Facial nerve palsy in children leads to significant functional impairment and facial asymmetry. While free gracilis muscle transfer (FGMT) is a cornerstone technique for smile reanimation in both pediatric and adult patients, its evaluation has mainly focused on the single metric of commissure excursion. This study seeks to evaluate the effectiveness of FGMT in restoring dynamic smiles in pediatric patients with facial palsy using image analysis. A retrospective review was conducted in children who underwent FGMT for facial palsy at a major children's hospital between 2007 and 2020. Data collection included pre- and postoperative chart reviews and image analysis. Anthropometric measurements were obtained using a machine learning-based smile analysis software. Primary outcomes included commissure excursion, commissure angle, dental show, and smile symmetry. Statistical analysis was performed using the Wilcoxon signed-rank test. A total of 31 patients with an average age of 10 years underwent FGMT for smile reanimation during the study period. The most common diagnosis was Moebius syndrome (48%). Donor nerves for gracilis neurotization included 18 ipsilateral trigeminal nerves (58.1%) and 12 contralateral facial nerves via cross-face sural nerve grafts (38.7%). Overall, 84% of patients demonstrated active gracilis contraction within a mean of 2.5 years postoperative follow-up. Commissure excursion increased by 9.7 mm at 1 year (p < 0.05), and symmetry significantly improved for commissure height, commissure excursion, upper lip height, and smile angle. There were no significant improvements in dental show, commissure angle, symmetry of dental show, and lower lip height. Furthermore, only 16% of patients demonstrated clinically symmetric smiles within the follow-up period. While FGMT effectively restores commissure excursion in pediatric patients with facial palsy, achieving multidimensional smile reanimation remains a challenge. New techniques in multi-vector free tissue transfer may help optimize FGMT outcomes in pediatric patients.

Corneal confocal microscopy is a valuable technique for assessing neuropathy; however, whether it can distinguish painful from painless neuropathy remains uncertain and existing evidence is based on the results of smaller studies. This study assessed the association of corneal nerve parameters with abnormalities identified by electromyography (EMG) and neuropathic pain in a large population with and without (pre)diabetes. In this study we included cross-sectional data for 3425 participants from the Maastricht Study. Wide-field corneal confocal microscopy (WF-CCM) was performed using fully automated analysis of three corneal nerve parameters: corneal nerve branch density (CNBD), corneal nerve fibre density (CNFD) and corneal nerve fibre length (CNFL). An axonal degeneration composite score comprising compound muscle action potential amplitudes (peroneal and tibial) and the sensory nerve action potential amplitude of the sural nerve was created by categorising EMG amplitudes as normal or indicating minor (≤10th percentile), moderate (≤5th percentile) or severe (≤2.5th percentile) abnormalities. Neuropathic pain was determined as a modified Douleur Neuropathique en 4 Questions (DN4) interview score ≥3. The mean age of the participants was 59.2 years; 51.6% were female, 15% had prediabetes (defined as impaired fasting glucose, impaired glucose tolerance or both) and 19% had type 2 diabetes. The median diabetes duration was 3.0 years. Regression analyses revealed statistically significant associations between the axonal degeneration EMG score and WF-CCM parameters (CNFL: β=-0.51 [95% CI -0.78, -0.24]; CNFD: β=-1.56 [95% CI -3.04, -0.08]; CNBD: β=-3.08 [95% CI -5.51, -0.64]; all p<0.05) but no statistically significant associations between neuropathic pain and WF-CCM parameters (CNFL: β=-0.06; CNFD: β=-1.15; CNBD: β=-0.22; all p>0.1). The study found associations between the axonal degeneration EMG score and WF-CCM, but no associations were observed between neuropathic pain and WF-CCM parameters, suggesting that WF-CCM has limited value in assessing neuropathic pain.

