Nerve Fibers Research Articles

From Sudoscan to bedside: theory, modalities, and application of electrochemical skin conductance in medical diagnostics

The human body has two main types of sweat glands: apocrine and eccrine. Eccrine glands are widely distributed across the skin, including areas with hair. While the eccrine glands on palms and soles help improve grip, those on the rest of the body primarily aid in thermoregulation. Sudomotor function, which controls sweating, is regulated by the sympathetic division of the autonomic nervous system through cholinergic and adrenergic pathways. The activation of eccrine glands involves intricate processes, including neurotransmitter binding, ion channel modulation, and voltage generation. Sudoscan technology utilizes electrochemical skin conductance (ESC) to non-invasively measure sudomotor function. This method, which has been standardized for accuracy, has established normative benchmarks and has proven reliable across diverse populations. Sudoscan’s diagnostic performance is comparable to invasive methods such as intraepidermal nerve fiber density testing, making it a valuable tool for diagnosing small fiber neuropathy. Moreover, it has been shown to correlate with corneal nerve fiber length, providing insights into various neuropathic conditions. Compared to traditional sudomotor function tests, Sudoscan proves superior in terms of its accessibility, simplicity, and reliability, with the potential to replace or complement existing diagnostic methods. It is important to differentiate ESC, as measured by Sudoscan, from other skin conductance measures, such as galvanic skin response (GSR) or electrodermal activity (EDA). Although these methods share a common physiological principle, ESC is specifically designed for diagnosing sudomotor function, unlike GSR/EDA, which is typically used for continuous monitoring. Sudoscan’s success has led to its integration into consumer health devices, such as the BodyScan from Withings, showcasing its versatility beyond clinical settings. Future research may explore ESC applications in diverse medical fields, leveraging real-world data from integrated consumer devices. Collaborative efforts between researchers and engineers promise to offer new insights into sudomotor function and its implications for broader health monitoring. This study provides a comprehensive overview of ESC, including topics such as eccrine gland physiology, sudomotor function, Sudoscan technology, normative benchmarks, diagnostic comparisons, and potential future applications.

Nanoparticle-mediated synergistic disruption of tumor innervation and redox homeostasis for potent antineoplastic therapy

Innervation is closely linked to several biological processes that promote tumor growth, making it an increasingly promising therapeutic target. In this study, biomimetic hollow MnO2 nanocarriers camouflaged with tumor cell membranes (HMLC) are developed to encapsulate lidocaine, an innervation inhibitor, for effective antineoplastic therapy. This approach aims to suppress nerve fiber growth and induce intracellular redox imbalance. Benefiting from the tumor-homing effect, HMLC accumulates in cancerous tissue during circulation and is endocytosed by tumor cells through homologous membrane fusion. Once inside the cells, MnO2 can be degraded by the overproduced glutathione and H2O2, leading to the tumor-specific release of Mn2+ and lidocaine. The Mn2+-mediated Fenton-like reaction promotes the accumulation of reactive oxygen species, and the resulting oxidative stress, combined with glutathione depletion, exacerbates redox imbalance. Simultaneously, the released lidocaine downregulates nerve growth factor and neuronatin. The reduction in nerve growth factor significantly inhibits nerve fiber formation and infiltration in tumor tissue, while the decrease in neuronatin reduces intracellular Ca2+, which helps prevent metastasis. Overall, this strategy highlights the potential of nanoparticle-based tumor innervation disruptors in antineoplastic therapy.

Promotion of nerve regeneration and motor function recovery in SCI rats using LOCAS-iPSCs-NSCs

