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 & 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 < .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.

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.

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.

To evaluate the relationship between the diabetic profile and human β-nerve growth factor (HβNGF), calcitonin gene-related peptide (CGRP), endothelin-1 (ET-1), and von Willebrand factor (VWF) in distinguishing painful from painless diabetic neuropathy. A case-control study. Department of Diabetic Foot, Baqai Institute of Diabetes and Endocrinology, Karachi, Pakistan, from October 2023 to August 2024. A total of 150 patients with Type I or II diabetes were recruited after IRB approval. Following informed consent, data on demographics, clinical examination, nerve conduction studies (peroneal, tibial, median, and sural nerves), and biochemical parameters (FBS, RBS, HbA1c, HβNGF, CGRP, ET-1, and VWF) were collected. Based on the NCS and DN4 questionnaire, participants were categorised into controls (no neuropathy), painless neuropathy, and painful neuropathy groups. Data were analysed using IBM SPSS version 23.0, with p <0.05 considered significant. Patients with painful neuropathy exhibited significantly lower VWF levels (p = 0.002) and higher fasting blood glucose (p = 0.01). Age, BMI, weight, and duration of diabetes differed significantly among the groups. Logistic regression identified duration of diabetes as the only independent predictor of painful neuropathy in both univariate (OR = 1.30) and multivariate analyses (OR = 1.47). FBS showed a positive correlation with diabetes duration (r = 0.188, p = 0.02). The duration of diabetes independently predicts painful diabetic neuropathy. Reduced VWF levels in patients with painful neuropathy suggest a potential role as a diagnostic biomarker. Further longitudinal studies are recommended. Diabetes mellitus, Diabetic peripheral neuropathy, β-Nerve growth factor, CGRP, Endothelin-1, von Willebrand factor.

Neuromuscular ultrasound and nerve conduction studies as complementary tools for screening of diabetic peripheral neuropathy.

This study investigates the relationship between National Cancer Institute Common Terminology Criteria (NCI-CTC) for grading bortezomib-induced peripheral neuropathy (BIPN) and objective motor/sensory nerve dysfunctions assessed by nerve conduction studies (NCS). It also evaluates the correlation between specific nerve conduction abnormalities and progression- free survival (PFS). Thirty-three patients with multiple myeloma developing peripheral neuropathy during bortezomib treatment were enrolled. Participants were grouped based on NCI-CTC toxicity scores (< 2, n=17; ≥ 2, n=16). Comprehensive NCS were performed, assessing compound muscle action potentials (CMAP), motor conduction velocities (MCV), sensory nerve action potentials (SNAP), and sensory conduction velocities (SCV) across ulnar, median, tibial, peroneal, sural, and superficial peroneal nerves. Correlation analyses were used to examine the association between NCS parameters and PFS. Patients with higher NCI-CTC grades (≥ 2) exhibited significant reductions in motor and sensory nerve conduction parameters. Notably, the peroneal nerve showed significant decreases in CMAP (p=0.0059) and MCV (p=0.0223). The superficial peroneal nerve displayed a significant reduction in SCV (p=0.0189). A strong positive correlation was found between median nerve SNAP and longer PFS (r=0.558, p=0.001). The findings indicate that higher clinical grades of BIPN (NCI-CTC ≥ 2) are associated with objective neurophysiological evidence of worsened nerve function, with the peroneal nerve being particularly affected. The correlation between median nerve SNAP and PFS suggests that NCS parameters could potentially serve as prognostic markers in patients with BIPN. Bortezomib-induced neurotoxicity leads to significant impairments in both motor and sensory nerve conduction. Median nerve SNAP shows promise as a predictor for PFS, underscoring the potential value of NCS in monitoring neurotoxicity and guiding clinical management in patients receiving bortezomib.