Clinical and sonographic sequelae of sural nerve biopsy

This report discusses a patient in his late 60s with a diagnosis of eosinophilic granulomatosis with polyangiitis (EGPA) who was found to have radiological periaortitis. He presented with acute mononeuritis multiplex and constitutional symptoms. Investigations revealed marked eosinophilia, positive myeloperoxidase (MPO) antibodies and imaging evidence of periaortitis. Nerve conduction studies showed axonal mononeuropathies, and a sural nerve biopsy confirmed a vasculitic neuropathy with eosinophilic infiltrates. He was treated with high-dose corticosteroids and intravenous cyclophosphamide, with substantial neurological improvement, and later transitioned to maintenance azathioprine. His course was complicated by a pulmonary embolism. Radiological follow-up demonstrated remission of periaortitis. This case emphasises the diagnostic challenges of distinguishing EGPA from mimics such as IgG4-related disease and highlights the importance of recognising rare large-vessel involvement in EGPA and underlines the need for vigilance regarding thromboembolic complications.

Chronic tendinopathy is typified by persistent tendon-associated pain, transmitted by local nociceptive neurons. However, the regulatory function of somatosensory neurons in the development of tendinopathy is unknown. Here, we show that sensory neurons grow into the tendon proper across preclinical models of chronic tendinopathy to serve a protective function against tendinopathic changes through interactions with resident tenocytes and infiltrating macrophages. Retrograde neuronal tracing combined with single-cell RNA sequencing (scRNA-seq) of dorsal root ganglion neurons revealed a tendon-specific innervation profile, including calcitonin gene-related peptide (CGRP)-positive nociceptors among other sensory neuron types. We further evaluated these findings in three complementary surgical and transgenic mouse models of disrupted sensory nerve growth. Conditional deletion of nerve growth factor (Ngf) in macrophages (NgfCsfr1) or inactivation of its high-affinity receptor, tropomyosin receptor kinase A (TrkA), on sensory neurons exacerbated tendinopathic changes. Subsequently, a "sensory-only" sural nerve denervation model phenocopied these results, including heightened macrophage infiltration and tenocyte apoptosis. scRNA-seq of tendinous tissue identified defective tenocyte differentiation and altered macrophage migration and polarization with tendon denervation. Last, neuron-tendon interaction analyses implicated neuron-derived fibroblast growth factor 1 (FGF1) as a preventative factor for tendon degeneration, a finding supported by tendon organ culture and in vivo assessment. Consistent with a conserved mechanism, human tendinopathy specimens showed FGF1 immunoreactivity associated with tendon-innervating nerve fibers. Collectively, our findings demonstrate that peripheral afferent neural networks exert a protective effect in preclinical tendinopathy models by secreting FGF1 and that targeting this pathway may offer therapeutic strategies to prevent tendinopathic changes.

Bone autografts are commonly used to augment arthrodesis sites and enhance the biologic environment necessary for successful fusion. Autogenous bone may be harvested from several donor locations, including the anterior and posterior iliac crest, proximal and distal tibia, and notably the calcaneus. Complication rates of calcaneal graft harvest have varied widely in the literature with several different techniques from open to percutaneous methods. The purpose of this study was to assess optimal zones of graft volume while minimizing donor-site morbidity. Twenty, ten matched-pairs, fresh-frozen cadaveric below-knee specimens were used for this study. The posterior tuber of the calcaneus was measured in height and equally divided into 3 distinct zones. A 7-mm Medline bone graft harvester was inserted perpendicular to the lateral calcaneal wall and advanced in a single pass to obtain cancellous autograft from the calcaneus. Graft volume as well as distance to adjacent structures at risk were measured. We found no statistical significance in graft volume among the three zones; however, we did note a significant difference in distance from the sural nerve between zones 1 and 2, and between zones 1 and 3. We found an average volume of 0.59, 0.41, and 0.61 grams3 for zones 1, 2, and 3, respectively. These findings suggest calcaneal bone graft harvest remains a safe procedure and enables to obtain consistent graft volume. Further clinical studies are recommended to confirm these results and guide future surgical practices.Level of Evidence: Level IV: Cadaveric study.

