Point prevalence of motor neuropathy in children and adolescents with type 1 diabetes mellitus 

Point prevalence of motor neuropathy in children and adolescents with type 1 diabetes mellitus | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Point prevalence of motor neuropathy in children and adolescents with type 1 diabetes mellitus Joana Helena Bourbon Lopes, Jacinta Rodrigues Fonseca, Fernando Silveira, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6514477/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 26 Feb, 2026 Read the published version in Journal of Diabetes & Metabolic Disorders → Version 1 posted You are reading this latest preprint version Abstract Purpose Our objective is to conduct a screening for motor neuropathy in children and adolescents with type 1 diabetes to assess its point prevalence and to analyse potential risk factors associated with any positive motor neuropathy diagnosis. Methods This is a cross-sectional study involving children aged 12 to 18 years who have been diagnosed with diabetes for five or more years and are receiving treatment with an insulin pump. All participants underwent a neurological examination and were questioned about symptoms of neuropathy. A nerve conduction study was conducted to evaluate the median, ulnar, common peroneal, and tibial motor nerves. Sensory nerves were also examined. The F-wave response of the tibial nerve was analysed, and needle electromyography was performed on a proximal and distal muscle of the lower limb. Results A total of 29 children completed the study (mean age: 15.34 ± 1.56 years; mean duration of diabetes: 11.93 ± 2.84 years; HbA1c levels: 7.50 ± 1.17%). Results were normal, indicating adequate motor nerve integration and excluding the presence of motor neuropathy as well as peripheral neuropathy, even at subclinical level. Conclusion In our studied population, which receives tight monitoring and support for diabetes management, using nerve conduction studies to detect early subclinical motor neuropathy shows no clear benefit. This finding was consistent even among individuals with poor metabolic control, altered albumin/creatinine ratio, and diabetes duration over 10 years, with no abnormalities observed. We recommend following the latest guidelines provided by the American Diabetes Association (ADA). Motor neuropathy nerve conduction studies type I diabetes mellitus paediatrics Figures Figure 1 Background Type 1 diabetes(T1DM) Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by insulitis, an inflammatory lesion caused by autoreactive T-cells that infiltrate the islets, leading to the destruction of β-cells and ultimately resulting in insulin deficiency[ 1 – 3 ]. The most common symptoms resulting from hyperglycaemia include polyuria, weight loss, polydipsia, and, in some cases, diabetic ketoacidosis. Diagnosis is based on clinical symptoms and glucose monitoring[ 4 – 6 ]. T1DM progresses through three stages. Stage 1, known as preclinical type 1 diabetes, is marked by the presence of two or more autoantibodies despite normal blood glucose levels. Stages 2 and 3 indicate a progression from dysglycemia to overt symptomatic hyperglycaemia[ 5 ]. It is the most common chronic endocrine disease among the paediatric population[ 7 ]. Diabetic peripheral neuropathy Prolonged T1DM can cause early microvascular complications like retinopathy, nephropathy, and neuropathy, while macrovascular consequences like arteriosclerosis tend to occur later[ 8 ]. Diabetic neuropathies affect the nervous system, causing various symptoms due to abnormalities in sensory, motor, and autonomic nerve fibres, which are classified based on clinical features[ 9 ]. Chronic sensorimotor distal symmetric polyneuropathy (DSPN) and autonomic neuropathy are the two most common types of neuropathies[ 9 – 11 ]. Diabetic peripheral neuropathy (DPN) falls under the DSPN category. DPN is defined as symptoms or signs of peripheral nerve dysfunction in individuals with diabetes, excluding other causes[ 11 ]. It is a common complication that can lead to significant disability, reduced quality of life, and a substantial economic burden[ 12 ]. It is estimated that up to 50% of individuals with long-term diabetes may be affected by this complication[ 11 , 13 ]. This percentage could rise to 100% when more precise diagnostic methods, such as nerve conduction studies, are used[ 11 ]. The prevalence of these complications is likely underestimated, as they often remain subclinical in younger age groups[ 9 , 11 ]. Although younger age at onset, longer duration of diabetes, and a history of diabetic complications are recognised risk factors, the primary driver is chronic hyperglycemia[ 9 , 11 ]. This sustained metabolic imbalance leads to the formation of advanced glycation end products and activation of polyol, glycolysis and hexamine biological pathways which trigger oxidative stress at the cellular level, resulting in vascular and neuronal damage. Therefore, it is crucial to maintain good metabolic control[ 11 ]. DPN affects both myelinated and unmyelinated nerve fibres. Pain mainly results from damage to thin, unmyelinated fibres, while impairment of large, myelinated fibres can lead to gait instability, increasing fall risk[ 2 ]. Common symptoms like numbness, tingling, allodynia, and a shock-like sensation, indicate somatic involvement[ 11 ]. According to the American Diabetes Association (ADA), screening for DPN is recommended five years after diagnosis in type 1 diabetic patients. The frequency of this screening should be annual or semestral and must include clinical history and a physical examination[ 13 ]. Motor neuropathy and nerve conduction studies Motor involvement in DPN is often overlooked compared to sensory dysfunction[ 14 ]. However, motor impairment increases fall risk, affects gait and balance, and can lead to foot deformities like hammer toes, contributing to chronic irritation and ulceration[ 14 , 15 ]. Multiple studies using nerve conduction studies (NCS) have shown the ability to detect subclinical motor involvement, revealing reduced motor nerve conduction velocity (MNCV) and amplitude, indicative of nerve deterioration. Early MNCV reduction is linked to nodal dysfunction, axonal swelling, oxidative stress, and metabolic disturbances. Over time, axonal atrophy and segmental demyelination leads to conduction blocks. When detected early, these conditions can be reversed with proper metabolic control, including insulin administration; however, after a few months, these abnormalities become irreversible[ 14 ]. Studies emphasize the importance of NCS in detecting early motor dysfunction, revealing a high prevalence of subclinical neuropathy in diabetic patients and indicating that motor involvement is more frequent than previously recognised[ 10 , 14 , 16 ]. Longitudinal research demonstrates a significant increase in DPN over time, with subclinical cases nearly doubling after several years, underscoring the progressive nature of the condition[ 12 ]. These findings substantiate the hypothesis that NCS provide significant advantages for early screening and detection of motor neuropathy. By identifying nerve dysfunction before clinical symptoms emerge, these tests enable earlier interventions, potentially slowing progression and preventing severe motor complications. Although subclinical nerve function abnormalities may not directly predict the onset of clinical neuropathy, certain changes in nerve function indicate damage that, when combined with other local injuries, may become clinically significant[ 17 ]. Despite extensive research on peripheral neuropathy in type 1 diabetes, the pattern of nerve involvement remains controversial. The frequent involvement of the common peroneal nerve in some studies further suggests a