Severity Of Neuropathy Research Articles

Optimizing Diabetic Neuropathy Severity Classification Using Electromyography Signals Through Synthetic Oversampling Techniques

Electromyography signals are electrical signals generated by muscle activity and are very useful for analyzing the health conditions of muscles and nerves. Data imbalance is a prevalent issue in EMG signal data, especially when addressing patients with varied health conditions and restricted data availability. A major difficulty for machine learning models is class imbalance in datasets, which frequently leads to biased predictions favoring the dominant class and neglecting the minority classes. The data augmentation method employs the Synthetic Minority Over Sampling Technique (SMOTE) and Random Over Sampling (ROS) to address data imbalances and enhance the performance of classification models for underrepresented classes. This study employs an oversampling technique to enhance the efficacy of the XG Boost model. SMOTE exhibits better efficacy relative to competing methods; the application of appropriate oversampling techniques allows models to integrate patterns from both majority and often neglected minority data.

Factors associated with the development of recurrent and contralateral Charcot neuroarthropathy in individuals with diabetes mellitus: A scoping review.

Charcot neuroarthropathy (CN) can result in fractures and dislocations of the foot and ankle in individuals with diabetes and neuropathy, leading to ulceration, amputation and a poor quality of life. Additional episodes of acute CN can lead to extended periods of physical and psychosocial distress. The aim of this scoping review was to identify and synthesise the evidence relating to factors associated with the development of recurrent and contralateral Charcot neuroarthropathy (CN) in individuals with diabetes. A systematic search of four electronic databases was conducted from inception to February 06, 2023. All relevant study designs, except single case studies, that had been published in full in peer-reviewed journals were included. Studies were excluded if they were not published in English and did not provide data on individuals with diabetes. The search identified two studies that investigated factors associated with the development of recurrent CN, but none that related to the development of contralateral CN. Ten factors were investigated for association with recurrent CN development: age, body mass index, diabetes type and duration, glycated haemoglobin, anatomical site affected, duration of offloading applied to treat the primary CN episode, use of pharmacological intervention, severity of neuropathy, and skin temperature. However, no significant associations were reported. There is an alarming lack of evidence-based findings in this research area to guide practice. Clearly, more research in the form of rigorous prospective studies is urgently required to identify risk factors for the development of recurrent and contralateral CN in individuals with diabetes.

Vitamin D levels do not correlate with severity of idiopathic peripheral neuropathy.

Peripheral neuropathy (PN) is a common neurological condition in elderly adults. Vitamin D deficiency has been associated with diabetic and chemotherapy-induced neuropathy, but its role in idiopathic PN, in which no underlying cause of neuropathy can be identified, has not been investigated. Two hundred thirty patients with idiopathic PN enrolled in the Peripheral Neuropathy Research Registry (PNRR) at Johns Hopkins University School of Medicine had vitamin D testing information on record. Linear and logistic regressions were used to investigate the relationship between absolute vitamin D level or vitamin D insufficiency (<20 ng/mL) and both the severity of neuropathy as measured by the reduced total neuropathy score (TNSr) and severity of neuropathic pain. Sixteen (7%) patients were vitamin D insufficient (<20 ng/mL). Controlling for factors known to correlate with severity of neuropathy, there was no correlation between absolute vitamin D levels and TNSr (correlation coefficient 0.01, 95% CI -0.03 to 0.07, p = .59) and no association between vitamin D insufficiency and TNSr (correlation coefficient 0.3, 95% CI -2.8 to 3.4, p = .86). Vitamin D insufficiency was not associated with the presence of neuropathic pain (OR 4.1, 95% CI 0.6-26.0, p = .13), and there was no correlation between vitamin D levels and pain score (correlation coefficient 0.01, 95% CI -0.02 to 0.03, p = .59). In a single-center cohort of patients with idiopathic PN, there was no correlation between vitamin D levels and the severity of neuropathy or neuropathic pain.

Evaluating N-acetylcysteine as a Protective Agent Against Chemotherapy-induced Neuropathy in Breast Cancer: A Triple-blind, Randomized Clinical Trial.

