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Key Points Itch—also referred to as pruritus—is an unpleasant sensation that elicits an urge to scratch Neuropathic pruritus is caused by neuronal or glial damage CNS disorders rarely trigger pruritus, but pruritus is commonly associated with peripheral neuropathies and disorders of mixed or undetermined aetiology with neurological involvement Treatment for neuropathic pruritus is similar to that for neuropathic pain, but μ opioids can induce itch and are, therefore, contraindicated Pruritus is a very common condition, with almost one-third of the global population experiencing itch in a given week. Its origin is not always in the skin: damage to neurons or glia can induce neuropathic pruritus, which is often associated with neuropathic pain. Neuropathic pruritus is often difficult to treat and—if chronic—can severely impair quality of life. Here, Laurent Misery and colleagues review the role of the nervous system and neuropathic syndromes in pruritus, summarize the currently available therapeutic options, and propose therapeutic strategies for managing neuropathic pruritus. Pruritus, also known as itch, is a very common, unpleasant sensation that elicits an urge to scratch. Its origin is not always in the skin, and neuropathic itch that is caused by neuronal or glial damage is common, but poorly understood by both dermatologists and neurologists. Although pruritus has not been considered as serious a symptom as pain, it is difficult to treat and—if chronic—can severely impair quality of life. Neuropathic itch is often associated with other clinical symptoms, most commonly neuropathic pain, and hypersensitization to stimuli is present in both pruritus and pain of neuropathic origin. The shared aetiology can aid in finding suitable treatment for itch in some cases, but more detailed knowledge of the mechanisms of itch, along with standardized, well-controlled trials, is needed. Pruritus research is an emerging but currently very active field, and our understanding of this sensation is rapidly increasing. Here, we review new discoveries regarding the role of the nervous system and the contribution of different pathways in pruritus, discuss the different aetiologies of neuropathic itch, and outline currently available and potential strategies for managing neuropathic pruritus.

Purpose of Review Our goal is to examine the processes—both central and peripheral—that underlie the development of peripherally-induced neuropathic pain (pNP) and to highlight recent evidence for mechanisms contributing to its maintenance. While many pNP conditions are initiated by damage to the peripheral nervous system (PNS), their persistence appears to rely on maladaptive processes within the central nervous system (CNS). The potential existence of an autonomous pain-generating mechanism in the CNS creates significant implications for the development of new neuropathic pain treatments; thus, work towards its resolution is crucial. Here, we seek to identify evidence for PNS and CNS independently generating neuropathic pain signals. Recent Findings Recent preclinical studies in pNP support and provide key details concerning the role of multiple mechanisms leading to fiber hyperexcitability and sustained electrical discharge to the CNS. In studies regarding central mechanisms, new preclinical evidence includes the mapping of novel inhibitory circuitry and identification of the molecular basis of microglia-neuron crosstalk. Recent clinical evidence demonstrates the essential role of peripheral mechanisms, mostly via studies that block the initially damaged peripheral circuitry. Clinical central mechanism studies use imaging to identify potentially self-sustaining infra-slow CNS oscillatory activity that may be unique to pNP patients. Summary While new preclinical evidence supports and expands upon the key role of central mechanisms in neuropathic pain, clinical evidence for an autonomous central mechanism remains relatively limited. Recent findings from both preclinical and clinical studies recapitulate the critical contribution of peripheral input to maintenance of neuropathic pain. Further clinical investigations on the possibility of standalone central contributions to pNP may be assisted by a reconsideration of the agreed terms or criteria for diagnosing the presence of central sensitization in humans.