targeted approach in screening protocols, making NCS a valuable tool beyond standard neurological exams[ 8 , 10 ]. This method can be time-consuming, expensive, and uncomfortable for many paediatric patients. However, it is less dependent on patient cooperation, making it less subjective. In children and adolescents with T1DM, early signs of neuropathy are often minimal or absent, making clinical exams less reliable in this group[ 9 , 18 ]. Nerve conduction studies can therefore be a more effective diagnostic tool, as they can detect the condition at a subclinical stage. Objectives The main objective is to evaluate the point prevalence of motor neuropathy in children and adolescents with a 5-year or more diagnosis of type 1 diabetes using nerve conduction studies. We will analyse various biochemical and clinical parameters of each individual to evaluate their metabolic control. Subsequently, to potentially identify factors that may increase the risk of developing motor neuropathy, we intend to evaluate positive motor neuropathy diagnoses with these parameters. Methods This cross-sectional analytical study was conducted at the paediatric endocrinology department of the Centro Hospitalar Universitário S. João (CHUSJ), from September 2024 to March 2025. We reviewed all the children who attended the semester evaluation consultation for their T1DM diagnosis between September 2024 and January 2025. Among them, we found a total of 42 children who met our inclusion criteria: they were aged between 10 and 18 years, had been diagnosed with T1DM for over five years, and were being treated with an insulin pump. We then excluded any children who had been diagnosed with neuropathy due to causes other than T1DM, such as infections, connective tissue diseases, medications, or nutritional deficiencies. We also excluded children with a family history of hereditary neuropathy, those with types of diabetes other than type 1, and children using medications that could potentially affect peripheral nerve function. The total number of participants was determined based on a review of similar studies, the total number of children monitored at CHUSJ, and practical considerations such as time constraints and the availability required to conduct both NCS and neurological examinations. The study was approved by the Ethics committee of CHUSJ. Written informed consent was obtained from patients and their parents. Participants had the right to withdraw from the study at any time. Confidentiality and the well-being of patients were prioritized throughout the study. The enrolled children underwent a standardized and systematic summary neurological examination which included ankle, patellar, bicipital and tricipital reflex, assessment of muscular force, vibration and cutaneous sensation. All evaluations were conducted by a single individual to eliminate interobserver bias, thereby reducing variability in the application and interpretation of the neurological examination. Vibration was evaluated using a 128 Hz tuning fork placed on the dorsum of the great toe, just proximal to the nail bed and scored as (= 1) if present (= 0) if absent. The analysis of cutaneous touch sensation was conducted using the 10g Semmes-Weinstein monofilament on the plantar surface of the great toe and the bases of the first and fifth metatarsals on both feet. The monofilament was applied perpendicularly to intact skin with enough pressure to cause it to bend, maintaining contact for no longer than two seconds. The individuals were with their eyes closed and described whether they felt the pressure and where they felt it. The test was assessed in three specific sites, making three applications at each site while alternating between actual touches and simulated ones. Cutaneous sensation was considered present if at least two out of three responses were correct for each site, with a score of (= 1) if present and (= 0) if absent[ 19 ]. The assessment of muscular force involved extending and flexing the ankle, knee, and elbow, which was then graded using the Medical Research Council (MRC) scale from zero to five. Muscle power was classified as follows: normal for grades 4–5, reduced for grade 3, and severely reduced for grades 0–2. The reflexes were evaluated using a reflex hammer and scored as normal (= 0), present with reinforcement (= 1) and decreased or absent (= 2). Following the neurological summary examination, participants were inquired about the presence of various symptoms suggestive of neuropathy, including cramps, numbness, tingling, burning sensations, electric shock-like sensations, instability while walking, fatigue, hyperalgesia, and allodynia. The symptoms were classified as follows: (= 1) if present and (= 0) if absent. The electrophysiological test was done by the dantec keypoint electromyography machine by a single neurophysiologist who was blinded to the patient´s clinical and medical history. The exam was, in general, well tolerated by the children and adolescents. The temperature was checked each time before placing the electrodes, ensuring it was above 30°C. When necessary, arms and legs were warmed with hot water. The ground electrode was placed midway between the stimulation and the recording electrodes. Motor conduction studies were performed bilaterally on the median, ulnar, common peroneal, and tibial motor nerves. Conduction velocity (CV) on the tibial nerve was not measured, as it can be uncomfortable. Instead, we opted to measure the F wave response, which was recorded in both the right and left tibial nerves. This technique has a higher sensitivity as it studies also proximal conduction[ 20 ]. F minimal latency (m s) was considered normal if equal to or lower than 55 m s. Table 1 shows the reference cut-off values considered normal and routinely used in clinical practice. Considering these reference values, the electrophysiological findings were analysed by a neurologist trained in clinical neurophysiology and neuromuscular disorders. They were determined through a literature review by neurophysiology specialists, based on the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) guidelines and adapted to the Portuguese population[ 21 ]. Table 1 Reference values for nerve conduction studies that are considered normal. Nerve Stimuli Response registration Distal Latency (m s) Amplitude (M v) Velocity (m s⁻¹) Distance (cm) Peroneal Ankle Extensor digitorum brevis ≤ 6.0 ≥ 2.0* - Extensor digitorum brevis - - ≥ 40 Tibial Posterior to the medial malleolus Hallux abductor ≤ 6.0 ≥ 4.0* - Medianus wrist Abductor pollicis brevis ≤ 4.2 ≥ 4.0 ≥ 50 8.0 Ulnaris Wrist Abductor digiti minimi ≤ 3,6 ≥ 6,0 8–12 Below elbow Abductor digiti minimi ≥ 50 *Compare with the contralateral Needle electromyography (EMG) was conducted on all individuals for the right peroneus tertius and right vastus medialis, as this test shows greater sensitivity for axonal motor damage. The reduction in the amplitude of the compound muscle action potential (CMAP), with either normal or slightly decreased CV, or a modest increase in distal motor latency (DML) can support axonal damage[ 22 ]. Primary demyelination can be considered when there is a marked reduction in motor CV or grossly increased DMLs or minimum F-wave latencies[ 22 ]. Data were collected and analysed, including age, gender, height, weight, body mass index (BMI), duration of diabetes, haemoglobin A1c (HbA1c), fasting plasma glucose, lipid profile (HDL, LDL, total cholesterol, triglycerides), time in range (TIR) percentage, coefficient of variation, vitamin D levels, urea, creatinine, albuminuria and the spot albumin-to-creatinine ratio. Metabolic control was considered good if HbA1c levels were between 6.5% and 7.5%, moderate if between 7.6% and 9.0% and poor if above 9.0%[ 8 ]. Statistical Analysis