Introduction. Chemotherapy (CT) with platinum and taxane drugs often leads to chemotherapy-induced peripheral neuropathy (CIPN), which significantly impairs patients’ quality of life. CIPN is diagnosed based on symptoms and neurological examination, which underscores the need for objective biomarkers. Promising criteria for peripheral nerve damage are neurofilaments, in particular the light chain (NfL) and peripherin. NfL is released during axonal damage but is not specific to the peripheral nervous system. Peripherin, in contrast, is expressed exclusively in peripheral neurons and is considered a more specific marker; however, its detection is challenging. The aim of the study was to evaluate serum levels of neurofilament and peripherin using the ELISA method in patients with solid tumors undergoing CT. Materials and methods. The study included 66 patients with newly diagnosed solid tumors before starting CT with platinum or taxanes. Patients with known risk factors for polyneuropathy and those taking medications with neurotoxic effects were excluded. After treatment, 51 patients were examined. Neurological examination with assessment using the NCI-CTCAE and NDS scales, nerve conduction study (SRAR index, amplitude of the sural nerve action potential), and assessment of intraepidermal nerve fiber density were performed. Serum levels of NfL and peripherin were measured using ELISA before and approximately 4.5 months after CT. Preanalytical sample processing was standardized. Results. After the CT course all patients showed a significant increase in NfL levels (p 0.0003). The most pronounced increase in the indicator (~fivefold) was recorded in male patients (p 0.001) and in the group of patients with malignant neoplasms in the gastrointestinal tract (p = 0.001). The concentration of peripherin in all analyzed samples was zero, likely due to the low ELISA sensitivity. In patients with developed CIPN, the NfL level after treatment was significantly higher (p = 0.001); however, no prognostic value for predicting neuropathy was found (AUC = 0.526; p = 0.803). At the same time, a moderate negative correlation was found between the NfL level and the density of intraepidermal nerve fibers (r = –0.416; p = 0.012). No statistically significant association was found between NfL concentration and electrophysiological parameters (SRAR index and sural nerve action potential amplitude). Conclusion. NfL is a promising but insufficiently specific biomarker for monitoring patients with CIPN. The absence of a detectable level of peripherin by ELISA limits its clinical application and suggests the use of more sensitive analytical methods.

Background/Objectives: The peroneus longus tendon (PLT) is increasingly used as an autograft for anterior cruciate ligament reconstruction (ACLR). However, during PLT harvest, the necessity of distal peroneus longus-to-peroneus brevis (PL-to-PB) tenodesis for the potential preservation of donor ankle function and medial longitudinal arch alignment remains unclear. This study compared ankle function, donor-site morbidity, complications, and weight-bearing radiographic foot alignment after PLT harvest with and without distal tenodesis. Methods: Between January 2020 and December 2024, 92 primary ACLR cases using an ipsilateral PLT autograft were retrospectively screened; 60 patients with available bilateral weight-bearing comparative foot radiographs were included and categorized into a tenodesis group (n = 30) or a non-tenodesis group (n = 30). Ankle outcomes included American Orthopedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot and Foot and Ankle Disability Index (FADI) scores, ankle range of motion (ROM), and donor-site complications. Radiographic alignment was assessed using Meary's angle and calcaneal pitch angle on bilateral weight-bearing lateral foot radiographs, including side-to-side differences. Results: Follow-up duration was comparable between groups (18.5 ± 4.4 vs. 16.8 ± 3.4 months, p = 0.113). No patient demonstrated clinically relevant loss of ankle range of motion or strength at final follow-up. AOFAS (97.3 ± 4.9 vs. 95.0 ± 5.5, p = 0.078) and FADI (96.8 ± 5.2 vs. 95.3 ± 5.5, p = 0.091) scores were similarly high in the tenodesis and non-tenodesis groups, respectively. Sural nerve sensory disturbance occurred in 6/30 (20.0%) versus 5/30 (16.7%) patients (p = 0.739), and no harvest-site infection was observed. On weight-bearing radiographs, Meary's angle and calcaneal pitch angle did not differ significantly between groups on the operated side (Meary: 7.99 ± 6.76 vs. 4.76 ± 6.32°, p = 0.061; calcaneal pitch: 23.19 ± 5.94 vs. 21.41 ± 4.64°, p = 0.201) or intact side (Meary: 7.05 ± 6.89 vs. 5.36 ± 6.11°, p = 0.320; calcaneal pitch: 23.33 ± 5.43 vs. 22.00 ± 4.48°, p = 0.305). Side-to-side differences were small and comparable (Δ Meary: 0.94 ± 3.97 vs. -0.60 ± 3.58°, p = 0.120; Δ calcaneal pitch: -0.14 ± 3.35 vs. -0.59 ± 3.29°, p = 0.603). Conclusions: Distal PL-to-PB tenodesis did not appear to provide measurable advantages in donor-ankle patient-reported outcomes or weight-bearing radiographic foot alignment compared with no tenodesis after PLT harvest for ACLR.

Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive disorder caused by variants in the CYP27A1 gene, resulting in cholestanol accumulation in various tissues, including peripheral nerves. Polyneuropathy is common but often under-recognized in CTX. This study aimed to evaluate the cross-sectional area (CSA) of peripheral nerves in CTX. Six genetically confirmed CTX patients underwent clinical, electrophysiological, and ultrasonographic evaluations. Clinical severity was assessed using the Scale for the Assessment and Rating of Ataxia (SARA) and the Polyneuropathy Disability (PND) score. Nerve ultrasound was performed at standardized sites of the median, ulnar, tibial, and sural nerves, and at the supraclavicular brachial plexus. CSA values were compared with healthy controls. Nerve conduction studies (NCS) identified demyelinating polyneuropathy in three patients. However, ultrasound showed nerve enlargement in all six, including those with normal NCS. The supraclavicular brachial plexus was enlarged in every patient. In 5 adult patients, enlargement was most consistently observed in the median nerve (4 at the wrist and forearm; 5 at the cubital fossa and upper arm), the ulnar nerve at the upper arm (5), and the fibular nerve at the fibular head (4). This study demonstrates that nerve ultrasound can detect peripheral nerve enlargement in CTX, even in preclinical stages of polyneuropathy. Enlargement of peripheral nerves may be a sensitive marker of disease severity and peripheral nerve involvement. The role of nerve ultrasound as a diagnostic tool in CTX is promising, and future longitudinal studies are needed to determine its value in disease monitoring.

Cutaneous arteritis (CA) is a skin-limited medium-vessel vasculitis. Some patients with CA also exhibit extracutaneous manifestations, such as vasculitic peripheral neuropathy (VPN). VPN is likely underdiagnosed because nerve biopsies are invasive and often impractical. This study proposed the concept of provisional CA to better identify patients with neuropathic involvement and to evaluate the prevalence and electrophysiological features of VPN. We retrospectively analysed patients with provisional CA treated at the Severance Hospital between 2011 and 2024. Provisional CA was defined as skin-limited medium-vessel vasculitis with neuropathic symptoms in the lower limbs irrespective of a nerve biopsy. VPN was defined based on established clinical and electrophysiological criteria. Demographic, clinical, and laboratory data were collected from the electronic medical records. Thirty-six patients met the provisional CA criteria. The median age was 51.0 years, and 36.1% of the patients were male. Among these, 22 (61.1%) demonstrated electrophysiological evidence of VPN. Pure sensory neuropathy and sensorimotor involvement were observed in 59.1% and 40.9% of patients, respectively. The most frequently affected nerves were the peroneal (63.6%) and sural (54.5%) nerves. No significant differences were found between the patients with and without VPN in terms of age, sex, skin manifestations, or laboratory findings. VPN was prevalent in patients with provisional CA. Clinical features alone were insufficient to predict nerve involvement. Nerve conduction studies serve as a valuable diagnostic tool when a nerve biopsy is not feasible and may facilitate the earlier detection and management of neuropathic complications in skin-limited vasculitis.