Sandhoff disease (SD) is a subtype of GM2 gangliosidosis caused by pathogenic variants in Hexosaminidase B (HEXB). It most frequently presents in infancy or early childhood, whereas adult-onset disease is rare and remains incompletely characterized. Here, we describe an adult-onset case of SD presenting as motor neuron disease and provide clinical and mechanistic insights using patient-derived models. The patient was a 34-year-old man with compound heterozygous HEXB variants (c.1598G > A, p.Arg533His and c.1645G > A, p.Gly549Arg) who developed progressive lower limb weakness. Muscle biopsy demonstrated neurogenic changes consistent with denervation, and sural nerve biopsy revealed mild peripheral neuropathy. Nerve conduction studies and electromyography showed widespread neurogenic changes with mildly reduced sensory nerve action potential amplitudes, and leukocyte β-hexosaminidase activity was decreased. To investigate disease mechanisms, we generated induced pluripotent stem cells (iPSCs) from the patient and an isogenic CRISPR-Cas9-corrected control (ISO), and differentiated both lines into motor neurons (MNs). In the SD patient (SDHF)-derived MNs, we observed lysosomal expansion, increased apoptosis, reduced neuronal network excitability, and dysregulated lipidomic profiles. These phenotypes were attenuated in MNs derived from the ISO line, with multiple measures shifting toward those of control (CTL) MNs. Collectively, our findings expand the clinical spectrum of adult-onset SD and support an association between HEXB deficiency and the vulnerability of MNs, while underscoring the value of patient-derived iPSC models for mechanistic studies of lateonset SD.

To describe the clinical course, surgical management, and sensory outcomes of indirect corneal neurotization using an autologous sural nerve graft in a pediatric patient with congenital corneal anesthesia complicated by recurrent herpetic keratitis and neurotrophic keratopathy. Case report of a 6-year-old girl with severe unilateral corneal hypoesthesia secondary to recurrent herpes simplex virus keratitis and a history of deep anterior lamellar keratoplasty, who underwent indirect corneal neurotization. Serial postoperative assessments included visual acuity, slit-lamp examination, and Cochet-Bonnet esthesiometry. By mid-term follow-up (8 months), partial peripheral sensory recovery was observed, accompanied by restoration of ocular surface stability and improvement in best-corrected visual acuity to 20/40. At 1 year, asymmetric but clinically meaningful peripheral sensory improvement was documented, whereas central sensitivity remained markedly reduced. The corneal graft remained clear, and no further inflammatory complications occurred. Indirect corneal neurotization using a sural nerve graft resulted in significant peripheral sensory recovery and enhanced visual function in a pediatric patient with congenital corneal anesthesia and herpes simplex virus-related neurotrophic keratopathy. This case supports indirect corneal neurotization as a promising regenerative strategy capable of restoring corneal sensation and improving ocular surface stability in pediatric patients at risk of amblyopia.