Data are presented as arithmetic means ± standard deviations (SD). Three missing conduction velocity values were imputed using the mean after confirming a normal distribution (bolt in Table S1 - see Online Resource 1). This preserved the sample size. Two individuals had clinical analyses performed privately, with only confirmation of normal results available. One individual lacked TIR (%) and variation coefficient (%) due to the absence of FreeStyle Libre monitoring (hyphen in Table S1 - see Online Resource 1). Results Out of the 42 individuals assessed for eligibility, 2 were initially excluded from the study: one had Charcot-Marie-Tooth syndrome and the other had a cognitive disorder. Additionally, 3 individuals declined to participate. Ultimately, a total of 29 participants completed the study (Fig. 1 ). Of the 37 individuals who initially agreed to participate, a total of 8 did not attend the scheduled electromyography session. Some individuals gave no reason for their absence, while others were hesitant to miss classes solely for the purpose of the exam. Due to time constraints and scheduling logistics with the neurophysiology doctor, it was difficult to arrange the exam on the days when they had other appointments. If it had been possible, we would have achieved better adhesion. The mean age of the patients was 15.34 ± 1.56 years, 34.48% were female and 65.52% were male. The mean age duration of T1DM was 11,93 ± 2,84 years. The biochemical characteristics of the patients are shown in Table 2 . The HbA1c was 7.50 ± 1.17%, with 37% having values of HbA1c above 7.5%. In addition, 68% had a time in range (%) less than 70% and 61% had a coefficient of variation (%) greater than 36%. None of our patients had retinopathy, and only one individual showed an altered albumin/creatinine ratio. Table 2 Profile of biochemical parameters in study participants Parameters Cases (%) n = 29 1. BMI (Percentile) P97 (obesity) 1 (3%) 2. Fasting plasma glucose (mg dL⁻¹) (178 ± 40.86) 200 mg dL⁻¹ 8 (30%) 3. HbA1c (%) (59 ± 13 mmol/mol (7.5 ± 1.2%)) < 48 mmol/mol ( 9.0%) 3 (11%) Cases (%) n = 28 4. Spot urinary albumin/creatinine ratio (mg g ⁻¹) (7.15 ± 9.02) < 30 mg g⁻¹ (Normal) 27 (96%) 30–300 mg g⁻¹ (microalbuminuria present) 1 (4%) Spot urinary Albuminuria (mg L ⁻ ¹) (12.60 ± 23.61) 20mg L ⁻ ¹ (Albuminuria) 3 (11%) 5. Urea (mg dL ⁻ ¹) (28.57 ± 6.43) 10.00–50 mg dL ⁻ ¹ (Normal) 28 (100%) > 50 mg dL ⁻ ¹ 0 (0%) 6. Creatinine (mg dL ⁻ ¹) (0.66 ± 0.14) 0.67 mg dL ⁻ ¹- 1.17 mg dL ⁻ ¹ (Normal) 15 (54%) 1.17 mg dL ⁻ ¹ (Abnormal) 13 (46%) 1. Time in range(%) ( 57 ± 0.19) ≥ 70% (Normal) 9 (32%) 36% (Abnormal) 17 (61%) Cases n = 27 3. Total cholesterol (mg dL ⁻ ¹) (152.22 ± 28.10) ≤ 200 mg dL ⁻ ¹ (Normal) 24 (89%) > 200 mg dL ⁻ ¹ (Abnormal) 3 (11%) 4. HDL (mg dL ⁻ ¹) (55.65 ± 9.43) ≥ 35 mg dL ⁻ ¹ (Normal) 27 (100%) 130 mg dL ⁻ ¹ (Abnormal) 0 (0%) 6. Triglycerides (mg dL ⁻ ¹) ( 76.07 ± 51.06) ≤ 170 mg dL ⁻ ¹ (Normal) 24 (89%) > 170 mg dL ⁻ ¹ (Anormal) 3 (11%) Vitamin D (ng mL ⁻ ¹) (21.85 ± 8.52) > 20 ng mL ⁻ ¹ (Normal) 14 (52%) 12–20 ng mL ⁻ ¹ (insufficiency) 10 (37%) < 12 ng mL ⁻ ¹ (deficiency) 3 (11%) HbA1c Hemoglobin A1c or glycated hemoglo 1;HDL High-density;LDL Low-density lipoprotein, BMI body mass index; During the summary neurological examination, no abnormalities were found, except in four individuals who exhibited decreased patellar and achilles reflexes. Among these, one reported numbness in the legs. No other complaints were noted. Ultimately, all NCS results were normal. Table 3 summarises the mean values (± SD) for latency, velocity, and amplitude of the peroneal, tibial, median, and ulnar motor nerves. The full dataset is available as supplementary material (see Online Resource 1). Table 3 Nerve conduction study results (latency, amplitude, and velocity) presented as mean ± standard deviation. Nerve Latency (m s) Amplitude (M v) Velocity (m s⁻¹) Left Peroneal 4.11 ± 0.53 5.62 ± 2.17 49.61 ± 3.47 Right Peroneal 3.79 ± 0.35 6.33 ± 2.10 48.69 ± 3.26 Left Tibial 4,11 ± 0,54 11.39 ± 3.65 - Right Tibial 4.24 ± 0.56 11.47 ± 3.00 - Left Medianus 3.39 ± 0.33 8.46 ± 1.97 56.90 ± 3.50 Right Medianus 3.39 ± 0.34 9.35 ± 1.93 58.02 ± 2.66 Left Ulnaris 2.56 ± 0.29 8.68 ± 1.29 60.99 ± 4.43 Right Ulnaris 2.66 ± 0.30 8.62 ± 1.55 60.12 ± 4.90 The EMG results were also normal, indicating no axonal damage. Additionally, F minimum latency values were within the normal range (below 55 m s) at 45.59 ± 3.73 m s in the right tibialis and 45.77 ± 3.96 m s in the left tibialis. Discussion Our study found no evidence of subclinical motor neuropathy in any of the participants, suggesting that motor nerve function remained preserved in this population. This contrasts with previous studies that reported a higher prevalence of motor involvement. Abuelwafaa et al. 2019 studied 50 diabetic patients aged 10–18 years and found that 88% had electrophysiological evidence of peripheral neuropathy, primarily affecting motor function (68.2%) with no cases of pure sensory neuropathy. The most common finding was conduction slowing, particularly in the common peroneal nerve[ 10 ]. This finding is noted in other studies, highlighting the significance of motor involvement[ 16 , 23 ]. They used a stricter conduction velocity threshold of 46.7 m s⁻¹ compared to our 40 m s⁻¹, which may explain their higher prevalence rates[ 10 ]. This study was conducted in Sudan, where limited healthcare resources and poor diabetes management may have contributed to the increased prevalence of neuropathy. The mean HbA1c level in their population was 11.28 ± 2.75 %, compared toour study's mean of 7.50 ± 1.17 %. This indicaes poorer metabolic control, despite a shorter disease duration of 10.21 ± 3.93 years[ 10 ]. Singh et al. 2022 study, out of also 50 children aged 8–18 years, 56% exhibiting subclinical neuropathy on NCS, with 40% having pure motor, 2% pure sensory, and 14% mixed motor-sensory neuropathy[ 8 ]. The participants had poorer metabolic control with HbA1c of 9.14 ± 2.10 % nd the higher prevalence may also be due to ethnic and genetic differences, limited healthcare infrastructure and environmental factors in India. Glycaemic variability, including the frequency of hypoglycaemia and hyperglycaemia, and different diagnostic criteria may also contribute. The peroneal nerve was also the most affected, with significant risk factors including poor glycaemic control (HbA1c > 9 %)and diabetes duration of over five years[ 8 ]. However, this pattern is not consistently observed in other studies, leading to the belief that the development of neuropathy in childhood is neurophysiologically heterogeneous[ 7 , 12 , 17 ]. On the other hand, Walter-Holiner et al. 2018 conducted a cohort study with a 5-year follow-up, in Austria with a total of 38 patients aged 9–18 years[ 12 ]. At baseline, the prevalence of diabetic peripheral neuropathy (DPN) diagnosed through neurological examination was 13.2 %, hile nerve conduction velocity (NCV) testing detected DPN in 31.6 %, ndicating a high prevalence of subclinical cases. After five years, clinically diagnosed DPN increased to 34.2 % (= 0.039), while subclinical DPN rose to 63.2 % (= 0.002), with the most significant electrophysiological changes observed in the tibial sensory nerve[ 12 ]. Some research indicates that the motor nervous system is more resistant than the sensory nervous system. This difference may be due to anatomy: dorsal root ganglion neurons are outside the blood-brain barrier, while motor neurons are protected within the ventral horn of the spinal cord[ 7 , 24 , 25 ]. While not the main focus of this study, NCSs were also performed on the median, ulnar, and sural sensory nerves. These revealed no abnormalities, thus providing no evidence of diabetic peripheral neuropathy. In addition, they used reference