Background Neuropathic pain represents a significant public health concern due to its complex pathophysiology and the disability it can cause. Despite advancements in understanding its underlying mechanisms and potential treatments, challenges persist in achieving effective management. This bibliometric analysis aims to offer a comprehensive overview of research trends, key contributors, and existing gaps in the literature on neuropathic pain, providing valuable insights to guide future studies and enhance clinical approaches. Methods A bibliometric analysis was conducted using the Web of Science Core Collection (WoSCC) database. Key metrics, including publication trends, citation patterns, co-authorship networks, and keyword co-occurrence, were evaluated. Statistical analyses included average annual percentage change (APC) assessments and trend forecasting with an Auto Regressive Integrated Moving Average (ARIMA) model. Results A total of 9,974 studies published between 2005 and 2024 were included. Publications peaked between 2021 and 2022 but showed a slight decline thereafter, with forecasts predicting a steady increase from 2025 to 2030. Most papers were published in high-impact Q1 journals, reflecting the quality of research. Co-authorship analysis revealed central hubs of collaboration in the USA and China, with limited integration of smaller countries into the global research network. Keyword analysis identified multiple thematic clusters, including \"chronic pain,\" \"molecular mechanisms,\" and \"clinical management.\" Specific gaps were noted in understanding personalized therapeutic approaches, and non-pharmacological interventions. Conclusions This analysis underscores the critical need for continued research to address gaps in diagnosis, treatment, and management of neuropathic pain. Strengthening international collaborations and fostering multidisciplinary efforts will be pivotal in advancing this field.

Purpose of Review Researchers suggests that patients with COVID-19 develop neuropathic pain within weeks or months following infection and that patients with neuropathic pain and COVID-19 sometimes present with deterioration of neurologic complications and pain exacerbation. The objective of this systematic review is to discuss the case-reports having neuropathic pain during and after COVID-19 infection. Recent Findings Case reports that has described about patients getting neuropathy or neuropathic pain around the disease either immediately or late post COVID were included. The data was extracted and qualitatively synthesised. Literature was searched and 939 articles were found. 12 articles were screened as per the eligibility criteria and finally, 6 case reports on neuropathic pain in Covid-19 were selected from the database and manual search and finalised for analysis. 2 cases of herpes zoster and post herpetic neuralgia, 2 cases of intense burning pain, 1 case of trigeminal neuralgia and 1 of brachial plexopathy included for the review. Summary Covid 19 viral neurogenic invasion is something very newly discovered topic of discussion in the field of research. With the passage of time, more cases will emerge and more data will be available for research. The review is registered in Prospero with no. CRD42021257060.

Purpose of Review This manuscript summarizes novel clinical and interventional approaches in the management of chronic, nociceptive, and neuropathic pain. Recent Findings Pain can be defined as a feeling of physical or emotional distress caused by an external stimulus. Pain can be grouped into distinct types according to characteristics including neuropathic pain, which is a pain caused by disease or lesion in the sensory nervous system; nociceptive pain, which is pain that can be sharp, aching, or throbbing and is caused by injury to bodily tissues; and chronic pain, which is long lasting or persisting beyond 6 months. With improved understanding of different signaling systems for pain in recent years, there has been an upscale of methods of analgesia to counteract these pathological processes. Novel treatment methods such as use of cannabinoids, stem cells, gene therapy, nanoparticles, monoclonal antibodies, and platelet-rich plasma have played a significant role in improved strategies for therapeutic interventions. Summary Although many management options appear to be promising, extensive additional clinical research is warranted to determine best practice strategies in the future for clinicians.

Purpose of Review Topical therapeutic approaches in localized neuropathic pain (LNP) syndromes are increasingly used by both specialists and general practitioners, with a potentially promising effect on pain reduction. In this narrative review, we describe the available compounds for topical use in LNP syndromes and address their potential efficacy according to the literature. Recent Findings Local anaesthetics (e.g., lidocaine, bupivacaine and mepivacaine), as well as general anaesthetic agents (e.g., ketamine), muscle relaxants (e.g., baclofen), capsaicin, anti-inflammatory drugs (e.g., diclofenac), salicylates, antidepressants (e.g., amitriptyline and doxepin), α2 adrenergic agents (e.g., clonidine), or even a combination of them have been tested in various applications for the treatment of LNP. Few of them have reached a sufficient level of evidence to support systematic use as treatment options. Summary Relatively few systemic side effects or drug–drug interactions and satisfactory efficacy seem to be the benefits of topical treatments. More well-organized and tailored studies are necessary for the further conceptualization of topical treatments for LNP.