To evaluate the relationship between Pacinian corpuscle (PC) count on forefoot MRI in diabetic sensorimotor polyneuropathy (DSP) and large-fiber sensory dysfunction as quantified by nerve conduction studies (NCS). Thirty-nine patients with type 2 diabetes and neurologically confirmed DSP (mean age 67.9 ± 13.5 years; 29 males) underwent forefoot MRI and NCS, including compound muscle and sensory nerve action potentials (cMAP, sNAP) and conduction velocities of tibial, peroneal, and sural nerves. PC counts were assessed in the subcutaneous and deep regions of each digit. Spearman's rank correlation analysis examined the relationship between total PC counts and sural sNAP amplitudes. Based on motor and sensory amplitudes and age-adjusted conduction velocities of NCS, 10 patients were classified as having mild-to-moderate DSP, and 29 as having severe DSP. Severe DSP was associated with sensory large-fiber impairment, with 86.1% of patients showing abolished sural sNAP amplitudes. Total PC counts were significantly lower in severe cases compared to mild-to-moderate polyneuropathy (54.1 ± 40.6 vs 146.1 ± 43.2; p < 0.001). Spearman's rank correlation analysis revealed a strong positive association between PC counts and sural sNAP amplitudes (ρ = 0.638, p < 0.001). Likewise, patients with severe DSP had substantially reduced or absent sural sNAP amplitudes (median [range]: 0.1 [0.1-1.7] µV) and lower PC counts, while those with mild-to-moderate DSP showed both higher sural sNAP amplitudes (median [range]: 2.3 [0.9-11.4] µV) and PC counts (p < 0.001). Forefoot MRI-detected PC counts closely correlate with large-fiber sensory function in DSP, supporting their potential as noninvasive imaging biomarkers of polyneuropathy severity. Question DSP is linked to loss of PC on forefoot MRI; however, it remains unclear whether the number of PC correlates with DSP severity. Findings Forefoot MRI showed lower PC counts in patients with severe DSP than in those with mild-to-moderate disease and indicated a strong association between PC loss and electrophysiological measures of large-fiber sensory dysfunction. Clinical relevance MRI-based PC quantification is a promising imaging biomarker for large-fiber sensory dysfunction in DSP, complementing established clinical and electrophysiological methods for diagnosing and assessing DSP severity.

Synovial lipomatosis, also known as lipoma arborescens, is a rare benign condition characterized by villous fatty proliferation of the synovium with replacement of the subsynovial tissue by mature adipocytes. Although it predominantly affects the knee joint, involvement of the ankle is distinctly uncommon. We report the case of a 52-year-old woman who presented with progressive left ankle pain and swelling of 1 year duration, associated with mechanical symptoms and restriction of motion. Physical examination revealed a posterolateral ankle swelling with mild limitation of range of motion, while laboratory parameters and rheumatologic markers were within normal limits. Plain radiography demonstrated a soft-tissue swelling with a calcified/bony mass, and magnetic resonance imaging revealed diffuse synovial proliferation with associated bone marrow edema. The patient underwent open ankle arthrotomy with excision of a loose calcified body and synovectomy. Histopathological examination confirmed synovial lipomatosis, showing fibrocollagenous tissue lined by hyperplastic synovial membrane with infiltration of mature adipocytes in a myxoid stroma, without evidence of malignancy. Postoperatively, the patient achieved complete symptomatic relief with restoration of normal ankle function at 6 months of follow-up, and no recurrence was noted at 1 year. This case highlights synovial lipomatosis as an important differential diagnosis for chronic ankle swelling and supports surgical synovectomy as an effective treatment with excellent clinical outcome and low recurrence.

Background: Posterior ankle pain has varied etiologies, with sural nerve (SN) entrapment contributing to posterolateral ankle discomfort. The SN is a pure sensory nerve that innervates the lateral ankle and foot up to the fifth metatarsal. Although SN pathologies are known, specific clinical features and management of neuropathy affecting the lateral calcaneal branch of the sural nerve (LCBSN), which supplies the lateral heel, are less defined. This condition is often exacerbated by repetitive ankle dorsiflexion in sports or external compression from tight footwear. We hypothesized that LCBSN lesions cause a distinct pattern of heel pain that is uniquely aggravated by ankle dorsiflexion or shoe contact, thereby distinguishing this entity from other causes of posterior ankle pain. Methods: This retrospective case series included 23 patients. We reviewed records of 23 patients presenting with posterolateral ankle pain and localized LCBSN tenderness. Key diagnostic features included pain aggravation with ankle dorsiflexion or shoe contact, lacking motor deficits. Diagnosis was primarily confirmed by immediate, significant pain relief after local anesthetic injection around the LCBSN. Symptom severity (0-4 scale) and American Orthopaedic Foot &amp; Ankle Society (AOFAS)-hindfoot scores were assessed at 1 month and 1 year post-treatment. Surgical intervention was performed for recurrent pain after 6 months of conservative management. Results: Improvement ( P &lt; .05) in both symptoms and AOFAS-hindfoot scores was observed at 1-month and 1-year follow-ups. Six patients required surgical treatment for recurrent symptoms. Pathologic findings included arterial wall thickening with dense perineural adhesions and scarring (3 cases), neuroma formation (2 cases), and nerve entrapment due to adhesions (1 case). Conservative treatment was effective for the remaining patients. Conclusion: Accurate and timely diagnosis of LCBSN lesions is crucial for effective treatment and enabling prompt return to sports activities. A diagnostic, small volume local anesthetic injection may serve as a practical diagnostic adjunct and an initial therapeutic measure for this clinically significant condition.