values like ours for conduction velocity in motor nerves. And so given Austria’s advanced healthcare system, the high prevalence cannot be due to limited resources or poor metabolic monitoring, as shown in other studies. Their mean HbA1c was 8.1 ± 1.2 %, comparable toours, but with a shorter disease duration of 5.6 ± 3.2 years[ 12 ]. There were one or two individual measurements that were close to the reference range, particularly the common peroneal nerve velocity and F minimum latency. Notably, this phenomenon has been observed in taller individuals with no clinical symptoms and no changes in the physical and neurological exam. Studies indicate that taller people typically exhibit lower nerve conduction velocities and higher F wave latencies, which may represent a physiological variation rather than a pathological one[ 16 , 26 ]. Secondly, there may also be minor technical factors such as electrode positioning which can introduce small discrepancies in motor nerve assessments. These considerations highlight the need for cautious interpretation of borderline values to avoid overestimating pathological findings. In instances of isolated borderline values, it is crucial to consider the broader context, potential concomitant alterations like altered tibial F waves, altered needle electromyography, changes in physical neurological exam and the individual's height. For these individuals, a follow-up evaluation is recommended within a five-year period to determine whether there have been any significant changes in the values compared to the initial assessment. If any changes are observed, it may be appropriate to consider the onset of subclinical motor neuropathy. Consistent and reliable results were achieved through standardized neurological and electrophysiological assessments, which offered a comprehensive and objective evaluation of neuropathy in patients with T1DM. This also ensured comparability across different settings and populations. It is a relatively underexplored area, especially in our Portuguese population contributing to new knowledge to the field. In addition, by having a single examiner conduct the neurological exam, inter-observer variability was minimized, enhancing the study's internal validity. However, misinterpretation or subtle variations in reflex evaluations could account for the alterations observed in the four cases. Furthermore, all NCS and EMG assessments were performed by the same highly experienced neurophysiologist, blinded to the patient´s clinical and medical history. This approach minimized, once again, interobserver variability while also reducing observer bias. Some factors may limit the study´s generalisability. It was conducted in a single centre, CHUSJ, a hospital with experienced physicians and systematic treatment monitoring. This may not fully represent the broader paediatric T1DM population in other hospitals. This study may be subject to some healthy user bias, as some children or adolescents who chose not to participate had poorer metabolic control and appeared to be less concerned about their health. There are scarce reference values of electrophysiological results in a healthy paediatric population and so incorporating a healthy control group in a cohort study for comparison would improve external validity. However, it would be difficult to get approval from the ethics committee. Although we did not use a control group for reference and comparison, relying instead on fixed reference values, we could possibly say that our individual and mean ± SD values were very similar to those of control groups used as reference in many studies. There could be some doubt regarding the conduction velocity of the common peroneal nerve, which could eventually show statistical significance if analysed with values from control groups in other studies. Nonetheless, we wouldn't consider these individual values to be pathological, given the clinical context, the height of the patients, and additional findings such as normal tibial F waves and needle electromyography, which are more sensitive indicators[ 17 , 23 , 27 ]. Still, we did not take this approach because no similar study has been conducted in a Portuguese population with comparable characteristics. Using control groups from studies conducted in other countries could introduce bias due to population differences like genetic background, environmental factors, healthcare systems, and lifestyle that could influence the results. Conclusion This study indicates that, within our population, where patients receive thorough monitoring and support for their diabetes management, there is no discernible benefit of employing nerve conduction studies, like electromyography, for the purpose of diagnosing or detecting subclinical motor neuropathy. Even children and adolescents with poor metabolic control, altered albumin/creatinine ratios, and a long duration of diabetes exceeding 10 years showed no abnormalities in our study. There is still no consensus on the pattern of nerve involvement and histological abnormalities (demyelination or axonal degeneration), so further research is needed in this area to provide more conclusive information on the possibility of primary and secondary prevention and to improve quality of life. The varying prevalence rates presented are mostly due to the different criteria and lack of standardized characterization of DPN[ 23 ]. For, now we recommend using the electrophysiological diagnostic method only in accordance with the guidelines established by the American Diabetes Association (ADA). This recommendation applies specifically when clinical features are atypical or when a diagnosis remains uncertain after a comprehensive medical history and basic clinical assessments have been conducted[ 13 ]. Abbreviations ADA American Diabetes Association BMI Body Mass Index CHUSJ Centro Hospital Universitário S.João CMAP Compound Muscle Action Potential CV Conduction Velocity DPN Diabetic Peripheral Neuropathy DML Distal Motor Latency DSPN Distal Symmetric Polyneuropathy EMG Needle Electromyography HbA1c Haemoglobin A1c MNCV Motor Nerve Conduction Velocity NCS Nerve conduction studies SD Standard Deviations TIR Time in Range T1DM Type 1 Diabetes Mellitus Declarations Ethics approval and consent to participate The study was approved by the Ethics Committee of Centro Hospitalar Universitário S.João. Written informed consent was obtained from children and their parents. Consent for publication Not applicable. Availability of data and materials All data generated or analysed during this study are included in this published article [and its supplementary information files]. Competing interests The authors declare that they have no competing interests. Funding No financial support was received for our study. Authors' contributions JL was deeply involved in all stages of the study, including the conception and design, data acquisition, analysis and interpretation. Took the lead in drafting the manuscript. Conducted all neurological examinations for all participants during their semestral appointments. JF made significant contributions to the conception and design of the study, data acquisition, and overall interpretation of the results. Played a major role in critically revising the manuscript for important intellectual content FS made significant contributions to the conception of the study and the interpretation of data. Was actively involved in critically revising the manuscript for important intellectual content. Also played a key role in performing nerve conduction studies and needle electromyography for all participants, as well as in analysing the results. CC made significant contributions to the conception and design of the study, data acquisition and interpretation of data. Was involved in critically revising it for important intellectual content. All authors read and approved the final manuscript. Conflicts of interest All other authors state no conflict of interest. References DiMeglio LA, Evans-Molina C, Oram RA. Type 1 diabetes. Lancet. 