Chemotherapy-induced peripheral neuropathy (CIPN) is a significant clinical issue that affects patients' quality of life and can limit the dosing of chemotherapeutic agents. N-acetylcysteine (NAC) has been proposed as a potential chemoprotective agent against CIPN due to its antioxidant properties. This study aimed to investigate the efficacy of oral NAC in preventing and controlling taxane-induced neuropathy in patients with breast cancer. This randomized, triple-blind, placebo-controlled trial included 80 breast cancer patients undergoing taxane-based chemotherapy. Participants were divided into 2 groups: an intervention group receiving 1200mg of oral NAC in divided doses per day and a placebo group. Patients were evaluated for neuropathy grade and functional status at 1 and 12 weeks postintervention. Our analysis revealed no significant difference in the incidence and severity of neuropathy between the intervention and placebo groups at 1 (P=0.328) and 12 weeks (P=0.569) postchemotherapy. Baseline characteristics such as age, number of treatment cycles, and disease stage were similar between groups, indicating a homogeneous population. Oral NAC at a dose of 1200mg per day did not significantly reduce the incidence or severity of taxane-induced neuropathy. These findings suggest that the oral bioavailability of NAC may be insufficient to exert a protective effect and that future studies should consider alternative dosing strategies or routes of administration. The need for further research to optimize NAC's chemoprotective role in CIPN remains evident.

Evaluation of the Impact of Advanced Glycation End-Products on Peripheral Neuropathy Outcomes in Type 2 Diabetes.

Background: Type 2 diabetes (T2DM) affects over 500 million people worldwide, and over 50% of this group experience the most common complication, diabetic peripheral neuropathy (DPN). The presence of advanced glycation end-products (AGEs) has been linked with the development of DPN. The present study assessed AGE levels in participants with type 2 diabetes and explored the hypothesis that there may be increased AGE levels in more severe DPN. Methods: A total of 124 participants with T2DM were consecutively recruited, and they underwent skin autofluorescence, clinical assessment for peripheral neuropathy, peripheral nerve ultrasound, nerve conduction studies, and axonal excitability assessment. Results: AGE accumulation showed weak but significant correlations with neuropathy severity and reduced nerve conduction function. However, after adjusting for confounding variables, a linear regression analysis did not reveal significant associations between the AGE levels and neuropathy outcomes. Conclusions: The present study suggests that the accumulation of AGE is not associated with the clinical, electrophysiological, and morphological measures of neuropathy in T2DM.

Autonomic and Immune Stress Response Networks in Patients Living With HIV.

Stress response systems are frequently dysregulated in patients with chronic inflammatory disorders. Pre-clinical studies have demonstrated direct influences of the sympathetic and vagal/parasympathetic branches of the autonomic nervous system (ANS) on the immune system. However, these connections have not been examined in humans. We hypothesized that the subtype and severity of autonomic neuropathy (AN) would predict immune phenotypes with distinct clinical and demographic characteristics in people living with HIV. This is a cross-sectional study of 79 adult people with a history of well-controlled HIV on stable combination antiretroviral treatment (CART) recruited from a primary care clinic network within the Mount Sinai Health System in New York City. All participants underwent a standardized battery of autonomic function tests summarized as the Composite Autonomic Severity Score (CASS) and vagal and adrenergic baroreflex sensitivity (BRS-V and BRS-A). Immune profiling included: 1) measurement of interleukin-6 (IL-6) as part of the Olink assay Target 96 Inflammation Panel, 2) non-negative matrix factorization (NMF) clustering analyses on Olink immune biomarkers, and 3) mass cytometry (CyTOF) on a subset of participants with and without autonomic neuropathy (N = 10). Reduced activity of caudal vagal circuitry involved in the cholinergic anti-inflammatory pathway (CAP) predicted higher levels of IL-6 (Spearman's rho = -0.352, p=0.002). The comprehensive assessment of the ANS-immune network showed four immunotypes defined by NMF analyses. A pro-inflammatory immunotype defined by elevations in type 1 cytokines (IL-6, IL-17) and increased numbers of CD8+ T-cells was associated with autonomic neuropathy (AN). This association was driven by deficits in the cardiovascular sympathetic nervous system and remained strongly significant after controlling for the older age and greater burden of co-morbid illness among participants with this immunotype (aOR=4.7, p=0.017). Our results provide novel support for the clinical relevance of the CAP in patients with chronic inflammatory AN. These data also provide insight regarding the role of the sympathetic nervous system and aging in the progression and development of co-morbidities in patients with chronic HIV and support future research aimed at developing therapies focused on modulation of the sympathetic and parasympathetic/vagal nervous system.