Introduction: Acute Achilles tendon rupture is a frequent and disabling injury. When early functional rehabilitation protocols are standardized, the independent effect of surgical versus nonoperative management on rerupture and complications remains unclear, as does the influence of surgical technique. Methods: A systematic review and meta-analysis of parallel-group randomized controlled trials was performed, including adults with acute (≤ 14 days), unilateral, closed Achilles tendon rupture. Nonoperative management with functional bracing and early rehabilitation was compared with open or minimally invasive surgical repair, with both groups following equivalent rehabilitation protocols. Searches of PubMed, Embase, and Cochrane were conducted following PRISMA guidelines. Primary outcomes at 12 months were rerupture and complications, including deep infection, superficial infection, and sural nerve injury. Risk ratios were pooled using a random-effects model, with prespecified subgroup analyses by surgical technique. Results: Seven randomized controlled trials, including 1,003 patients, were analyzed; 410 underwent nonoperative treatment and 593 surgical repair (410 open, 183 MIS). Nonoperative management was associated with a significantly higher 12-month rerupture rate than surgery (RR 3.35; 95% CI 1.35–8.30). No significant differences were observed in deep or superficial infection rates. Sural nerve injury was significantly less frequent in the nonoperative group (RR 0.20; 95% CI 0.05-0.85). Subgroup analysis showed persistently higher rerupture rates with nonoperative treatment than with open surgery, while superficial infection rates were lower in the nonoperative group. Conclusion: When early functional rehabilitation is standardized, surgical repair reduces the risk of rerupture at 12 months, whereas nonoperative management is associated with fewer sural nerve injuries. Treatment selection should be individualized based on patientspecific risks and priorities.

To evaluate functional outcomes, quality of life, and complications after repair of acute Achilles tendon rupture using a minimally invasive Dresden technique. Achilles rupture is common, and management remains debated; minimally invasive approaches aim to preserve functional outcomes while reducing soft-tissue complications and sural nerve injury risk. Single-center case series (2015–2024) at a tertiary orthopedic institute. Adults with noninsertional acute ruptures (≤2 weeks) underwent repair with the Dresden technique, using minor instrument modifications and a standardized rehabilitation protocol. Outcomes included Foot and Ankle Outcome Score (FAOS), Achilles Tendon Total Rupture Score (ATRS), EuroQol 5-Dimension 5-Level questionnaire (EQ-5D-5L), Patient Reported Outcomes Measurement Information System (PROMIS), heel-rise test, calf circumference, maximum plantarflexion/dorsiflexion, and gravitational equinus angle. Thirty-one patients (mean age 37.0 ± 10.55 years; 64.5% male) completed follow-up. Mean scores: FAOS 99.03 ± 1.73, ATRS 98.29 ± 2.64, EQ-5D-5L 0.98 ± 0.03, PROMIS 61.0 ± 0.51 (range 60.3–61.5). Heel-rise: 24/31 (77.4%) maintained single-leg support. Complications: none for infection, wound dehiscence, rerupture, or deep vein thrombosis; two transient sural nerve-related symptoms resolved by 2 months. Plantarflexion: 25.42° (operated) vs 25.45° (nonoperated), mean difference 0.03° (SD 0.18), p &gt; 0.05. Dorsiflexion and gravitational equinus: no significant side-to-side differences. Calf circumference difference 1.08 cm (p &lt; 0.05), not correlated with functional scores (p &gt; 0.05). Very strong, statistically significant intercorrelations were observed among FAOS, ATRS, EQ-5D-5L, and PROMIS. The modified minimally invasive Dresden repair yielded excellent functional outcomes, high quality-of-life scores, and very low complication rates, with no meaningful deficits in ankle range of motion. Calf atrophy was small and not functionally relevant.