2018;391:2449–62. https://doi.org/10.1016/S0140-6736(18)31320-5 . Stoian A, Muntean C, Babă DF, et al. Update on biomarkers of chronic inflammatory processes underlying diabetic neuropathy. Int J Mol Sci. 2024;25. https://doi.org/10.3390/ijms251910395 . Pugliese A. Insulitis in the pathogenesis of type 1 diabetes. Pediatr Diabetes. 2016;17:31–6. https://doi.org/10.1111/pedi.12388 . Holt R, Devries JH, Hess-Fischl A, et al. The management of type 1 diabetes in adults. A consensus report by the American diabetes association (ADA) and the European association for the study of diabetes (EASD). 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Revisão relacionada a alguns aspetos técnicos e fisiológicos das ondas F e análise dos dados obtidos em um grupo de indivíduos diabéticos. Arq Neuropsiquiatr. 2001;59:192–7. Chen S, Andary M, Buschbacher R, et al. Electrodiagnostic reference values for upper and lower limb nerve conduction studies in adult populations. AANEM Pract Topic. 2016;54:371–7. Tankisi H, Pugdahl K, Fuglsang-Frederiksen A, et al. Pathophysiology inferred from electrodiagnostic nerve tests and classification of polyneuropathies. Suggested guidelines. Clin Neurophysiol. 2005;116:1571–80. https://doi.org/10.1016/j.clinph.2005.04.003 . Espirito B, Ferreira SN, Silva IN, et al. High prevalence of diabetic polyneuropathy in a group of brazilian children with type 1 diabetes mellitus. Lond J Pediatr Endocrinol Metabolism. 2005;18:1087–94. Zochodne DW, Verge VMK, Cheng C, et al. Does diabetes target ganglion neurones? Progressive sensory neurone involvement in long-term experimental diabetes. Brain. 2001;124:2319–34. Ramji N, Toth C, Kennedy J, et al. Does diabetes mellitus target motor neurons? Neurobiol Dis. 2007;26:301–11. https://doi.org/10.1016/j.nbd.2006.11.016 . Soudmand R, Ward LC, Swift TR. Effect of height on nerve conduction velocity. Neurology. 1989;32:407–10. Rota E, Quadri R, Fanti E et al. Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus. J Peripheral Nerv Syst 2005:348–53. Additional Declarations No competing interests reported. Supplementary Files ESM1.pdf Cite Share Download PDF Status: Published Journal Publication published 26 Feb, 2026 Read the published version in Journal of Diabetes & Metabolic Disorders → Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6514477","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":453140383,"identity":"2e052c6d-f00a-40f3-b544-baaf1ef7e9be","order_by":0,"name":"Joana Helena Bourbon Lopes","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA2klEQVRIie3RsQrCMBCA4ZTAuaSdz0VfoVLoJPgqF4RO0qUggktByCT4BOprOEYKnYqzUIf6AGLdHK2b4JCMgvm3Gz6OSxhzuX4yrjUtcAC91bGxJCCbphpHgSin4XsWZiKi0VUlcoezGK1IWOcxSlVEwChe+geWTozkohOkUzEAppPar1hm3nKmEmnebfHysvYVk2szkQoJCqm4pzJLMuUhdecr4MCtSP9Seg11jwwCeH9bYSa0gQT1pj0+u68c7u+P9nYYp73ctAY/By9HMoEvwiyIy+Vy/VsvyuNDzj/waroAAAAASUVORK5CYII=","orcid":"","institution":"Faculdade de Medicina Universiade do Porto","correspondingAuthor":true,"prefix":"","firstName":"Joana","middleName":"Helena Bourbon","lastName":"Lopes","suffix":""},{"id":453140384,"identity":"114246f5-2782-473f-9655-19efb296a2eb","order_by":1,"name":"Jacinta Rodrigues Fonseca","email":"","orcid":"","institution":"Faculdade de Medicina Universiade do Porto","correspondingAuthor":false,"prefix":"","firstName":"Jacinta","middleName":"Rodrigues","lastName":"Fonseca","suffix":""},{"id":453140385,"identity":"865764f3-db99-40e6-a1b2-a8fed2c51177","order_by":2,"name":"Fernando Silveira","email":"","orcid":"","institution":"Hospital de São João","correspondingAuthor":false,"prefix":"","firstName":"Fernando","middleName":"","lastName":"Silveira","suffix":""},{"id":453140386,"identity":"cf02fb07-399c-43e4-b7a2-ee008f5305c8","order_by":3,"name":"Cíntia Castro-Correia","email":"","orcid":"","institution":"Faculdade de Medicina Universiade do Porto","correspondingAuthor":false,"prefix":"","firstName":"Cíntia","middleName":"","lastName":"Castro-Correia","suffix":""}],"badges":[],"createdAt":"2025-04-23 16:38:22","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6514477/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6514477/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1007/s40200-026-01865-z","type":"published","date":"2026-02-26T15:59:09+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":82583204,"identity":"e80a6afc-4653-4bcc-9105-26e4b3702aa1","added_by":"auto","created_at":"2025-05-13 06:48:58","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":107678,"visible":true,"origin":"","legend":"\u003cp\u003eFlow diagram for participant recruitment\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-6514477/v1/b89d9f009ee3e239f732f002.jpeg"},{"id":103765617,"identity":"3be4b5d2-8b20-4f1a-b75a-acd41de7bde0","added_by":"auto","created_at":"2026-03-02 16:05:55","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1076713,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6514477/v1/dcaa9365-5f38-4a93-b5a7-4f0de2d93654.pdf"},{"id":82583205,"identity":"43f47145-f35c-4d38-b446-7ed3a43424ea","added_by":"auto","created_at":"2025-05-13 06:48:59","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"supplement","size":411669,"visible":true,"origin":"","legend":"","description":"","filename":"ESM1.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6514477/v1/3c65c38bea352f066d752043.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Point prevalence of motor neuropathy in children and adolescents with type 1 diabetes mellitus ","fulltext":[{"header":"Background","content":"\u003cdiv id=\"Sec2\" class=\"Section2\"\u003e \u003ch2\u003eType 1 diabetes(T1DM)\u003c/h2\u003e \u003cp\u003eType 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by insulitis, an inflammatory lesion caused by autoreactive T-cells that infiltrate the islets, leading to the destruction of β-cells and ultimately resulting in insulin deficiency[\u003cspan additionalcitationids=\"CR2\" citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The most common symptoms resulting from hyperglycaemia include polyuria, weight loss, polydipsia, and, in some cases, diabetic ketoacidosis. Diagnosis is based on clinical symptoms and glucose monitoring[\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eT1DM progresses through three stages. Stage 1, known as preclinical type 1 diabetes, is marked by the presence of two or more autoantibodies despite normal blood glucose levels. Stages 2 and 3 indicate a progression from dysglycemia to overt symptomatic hyperglycaemia[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIt is the most common chronic endocrine disease among the paediatric population[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eDiabetic peripheral neuropathy\u003c/h2\u003e \u003cp\u003eProlonged T1DM can cause early microvascular complications like retinopathy, nephropathy, and neuropathy, while macrovascular consequences like arteriosclerosis tend to occur later[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Diabetic neuropathies affect the nervous system, causing various symptoms due to abnormalities in sensory, motor, and autonomic nerve fibres, which are classified based on clinical features[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eChronic sensorimotor distal symmetric polyneuropathy (DSPN) and autonomic neuropathy are the two most common types of neuropathies[\u003cspan additionalcitationids=\"CR10\" citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Diabetic peripheral neuropathy (DPN) falls under the DSPN category. DPN is defined as symptoms or signs of peripheral nerve