Most Carpal Tunnel Releases Address Moderate or Severe Median Neuropathy.

The role of surgery in normal or very mild median neuropathy can be questioned given that surgery in the absence of pathophysiology may offer only nonspecific effects that can be achieved without surgery, which raises ethical concerns. It's also important to avoid misdiagnosis: given that mild median neuropathy is prevalent and generally well-accommodated, notable symptoms from mild median neuropathy can signal unhelpful thoughts and feelings of distress that are a more pressing health priority. We identified 38 studies that categorized electrodiagnostic (EDX) measured median neuropathy severity among people being evaluated for carpal tunnel syndrome. We converted the different EDX grades used into one general grading classification. The Kruskal-Wallis test was used to compare the ratio of moderate/severe to mild/normal EDX findings between tests ordered by a surgeon or a nonoperative clinician. The median (interquartile range) ratio of moderate/severe to mild/normal EDX findings of median neuropathy at the carpal tunnel was 1.2 (0.91 to 1.8) among tests ordered by nonoperative clinicians and 3.3 (1.5 to 5.3) among tests ordered by surgeons (P = .0023). Only 4.1% of the patients who had EDX testing ordered by a surgeon had no measurable neuropathy. There were zero patients with normal EDX findings in 10 of the 17 (59%) studies in surgeon practices and in 10 of the 21 (48%) in the practices of nonoperative clinicians. The observation that in case series documenting EDX severities of median neuropathy, surgeons are mostly treating and operating on moderate to severe pathophysiology, emphasizes that while mild median neuropathy is highly prevalent it is uncommonly considered for surgery. Level II, Prognostic study.

Update on Biomarkers of Chronic Inflammatory Processes Underlying Diabetic Neuropathy.

There is an increasing prevalence of diabetes mellitus (DM), particularly type 2 DM (T2DM), and its associated complications. T2DM is linked to insulin resistance, chronic inflammation, and oxidative stress, which can lead to both macrovascular and microvascular complications, including peripheral diabetic neuropathy (PDN). Inflammatory processes play a key role in the development and progression of T2DM and its complications, with specific markers like C-reactive protein (CRP), interleukins (ILs), and tumor necrosis factor (TNF)-α being associated with increased risk. Other key inflammatory markers such as nuclear factor kappa B (NF-κB) are activated under hyperglycemic and oxidative stress conditions and contribute to the aggravation of PDN by regulating inflammatory gene expression and enhancing endothelial dysfunction. Other important roles in the inflammatory processes are played by Toll-like receptors (TLRs), caveolin 1 (CAV1), and monocyte chemoattractant protein 1 (MCP1). There is a relationship between vitamin D deficiency and PDN, highlighting the critical role of vitamin D in regulating inflammation and immune responses. The involvement of macrophages in PDN is also suspected, emphasizing their role in chronic inflammation and nerve damage in diabetic patients. Vitamin D supplementation has been found to reduce neuropathy severity, decrease inflammatory markers, and improve glycemic control. These findings suggest that addressing vitamin D deficiency could offer therapeutic benefits for PDN. These molecular pathways are critical in understanding the pathogenesis of DM complications and may offer potential biomarkers or therapeutic targets including anti-inflammatory treatments, vitamin D supplementation, macrophage phenotype modulation, and lifestyle modifications, aimed at reducing inflammation and preventing PDN. Ongoing and more extensive clinical trials with the aim of investigating anti-inflammatory agents, TNF-α inhibitors, and antioxidants are needed to advance deeper into the understanding and treatment of painful diabetic neuropathy.

The 'vulnerable nerve'; surgically acquired neuropathy in distal humeral surgery patients and the role of a tourniquet.