BackgroundSpinal cord injury (SCI) is a severe traumatic spinal condition with a poor prognosis. In this study, a scaffold called linearly ordered collagen aggregates (LOCAS) was created and loaded with induced pluripotent stem cells (iPSCs)-derived neural stem cells (NSCs) from human umbilical cord blood derived mesenchymal stem cells (hUCB-MSCs) to treat SCI in a rat model.MethodsThe rats underwent a complete transection SCI resulting in a 3-mm break at either the T9 or T10 level of the spinal cord.ResultsScanning electron microscope analysis revealed a uniform pore structure on the coronal plane of the scaffold. The LOCAS had a porosity of 88.52% and a water absorption of 1161.67%. Its compressive modulus and stress were measured at 4.1 MPa and 205 kPa, respectively, with a degradation time of 10 weeks. After 12 weeks, rats in the LOCAS-iPSCs-NSCs group exhibited significantly higher BBB scores (8.6) compared to the LOCAS-iPSCs-NSCs group (5.6) and the Model group (4.2). The CatWalk analysis showed improved motion trajectory, regularity index (RI), and swing speed in the LOCAS-iPSCs-NSCs group compared to the other groups. Motor evoked potentials latency was lower and amplitude was higher in the LOCAS-iPSCs-NSCs group, indicating better neural function recovery. Histological analysis demonstrated enhanced neuronal differentiation of NSCs and nerve fiber regeneration promoted by LOCAS-iPSCs-NSCs, leading to improved motor function recovery in rats. The LOCAS scaffold facilitated ordered neurofilament extension and guided nerve regeneration.ConclusionsThe combination of LOCAS and iPSCs-NSCs demonstrated a positive therapeutic impact on motor function recovery and tissue repair in rats with SCI. This development offers a more resilient bionic microenvironment and presents novel possibilities for clinical SCI repair.

Three-dimensional visualization of uterine nerve fiber distribution using fluorescence micro-optical sectioning tomography (fMOST): A pilot study.

This study aimed to observe and quantitatively analyze the morphology and distribution of uterine nerve fibers using fluorescence micro-optical sectioning tomography (fMOST). The goal was to provide an accurate morphological reference for pathological evaluations of uterine nerves. Using fMOST technique, we observed and analyzed the distribution of nerve fibers within the uterus. Our findings revealed a radial dispersion of nerve fibers radiating from myometrium to endometrium. The cervix uteri region exhibited a high density of nerve fibers, displaying terminations in a flower spray pattern. In contrast, nerve fibers in corpus uteri were comparatively sparse. However, we identified a unique "vine-like" pattern of a single nerve fiber extending from myometrium to endometrial layer in areas with concentrated nerves. The fMOST technique is able to effectively elucidate the morphology and distribution of uterine nerve fibers. This method enables three-dimensional visualization of nerves in myometrium and offers a novel approach to observe the pathological changes in uterine nerves.

Glucose-lowering medication associated with weight loss may limit the progression of diabetic neuropathy in type 2 diabetes.

Obesity is a major risk factor for diabetic peripheral neuropathy (DPN) in type 2 diabetes (T2D). This study investigated the effect of glucose lowering medication associated with weight change on DPN. Participants with T2D were grouped based on whether their glucose lowering medications were associated with weight gain (WG) or weight loss (WL). They underwent clinical, metabolic testing and assessment of neuropathic symptoms, vibration perception threshold (VPT), sudomotor function and corneal confocal microscopy (CCM) at baseline and follow-up between 4 and 7 years. Of 76 participants, 69.7% were on glucose lowering medication associated with WG, and 30.3% were on glucose lowering medication associated with WL. At baseline, participants in the WG group had a significantly longer duration of diabetes (p < .01), higher douleur neuropathique en 4 (DN4) score (p < .0001) and VPT (p = .01) compared with those in the WL group. Over a 56-month period, participants in the WG group showed no significant change in body weight (p = .11), HbA1c (p = .18), triglycerides (p = .42), DN4 (p = .11), VPT (p = .15) or Sudoscan (p = .43), but showed a decline in corneal nerve fiber density (CNFD), corneal nerve branch density (CNBD) and corneal nerve fiber length (CNFL) (p < .0001). Participants in the WL group showed a reduction in weight (p = .01) and triglycerides (p < .05), no change in DN4 (p = .30), VPT (p = .31) or Sudoscan (p = .17) and a decline in the corneal nerve branch density (p < .01). Participants treated with glucose lowering medication associated with weight gain had worse neuropathy and greater loss of corneal nerves during follow-up, compared to patients treated with medication associated with weight loss.

