We then tested what range of stimuli produce dynamic stimulus-response relationships for different outcome measures in naive mice. We finally used this assay to show that nerve injury produces modality-specific sex differences in pain behavior. Our improved assay opens new avenues to study the basis of modality-specific abnormalities in pain behavior.