The complication of neuropathy is high in patients undergoing distal humerus surgery. Tourniquets (TQs) are typically used but can lead to nerve injury. We present a comparative study of a pre-intervention group (n = 38) and a post-intervention group (n = 38) undergoing distal humerus surgery between November 2020 and July 2023. The intervention included TQ discontinuation and the introduction of intravenous tranexamic acid at induction. Our analysis encompasses patient, anaesthetic, and surgical variables, as well as the rates and severity of neuropathy. Post-intervention, the rate of surgically acquired or deterioration in nerve injury improved from 15.8% (n = 6) to 2.6% (n = 1). Pre-intervention, the mean TQ duration was significantly longer for patients with post-operative neuropathy versus those without (120 min, SD = 29 vs. 88 min, SD = 38, p = 0.032). Surgery duration was not significantly longer without a TQ but was associated with a greater reduction in haemoglobin (12.7 g/L, SD = 10.9 vs. 25.2 g/L, SD = 15.5, p = 0.03). Trauma patients have a high risk of acquiring a nerve injury following elbow surgery or deterioration of a pre-surgical nerve injury, which emphasises the concept of vulnerable nerves. The cessation of using a TQ was associated with a lower nerve injury rate, with no cases of major nerve injury and no significant increase in surgical time.

Interconnections between diabetic corneal neuropathy and diabetic retinopathy: diagnostic and therapeutic implications.

Diabetic corneal neuropathy and diabetic retinopathy are ocular complications occurring in the context of diabetes mellitus. Diabetic corneal neuropathy refers to the progressive damage of corneal nerves. Diabetic retinopathy has traditionally been considered as damage to the retinal microvasculature. However, growing evidence suggests that diabetic retinopathy is a complex neurovascular disorder resulting from dysfunction of the neurovascular unit, which includes both the retinal vascular structures and neural tissues. Diabetic retinopathy is one of the leading causes of blindness and is frequently screened for as part of diabetic ocular screening. However, diabetic corneal neuropathy is commonly overlooked and underdiagnosed, leading to severe ocular surface impairment. Several studies have found that these two conditions tend to occur together, and they share similarities in their pathogenesis pathways, being triggered by a status of chronic hyperglycemia. This review aims to discuss the interconnection between diabetic corneal neuropathy and diabetic retinopathy, whether diabetic corneal neuropathy precedes diabetic retinopathy, as well as the relation between the stage of diabetic retinopathy and the severity of corneal neuropathy. We also endeavor to explore the relevance of a corneal screening in diabetic eyes and the possibility of using corneal nerve measurements to monitor the progression of diabetic retinopathy.

Three-Dimensional Microarchitecture of Lamina Cribrosa Pores in High and Normal Tension Glaucoma Using Optical Coherence Tomography.

The lamina cribrosa (LC) pores of patients with high-tension glaucoma (HTG) appear to take a more tortuous pathway than the LC pores of patients with non-glaucomatous (NG). To compare the LC pore microarchitecture in patients with HTG, normal tension glaucoma (NTG), and NG, by reconstructions of the LC made from tomographic images. Spectral domain-optical coherence tomography images of 52 eyes (18 NG, 18 HTG, and 16 NTG) of 29 patients were analyzed. Pores were traced using segmentation software. Pore length, tortuosity, and verticality were the 3 quantitative parameters compared among the 3 groups. Correlation analyses were performed to determine the effects of covariates on the 3 quantitative parameters. Pore tortuosity in HTG (1.419 ± 0.093) was significantly higher ( P = 0.011) than in NG (1.347 ± 0,034) but did not differ from that of NTG eyes ( P = 0.251). In addition, NTG had significantly shorter pores ( P = 0.005) than NG. No difference in pore tortuosity or verticality was found between NG and NTG ( P = 0.587 and P = 0.120, respectively). Pore verticality and length in HTG eyes did not significantly differ from that of NG eyes ( P = 0.049 and P = 0.033, respectively) and NTG eyes ( P = 0.827 and P = 0.968, respectively). All of the quantitative parameters measured were not correlated with age but were associated with glaucoma severity (Visual Field Index, mean deviation, retinal nerve fiber layer, and ganglion cell complex), except for pore verticality, which was not correlated with retinal nerve fiber layer. The LC pores of patients with HTG appear to be more tortuous than the pores of patients with NG, and the pores of patients with NTG are shorter than those of patients with NG. Changes in pore parameters appear to be associated with the severity of glaucomatous optic neuropathy.