dysfunction in individuals with diabetes, excluding other causes[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. It is a common complication that can lead to significant disability, reduced quality of life, and a substantial economic burden[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIt is estimated that up to 50% of individuals with long-term diabetes may be affected by this complication[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. This percentage could rise to 100% when more precise diagnostic methods, such as nerve conduction studies, are used[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. The prevalence of these complications is likely underestimated, as they often remain subclinical in younger age groups[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAlthough younger age at onset, longer duration of diabetes, and a history of diabetic complications are recognised risk factors, the primary driver is chronic hyperglycemia[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. This sustained metabolic imbalance leads to the formation of advanced glycation end products and activation of polyol, glycolysis and hexamine biological pathways which trigger oxidative stress at the cellular level, resulting in vascular and neuronal damage. Therefore, it is crucial to maintain good metabolic control[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eDPN affects both myelinated and unmyelinated nerve fibres. Pain mainly results from damage to thin, unmyelinated fibres, while impairment of large, myelinated fibres can lead to gait instability, increasing fall risk[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eCommon symptoms like numbness, tingling, allodynia, and a shock-like sensation, indicate somatic involvement[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAccording to the American Diabetes Association (ADA), screening for DPN is recommended five years after diagnosis in type 1 diabetic patients. The frequency of this screening should be annual or semestral and must include clinical history and a physical examination[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e].\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eMotor neuropathy and nerve conduction studies\u003c/h3\u003e\n\u003cp\u003eMotor involvement in DPN is often overlooked compared to sensory dysfunction[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. However, motor impairment increases fall risk, affects gait and balance, and can lead to foot deformities like hammer toes, contributing to chronic irritation and ulceration[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eMultiple studies using nerve conduction studies (NCS) have shown the ability to detect subclinical motor involvement, revealing reduced motor nerve conduction velocity (MNCV) and amplitude, indicative of nerve deterioration. Early MNCV reduction is linked to nodal dysfunction, axonal swelling, oxidative stress, and metabolic disturbances. Over time, axonal atrophy and segmental demyelination leads to conduction blocks. When detected early, these conditions can be reversed with proper metabolic control, including insulin administration; however, after a few months, these abnormalities become irreversible[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eStudies emphasize the importance of NCS in detecting early motor dysfunction, revealing a high prevalence of subclinical neuropathy in diabetic patients and indicating that motor involvement is more frequent than previously recognised[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Longitudinal research demonstrates a significant increase in DPN over time, with subclinical cases nearly doubling after several years, underscoring the progressive nature of the condition[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThese findings substantiate the hypothesis that NCS provide significant advantages for early screening and detection of motor neuropathy. By identifying nerve dysfunction before clinical symptoms emerge, these tests enable earlier interventions, potentially slowing progression and preventing severe motor complications. Although subclinical nerve function abnormalities may not directly predict the onset of clinical neuropathy, certain changes in nerve function indicate damage that, when combined with other local injuries, may become clinically significant[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eDespite extensive research on peripheral neuropathy in type 1 diabetes, the pattern of nerve involvement remains controversial. The frequent involvement of the common peroneal nerve in some studies further suggests a targeted approach in screening protocols, making NCS a valuable tool beyond standard neurological exams[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThis method can be time-consuming, expensive, and uncomfortable for many paediatric patients. However, it is less dependent on patient cooperation, making it less subjective. In children and adolescents with T1DM, early signs of neuropathy are often minimal or absent, making clinical exams less reliable in this group[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. Nerve conduction studies can therefore be a more effective diagnostic tool, as they can detect the condition at a subclinical stage.\u003c/p\u003e\n\u003ch3\u003eObjectives\u003c/h3\u003e\n\u003cp\u003eThe main objective is to evaluate the point prevalence of motor neuropathy in children and adolescents with a 5-year or more diagnosis of type 1 diabetes using nerve conduction studies. We will analyse various biochemical and clinical parameters of each individual to evaluate their metabolic control. Subsequently, to potentially identify factors that may increase the risk of developing motor neuropathy, we intend to evaluate positive motor neuropathy diagnoses with these parameters.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003eThis cross-sectional analytical study was conducted at the paediatric endocrinology department of the Centro Hospitalar Universit\u0026aacute;rio S. Jo\u0026atilde;o (CHUSJ), from September 2024 to March 2025.\u003c/p\u003e \u003cp\u003eWe reviewed all the children who attended the semester evaluation consultation for their T1DM diagnosis between September 2024 and January 2025. Among them, we found a total of 42 children who met our inclusion criteria: they were aged between 10 and 18 years, had been diagnosed with T1DM for over five years, and were being treated with an insulin pump. We then excluded any children who had been diagnosed with neuropathy due to causes other than T1DM, such as infections, connective tissue diseases, medications, or nutritional deficiencies. We also excluded children with a family history of hereditary neuropathy, those with types of diabetes other than type 1, and children using medications that could potentially affect peripheral nerve function.\u003c/p\u003e \u003cp\u003eThe total number of participants was determined based on a review of similar studies, the total number of children monitored at CHUSJ, and practical considerations such as time constraints and the availability required to conduct both NCS and neurological examinations.\u003c/p\u003e \u003cp\u003e The study was approved by the Ethics committee of CHUSJ. Written informed consent was obtained from patients and their parents. Participants had the right to withdraw from the study at any time. Confidentiality and the well-being of patients were prioritized throughout the study.\u003c/p\u003e \u003cp\u003eThe enrolled children underwent a standardized and systematic summary neurological examination which included ankle, patellar, bicipital and tricipital reflex, assessment of muscular force, vibration and cutaneous sensation. All evaluations were conducted by a single individual to eliminate interobserver bias, thereby reducing variability in the application and interpretation of the neurological examination.