Neuronal Intranuclear Inclusion Disease with a Corneal Disorder: A Case Report

Background: Neuronal intranuclear inclusion disease (NIID) is a progressive neurodegenerative disorder characterized by the formation of intranuclear inclusions in cells. Adult-type NIID usually develops in elderly patients with various clinical manifestations and is sometimes accompanied by ocular symptoms. A case of adult-onset NIID with early and unique manifestations, including a progressive corneal defect and retinal changes, which are concerning at a young age, is reported. Case Presentation: A 29-year-old woman with adult sporadic NIID presented to our department with a progressive corneal disorder. Her neurological symptoms started at the age of 22 years, and she was diagnosed with NIID by skin biopsy and genetic testing. Ocular examination revealed bilateral corneal superficial punctate keratitis, right corneal opacity, decreased vision, nocturnal lagophthalmos, and early retinal changes. Corneal nerve fiber atrophy was detected by in vivo confocal microscopy. With a Cochet–Bonnet aesthesiometer, the progression of NIID and decreased corneal sensation were confirmed. Findings consistent with neurotrophic keratitis and keratoconjunctivitis due to nocturnal lagophthalmos were both suggested as being complications of her underlying NIID. Treatment with punctal plugs, sodium hyaluronate eye drops, diquafosol sodium eye drops, systemic and local antivirals, and local steroid medications resulted in the gradual improvement in the irregularity and opacity of the epithelium. Conclusions: NIID may lead to neurotrophic keratopathy due to impairment of the corneal sensory nerves. Nocturnal lagophthalmos is a remarkable finding in a case of NIID. The findings in the present case highlight the complex and multifaceted nature of NIID, with neurological and ocular manifestations requiring a multidisciplinary approach to management.

Evaluation of retinal nerve fiber layer and choroidal structure in obese children and adolescents

Aim: Obesity-related vascular damage and endothelial dysfunction have deleterious effects on the ocular vasculature. It was aimed to examine optical coherence tomography (OCT) parameters in obese and overweight children and to define their relationship with metabolic markers in this study. Methods: The patient group consisted of 26 obese, 24 overweight patients aged between 8 and 18 years. The control group consisted of 25 healthy children with normal body mass index (BMI). This was a cross-sectional observational study. Serum glucose, lipid parameters, and homeostasis model assessment of insulin resistance (HOMA-IR) were investigated. Measurement of choroidal thickness was performed with Cirrus HD-OCT (Carl Zeiss Meditec Inc., Dublin, CA, USA). Retinal nerve fiber layer (RNFL) thickness was determined by an automatic computer algorithm without the need for user measurement. Results: There were no differences in subfoveal, nasal, temporal choroidal thickness, and RNFL between obese, overweight, and control groups (p&gt;0.05). A positive (linear) moderate relationship was found between RNFL and the HOMA-IR of 26 patients in the obese group (r=0.389) (p=0.049). A positively weak correlation was found between height and RNFL in obese patient group (r=0.264, p=0.028). Conclusion: In the study, RNFL thickness increased as HOMA-IR level increased in obese children and adolescents. RNFL decreased as the height increased in obese children and adolescents. We believe that more comprehensive data about the effect of obesity on RNFL and choroidal thickness will be obtained with prospective studies in which the obese patient group with insulin resistance is taken separately and disease durations are defined, and long-term patient follow-up is performed.

Posterior short ciliary arteries ischemia following embolization of anterior ethmoid artery to treat dural arteriovenous fistulas: a case report

BackgroundThe Onyx™ Liquid Embolic System is a non-adhesive liquid embolic agent, which has been proved by the US FDA for embolization of lesions in the peripheral and neurovasculature since 2005. We reported a case of ischemic optic neuropathy after using Onyx-18 to embolize the anterior ethmoid arteries that feeding dural arteriovenous fistulas (DAVF).Case presentationA 57-year-old Asian male presented with anterior cranial fossa DAVF underwent embolotherapy by delivering Onyx-18 through a microcatheter into the anterior ethmoid arteries under angiography guidance. The interventional procedure was successful and no clear evidence was found pointing to untargeted occlusive embolus. But after the surgery the patient experienced delayed painless vision loss in the right eye (RE). The fundoscopy showed unilateral papilledema with pale optic disc in RE, accompanied by significant edema and thickening in the retinal nerve fiber layer (RNFL) of macula. The fundus fluorescence angiography showed that most of the optic disc in RE had postponed or absent fluorescence filling. Visual evoked potential (VEP) confirmed that the amplitude of the P100 component was decreased in RE without significant prolongation of the latency. The patient was diagnosed with anterior ischemic optic neuropathy, but immediate pulse steroid therapy failed to rescue his vision.ConclusionPreoperative evaluation of the patient’s hemodynamic status and fundus examination are essential for assessing the risk of ischemic ocular complications, and the non-adhesive liquid embolic agent Onyx-18 should be used cautiously during endovascular embolization of intracranial artery.

Sphingomyelin Inhibits Hydrolytic Activity of Heterodimeric PLA2 in Model Myelin Membranes: Pharmacological Relevance.

In this work, the heterodimeric phospholipase A2, HDP-2, from viper venom was investigated for its hydrolytic activity in model myelin membranes as well as for its effects on intermembrane exchange of phospholipids (studied by phosphorescence quenching) and on phospholipid polymorphism (studied by 1H-NMR spectroscopy) to understand the role of sphingomyelin (SM) in the demyelination of nerve fibers. By using well-validated in vitro approaches, we show that the presence of SM in model myelin membranes leads to a significant inhibition of the hydrolytic activity of HDP-2, decreased intermembrane phospholipid exchange, and reduced phospholipid polymorphism. Using AutoDock software, we show that the NHδ+ group of the sphingosine backbone of SM binds to Tyr22(C=Opbδ-) of HDP-2 via a hydrogen bond which keeps only the polar head of SM inside the HDP-2's active center and positions the sn-2 acyl ester bond away from the active center, thus making it unlikely to hydrolyze the alkyl chains at the sn-2 position. This observation strongly suggests that SM inhibits the catalytic activity of HDP-2 by blocking access to other phospholipids to the active center of the enzyme. Should this observation be verified in further studies, it would offer a tantalizing opportunity for developing effective pharmaceuticals to stop the demyelination of nerve fibers by aberrant PLA2s with overt activity - as observed in brain degenerative diseases - by inhibiting SM hydrolysis and/or facilitating SM synthesis in the myelin sheath membrane.

Corneal nerve loss in adolescents with obesity and acanthosis nigricans.

Obesity and related metabolic abnormalities in adults are associated with peripheral neuropathy. Acanthosis nigricans (AN) is associated with insulin resistance, fatty liver, hyperlipidemia and glucose intolerance, all of which are risk factors for neuropathy. The aim of this study was to investigate if obese adolescents with AN have evidence of small nerve fiber damage. Adolescents with obesity with and without AN underwent body composition analysis, assessment of vibration perception threshold (VPT), monofilament sensitivity and corneal confocal microscopy (CCM) to quantify corneal nerve fiber density (CNFD), branch density (CNBD), length (CNFL) and inferior whorl length (IWL). Forty-six participants with obesity with (n = 31) and without (n = 15) AN aged 15(14-17) years were compared to 20 healthy controls aged 13(12-14) years. There was no difference in VPT, monofilament sensitivity and CCM measures between adolescents with obesity and controls. However, adolescents with AN had a significantly higher weight (P = 0.022), fat% (P = 0.029) and fat-muscle ratio (P = 0.012) with a lower CNFD (P = 0.045) compared to those with obesity without AN. Adolescents with obesity and acanthosis nigricans have a higher fat mass and small nerve fibre loss, indicative of a sub-clinical neuropathy.

Cribriform Plate Foramina Count in Patients With Acquired and Congenital Anosmia.

Cribriform foramina provide the openings for olfactory nerve fibers to cross from the nasal cavity to the olfactory bulb. Disruption of the olfactory nerve fibers is known to affect olfactory function, but little is known about the potential effects on the number of cribriform foramina in congenital anosmia. This pilot study aimed to investigate whether there was a reduction in foramina in patients with acquired and congenital anosmia (including both Kallmann syndrome and isolated congenital anosmia) compared to controls with normal olfactory function. Paranasal CT image stacks were analyzed from 20 patients with congenital anosmia (n = 6), acquired anosmia (n = 6), or normal olfactory function (n = 8). Cribriform foramina were counted by three observers from the slice revealing the crista galli and the ethmoidal slits. The two closest values for each subject were analyzed in comparison across the three groups using one-way analysis of variance. Patients with congenital, but not acquired, anosmia had significantly fewer cribriform foramina (x̄ ± SE = 10.17 ± 1.23) compared to healthy, normosmic controls (x̄ ± SE = 19.88 ± 2.01). There was no significant difference in foramina count between congenital and acquired anosmics (x̄ ± SE = 15.83 ± 3.47). In this pilot study, a reduced number of cribriform foramina was found in individuals with congenital anosmia. Examination of cribriform foramina could be helpful in counseling patients with olfactory loss. Further investigation in larger studies with additional cohorts is warranted.

The Evolving Landscape of Small Fiber Neuropathy.

Small fiber neuropathy (SFN) belongs to a heterogeneous group of disorders in which thinly myelinated Aδ and unmyelinated C-fibers are primarily affected, leading to neuropathic pain and autonomic symptoms. SFN can be associated with systemic conditions such as diabetes, autoimmune diseases, exposure to drugs and toxins, and infection, with the list of associated diseases continuing to expand. Variants in the SCN9A, SCN10A, and SCN11A genes encoding Nav 1.7, Nav 1.8, and Nav 1.9 sodium channel subunits, as well as in the TRPA1 gene, have been found in SFN patients, expanding the spectrum of underlying conditions and enhancing our understanding of pathophysiological mechanisms. There is also growing interest in immune-mediated forms that could help identify potentially treatable subgroups. According to international criteria, diagnosis is established through clinical examination, the assessment of intraepidermal nerve fiber density, and/or quantitative sensory testing. Autonomic functional tests allow for a better characterization of dysautonomia in SFN, which can be subclinical. Other tests can support the diagnosis. Currently, the management of SFN prioritizes treating the underlying condition, if identified, within a multidisciplinary approach that combines symptomatic pain therapy, lifestyle changes, and biopsychological interventions. Emerging insights from the molecular characterization of SFN channelopathies hold promise for improving diagnosis, potentially leading to the discovery of new drugs and refining trial designs in the future. This article reviews the clinical presentation, diagnostic workup, and advancing knowledge of associated conditions and interventional management of SFN.

Application of optical coherence tomography in neurodegenerative diseases: a focus on Parkinson’s, Alzheimer’s, and Schizophrenia in Bulgarian patients

This study investigates retinal alterations in patients with Alzheimer’s disease (AD), Parkinson’s disease (PD), and schizophrenia (SZ) using Optical Coherence Tomography (OCT). The primary objective was to determine whether these neurodegenerative diseases manifest in measurable retinal changes and to assess the impact of disease duration, medication use, and cognitive decline on these alterations. A cross-sectional observational design was employed, including 132 patients and age- and gender-matched controls. OCT imaging was performed using the Topcon 3D OCT-1 Maestro 2, focusing on the retinal nerve fibre layer (RNFL), ganglion cell complex (GCC), and macular thickness. Significant retinal thinning was observed in the AD and PD groups, correlating with disease severity and cognitive decline, and was more pronounced with longer disease duration. In contrast, no significant retinal changes were identified in the SZ group. The study also explored the effects of different drug classes, revealing correlations between specific medications and retinal parameters, particularly in the AD and PD cohorts. To our knowledge, this is the first study of its kind conducted with Bulgarian patients. These findings suggest that OCT may serve as a non-invasive biomarker for neurodegeneration in AD and PD, though its utility in SZ remains limited. Future research should aim to standardize OCT protocols, further investigate the potential of retinal imaging in tracking neurodegenerative disease progression, and explore its integration with other neuroimaging techniques for a more comprehensive diagnostic and monitoring approach.

Early life cisplatin exposure induces nerve growth factor mediated neuroinflammation and chemotherapy induced neuropathic pain.

Chemotherapy-induced neuropathic pain (CINP) is a common adverse health related comorbidity that manifests later in life in paediatric cancer patients. Current analgesia is ineffective, aligning closely with our lack of understanding of CINP. The aim of this study was to investigate how cisplatin induces nerve growth factor mediated neuroinflammation and nociceptor sensitisation. In a rodent model of cisplatin induced survivorship pain, cisplatin induced a neuroinflammatory environment in the dorsal root ganglia (DRG) demonstrated by nerve growth factor (NGF) positive macrophages infiltrating into the DRG. Cisplatin treated CD11b/F480 positive macrophages expressed more NGF compared to vehicle treated. Primary DRG sensory neuronal cultures demonstrated enhanced NGF-dependent TRPV1 mediated nociceptor activity after cisplatin treatment. Increased nociceptor activity was also observed when cultured DRG neurons were treated with conditioned media from cisplatin activated macrophages. Elevated nociceptor activity was dose-dependently inhibited by a neutralising NGF antibody. Intraperitoneal administration of a NGF neutralising antibody reduced cisplatin-induced mechanical hypersensitivity and aberrant nociceptor intraepidermal nerve fibre density. These findings identify that a monocyte/macrophage driven NGF/TrkA pathway is a novel analgesic target for adult survivors of childhood cancer.