Evaluation of Peripheral Neuropathy in Rat Models of Metabolic Syndrome and Diabetes Mellitus.

The dynamics of nephropathy development in rats with type 2 diabetes mellitus, caused by a high-fat diet and the streptozotocin administration (25 mg/kg), and metabolic syndrome, caused by addition of 20% fructose solution to the diet, was evaluated during the experiment. Models with moderate severity of metabolic changes without significant changes in body weight were obtained after 24 weeks. To study neuropathy severity, the method of electroneuromyography was used; the velocities of motor and sensory excitation propagation along the caudal nerve fibers were measured. In modeled diabetes mellitus against the background of hyperglycemia, a marked decrease in motor and sensory propagation rates was observed, and an increase in the response durations was noted from week 12 to week 24, indicating pronounced neuropathy. In the fructose model, the motor response duration increased from week 12, which possibly indicates the development of peripheral neuropathy.

Moderate-severe peripheral neuropathy in diabetes associated with an increased risk of dry eye disease.

This study establishes an increased risk of developing dry eye disease (DED) in patients with diabetic peripheral neuropathy using validated diagnostic criteria for both conditions. The disruption of ocular surface homeostasis has been associated with diabetes. However, it remains unclear if this association is independently influenced by peripheral neuropathy secondary to diabetes. This study aimed to investigate the clinical signs and symptoms of DED and their association with the severity of peripheral neuropathy in participants with type 2 diabetes. This prospective cross-sectional study recruited 63 participants with type 2 diabetes. All participants underwent a detailed assessment of DED using dry eye questionnaires (Ocular Surface Disease Index, Dry Eye Questionnaire-5), tear osmolarity, lipid layer thickness, noninvasive keratographic tear breakup time, phenol red thread test (PRT), and ocular surface staining. Corneal nerve morphology was imaged using corneal confocal microscopy. Based on the Total Neuropathy Scale, participants were stratified into no/mild (n = 48) and moderate/severe (n = 15) neuropathy groups. Dry eye disease was diagnosed in 31 participants (50%) of the total cohort, and the odds of developing DED in the moderate/severe neuropathy group were four times (95% confidence interval, 1.10 to 13.80; p=0.030) higher compared with the no/mild neuropathy group. The Dry Eye Questionnaire-5 scores were significantly higher (p=0.020), and PRT values (p=0.048) and corneal nerve fiber length (p<0.001) were significantly reduced in the moderate/severe neuropathy group compared with the no/mild neuropathy group. In regression analysis, neuropathy scores were independently associated with PRT measurements ( β = -0.333, p=0.023) and nerve fiber length ( β = -0.219, p=0.012) while adjusting for age, gender, hemoglobin A 1c , and duration of diabetes. Type 2 diabetic patients with peripheral neuropathy have a risk of developing DED, which increases with the severity of neuropathy. The observation that worsening peripheral neuropathy is associated with reduced tear secretion suggests that it may contribute to aqueous insufficiency.

Central neurodegeneration in Kennedy’s disease accompanies peripheral motor dysfunction

Spinal and bulbar muscular atrophy (SBMA), or Kennedy’s disease (KD), is a rare hereditary neuromuscular disorder demonstrating commonalities with amyotrophic lateral sclerosis (ALS). The current study aimed to define functional and central nervous system abnormalities associated with SBMA pathology, their interaction, and to identify novel clinical markers for quantifying disease activity. 27 study participants (12 SBMA; 8 ALS; 7 Control) were recruited. SBMA patients underwent comprehensive motor and sensory functional assessments, and neurophysiological testing. All participants underwent whole-brain structural and diffusion MRI. SBMA patients demonstrated marked peripheral motor and sensory abnormalities across clinical assessments. Increased abnormalities on neurological examination were significantly associated with increased disease duration in SBMA patients (R2 = 0.85, p < 0.01). Widespread juxtacortical axonal degeneration of corticospinal white matter tracts were detected in SBMA patients (premotor; motor; somatosensory; p < 0.05), relative to controls. Increased axial diffusivity was significantly correlated with total neuropathy score in SBMA patients across left premotor (R2 = 0.59, p < 0.01), motor (R2 = 0.63, p < 0.01), and somatosensory (R2 = 0.61, p < 0.01) tracts. The present series has identified involvement of motor and sensory brain regions in SBMA, associated with disease duration and increasing severity of peripheral neuropathy. Quantification of annualized brain MRI together with Total Neuropathy Score may represent a novel approach for clinical monitoring.