Pain is an important innate defense mechanism that can dramatically alter a person’s quality of life. Understanding the microbiological and physiological effects of pain may be important in the pursuit of novel pain interventions. The three descriptors of pain recognized by the International Association for the Study of Pain are nociceptive, neuropathic, and nociplastic pain. Our review examined the current understanding of all three pain types, focusing on the key molecules involved in the manifestation of each type as well as physiological effects. Additionally, we compared the differences in painful and painless neuropathies and discussed the neuroimmune interaction involved in the manifestation of pain.

Recently, the International Association for the Study of Pain (IASP) released clinical criteria and a grading system for nociplastic pain affecting the musculoskeletal system. These criteria replaced the 2014 clinical criteria for predominant central sensitization (CS) pain and accounted for clinicians’ need to identify (early) and correctly classify patients having chronic pain according to the pain phenotype. Still, clinicians and researchers can become confused by the multitude of terms and the variety of clinical criteria available. Therefore, this paper aims at (1) providing an overview of what preceded the IASP criteria for nociplastic pain (‘the past’); (2) explaining the new IASP criteria for nociplastic pain in comparison with the 2014 clinical criteria for predominant CS pain (‘the present’); and (3) highlighting key areas for future implementation and research work in this area (‘the future’). It is explained that the 2021 IASP clinical criteria for nociplastic pain are in line with the 2014 clinical criteria for predominant CS pain but are more robust, comprehensive, better developed and hold more potential. Therefore, the 2021 IASP clinical criteria for nociplastic pain are important steps towards precision pain medicine, yet studies examining the clinimetric and psychometric properties of the criteria are urgently needed.

Purpose of Review This review presents the most current information about the epidemiology of complex regional pain syndrome (CRPS), classification and diagnostic criteria, childhood CRPS, subtypes, pathophysiology, conventional and less conventional treatments, and preventive strategies. Recent Findings CRPS is a painful disorder with multifactorial pathophysiology. The data describe sensitization of the central and peripheral nervous systems, inflammation, possible genetic factors, sympatho-afferent coupling, autoimmunity, and mental health factors as contributors to the syndrome. In addition to conventional subtypes (type I and type II), cluster analyses have uncovered other proposed subtypes. Prevalence of CRPS is approximately 1.2%, female gender is consistently associated with a higher risk of development, and substantial physical, emotional, and financial costs can result from the syndrome. Children with CRPS seem to benefit from multifaceted physical therapy leading to a high percentage of symptom-free patients. The best available evidence along with standard clinical practice supports pharmacological agents, physical and occupational therapy, sympathetic blocks for engaging physical restoration, steroids for acute CRPS, neuromodulation, ketamine, and intrathecal baclofen as therapeutic approaches. There are many emerging treatments that can be considered as a part of individualized, patient-centered care. Vitamin C may be preventive. Summary CRPS can lead to progressively painful sensory and vascular changes, edema, limb weakness, and trophic disturbances, all of which substantially erode healthy living. Despite some progress in research, more comprehensive basic science investigation is needed to clarify the molecular mechanisms of the disease so that targeted treatments can be developed for better outcomes. Incorporating a variety of standard therapies with different modes of action may offer the most effective analgesia. Introducing less conventional approaches may also be helpful when traditional treatments fail to provide sufficient improvement.

Purpose of Review Painful diabetic neuropathy (PDN) manifests with pain typically in the distal lower extremities and can be challenging to treat. The authors appraised the literature for evidence on conservative, pharmacological, and neuromodulation treatment options for PDN. Recent Findings Intensive glycemic control with insulin in patients with type 1 diabetes may be associated with lower odds of distal symmetric polyneuropathy compared to patients who receive conventional insulin therapy. First-line pharmacologic therapy for PDN includes gabapentinoids (pregabalin and gabapentin) and duloxetine. Additional pharmacologic modalities that are approved by the Food and Drug Administration (FDA) but are considered second-line agents include tapentadol and 8% capsaicin patch, although studies have revealed modest treatment effects from these modalities. There is level I evidence on the use of dorsal column spinal cord stimulation (SCS) for treatment of PDN, delivering either a 10-kHz waveform or tonic waveform. Summary In summary, this review provides an overview of treatment options for PDN. Furthermore, it provides updates on the level of evidence for SCS therapy in cases of PDN refractory to conventional medical therapy.