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.

Background: The plantaris muscle (PM) shows substantial variability in its proximal belly attachments. Although often deemed vestigial, specific variants may narrow or reshape the popliteal corridor and contribute to vascular (popliteal artery entrapment syndromes, PAES) and neural conflict (TN, CPN, sural nerves). Despite abundant anatomical descriptions of the plantaris, its contribution to neurovascular compression has not been organised into a classification-linked, imaging-integrated framework. Objective: To synthesise adult and foetal anatomical data with clinical-radiological evidence into a classification-linked framework that stratifies vascular and neural compression risk by proximal PM variants, and to propose an integrated risk matrix and variant-directed diagnostic/operative pathway. Methods: Narrative, classification-centred review centred on the Olewnik schema (Types I-VI) and multi-headed/accessory variants. We mapped variant geometry to (1) physiological compromise on provoked Doppler US and (2) anatomical correlates on MRI/MR angiography (MRA) (axial "band sign"), deriving graded risk for vascular and neural axes and an integrated, action-oriented grade per limb. Results: Baseline risk is low for canonical/compact footprints (Type I-IA, Type V), moderate for capsular-junction patterns (Types II/III), and potentially higher-risk for lateral linkage (Type IV; iliotibial band (ITB)/Kaplan fibres continuity) and multi-headed configurations (duplication, bifurcation, ≥3-4 heads; accessory proximal slips). The integrated matrix upgrades risk for a clear band sign, reproducible compromise on provoked Doppler US, or multi-headed/Type IV anatomy and downgrades when rigorous provocation is negative and muscle volume is small. We provide a variant-indexed imaging checklist, common pitfalls (e.g., Type IV misread as ITB thickening; multi-headed variants misread as cyst/tumour), and operative checkpoints to target capsular clefts, lateral bands, tunnels, and accessory slips. Conclusions: A classification-linked, imaging-integrated approach clarifies which proximal PM variants are plausibly associated with neurovascular entrapment (based on case-level evidence) and aligns work-up with targeted decompression and may improve diagnostic precision and inform surgical planning. Clinical relevance: The framework operationalises variant naming in reports, standardises dynamic provocation and axial mapping, and prioritises variants considered higher risk (Type IV; multi-headed) for early multidisciplinary review. Given that most clinical signals derive from case reports/series (Level IV), these recommendations are inferential and should be applied with clinical judgement.