Comparative Analysis of Diabetic Neuropathy Examination Scores and Nerve Conduction Velocity in Patients with Diabetic Neuropathy

Background: Diabetic neuropathy is a prevalent consequence of diabetes, resulting in substantial morbidity. Precise evaluation is essential for prompt intervention and control. The study assessed the correlation and effectiveness of the Diabetic Neuropathy Examination (DNE) scores and Nerve Conduction Velocity (NCV) as diagnostic tools in individuals with diabetic neuropathy. Methods: An observational research was done, comprising 200 diabetic patients who were diagnosed with diabetic sensory-motor polyneuropathy. Participants completed Dynamic Neuromuscular Examination (DNE) grading and Nerve Conduction Velocity (NCV) testing. The data were analysed using SPSS version 20.0. Results: The study found a considerable negative correlation (r = -0.68, p &lt; 0.001) between DNE scores and NCV results. Higher DNE scores were associated with lower NCV values. Specifically, 20% of participants had mild neuropathy, 40% had moderate neuropathy, and 40% had severe neuropathy according to DNE scores. NCV testing revealed that 65% of participants had abnormal nerve conduction, with 25% showing mild reduction, 25% moderate reduction, and 15% severe reduction. Multivariate regression confirmed that DNE scores are significant predictors of NCV outcomes (Beta = -0.52, p &lt; 0.001), even after adjusting for confounding variables such as gender, age, diabetes duration, and HbA1C levels. Conclusion: DNE scoring is a reliable tool for assessing neuropathy severity in diabetic patients, correlating well with NCV results. Integrating DNE scoring in routine clinical practice can enhance the early detection and management of diabetic neuropathy. Recommendations: Routine use of DNE scoring along with NCV testing is recommended for comprehensive evaluation of diabetic neuropathy. Further research should explore additional diagnostic tools to improve early detection and intervention. Keywords: Diabetic Neuropathy, Diabetic Neuropathy Examination Score, Nerve Conduction Velocity Testing, Diabetic Polyneuropathy, Neuropathy Assessment..

Effectiveness of an intervention (effleurage and petrissage) on the severity of chemotherapy-induced peripheral neuropathy (CIPN) among patients: A randomized control pilot trial.

Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-dependent, nerve-damaging adverse reaction with reported prevalence rates of 68.1% at the first month after starting chemotherapy; 60.0 % at the third month; and 30% at the sixth month. To determine the effectiveness of an intervention (effleurage and petrissage) on severity of CIPN among patients receiving platinum-based chemotherapy. Sixty patients receiving either a third or fourth cycle of platinum-based chemotherapy were randomly assigned to one of two groups with a pre- and post-test design. The interventional group received effleurage and petrissage prior to chemotherapy for a period of one month. Comparisons of CIPN levels among both groups were done at Day 7, 14, 21, and 1 month using the FACT/ GOG-Ntx subscale. Prior to intervention, the mean score (+SD) of CIPN in the intervention group was 17.17 (+4.907) and 17.10 (+ 4.421) in the control group (T = 0.055, P value 0.956). The post-test scores following intervention at 1 month, was a mean score (+SD) for CIPN in the intervention group of 10.70 (±2.855) and 16.27 (±3.039) in the control group (P value 0.000). This pilot result supports that the intervention (effleurage and petrissage) can be effective in reducing CIPN severity levels among patients receiving platinum-based chemotherapy.

Reduced Thalamic γ-Aminobutyric Acid (GABA) in Painless but Not Painful Diabetic Peripheral Neuropathy.