\u003c/p\u003e \u003cp\u003eVibration was evaluated using a 128 Hz tuning fork placed on the dorsum of the great toe, just proximal to the nail bed and scored as (=\u0026thinsp;1) if present (=\u0026thinsp;0) if absent.\u003c/p\u003e \u003cp\u003eThe analysis of cutaneous touch sensation was conducted using the 10g Semmes-Weinstein monofilament on the plantar surface of the great toe and the bases of the first and fifth metatarsals on both feet. The monofilament was applied perpendicularly to intact skin with enough pressure to cause it to bend, maintaining contact for no longer than two seconds. The individuals were with their eyes closed and described whether they felt the pressure and where they felt it. The test was assessed in three specific sites, making three applications at each site while alternating between actual touches and simulated ones. Cutaneous sensation was considered present if at least two out of three responses were correct for each site, with a score of (=\u0026thinsp;1) if present and (=\u0026thinsp;0) if absent[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe assessment of muscular force involved extending and flexing the ankle, knee, and elbow, which was then graded using the Medical Research Council (MRC) scale from zero to five. Muscle power was classified as follows: normal for grades 4\u0026ndash;5, reduced for grade 3, and severely reduced for grades 0\u0026ndash;2.\u003c/p\u003e \u003cp\u003eThe reflexes were evaluated using a reflex hammer and scored as normal (=\u0026thinsp;0), present with reinforcement (=\u0026thinsp;1) and decreased or absent (=\u0026thinsp;2).\u003c/p\u003e \u003cp\u003eFollowing the neurological summary examination, participants were inquired about the presence of various symptoms suggestive of neuropathy, including cramps, numbness, tingling, burning sensations, electric shock-like sensations, instability while walking, fatigue, hyperalgesia, and allodynia. The symptoms were classified as follows: (=\u0026thinsp;1) if present and (=\u0026thinsp;0) if absent.\u003c/p\u003e \u003cp\u003eThe electrophysiological test was done by the dantec keypoint electromyography machine by a single neurophysiologist who was blinded to the patient\u0026acute;s clinical and medical history. The exam was, in general, well tolerated by the children and adolescents. The temperature was checked each time before placing the electrodes, ensuring it was above 30\u0026deg;C. When necessary, arms and legs were warmed with hot water. The ground electrode was placed midway between the stimulation and the recording electrodes.\u003c/p\u003e \u003cp\u003eMotor conduction studies were performed bilaterally on the median, ulnar, common peroneal, and tibial motor nerves. Conduction velocity (CV) on the tibial nerve was not measured, as it can be uncomfortable. Instead, we opted to measure the F wave response, which was recorded in both the right and left tibial nerves. This technique has a higher sensitivity as it studies also proximal conduction[\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. F minimal latency (m s) was considered normal if equal to or lower than 55 m s.\u003c/p\u003e \u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e shows the reference cut-off values considered normal and routinely used in clinical practice. Considering these reference values, the electrophysiological findings were analysed by a neurologist trained in clinical neurophysiology and neuromuscular disorders. They were determined through a literature review by neurophysiology specialists, based on the American Association of Neuromuscular \u0026amp; Electrodiagnostic Medicine (AANEM) guidelines and adapted to the Portuguese population[\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e].\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eReference values for nerve conduction studies that are considered normal.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"7\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNerve\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eStimuli\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eResponse registration\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eDistal Latency (m s)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAmplitude (M v)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eVelocity (m s⁻\u0026sup1;)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003eDistance (cm)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e \u003cp\u003ePeroneal\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\" morerows=\"1\" rowspan=\"2\"\u003e \u003cp\u003eAnkle\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eExtensor digitorum brevis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;6.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;2.0*\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eExtensor digitorum brevis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;40\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTibial\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePosterior to the medial malleolus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eHallux abductor\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;6.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;4.0*\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMedianus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ewrist\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAbductor pollicis brevis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;4.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;4.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;50\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e8.0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e \u003cp\u003eUlnaris\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eWrist\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAbductor digiti minimi\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;3,6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;6,0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003e8\u0026ndash;12\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eBelow elbow\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAbductor digiti minimi\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;50\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e\n\u003ch3\u003e*Compare with the contralateral\u003c/h3\u003e\n\u003cp\u003eNeedle electromyography (EMG) was conducted on all individuals for the right peroneus tertius and right vastus medialis, as this test shows greater sensitivity for axonal motor damage. The reduction in the amplitude of the compound muscle action potential (CMAP), with either normal or slightly decreased CV, or a modest increase in distal motor latency (DML) can support axonal damage[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e].\u003c/p\u003e \u003cp\u003ePrimary demyelination can be considered when there is a marked reduction in motor CV or grossly increased DMLs or minimum F-wave latencies[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eData were collected and analysed, including age, gender, height, weight, body mass index (BMI), duration of diabetes, haemoglobin A1c (HbA1c), fasting plasma glucose, lipid profile (HDL, LDL, total cholesterol, triglycerides), time in range (TIR) percentage, coefficient of variation, vitamin D levels, urea, creatinine, albuminuria and the spot albumin-to-creatinine ratio. Metabolic control was considered good if HbA1c levels were between 6.5% and 7.5%, moderate if between 7.6% and 9.0% and poor if above 9.0%[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eStatistical Analysis\u003c/h2\u003e \u003cp\u003eData are presented as arithmetic means\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviations (SD). Three missing conduction velocity values were imputed using the mean after confirming a normal distribution (bolt in Table \u003cspan refid=\"MOESM1\" class=\"InternalRef\"\u003eS1\u003c/span\u003e- see Online Resource 1). This preserved the sample size. Two individuals had clinical analyses performed privately, with only confirmation of normal results available. One individual lacked TIR (%) and variation coefficient (%) due to the absence of FreeStyle Libre monitoring (hyphen in Table \u003cspan refid=\"MOESM1\" class=\"InternalRef\"\u003eS1\u003c/span\u003e- see Online Resource 1).