Summary:Segmental peripheral nerve injuries, particularly those involving long nerve gaps, pose a significant challenge in reconstructive surgery. Conventional strategies, such as nerve autografts or processed allografts, are often limited by inadequate length or poor regenerative outcomes, especially in traumatized wound beds. Nerve flaps offer the theoretical advantage of enhanced axonal regeneration through improved perfusion and support of Schwann cell viability but are rarely used due to technical complexity and limited donor options. We present a unique case of a free sural nerve flap used to reconstruct a 7-cm segmental defect of the tibial nerve following blast trauma in a 23-year-old man. A composite flap consisting of the sural nerve and lesser saphenous vein was harvested with preservation of the bridging adipofascial tissue to maintain perfusion to the nerve. The lesser saphenous vein was anastomosed to the retrograde peroneal artery distally and ligated proximally, whereas the sural nerve was divided and used as a double-barrel cable graft across the defect. Intraoperative Doppler and SPY angiography confirmed perfusion of the nerve through the preserved adipofascial connections. The patient was recently seen in our clinic at 17 weeks postoperation. He demonstrated undetectable 2-point discrimination in all nerve distributions of his foot but is ambulatory. This case demonstrates the feasibility and potential utility of a free vascularized sural nerve flap for reconstructing extensive peripheral nerve defects, particularly in cases where standard techniques are inadequate.

Cerebellar ataxia, neuropathy, and vestibular areflexia syndrome (CANVAS) is caused by biallelic pathogenic repeat expansions in the RFC1 gene. Chronic cough can precede the neurological features of CANVAS by decades and, in some instances, may be the sole clinical manifestation. However, the prevalence of biallelic RFC1 repeat expansions among patients with unexplained chronic cough (UCC), as well as the diagnostic utility of targeted neurological screening in this setting, remains unclear. In this 6-month pilot study, 13 consecutive patients with UCC underwent a standardized neurological evaluation and screening nerve conduction studies (NCS) during a single clinical visit. All patients were subsequently tested for RFC1 repeat expansions. Those carrying biallelic pathogenic expansions (RFC1+) were further assessed with extended NCS, electrochemical skin conductance (ESC), and thermal quantitative sensory testing (QST). Three patients (23%) were RFC1+. Clinical and demographic features did not significantly differ between RFC1+ and RFC1- groups. All RFC1+ individuals exhibited marked bilateral reduction in radial and sural sensory nerve action potential (SNAP) amplitudes. In contrast, only two RFC1- patients showed reduced sural SNAPs. QST revealed impaired cold detection thresholds with preserved warm detection in all RFC1+ cases, while ESC results were normal. These findings suggest that standardized neurological and electrophysiological assessment can detect subclinical sensory neuropathy in UCC patients lacking overt neurological symptoms, thereby identifying those more likely to carry RFC1 expansions. The observed 23% prevalence supports incorporating RFC1 testing into the diagnostic approach for selected UCC patients, particularly when radial SNAP amplitudes are reduced.

Intraneural ganglion cysts (IGCs) are mucinous lesions that originate from adjacent synovial joints. According to the articular theory, synovial fluid tracks from a joint into the parent nerve through an articular branch. In uncommon sites such as the sural nerve, this connection can be difficult to identify. This report illustrates the use of a preoperative intra-articular fluorescein injection as a tool to identify the articular branch during surgery. A 60-year-old woman presented with lateral foot pain, numbness, and a palpable mass along the left sural distribution. MRI showed a large cyst extending along the course of the sural nerve with connection to the subtalar joint. Fluorescein was injected preoperatively into this joint to detect the articular branch intraoperatively with ultraviolet illumination. The connection was transected at the joint origin, and the cyst was decompressed, preserving the parent nerve. Postoperatively, the patient had complete pain relief and sensory recovery, and MRI at 3 and 8 months confirmed resolution of the cyst. Sural IGCs conform to the articular theory and can be managed effectively by transection of the articular branch. Preoperative intra-articular fluorescein injection is a useful tool to detect the articular branch that can be difficult to find in sural IGCs. https://thejns.org/doi/10.3171/CASE251018.