Alterations in the structure, function, and microcirculation of the thalamus, a key brain region involved in pain pathways, have previously been demonstrated in patients with Painless- and Painful-diabetic peripheral neuropathy (DPN). However, thalamic neurotransmitter levels including GABA (inhibitory neurotransmitter) and glutamate (excitatory neurotransmitter) in different DPN phenotypes are not known. We performed a Magnetic Resonance Spectroscopy study and quantified GABA and glutamate levels within the thalamus, in a carefully characterised cohort of participants with Painless- and Painful-DPN. Participants with DPN (Painful- and Painless combined) had a significantly lower GABA:H2O ratio compared to those without DPN (Healthy volunteers [HV] and diabetes without DPN [No-DPN]). Participants with Painless-DPN had the lowest GABA:H2O ratio, which reached significance compared with HV and No-DPN, but not Painful-DPN. There was no difference in GABA:H2O in Painful-DPN compared with all other groups. A significant correlation with GABA:H2O and neuropathy severity was also seen. This study demonstrates that lower levels of thalamic GABA in participants with Painless-DPN may reflect neuroplasticity due to reduced afferent pain impulses. Whereas partially preserved levels of GABA in Painful-DPN may indicate that central GABAergic pathways are involved in the mechanisms of neuropathic pain in diabetes.

Eleven neurology-related proteins measured in serum are positively correlated to the severity of diabetic neuropathy

About 20% of patients with diabetes suffer from chronic pain with neuropathic characteristics. We investigated the multivariate associations between 92 neurology-related proteins measured in serum from 190 patients with painful and painless diabetic neuropathy. Participants were recruited from the Pain in Neuropathy Study, an observational cross-sectional multicentre study in which participants underwent deep phenotyping. In the exploration cohort, two groups were defined by hierarchical cluster analyses of protein data. The proportion of painless vs painful neuropathy did not differ between the two groups, but one group had a significantly higher grade of neuropathy as measured by the Toronto Clinical Scoring System (TCSS). This finding was replicated in the replication cohort. Analyzing both groups together, we found that a group of 11 inter-correlated proteins (TNFRSF12A, SCARB2, N2DL-2, SKR3, EFNA4, LAYN, CLM-1, CD38, UNC5C, GFR-alpha-1, and JAM-B) were positively associated with TCSS values. Notably, EFNA4 and UNC5C are known to be part of axon guidance pathways. To conclude, although cluster analysis of 92 neurology-related proteins did not distinguish painful from painless diabetic neuropathy, we identified 11 proteins which positively correlated to neuropathy severity and warrant further investigation as potential biomarkers.

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.

Hubungan Neuropati Diabetikum dengan Kualitas Tidur Pada Pengidap DM Tipe 2 di Rumah Sakit Baladhika Husada Jember

Diabetic neuropathy is a complication of type 2 diabetes mellitus which is caused by lesions or nerve dysfunction in the lower extremities due to chronic hyperglycemia through peripheral and central mechanisms which can cause symptoms of tingling, numbness, numbness, pain, burning sensation, etc. sleep, thus affecting the sleep quality of people with type 2 diabetes mellitus. This aim is to analyze the relationship between diabetic neuropathy and sleep quality in people with type 2 diabetes mellitus at the Baladhika Husada Hospital, Jember. This research uses a correlation research design with a Cross-Sectional Study approach with a sample size of 43 respondents taken using the Pusposive Sampling technique. The statistical test results for diabetic neuropathy with sleep quality using the Spearman Rho test showed that the p value was 0.002 and r = 0.456, which means that diabetic neuropathy has a sufficient relationship with sleep quality. There is a negative relationship between diabetic neuropathy and the sleep quality of type 2 diabetes mellitus patients, so it can be said that increasing the severity of diabetic neuropathy will also affect the sleep quality of sufferers. The results of this research can be used as a guide for sufferers of type 2 diabetes mellitus with diabetic neuropathy to increase self-awareness in paying attention to lifestyle, maintaining diet, and routinely controlling medication in health services, in order to reduce the symptoms of diabetic neuropathy so as to improve the quality of sleep of sufferers.