Epidemiological, Clinical, and Histopathological Features of the Head and Neck Region Schwannomas-Our Experience in the Western Part of Romania with Surgical Insights.

Schwannomas are benign solitary, slow-growing, encapsulated, asymptomatic tumors arising from Schwann's sheath of nervous fibers. The current paper presents all the cases diagnosed with different types of schwannomas in the head and neck region between January 2009 and December 2023 in the Western part of Romania. In this period, ten cases of schwannoma were identified. The pathological exams were performed at the Department of Pathology using morphological Hematoxylin-Eosin staining. In addition, immunohistochemical reactions were used in order to confirm the diagnosis. Demographic and clinical data, imaging features, surgical approach, and morphological and immunohistochemical aspects are presented. The results also display an impressive clinical picture of a gigantic ancient schwannoma. This retrospective study describes our experience with head and neck schwannomas, the diagnostic methods available, the surgical decisions, and the histopathological aspects while analyzing the data and reviewing the published specialized literature in the English language.

From Organotypic Mouse Brain Slices to Human Alzheimer’s Plasma Biomarkers: A Focus on Nerve Fiber Outgrowth

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory loss and progressive deterioration of cognitive functions. Being able to identify reliable biomarkers in easily available body fluids such as blood plasma is vital for the disease. To achieve this, we used a technique that applied human plasma to organotypic brain slice culture via microcontact printing. After a 2-week culture period, we performed immunolabeling for neurofilament and myelin oligodendrocyte glycoprotein (MOG) to visualize newly formed nerve fibers and oligodendrocytes. There was no significant change in the number of new nerve fibers in the AD plasma group compared to the healthy control group, while the length of the produced fibers significantly decreased. A significant increase in the number of MOG+ dots around these new fibers was detected in the patient group. According to our hypothesis, there are factors in the plasma of AD patients that affect the growth of new nerve fibers, which also affect the oligodendrocytes. Based on these findings, we selected the most promising plasma samples and conducted mass spectrometry using a differential approach and we identified three putative biomarkers: aldehyde-dehydrogenase 1A1, alpha-synuclein and protein S100-A4. Our method represents a novel and innovative approach for translating research findings from mouse models to human applications.

Differential diagnosis of optic neuritis and anterior ischemic optic neuropathy

Background. Acute anterior ischemic neuropathy and optic neuritis are among the most common diseases that are the most frequent cause of both reversible and persistent visual acuity reduction. There is a sudden loss of vision, the clinical picture is often similar, and the restoration of visual functions and the prevention of complications in the form of optic nerve atrophy and disease relapses depend on a correct diagnosis and timely prescribed therapy. A significant level of medico-social and economic losses for society in all regions of the world is related to complications, namely the occurrence of optic nerve atrophy due to both optic nerve inflammation (neuritis) and ischemic optic neuropathy. The purpose was to determine the differential signs of optic neuritis and anterior ischemic optic neuropathy. Materials and methods. Eighty-five patients were examined, 52 (61.2 %) women and 33 (38.8 %) men. Seventy-one (83.5 %) participants were employed. The patients were divided into two groups: the first one — 38 patients with optic neuritis (papillitis); the second one — 47 people with ischemic optic neuropathy. General ophthalmological examinations were carried out. Results. Computed perimetry showed the presence of scotoma and quadrantanopia, both in anterior optic neuropathy (typical altitudinal scotomas) and optic neuritis (peripheral and central scotomas). The difference in the indicators of the electrical activity of the visual analyzer according to phosphene between the groups was 15.8 % (p &lt; 0.05), which indicates a more significant increase in the functional activity of the visual analyzer in the group with anterior optic vascular neuropathy. Thinning of the peripapillar nerve fiber layer and partial atrophy of the optic nerve were noted 2 times less often in patients with anterior vascular ischemic neuropathy — 7 (16.3 %) vs. 14 (33.3 %) in those with partial atrophy of the optic nerve (Pearson’s χ2 = 22.59, p = 0.00001). Conclusions. The issue of early differential diagnosis of anterior optic ischemic neuropathy and optic neuritis is relevant, which determines the prognosis of the disease, allows increasing the effectiveness of treatment and preventing irreversible consequences. The therapeutic effect of treating the consequences of damage to the optic nerve is not stable and is weak, and success is not always achieved. First of all, the treatment of the underlying disease is indicated. Computed perimetry showed the presence of scotoma and quadrantanopia in both anterior optic neuropathy (typical altitudinal scotomas) and optic neuritis (peripheral and central scotomas).

