A false-positive hepatitis serology result may not be solely due to intravenous immunoglobulins (IVIG) administration but may also result from cross-reacting antibodies from other infections, autoimmune diseases, recent hepatitis B vaccination, or interactions with rheumatoid factor or biotin. Furthermore, technical errors, such as faulty reagents or unsuitable testing methods, as well as certain patient groups, for example, those with certain chronic diseases, can also contribute to false-positive results. More likely than interference from IVIGs, the false-positive hepatitis serology result in one of the studies we read is due to Henoch-Schönlein pupura.

Introduction/Aims: Quantitative analysis of nerve echogenicity can support the diagnosis of mono- and polyneuropathies, for instance by distinguishing inflammatory-demyelinating from axonal damage. However, echogenicity is mainly assessed qualitatively and examiner-dependently. This study aimed to establish quantitative reference data for grayscale values of peripheral nerves in the upper and lower extremities of healthy children and adolescents to provide a clinical benchmark. Methods: We retrospectively analyzed ultrasound data from 211 healthy children aged two to seventeen years who had undergone standardized examinations of 15 peripheral nerve sites. Grayscale analysis (0-255 levels per pixel) was performed within manually defined regions of interest (ROIs) using ImageJ (version 1.52). Echogenicity values were correlated with age, weight, height, and body mass index (BMI). Results: Echogenicity showed no significant overall association with biometric parameters. Mean grayscale values ranged from 85.23 ± 2.16 for the tibial nerve at the medial malleolus to 134.62 ± 2.69 for the sural nerve. Gain settings below 60 resulted in significantly lower grayscale values, whereas measurements with gain ≥ 60 were stable and comparable. Discussion: We propose reference grayscale ranges for peripheral nerves in healthy children and adolescents as a practical benchmark for clinical use and future studies. Due to technical constraints-particularly retrospective image processing and non-lossless data export-each laboratory should establish its own reference dataset, or multicentric parameters should be established. As our sample consisted predominantly of Caucasian participants, ethnic differences should be considered when applying these values to other populations.

Pathogenic variants in the PMP22 gene can lead to hereditary peripheral demyelinating neuropathies of varying severity, including hereditary neuropathy with liability to pressure palsies (HNPP), Charcot-Marie-Tooth disease types 1A and 1E (CMT1A, CMT1E), Roussy-Lévy syndrome, and Dejerine-Sottas disease (DSS). This study describes a novel deep intronic variant c.179-2809A>G in the PMP22 gene, identified in two unrelated Avar families from Dagestan republic, Russia. This variant was identified in nine patients. In seven cases, it was detected in a heterozygous state, leading to the development of HNPP. In two cases, this variant was found in a homozygous state, resulting in a more severe CMT1A phenotype (Dejerine-Sottas disease). The performed functional analysis allowed us to characterize the deleterious effect of this variant and propose an approach for personalized antisense therapy. This work demonstrates that, in Avar people with HNPP traits, variant c.179-2809A>G should be considered as disease-causing and included in standard genetic testing.

(1) Background: Creutzfeldt-Jakob disease (CJD) is a progressive neurodegenerative disorder, characterized by cognitive decline, and motor and psychiatric symptoms; it primarily affects the central nervous system; however, peripheral nervous system involvement has rarely been described, particularly as an atypical presentation. (2) Methods: A 78-year-old Caucasian man, a retired farmer with no family history of neurological disease, presented with diarrhea followed by progressive lower limb weakness, which eventually evolved into encephalopathy and generalized areflexia. An initial diagnosis of inflammatory neuropathy was considered; the diagnostic assessment included blood and cerebrospinal fluid testing, a CT whole body scan, brain MRI, neuropsychological testing, electroencephalography, a nerve conduction study and electromyography. (3) Results: Neurophysiological studies demonstrated an acute asymmetrical sensorimotor, predominantly axonal polyneuropathy, initially suggestive of an axonal form of inflammatory polyradiculoneuritis. This pattern was confirmed on follow-up neurophysiological assessment performed three weeks later. Unexpectedly, the diagnostic course ultimately led to a diagnosis of sporadic Creutzfeldt-Jakob disease, confirmed by post-mortem neuropathological examination. Based on these findings, we conducted a literature review to summarize the current evidence on CJD-related neuropathy. (4) Conclusions: Our case emphasizes the importance of maintaining clinical suspicion for CJD even in patients presenting with progressive lower limb weakness and suggests that peripheral neuropathy may be concomitant or even precede the CNS manifestations. Careful consideration is required to avoid misdiagnosis of inflammatory neuropathy in the context of neurodegenerative diseases such as CJD.

Small fiber neuropathy (SFN) is an early and common manifestation of diabetic polyneuropathy in type 2 diabetes mellitus (T2DM), often presenting with pain, dysesthesia, and autonomic dysfunction. Conventional diagnostic methods primarily assess large nerve fibers and may miss early small fiber damage, while skin biopsy, though considered the reference standard, is invasive. Corneal confocal microscopy (CCM) offers a rapid, noninvasive alternative for visualizing and quantifying small nerve fiber pathology in vivo. This was a monocentric observational study including 80 adults with T2DM (18-75 years), conducted at Alexandrovska Hospital, Sofia. Peripheral neuropathy was evaluated using a modified Neuropathy Disability Score and CCM-derived corneal nerve fiber density (CNFD), length (CNFL), and branching density (CNBD). Autonomic and sudomotor function were assessed by cardiovascular reflex tests and Sudoscan. Additional measures included vibration perception threshold, carotid intima-media thickness, body composition analysis, and laboratory parameters. Autonomic neuropathy was present in 66.7% and peripheral neuropathy in 57.5% of participants. Affected patients were older and had higher BMI and longer diabetes duration; peripheral neuropathy was additionally associated with higher HbA1c. Corneal nerve parameters negatively correlated with diabetes duration, HbA1c, intima-media thickness, and vibration threshold. Patients with diabetic retinopathy showed significantly reduced CNFD and CNFL. ROC analysis demonstrated significant discriminative ability of the HRV index for identifying peripheral neuropathy and of CNFD for detecting sudomotor dysfunction. These findings support CCM as a valuable, noninvasive marker of small fiber damage, closely linked to metabolic control, vascular impairment, and both sensory and autonomic dysfunction in T2DM.