Quantitative sensory testing (QST) is increasingly used to stratify patients with peripheral neuropathic pain into sensory phenotypes that may reflect distinct underlying pain mechanisms. Yet, their correspondence with objective measures of peripheral nerve damage remains unclear. This study investigated whether QST-based phenotypes are associated with objective measures of peripheral nerve damage in patients with painful polyneuropathy. We retrospectively analyzed data from 130 patients with painful polyneuropathy, who underwent nerve conduction studies, distal leg skin biopsy, and QST at the foot dorsum. Using an established algorithm, patients were classified into 4 QST sensory phenotypes: Sensory Loss, Mechanical Hyperalgesia, Thermal Hyperalgesia, and Healthy. We assessed sural sensory nerve action potential (SNAP) amplitude, intraepidermal nerve fiber density using PGP9.5, TRPV1, and GAP43 immunostaining, as well as TRPV1 and GAP43/PGP9.5 ratios. These parameters were compared across QST phenotypes. Associations were analyzed using multinomial logistic regression models. Patients with the Sensory Loss phenotype-the most prevalent subgroup-had significantly lower sural SNAP amplitudes and intraepidermal nerve fiber densities of PGP9.5, TRPV1, and GAP43, compared with the other phenotypes. Compared with Sensory Loss, Mechanical Hyperalgesia demonstrated higher sural SNAP amplitudes (P < 0.0001), TRPV1/PGP9.5 (P = 0.018), and GAP43/PGP9.5 ratios (P = 0.011), whereas Thermal Hyperalgesia was associated with higher sural SNAP amplitudes (P = 0.041) and PGP9.5 intraepidermal nerve fiber density (P = 0.025). Our study demonstrates that QST-based phenotypes are associated with distinctive patterns of peripheral nerve damage in patients with painful polyneuropathy. These findings suggest that QST phenotyping may capture different aspects of underlying pain mechanisms, supporting its value for mechanism-based patient stratification.

Objective: To assess irisin hormone in diabetic peripheral neuropathy and to assess the relation between irisin hormone and nerve conduction study. Study Design: Meta-analysis of observational studyPlace and Duration of Study: This study was conducted at the Marjan Teaching Hospital in Babil City in Endocrinology and Diabetes Center from 1st January 2025 to 31st March 2025. Methods: Forty one diabetic patients divided into two groups, 22 patients with diabetic peripheral neuropathy and 19 patients without diabetic peripheral neuropathy. Patients with diabetic peripheral neuropathy are diagnosed based on history and clinical examination with assistance of Michigan Neuropathy Screening Instrument scoring system. Serum irisin, nerve conduction study of sural nerve (amplitude, velocity) and sural/radial amplitude ratio are doing for all patients. Results: Irisin hormone level was significantly lower in patients with diabetic peripheral neuropathy (143.18 pg/ml) than patient without diabetic peripheral neuropathy (203.29 pg/ml), (p=0.0001) and the relation between irisin hormone and sural nerve conduction study and sural/radial amplitude ratio in both groups show no significant correlation. Conclusion: The irisin hormone level is significantly decreased in DPN patients. There is no significant correlation between irisin and nerve conduction study of sural nerve and sural/radial amplitude ratio.

Recovery after axotomy of a peripheral nerve is dependent on regrowth of axons from the point of injury to distal sensorimotor tissues and can be complicated by nerve branching. Little is known about regeneration of sensory axons that encounter branch points distal to injuries. The experiments reported here focused on this question and sought to assess the fidelity of sensory axon regeneration, where fidelity is defined as an axon that originally innervated a distal branch of the sciatic nerve regenerated into that same distal branch after injury, with serial retrograde labeling. Rats with segmental sciatic nerve injuries were treated with linear or branched grafts, with retrograde labels injected into the peroneal and sural branches of the sciatic nerve prior to injury and 12 weeks after. Lumbar dorsal root ganglia 4 and 5 were collected after 12 weeks and were imaged to determine the fidelity of sensory axon regeneration. Results show that the fidelity of sensory regeneration into these two branches differed by the branch and the graft type. Interestingly, the fidelity of sensory axon reinnervation was greater into the peroneal nerve, which is a mixed sensorimotor nerve, compared to the sural nerve, which is a sensory nerve. This occurred in both graft types and suggests that the fidelity of sensory regeneration is improved into mixed branches distal to the PNI compared to sensory branches and supports why regeneration of segmental branched defects may be superior using anatomically matching branched grafts.

The activation of classical and/or lectin complement pathway for the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy.