Peripheral Nerve Function Research Articles

A finite element model for biomechanical characterization of exvivo peripheral nerve dysfunction during stretch.

Peripheral nerve damage can cause debilitating symptoms ranging from numbness and pain to sensory loss and atrophy. To uncover the underlying mechanisms of peripheral nerve injury, our research aims to develop a relationship between biomechanical peripheral nerve damage and function through finite element modeling. A noncontact, exvivo electrophysiology chamber, capable of axially stretching explanted nerves while recording electrical signals, was used to investigate peripheral nerve injury. Successive stretch trials were run on eight sciatic nerves (four females and four males) excised from Sprague-Dawley rats. Nerves were stretched until 50% compound action potential (CAP) amplitude reduction was obtained. A constitutive model developed by Raghavan and Vorp was suitable for rat sciatic nerves, with an average α and β of 0.183 MPa and 1.88 MPa, respectively. We then generated 95% confidence intervals for the stretch at which specific CAP amplitude reductions would occur, which compares well to previous studies. We also developed a finite element model that can predict stretch-induced signaling deficits, applicable for complex nerve geometries and injuries. This relationship between nerve biomechanics and function can be expanded upon to create a clinical model for peripheral nerve dysfunction due to stretch.

P66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Natural polymeric biomaterials for managing peripheral nerve injuries : a novel approach for tissue repair and reconstruction.

Peripheral nerve injury serves as a major challenge to clinicians and researchers due to the complexity and functions of peripheral nerves that play the crucial role of transmitting signals between spinal cord and other human body tissues. Biomaterials offer promising solutions for regeneration of nerve tissues owing to their biodegradability, and biocompatibility. They can be fabricated as hydrogels, scaffolds, nanofibrous matrices, and nanoparticles that can facilitate the release of therapeutic molecules to reduce inflammation and promote neuronal growth. Managing peripheral nerve injuries through natural polymeric based biomaterials represents as a novel approach for tissue repair and reconstruction in the field of regenerative medicine. This correspondence will give an insight into the different types of natural polymeric biomaterials that can be efficiently used in managing peripheral nerve injuries.

Peripheral Neuropathic Pain.

This article synthesizes current knowledge on neuropathic pain, with a brief review of mechanisms, diagnostic approaches, and treatment strategies to help neurologists provide effective and individualized care for patients with this complex condition. The most promising developments in peripheral neuropathic pain are related to the molecular biology of the peripheral nervous system. Systematic molecular and genetic analyses of peripheral nerve terminals and dorsal root ganglia have advanced our understanding of the genetics of function and disease of peripheral nerves, as well as their physiology and clinical manifestations. Peripheral neuropathic pain, similar to central neuropathic pain, is primarily influenced by the biology and pathophysiology of the underlying structures, peripheral sensory nerves, and their central pathways. The clinical course is widely variable in sensory symptoms and intensities, natural history, and response to treatments.

Gastrodin alleviates diabetic peripheral neuropathy by regulating energy homeostasis via activating AMPK and inhibiting MMP9

BackgroundDiabetic peripheral neuropathy (DPN) is a serious complication of diabetes that lacks effective treatment. Gastrodin, the primary bioactive compound derived from Rhizoma Gastrodiae, has a long history in treating epilepsy and various central nervous system disorders. However, its effect on DPN remains uncertain. PurposeThis study aims to explore the therapeutic potential and underlying mechanisms of gastrodin in the treatment of DPN. MethodDPN model rats were induced with streptozotocin (STZ) injection and divided into four groups receiving either gastrodin at two doses (30 and 60 mg kg-1 per day), α-lipoic acid (positive drug, 60 mg kg-1 per day), or placebo. Healthy rats were administrated with placebo. The administrations began eight weeks post-STZ injection and continued for six weeks. Following a comprehensive evaluation of the neuroprotective effects, a systematic pharmacology-based approach was subsequently employed to investigate the underlying mechanism of gastrodin in vivo and in vitro. ResultsGastrodin was demonstrated to effectively enhance peripheral nerve function and reduce pathological damages in DPN rats. Furthermore, gastrodin facilitated the expression of remyelination-related proteins and mitigated oxidative stress in DPN rats. Transcriptomic analysis indicated that the modulation of energy metabolism was pivotal in the neuroprotective effect of gastrodin, corroborated by targeted metabolomic analysis using high-performance ion chromatography coupled with mass spectrometry. Using network pharmacology analysis, 12 potential targets of gastrodin were identified. Among these, matrix metallopeptidase 9 (MMP9) was further validated as the primary target through molecular docking and cellular thermal shift assays. Functional Analysis of the potential targets underscored the pivotal role of AMPK signaling, and gastrodin demonstrated the capability to activate AMPK and inhibit MMP9 in vivo. In vitro studies further found that gastrodin enhanced antioxidant capacity and mitochondrial function of high glucose-cultured rat Schwann cells RSC96 in an AMPK-dependent manner. Inhibition of AMPK hindered the decrease of MMP9 induced by gastrodin in vitro. ConclusionThis study revealed the new role of gastrodin in alleviating DPN by restoring the homeostasis of energy metabolism through activating AMPK and inhibiting MMP9. These findings highlight gastrodin's potential as a novel therapeutic candidate against DPN, and underscores an appealing strategy of regulating energy metabolism for DPN therapy.

Schwann cell-derived exosomes ameliorate peripheral neuropathy induced by ablation of dicer in Schwann cells.

MicroRNAs (miRNAs) in Schwann cells (SCs) mediate peripheral nerve function. Ablating Dicer, a key gene in miRNA biogenesis, in SCs causes peripheral neuropathy. Exosomes from healthy SCs (SC-Exo) ameliorate diabetic peripheral neuropathy in part via miRNAs. Thus, using transgenic mice with conditional and inducible ablation of Dicer in proteolipid protein (PLP) expressing SCs (PLP-cKO), we examined whether SC-Exo could reduce peripheral neuropathy in PLP-cKO mice. PLP-cKO mice at the age of 16 weeks (8 week post-Tamoxifen) were randomly treated with SC-Exo or saline weekly for 8 weeks. Age-and sex-matched wild-type (WT) littermates were used as controls. Peripheral neurological functions, sciatic nerve integrity, and myelination were analyzed. Quantitative RT-PCR and Western blot analyses were performed to examine miRNA and protein expression in sciatic nerve tissues, respectively. Compared to the WT mice, PLP-cKO mice exhibited a significant decrease in motor and sensory conduction velocities, thermal sensitivity, and motor coordination. PLP-cKO mice exhibited substantial demyelination and axonal damage of the sciatic nerve. Treatment of PLP-cKO mice with SC-Exo significantly ameliorated the peripheral neuropathy and sciatic nerve damage. PLP-cKO mice showed a substantial reduction in a set of Dicer-related miRNAs known to regulate myelination, axonal integrity, and inflammation such as miR-138, -146a and - 338 in the sciatic nerve. In addition, PLP-cKO mice exhibited significant reduction of myelin forming proteins, early growth response 2 (EGR2) and sex determining region Y-box10 (Sox10), but significantly increased myelination inhibitors, Notch1, c-Jun, and Sox2 and the axonal growth inhibitor phosphatase and tens in homolog (PTEN). However, SC-Exo treatment reversed the PLP-cKO altered miRNAs and proteins. This study demonstrates that exogenous SC-Exo ameliorate peripheral neuropathy induced by Dicer ablation in PLP expressing SCs. The therapeutic benefit may be mediated by the SC-Exo altered miRNAs and their targeted genes.

The Association between the Severity of Distal Sensorimotor Polyneuropathy and Increased Carotid Atherosclerosis in Individuals with Type 2 Diabetes.

Diabetes contributes to a spectrum of complications encompassing microvascular and macrovascular disorders. This study aimed to explore the correlation between distal sensorimotor polyneuropathy (DSPN) severity and heightened carotid atherosclerosis among individuals with type 2 diabetes mellitus (T2DM). Method: Participants underwent comprehensive assessments including nerve conduction studies (NCS), Toronto Clinical Neuropathy Score (TCNS) evaluations, assessment of cardiometabolic risk factors, and carotid sonography studies covering dynamic and morphological parameters. The resistance index (RI), pulsatility index (PI), peak systolic velocity (PSV), and end-diastolic velocity (EDV) in both the common carotid artery (CCA) and internal carotid artery (ICA), carotid intima-media thickness (IMT), and carotid plaque score (CPS) were also measured. Peripheral nerve function severity was assessed using composite amplitude scores (CAS) derived from NCS. Individuals with DSPN exhibited lower EDV in the CCA and ICA (p < 0.0001 and p = 0.002), higher PI and RI in both CCA and ICA (all p < 0.0001), and higher CPS (p = 0.002). They also demonstrated a higher prevalence of retinopathy as an underlying condition, higher index HbA1c, and reduced estimated glomerular filtration rate (eGFR) (all p < 0.0001). Multiple linear regression analysis revealed significant associations where eGFR, ICA-PI, index HbA1c, waist circumference, and age were correlated with CAS. Meanwhile, diabetes duration, waist circumference, age, and index HbA1c showed significant associations with TCNS. Our study suggests that individuals with T2DM who exhibit more severe carotid atherosclerosis may not only be at increased risk of developing DSPN but also may experience greater severity of DSPN. PI in both the CCA and ICA, along with the CPS, serve as surrogate biomarkers for DSPN severity.

Maltol Improves Peripheral Nerve Function by Inhibiting Schwann Cell Apoptosis via the PERK/eIF2α/CHOP Pathway and MME Upregulation in Diabetic Peripheral Neuropathy.

Diabetic peripheral neuropathy (DPN) is the most prevalent chronic complication among diabetic patients and a primary risk factor contributing to the deterioration of diabetic foot conditions. The pathogenesis of DPN remains complex and not fully understood, and there are hardly any effective treatment drugs. Maltol (3-hydroxy-2-methyl-4-pyranone) has demonstrated antioxidant and anti-inflammatory properties. However, the potential role of maltol in the treatment of DPN remains unclear. This study aimed to assess maltol's effects on DPN rats and high glucose (HG)/palmitic acid (PA)-induced rat Schwann cells (RSC96). The results indicated maltol's capacity to enhance peripheral nerve function in DPN rats. In RSC96 cells stimulated with high HG and PA, maltol treatment reduced DPN markers and apoptosis-related proteins. Functional enrichment analysis of differentially expressed genes revealed that endoplasmic reticulum (ER) stress pathways were involved in this process. Western blot results demonstrated the activation of ER stress pathway in HG/PA-induced RSC96 cells, with maltol attenuating ER stress-related protein expression. Furthermore, the knockdown of Membrane metallo-endopeptidase (MME) reversed maltol's effects on apoptosis-related protein expression, suggesting a potential therapeutic role for maltol via MME in treating DPN. These findings indicate that maltol may hold promise as a therapeutic agent for DPN treatment.

C-peptide: an essential ally in microvascular complications of type 2 diabetes mellitus and obesity

BackgroundIn order to investigate microvascular complications in metabolic diseases, we aimed to investigate cerebral and peripheral microcirculation in relation to peripheral neuropathy and laboratory biomarkers in type 2 diabetes mellitus (T2DM) and obesity.MethodsBased on the degree of neuropathy (NP), study participants (40 T2DM and 30 obese individuals) were classified into no-NP, mild-NP and severe-NP subgroups. After the injection of Technetium-99 m hexamethylpropylene amine oxime, both T2DM and obese participants underwent single-photon emission computed tomography/computed tomography ([99mTc]Tc-HMPAO SPECT/CT) and SPECT-only examinations to assess lower limb and brain perfusion; respectively. Peripheral nerve function was evaluated with a neurometer and glycaemic markers were measured from plasma in both groups.ResultsCompared to the obese individuals, lower extremity perfusion was significantly reduced in the diabetic subjects (p < 0.005), while it showed a positive correlation with C-peptide levels and negative association with HbA1c values. A U-shape pattern of peripheral microcirculation was observed between the NP groups, indicating a surprisingly better perfusion in the severe-NP group than in the mild one, with the highest levels in obese patients. Since changes in the C-peptide levels exhibited a similar U-shaped trend across the NP subgroups, we suggest a positive correlation between C-peptide levels and the extent of peripheral perfusion. Although, C-peptide values and cerebral microcirculation correlated positively (rho = 0.27), brain perfusion did not show any differences neither between the diabetic and the obese patients, nor between the NP subgroups (at p < 0.05).ConclusionsEstablishing the link between neuropathy and peripheral microcirculation, C-peptide seems to be a promising biomarker for the prediction of microvascular alterations in metabolic diseases. Of note, the dominance of metabolic factors over microvascular damage in the development of obesity-related neuropathy should be emphasized as well.

Serine and glycine physiology reversibly modulate retinal and peripheral nerve function

Metabolic homeostasis is maintained by redundant pathways to ensure adequate nutrient supply during fasting and other stresses. These pathways are regulated locally in tissues and systemically via the liver, kidney, and circulation. Here, we characterize how serine, glycine, and one-carbon (SGOC) metabolism fluxes across the eye, liver, and kidney sustain retinal amino acid levels and function. Individuals with macular telangiectasia (MacTel), an age-related retinal disease with reduced circulating serine and glycine, carrying deleterious alleles in SGOC metabolic enzymes exhibit an exaggerated reduction in circulating serine. A Phgdh+/- mouse model of this haploinsufficiency experiences accelerated retinal defects upon dietary serine/glycine restriction, highlighting how otherwise silent haploinsufficiencies can impact retinal health. We demonstrate that serine-associated retinopathy and peripheral neuropathy are reversible, as both are restored in mice upon serine supplementation. These data provide molecular insights into the genetic and metabolic drivers of neuro-retinal dysfunction while highlighting therapeutic opportunities to ameliorate this pathogenesis.

Knowledge, attitudes, and practices on leprosy among dermatology residents in the Philippines

Introduction: leprosy is a chronic bacterial infection caused by Mycobacterium leprae and Mycobacterium lepromatosis, primarily affecting the skin and peripheral nerves. Dermatologists play an important role in diagnosing and treating patients affected with leprosy and are equipped with adequate knowledge about the clinical presentation and management of patients with leprosy. Methods: a cross-sectional study was conducted on the knowledge, attitudes, and practices of leprosy among dermatology residents in the Philippines using a selfadministered online questionnaire. The study was conducted in two phases: Phase I was the development of the questionnaire, and Phase II was the survey proper, where the questionnaire was administered to dermatology residents in the Philippines via convenience sampling. Descriptive statistics appropriate for the study variables were used. Results: in Phase I of the study, a questionnaire was validated by three leprosy and infectious disease experts and pilot-tested on ten dermatology graduates in the year 2022, showing that items had high scores for validity and reliability. Phase II involved administering the survey to dermatology residents. Data showed that overall, 46 of 118 participants (38.98%) obtained a satisfactory score of 80% and higher on knowledge, 101 of 118 (85.59%) exhibited a positive attitude, and 116 of 118 (98.31%) had adequate practices. Moreover, first-year residents exhibit lower attitude scores than those in higher years, and no significant differences in knowledge and practices were found based on the practice setting. Conclusion: results of the study show that less than half of the included resident dermatologists had satisfactory knowledge of leprosy. However, we identified gaps in these physician’s knowledge, mainly in peripheral assessment nerve function, doses, and duration of treatment for leprosy peoples. On the other hand, participants were noted to have an overall positive attitude towards leprosy and adequate practices.

Age related changes in skin sensitivity assessed with smartphone vibration testing

The capacity to perceive tactile input at the fingertips, referred to as tactile sensitivity, is known to diminish with age due to regressive changes to mechanoreceptor density and morphology. Sensitivity is measured as perceptual responses to stimuli of varying intensity. Contrary to traditional sensitivity monitoring instruments, smartphones are uniquely suited for remote assessment and have shown to deliver highly calibrated stimuli along a broad spectrum of intensity, which may improve test reliability. The aim of this study was to evaluate a vibration-emitting smartphone application, the Vibratus App, as a mode of estimating tactile sensory thresholds in the aging adult. The peripheral nerve function of 40 neurologically healthy volunteers (ages 18–71) was measured using monofilaments, a 128-Hz tuning fork, the Vibratus App, and nerve conduction studies (NCS). Between group differences were analyzed to determine each measurement’s sensitivity to age. Spearman correlation coefficients depicted the associative strength between hand-held measurements and sensory nerve action potential (SNAP) amplitude. Inter-rater reliability of traditional instruments and the software-operated smartphone were assessed by intraclass correlation coefficient (ICC2,k). Measurements taken with Vibratus App were significantly different between age groups (p < 0.001). The inter-rater reliability of monofilament, smartphone vibration, and tuning fork testing was moderate to good (ICC2,k = 0.65, 0.69, and 0.79, respectively). The findings of this study support further investigation of smartphones as sensitivity monitoring devices for at home monitoring of skin sensitivity.

Romberg's test revisited: Changes in classical and advanced sway metrics in patients with pure sensory neuropathy

ObjectivesThe Romberg test, undoubtedly a classical and well-established method in physical neurological assessment of patients with sensory ataxia, has long been suspected to be prone to several limitations. Here, we quantified upright stance before and after visual deprivation in a selected cohort of patients with pure sensory neuropathy. MethodsStatic balance was assessed in sensory neuropathy patients during quiet stance on a force platform under different visual and proprioceptive feedback conditions. Sural nerve neurography was employed to evaluate the severity of peripheral neuropathy. Conventional and advanced postural sway metrics were investigated to draw a quantitative analogy to the clinical Romberg test. ResultsPosturographic analyses showed that patients displayed Romberg and vestibular Romberg quotient values around 2, indicating an approximately twofold increase in body sway in the absence of vision. However, the diagnostic discrimination ability between patients and controls was only modest. Even less impactful were the diagnostic contributions of frequency domain and non-linear sway analyses. This was primarily attributed to the heightened body sway exhibited by patients with sensory neuropathy under 'eyes open' conditions, diminishing the contrast with the 'eyes closed' condition as assessed in the classical Romberg test. ConclusionWe conclude that the Romberg test, even in its quantitative form with the aid of an apparatus, had an unsatisfactory classification value in terms of distinguishing patients from healthy controls. Instead, it should be interpreted within the comprehensive context of the broader neurological examination and the electrodiagnosis of peripheral nerve function.

Longitudinal Assessment of Blood-Based Inflammatory, Neuromuscular, and Neurovascular Biomarker Profiles in Intensive Care Unit-Acquired Weakness: A Prospective Single-Center Cohort Study.

The diagnosis of intensive care unit (ICU)-acquired weakness (ICUAW) and critical illness neuromyopathy (CINM) is frequently hampered in the clinical routine. We evaluated a novel panel of blood-based inflammatory, neuromuscular, and neurovascular biomarkers as an alternative diagnostic approach for ICUAW and CINM. Patients admitted to the ICU with a Sequential Organ Failure Assessment score of ≥ 8 on 3 consecutive days within the first 5 days as well as healthy controls were enrolled. The Medical Research Council Sum Score (MRCSS) was calculated, and motor and sensory electroneurography (ENG) for assessment of peripheral nerve function were performed at days 3 and 10. ICUAW was defined by an MRCSS < 48 and CINM by pathological ENG alterations, both at day 10. Blood samples were taken at days 3, 10, and 17 for quantitative analysis of 18 different biomarkers (white blood cell count, C-reactive protein, procalcitonin, C-terminal agrin filament, fatty-acid-binding protein 3, growth and differentiation factor 15, syndecan 1, troponin I, interferon-γ, tumor necrosis factor-α, interleukin-1α [IL-1α], IL-1β, IL-4, IL-6, IL-8, IL-10, IL-13, and monocyte chemoattractant protein 1). Results of the biomarker analysis were categorized according to the ICUAW and CINM status. Clinical outcome was assessed after 3 months. Between October 2016 and December 2018, 38 critically ill patients, grouped into ICUAW (18 with and 20 without) and CINM (18 with and 17 without), as well as ten healthy volunteers were included. Biomarkers were significantly elevated in critically ill patients compared to healthy controls and correlated with disease severity and 3-month outcome parameters. However, none of the biomarkers enabled discrimination of patients with and without neuromuscular impairment, irrespective of applied classification. Blood-based biomarkers are generally elevated in ICU patients but do not identify patients with ICUAW or CINM. ClinicalTrials.gov identifier: NCT02706314.

CLINICAL-EXPERIMENTAL JUSTIFICATION OF PATHOGENETIC TREATMENT OF DIABETIC DAMAGE OF THE PERIPHERAL NERVOUS SYSTEM

Background. Diabetes mellitus is a chronic endocrinological disease that, in addition to the somatic sphere, affects all departments and levels of the nervous system. At the same time, its prevalence is increasing every year. Most often, neurological manifestations concern the peripheral nervous system in the form of sensory-motor polyneuropathies. Aim: To clinically and experimentally study the effectiveness of the complex scheme of prevention and treatment of diabetic polyneuropathy, which is composed taking into account the pathogenetic mechanisms of the studied pathology. To find out the clinical features of the course of the disease and electrophysiological patterns. Under experimental conditions, to study the dynamics of changes in the indicators of sensitivity (nociception) and motor function of peripheral nerves in case of diabetic nerve damage. Materials and methods. In the work, streptozotocin-induced diabetic polyneuropathy was reproduced in rats in a chronic experiment. The formation of the latter was confirmed by a morphological study of the sciatic and tail nerves with the determination of edema and degeneration of Schwann cells, as well as segmental demyelination and spasm of precapillary arterioles. Nicergoline, alpha-lipoic acid, group B vitamins, NG-nitro-L-arginine were used for therapeutic or preventive purposes in groups of animals. The speed of conduction of excitation along the tail nerve was studied. In addition, the "hot plate" test was used. In the clinical part of the work, 43 patients with diabetic polyneuropathy were examined. In addition to the clinical and neurological examination; assessed the severity of polyneuropathies according to the scale of neuropathy symptoms, as well as stimulation electroneuromyography.The patients were divided into groups: the first received a developed treatment complex, the second received conventional treatment. Results. The obtained data indicate the feasibility of using direct (NG-nitro-L-arginine) and indirect (nicergoline - "Sermion" and LC - "Alpha-lipon") inhibitors of nitric oxide synthesis, as well as the complex of vitamin preparations "Neovitam", taking into account their reparative and antioxidant properties, in the clinic in patients with diabetic polyneuropathy with a therapeutic, and possibly preventive purpose. The positive experimental and clinical effects of the developed DPP prevention and treatment scheme are associated with the development of antioxidant and reparative effects, as well as the restoration of the myelin sheath of peripheral nerves, since demyelination contributes to the development of the clinic of polyneuropathy. Conclusion. Patients with diabetic polyneuropathy who received a complex treatment scheme achieved probable clinical, neurological and neurophysiological improvement. On the basis of experimental research, the probable mechanisms of this kind of improvement due to the restoration of myelin, blood circulation, antioxidant and reparative effects have been proven.

Anti-sulfatide antibody associated GBS with headache and abdominal pain: a case report

BackgroundGuillain‒Barre syndrome (GBS) is an acute inflammatory peripheral neuropathy caused by autoimmunity. Gangliosides and sulfatides are important components of peripheral nerves. Anti-sulfatide antibody-mediated complement is associated with acute sensorimotor peripheral neuropathy in GBS, which is characterized by pain and paresthesias.Case presentationThe child was a 7-year-old girl with headache and abdominal pain, followed by limb numbness and pain. Cranial imaging showed ventricular dilatation, peripheral nerve function conduction examination showed polyradiculopathy, and cerebrospinal fluid tests showed normal cell counts but elevated protein levels, all of which led to the diagnosis of GBS. After treatment with intravenous immunoglobulin (400 mg/kg × 5 days), the symptoms did not improve, and muscle strength progressively worsened, accompanied by paroxysmal complexion flushing, heart rate fluctuation, hyperhidrosis, and a progressive increase in cerebrospinal fluid protein (up to 3780.1 mg/L). On the basis of these findings combined with serum anti-sulfatide IgM positivity, anti-sulfatide antibody-related GBS was considered, and treatment with low-dose prednisolone (1 mg/kg/d) led to symptom improvement.ConclusionsAnti-sulfatide antibody-associated GBS is associated with small fiber peripheral neuropathy. The main manifestations are pain, paresthesias and autonomic dysfunction. In addition to the dysfunction of spinal nerve root absorption caused by increased cerebrospinal fluid protein, autonomic dysfunction may be involved in pain. When the therapeutic effect of immunoglobulin is not satisfactory, a low dose and short course of corticosteroids can be considered, and the prognosis is good.

A case control study of the relationship between persistent serum creatine kinase elevation and polyneuropathy

Creatine kinase (CK) has been associated with neuropathy, but the mechanisms are uncertain. We hypothesized that peripheral nerve function is impaired in subjects with persistent CK elevation (hyperCKemia) compared to age- and sex matched controls in a general population. The participants were recruited from the population based Tromsø study in Norway. Neuropathy impairment score (NIS), nerve conduction studies (NCS) and electromyography (EMG) in subjects with persistent hyperCKemia (n = 113; 51 men, 62 women) and controls (n = 128; 61 men, 67 women) were performed. The hyperCKemia group had higher NIS score than the controls (p = 0.050). NCS of the tibial nerve showed decreased compound motor action potential amplitude (p < 0.001), decreased motor conduction velocity (p < 0.001) and increased F-wave latency (p = 0.044). Also, reduced sensory amplitudes of the median, ulnar, and sural nerves were found. EMG showed significantly increased average motor unit potential amplitude in all examined muscles. CK correlated positively with glycated hemoglobin and non-fasting glucose in the hyperCKemia group, although not when controlled for covariates. The length dependent polyneuropathy demonstrated in the hyperCKemia group is unexplained, but CK leakage and involvement of glucose metabolism are speculated on.