Current consensus guidelines for the electrodiagnosis of polyneuropathy derive from highly standardized investigations performed in specialist centers, raising the question of whether they are equally applicable in everyday general neurology outpatient settings. This multicenter study evaluated the consistency of electrodiagnostic findings in chronic axonal polyneuropathy across different clinics. We retrospectively collected sural sensory nerve action potential (SNAP) and peroneal compound muscle action potential (CMAP) amplitude data from 62 patients with cryptogenic axonal polyneuropathy. Recordings were obtained both in general neurology outpatient clinics and in a specialized neuromuscular center in the Netherlands. After excluding technically inadequate waveforms, we assessed agreement and inter-center variability using Bland-Altman plots, standard error of measurement (SEM), intraclass correlation coefficients (ICC), relative inter-trial variation (RIV), concordance rates, and Krippendorff's α. In quality review, 22% of sural and 2% of peroneal recordings from general neurology clinics were either reclassified or excluded because of a technically inadequate waveform. Inter-center variability was substantial for sural SNAP (ICC 0.49; RIV -200% to 200%; SEM 81%) and peroneal CMAP amplitudes (ICC 0.82; RIV -78% to 110%; SEM 37%). Agreement was poor for the classification of sural SNAP (concordance rate 69%; Krippendorff's α 0.36) and peroneal CMAP (concordance rate 73%; Krippendorff's α 0.45) as normal/abnormal, and for the electrodiagnosis of polyneuropathy (concordance rate 71%; Krippendorff's α -0.15). In everyday clinical practice, substantial variability in sural SNAP and peroneal CMAP amplitudes limits consistent electrodiagnosis of polyneuropathy. Our findings underscore the necessity of rigorous quality control during nerve conduction studies.

'Hyperglycaemia in pregnancy' (HIP) is one of the most common antenatal complications, affecting about one in six pregnancies globally. HIP is sub-classified into two categories, namely 'gestational diabetes mellitus' (GDM) and 'overt diabetes mellitus' (ODM). Pregnancy is characterised by the accumulation of adipose tissue and a growing placenta, acting as endocrine organs, thus intensifying the hyperglycaemic environment and building up oxidative stress by dysregulation of metabolic pathways, instigating peripheral neuropathy. Due to paucity in existing literature on neurological influences of GDM and ODM, this follow-up study was planned to detect subclinical peripheral neuropathy by nerve conduction studies (NCS) and its correlation with biochemical parameters among them. Thirty-nine pregnant women were divided into three groups: control, GDM and ODM. The NCS (sural and ulnar nerves) and biochemical parameters, that is, fasting plasma glucose (FPG), glycated haemoglobin (HbA1c), serum fasting insulin, homeostatic model assessment of insulin resistance (HOMA-IR), serum chromium, serum N-carboxy-methyl lysine, total cholesterol, low-density lipoprotein, triglycerides and high-density lipoprotein, were recorded during different stages of gestation, that is, 24-28 weeks (first visit), 32-38 weeks (second visit) and 6-12 weeks after parturition (third visit). Nerve conduction studies reveal significant alterations in diabetic pregnant groups compared to control pregnant women, particularly in sensory latencies and amplitudes of the sural and ulnar nerves. Significant hyperglycaemia (FPG, HbA1c), hyperinsulinaemia, and elevated HOMA-IR in GDM and ODM groups confirm insulin resistance and poor glycaemic control during pregnancy and postpartum. Chromium levels were markedly lower in diabetics (p = .001). This study necessitates ongoing metabolic and neurological monitoring in GDM and ODM after childbirth. Early screening and focused interventions, including micronutrient supplementation and lifestyle modifications, may help avert progression to overt neuropathy and mitigate long-term complications.

Background and Objectives: Peripheral nerve adaptation to different pathological conditions is accompanied by the remodelling of the nerve's extracellular matrix (ECM). Ischemic conditions caused by peripheral vascular disease are known to affect the function of peripheral nerves; however, the morphological changes to their ECM remain insufficiently examined and understood. Bearing in mind that alterations in collagen I, collagen IV, and laminin content may compromise peri- and endoneurial integrity, the aim of our study was to analyse whether peripheral vascular disease (PVD) induces distinct ECM alterations in the human sural nerve compared with the adaptive remodelling observed in ageing. Materials and Methods: The study aimed to determine the amount of type I and IV collagen and laminin in the perineurium and endoneurium of human peripheral nerves from patients with PVD and to compare the results with those of the age-matched controls. Twenty human sural nerves were harvested from cadavers and amputated limbs-10 from each-and were further distributed into two age groups: below and over 75 years of age. The sural nerve tissue samples were stained immunohistochemically for collagen I, collagen IV, and laminin. We measured the percentage content of these ECM components in the perineurium and endoneurium. For morphometric analysis, we used ImageJ software v1.54d. Results: Perineurial collagen type I and laminin were decreased in the older PVD group, relative to both the younger PVD and the older age group. Within the endoneurium, the expression of collagen type IV was higher in older PVD patients, while both collagen type I and laminin were deposited in lower amounts in the same group compared with the younger PVD group. Conclusions: These findings suggest that age-related ECM remodelling in the peripheral nerve may be impaired under ischemic conditions in older adults, with implications for surgical grafting strategies or neural conduit therapies aimed at promoting functional regeneration.

Peripheral nerve blockade of the lower extremity focuses on two major nerves: the sciatic and femoral. Both nerves lie near large vascular structures and can require significant volumes of injectate to produce a reliable analgesic blockade. Moreover, blockade of these nerves leads to corresponding muscle weakness that can be unnecessary or even undesirable for recovery following surgery.New-generation, high-resolution ultrasound (US) probes facilitate the visualization of selective nerves in the lower extremity. Therefore, blockade of these nerves can be performed at multiple locations that can be individualized for specific patients undergoing forefoot and midfoot surgeries. This article describes an educational approach for selective lower extremity blocks of the saphenous, tibial, sural, superficial peroneal, and deep peroneal nerves with corresponding clinical applications for common forefoot and midfoot surgeries. These techniques are presented in a stepwise approach with surface and corresponding US anatomy. Cadaveric dissections are also included with some of the described techniques to emphasize the anatomical relationships. Each of these techniques, in this educational review, begins with easily identifiable surface landmarks and follows a stepwise approach.Understanding of these lower extremity selective nerve blocks allows for targeted low-volume blockade of specific sensory distributions, individualized to each patient.

To explore the pathological changes of peripheral neuropathy in Sjogren's syndrome and the role of macrophages in it. Methods: Sural nerve biopsy was performed in 12 patients diagnosed with primary Sjogren's syndrome associated peripheral nervous system involvement (pSS-PN) and 3 traumatic amputees. First, we collected clinical data and electromyography (EMG) findings from 12 pSS-PN patients. Histological assessment of sural nerve specimens was subsequently performed using hematoxylin-eosin (HE) and neurofilament protein (NF) staining under light microscopy. The ultrastructural changes of peripheral nerves were observed by transmission electron microscopy (TEM). Macrophage types were labeled with CD206 and iNOS antibodies by immunohistochemistry and immunofluorescence. The 3 control cases underwent HE staining, CD68 IHC, and TEM. Patients with pSS-PN typically present with symptoms such as neuropathic pain, limb weakness, and sensory disturbances. HE and NF staining revealed mild-to-severe damage to both myelinated and unmyelinated fibers in peripheral nerves, with some cases showing predominant small‑vessel inflammation. Immunohistochemistry and immunofluorescence demonstrated infiltration of CD68⁺ macrophages-predominantly of the M2 phenotype-around small vessels and within nerve bundles. Electron microscopy further illustrated that macrophages progressively strip and engulf myelin sheaths, leaving bare axons. In addition, inflammatory cell infiltration within vasa nervorum led to blood‑cell stasis, endothelial damage, platelet aggregation, and eventual vascular obstruction and collapse. These clinicopathological observations establish vasculitic peripheral neuropathy as the predominant form of pSS‑PN. This prominent infiltration of M2 macrophages in the affected nerves suggests that they play a pivotal role in the pathogenesis of pSS‑PN, potentially offering a novel therapeutic direction for this condition. Key Points • Vasculitic peripheral neuropathy is the main pattern of pSS‑PN, with M2 macrophages heavily infiltrating affected nerves. • Ultrastructural evidence shows macrophages actively stripping myelin sheaths, leading to axonal exposure. • These findings highlight M2 macrophages as a potential new therapeutic direction for pSS-PN.