YokoCo

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.

The use of high definition transcranial direct current stimulation (HD-tDCS) has shown analgesic effects in some chronic pain patients, but limited anti-nociceptive effects in healthy asymptomatic subjects. This double-blinded sham-controlled study assessed the effects of HD-tDCS applied on three consecutive days on central pain mechanisms in healthy participants with (N=40) and without (N=40) prolonged experimental pain induced by intramuscular injection of nerve growth factor into the right hand on Day1. Participants were randomly assigned to Sham-tDCS (N=20 with pain, N=20 without) or Active-tDCS (N=20 with pain, N=20 without) targeting simultaneously the primary motor cortex and dorsolateral prefrontal cortex for 20 min with 2mA stimulation intensity. Central pain mechanisms were assessed by cuff-algometry on the legs measuring pressure pain sensitivity, temporal summation of pain (TSP) and conditioned pain modulation (CPM), at baseline and after HD-tDCS on Day2 and Day3. Based on subject's assessment of received HD-tDCS (sham or active) they were effectively blinded. Compared with Sham-tDCS, Active-tDCS did not significantly reduce the average NGF-induced pain intensity. Tonic pain-induced temporal summation at Day2 and Day3 was significantly lower in the NGF-pain group under Active-tDCS compared to the pain group with Sham-tDCS (P≤0.05). No significant differences were found in the cuff pressure pain detection/tolerance thresholds or CPM effect across the 3 days of HD-tDCS in any of the four groups. HD-tDCS reduced the facilitation of TSP caused by tonic pain suggesting that efficacy of HD-tDCS might depend on the presence of sensitized central pain mechanisms.