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Pain and distress are common in children undergoing medical procedures, exposing them to acute and chronic biopsychosocial impairments if inadequately treated. Clinical hypnosis has emerged as a potentially beneficial treatment for children's procedural pain and distress due to evidence of effectiveness and potential superiority to other psychological interventions. However, systematic reviews of clinical hypnosis for children's procedural pain and distress have been predominantly conducted in children undergoing oncology and needle procedures and are lacking in broader paediatric contexts. This scoping review maps the evidence of clinical hypnosis for children's procedural pain and distress across broad paediatric contexts while highlighting knowledge gaps and areas requiring further investigation.

Small-fiber neuropathy (SFN) is a disorder that exclusively affects the small nerve fibers, sparing the large nerve fibers. Thinly myelinated Aδ-fibers and unmyelinated C-fibers are damaged, leading to development of neuropathic pain, thermal dysfunction, sensory symptoms, and autonomic disturbances. Although many SFNs are secondary and due to immunological causes or metabolic disturbances, the etiology is unknown in up to half of the patients. Over the years, this proportion of "idiopathic SFN" has decreased, as familial and genetic causes have been discovered, thus shifting a proportion of once "idiopathic" cases to the genetic category. After the discovery of SCN9A-gene variants in 2012, SCN10A and SCN11A variants have been found to be pathogenic in SFN. With improved accessibility of SFN diagnostic tools and genetic tests, many non-SCN variants and genetically inherited systemic diseases involving the small nerve fibers have also been described, but only scattered throughout the literature. There are 80 SCN variants described as causing SFN, 8 genes causing hereditary sensory autonomic neuropathies (HSAN) described with pure SFN, and at least 7 genes involved in genetically inherited systemic diseases associated with SFN. This systematic review aims to consolidate and provide an updated overview on the genetic variants of SFN to date—SCN genes and beyond. Awareness of these genetic causes of SFN is imperative for providing treatment directions, prognostication, and management of expectations for patients and their health-care providers.

There is a common symptom pattern with most chronic low back pain (CLBP), suggesting that there is a common underlying etiology, belying the term "nonspecific." Many studies of CLBP and its treatment have been conducted with the assumption of nonspecificity, and as a result, treatment has not been focused, thus there has not been a significant change in CLBP prevalence over the past several decades. It is the thesis of this study to show that there is an underlying, specific cause of CLBP and that the presumption that CLBP is nonspecific is misdirected. The lumbosacropelvic (LSP) region, including the sacroiliac joint (SIJ), is part of a neuromusculoskeletal (NMSK) feedback system, and it is proposed here that CLBP is the result of a change in the feedback (afferent) aspect in that system.

Headaches occur when cerebrospinal fluid (CSF) pressure drops following dural puncture or trauma or spontaneously. As the features of these headaches and their accompanying symptoms might not be typical, low CSF pressure headache syndromes, and spontaneous intracranial hypotension in particular, are often misdiagnosed and underdiagnosed.

Despite development of protocols to differentiate human pluripotent stem cells (hPSCs), those used to produce sensory neurons remain difficult to replicate and result in heterogenous populations. There is a growing clinical burden of chronic pain conditions, highlighting the need for relevant human cellular models. This study presents a hybrid differentiation method to produce nociceptive sensory neurons from hPSCs. Lines harboring an inducible construct were patterned toward precursors with small molecules followed by overexpression. Neurons expressed key markers, including and , with single-cell RNA sequencing, revealing populations of nociceptors expressing and channels. Physiological profiling with multi-electrode arrays revealed that neurons responded to noxious stimuli, including capsaicin. Finally, we modeled pain-like states to identify genes and pathways involved in pain transduction. This study presents an optimized method to efficiently produce nociceptive sensory neurons and provides a tool to aid development of chronic pain research.