Imprint of preterm birth with very low birth weight on optic disc OCT in adulthood-A two-country birth cohort study.

To determine the pattern, degree and prevalence of optic disc optical coherence tomography (OCT) alterations in adults born preterm with very low birth weight (VLBW; birth weight < 1500 g). Optic disc OCT was assessed in 98 VLBW participants and 139 term-born controls from birth cohorts in Finland and Norway at the mean age of 36 years. The participants had not been treated for retinopathy of prematurity and had no diagnosed brain abnormality. OCT assessment included parameters for optic disc size, neural rim and peripapillary retinal nerve fibre layer thickness (pRNFLT), and for the foveal developmental stage. Background data, visual acuity, refractive error and intraocular pressure were recorded. In the VLBW group, optic disc neural rim and pRNFLT were significantly decreased, most frequently in the nasal and inferior sectors. In 40% (95% CI: 33-47) of the VLBW eyes, nerve fibre thickness of at least one optic disc sector was below the fifth percentile of the control group, including 9% (95% CI: 6-14) subgroup falling below the first percentile, that is, clinically below normal limits. VLBW participants with nerve fibre thickness below the fifth percentile did not differ by perinatal data or foveal developmental stage from the other VLBW participants. All participants had normal visual acuity. A moderate decrease of the optic disc neural rim and pRNFLT is frequently seen in clinically healthy adults born preterm with VLBW. Awareness of the VLBW-related optic disc nerve fibre shallowness especially in the inferior and nasal sectors is important while evaluating acquired optic disc pathology in adulthood.

Brachial and Lumbosacral Plexopathies.

The brachial and lumbosacral plexuses are complex neural structures that transmit sensory, motor, and autonomic information between the spinal cord and the extremities. Plexus disorders can be particularly disabling because lesions in the plexus usually affect large groups of nerve fibers originating from several spinal levels. Electrodiagnostic studies are often required to confirm a plexus lesion and determine the extent of injury and prognosis. Magnetic resonance is the imaging modality of choice for detecting intrinsic nerve abnormalities; recently, high-resolution ultrasound has emerged as an alternative method for dynamic evaluation and visualization of internal nerve architecture. Once a plexopathy is confirmed, the list of possible etiologies is relatively limited and includes traumatic and nontraumatic causes. Treatment relies on symptom management and physical rehabilitation unless a treatable underlying condition is found. Surgical approaches, including nerve grafts or tendon transfers, may improve limb function when spontaneous recovery is suboptimal.

Comparative assessment of neurotrophic proteins in vibration disease

Introduction. The problem of health impairment due to the impact of physical factors, including vibration disease (VD), retains medical and social relevance due to the significant specific gravity in the structure of occupational morbidity and high prevalence. Under vibration exposure, the acid-base equilibrium, immune status are disturbed, rheological properties and properties of the neurohumoral system, as well as functional indices of the central and peripheral nervous system change. Neurotrophins are known to play an important role in regulating the development and functioning of the central and peripheral nervous systems. In this regard, research is needed to determine in VD patients the levels of neurospecific proteins, which may serve as one of the markers for tracing changes in the nervous system in workers. The aim of the study was to identify the peculiarities of changes in neurospecific proteins (BDNF, S100β, and MBP) in the serum of patients with VD of different genesis. Materials and methods. Serum concentrations of neurotrophic proteins: brain neurotrophic factor – BDNF, S100β protein and myelin basic protein (MBP) were studied by solid-phase enzyme-linked immunoassay. Results. There was an increase in serum BDNF, S100β protein, and MBP concentrations in persons with VD due to combined exposure to local and general vibration, and an increase in MBP was observed in patients with VD due to exposure to local vibration. Limitations. The limitations of this work are small groups of employees. Conclusion. As a result of studies, it can be assumed that in VD due to exposure to combined vibration, changes are observed in the peripheral and central parts of the nervous system, and in VD due to local vibration, disorders seem to be mainly associated with the peripheral nervous system. The general pattern of the revealed disorders in the content of MBP lies in the neurodestructive processes occurring in the nerve fibers in patients with VD, regardless of genesis. Summarizing the above mentioned, the validity of studying the concentration of neurospecific proteins in vibration disease occurring with damaging processes in the nervous tissue should be recognized.