Back pain is a common presentation in healthcare settings. The most serious cause is cauda equina syndrome (CES), a surgical emergency caused by acute compression of the lumbosacral nerve roots. In the UK, diagnosis requires a thorough clinical examination and emergency magnetic resonance imaging (MRI). Once confirmed on imaging, definitive treatment is urgent surgical decompression usually within 24 hours. Delays in diagnosis or treatment can lead to life-changing consequences including bowel and bladder incontinence, sexual dysfunction, lower limb paralysis and chronic pain. This narrative review provides a 2025 update to the 2023 review published in this journal. It covers the anatomy, epidemiology, aetiology, pathophysiology, classification, clinical presentation, examination, investigations, differentials, treatment, and management of CES. Major updates are based on the new UK 2025 Getting It Right First Time (GIRFT) interactive pathway. Important changes include: (1) the standardisation and timing of red flag symptoms, (2) the use of bladder scans as a rule-in rather than rule-out investigation, (3) aim for 24-hour MRI local diagnostic capabilities with standardized imaging sequences and proximal scanning in absence of cauda equina compression, (4) declassification of CES, (5) emphasis on all patients with established CES to receive urgent decompressive surgery as National Confidential Enquiry into Patient Outcome and Death (NCEPOD) level 1/2. This review uses the authors' experience of suspected CES pathway improvement to propose a pathway for the management of suspected CES in the emergency department at district general hospitals without 24-hour MRI capability based on the most recent national GIRFT guidelines.

The purpose of this narrative review is to provide a clinic-ready synthesis of contemporary concepts in peripheral neuropathy, spanning epidemiology, diagnosis, and treatment, with emphasis on high-yield advances applicable to daily practice. The authors integrate pragmatic tools-including a diagnostic algorithm, suggested initial laboratory panels, and commonly used outcome measures-to support clinical decision-making. However, this review is intended as a clinic-oriented synthesis rather than a formal practice guideline. Peripheral neuropathy can be systematically categorized into seven pathophysiologic phenotypes-(1) distal "dying-back" axonopathy, (2) neuronopathy (ganglionopathy), (3) demyelinating neuropathies, (4) small-fiber neuropathy, (5) autonomic neuropathy, (6) ischemic/infiltrative/inflammatory axonopathies, and (7) focal compressive/entrapment neuropathies. An organized evaluation and management around this phenotype-first structure, combined with a structured stepwise escalation algorithm (from bedside pattern recognition to targeted laboratory testing, electrodiagnostics, selective imaging, small-fiber assessment, and immune work-up when indicated), bridges fragmented evidence into a clinic-ready decision-support framework that improves diagnostic precision, rational test utilization, and therapeutic alignment. Beyond optimizing pharmacologic care, neuromodulation may expand options in carefully selected patients. For painful diabetic peripheral neuropathy (DPN), high‑frequency (10 kHz) spinal cord stimulation (SCS) has been evaluated in randomized comparative studies against optimized medical management and has been associated with sustained pain reduction and functional improvement through 24 months in follow‑up reports, supporting consideration in medication‑refractory cases where access and patient factors permit. Ultrasound ‑guided pulsed radiofrequency (PRF)-a nondestructive, field‑based neuromodulation that limits tip temperature to <42 °C-has been studied in small randomized trials and observational cohorts for focal entrapment‑type neuropathic pain after positive diagnostic blocks; reported benefits are generally short‑ to mid‑term with heterogeneous protocols, so certainty varies by indication. For hereditary transthyretin amyloid polyneuropathy (ATTRv), disease‑modifying approaches-including nucleic acid-based therapies-are increasingly integrated into contemporary care. Overall, these developments support earlier pattern recognition, more precise phenotyping, and rational escalation while using standardized outcome measures to track response.

This case report describes the successful use of ofatumumab, a fully humanized anti-CD20 monoclonal antibody, in a 62 years old male with monoclonal gammopathy of undetermined significance (MGUS) associated chronic inflammatory demyelinating polyneuropathy. The patient presented with acute limb weakness, glove-like paresthesia, and respiratory involvement, alongside elevated anti-ganglioside antibodies (anti-GM4 IgM and IgG) and λ-type IgM-M proteinemia. Despite initial therapies including intravenous immunoglobulin, efgartigimod, and immunosuppressants, he experienced recurrent relapses. Treatment with ofatumumab combined with methylprednisolone resulted in complete peripheral CD19+ B cell depletion, improved nerve conduction velocities, and sustained clinical remission. The findings highlight the efficacy of ofatumumab in targeting pathogenic CD20+ B cell clones, thereby disrupting autoantibody production implicated in immune mediated peripheral nerve injury. This case underscores the potential of B cell directed therapy for refractory MGUS associated neuropathies, offering a novel approach when conventional immunotherapies fail. Further multicenter studies are warranted to establish standardized protocols and optimize long term outcomes through combination regimens targeting both B cell and plasma cell compartments.