Association of Chemotherapy-Induced Peripheral Neuropathy with Diet Quality Among Post-Treatment Cancer Survivors

Nutrition is essential for peripheral nerve function, yet dietary factors associated with chronic chemotherapy-induced peripheral neuropathy (CIPN) remain poorly characterized. The purpose of this cross-sectional study was to determine differences in diet quality and macronutrients for cancer survivors with and without CIPN. Cancer survivors (e.g., ≥3 months post platinum and/or taxane-based neurotoxic chemotherapy) with (i.e., ≥1/4 PRO-CTACE™ Numbness and Tingling Severity) and without CIPN completed the VioScreen Research Graphical Food Frequency Questionnaire. The association among diet (Healthy Eating Index [HEI]), macronutrient intake (average percent caloric intake), and CIPN severity were analyzed using generalized linear regression models, adjusting for caloric intake, body mass index, age, and sex. Results revealed that for each one-point increase in diet quality, PRO-CTCAE severity decreased by −0.06 (95% CI: −0.10, −0.02, P < 0.01). Participants without CIPN reported higher diet quality than those with CIPN (HEI mean: 70.11 vs 68.45) (OR = 0.94, P = 0.03, 95% CI: 0.89, 0.99). Participants with CIPN had significantly higher carbohydrate consumption than participants without CIPN (OR = 1.11, P = 0.04, 95% CI: 1.01, 1.22). There were no significant differences in consumption of proteins or fats between groups. Further research should be pursued to discover the potential benefits of dietary interventions for CIPN management among cancers survivors.

Effects of Temporal Processing on Speech-in-Noise Perception in Middle-Aged Adults.

Auditory temporal processing is a vital component of auditory stream segregation, or the process in which complex sounds are separated and organized into perceptually meaningful objects. Temporal processing can degrade prior to hearing loss, and is suggested to be a contributing factor to difficulties with speech-in-noise perception in normal-hearing listeners. The current study tested this hypothesis in middle-aged adults-an under-investigated cohort, despite being the age group where speech-in-noise difficulties are first reported. In 76 participants, three mechanisms of temporal processing were measured: peripheral auditory nerve function using electrocochleography, subcortical encoding of periodic speech cues (i.e., fundamental frequency; F0) using the frequency following response, and binaural sensitivity to temporal fine structure (TFS) using a dichotic frequency modulation detection task. Two measures of speech-in-noise perception were administered to explore how contributions of temporal processing may be mediated by different sensory demands present in the speech perception task. This study supported the hypothesis that temporal coding deficits contribute to speech-in-noise difficulties in middle-aged listeners. Poorer speech-in-noise perception was associated with weaker subcortical F0 encoding and binaural TFS sensitivity, but in different contexts, highlighting that diverse aspects of temporal processing are differentially utilized based on speech-in-noise task characteristics.

Real time monitoring peripheral nerve function with ICG and BDA-ICG by NIR-II fluorescence imaging

Neuroanatomical tract tracers are important for studying axoplasmic transport and the complex interconnections of the nervous system. Though traditional fluorescent tracers are widely used, they have several prominent drawbacks when imaging, including low resolutions and low tissue penetrations and inability to be supervised dynamically within a long peripheral nerve during the long term. Here, we explored the potential of ICG as a neural tracer for axoplasmic transport and for the first time demonstrated that ICG could be used to detect transport function within peripheral nerve by near-infrared region II (NIR-II) imaging. On basis of this finding, a novel bi-directional neural tracer biotinylated dextran amine-indocyanine green (BDA-ICG) was prepared and characterized with better long-term stability and higher nerve-to-background ratio than ICG in vivo, and successfully imaged the injured peripheral nerve from the healthy one within 24 h. Our results show that BDA-ICG are promising neural tracers and clinically available dyes with NIR-II emission tail characteristics as ICG.