\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eOut of the 42 individuals assessed for eligibility, 2 were initially excluded from the study: one had Charcot-Marie-Tooth syndrome and the other had a cognitive disorder. Additionally, 3 individuals declined to participate. Ultimately, a total of 29 participants completed the study (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eOf the 37 individuals who initially agreed to participate, a total of 8 did not attend the scheduled electromyography session. Some individuals gave no reason for their absence, while others were hesitant to miss classes solely for the purpose of the exam. Due to time constraints and scheduling logistics with the neurophysiology doctor, it was difficult to arrange the exam on the days when they had other appointments. If it had been possible, we would have achieved better adhesion.\u003c/p\u003e \u003cp\u003eThe mean age of the patients was 15.34\u0026thinsp;\u0026plusmn;\u0026thinsp;1.56 years, 34.48% were female and 65.52% were male. The mean age duration of T1DM was 11,93\u0026thinsp;\u0026plusmn;\u0026thinsp;2,84 years. The biochemical characteristics of the patients are shown in Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e. The HbA1c was 7.50\u0026thinsp;\u0026plusmn;\u0026thinsp;1.17%, with 37% having values of HbA1c above 7.5%. In addition, 68% had a time in range (%) less than 70% and 61% had a coefficient of variation (%) greater than 36%. None of our patients had retinopathy, and only one individual showed an altered albumin/creatinine ratio.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eProfile of biochemical parameters in study participants\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eParameters\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCases (%)\u003c/p\u003e \u003cp\u003en\u0026thinsp;=\u0026thinsp;29\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e1. BMI (Percentile)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt; P3 (Underweight)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eP3 - P85 (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21 (72%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eP85 - P97 (Excess weight)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e7 (24%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt; P97 (obesity)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (3%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e2. Fasting plasma glucose (mg dL⁻\u0026sup1;) (178\u0026thinsp;\u0026plusmn;\u0026thinsp;40.86)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;100 mg dL⁻\u0026sup1;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (4%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e100\u0026ndash;125 mg dL⁻\u0026sup1;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (4%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e126\u0026ndash;200 mg dL⁻\u0026sup1;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e19 (70%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;200 mg dL⁻\u0026sup1;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8 (30%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e3. HbA1c (%) (59\u0026thinsp;\u0026plusmn;\u0026thinsp;13 mmol/mol (7.5\u0026thinsp;\u0026plusmn;\u0026thinsp;1.2%))\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;48 mmol/mol (\u0026lt;\u0026thinsp;6.5%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e48\u0026ndash;59 mmol/mol (6.5% -7.5%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e16 (59%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e60\u0026ndash;75 mmol/mol (7.6% \u0026minus;\u0026thinsp;9.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e7 (26%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e75 mmol/mol (\u0026gt;\u0026thinsp;9.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCases (%)\u003c/p\u003e \u003cp\u003en\u0026thinsp;=\u0026thinsp;28\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e4. Spot urinary albumin/creatinine ratio (mg g ⁻\u0026sup1;) (7.15\u0026thinsp;\u0026plusmn;\u0026thinsp;9.02)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;30 mg g⁻\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e27 (96%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e30\u0026ndash;300 mg g⁻\u0026sup1; (microalbuminuria present)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1 (4%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003eSpot urinary Albuminuria (mg L\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (12.60\u0026thinsp;\u0026plusmn;\u0026thinsp;23.61)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;20 mg L\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e25 (89%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;20mg L\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Albuminuria)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e5. Urea (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (28.57\u0026thinsp;\u0026plusmn;\u0026thinsp;6.43)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e10.00\u0026ndash;50 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e28 (100%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;50 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e6. Creatinine (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (0.66\u0026thinsp;\u0026plusmn;\u0026thinsp;0.14)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e0.67 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;- 1.17 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e15 (54%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0,67 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; \u0026amp; \u0026gt; 1.17 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e13 (46%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e1. Time in range(%) ( 57\u0026thinsp;\u0026plusmn;\u0026thinsp;0.19)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;70% (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e9 (32%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;70% (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e19 (68%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e2. Variation coefficient (%) (38\u0026thinsp;\u0026plusmn;\u0026thinsp;0.06)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;36% (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e11 (39%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;36% (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17 (61%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCases\u003c/p\u003e \u003cp\u003en\u0026thinsp;=\u0026thinsp;27\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e3. Total cholesterol (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (152.22\u0026thinsp;\u0026plusmn;\u0026thinsp;28.10)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;200 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e24 (89%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;200 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e4. HDL (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (55.65\u0026thinsp;\u0026plusmn;\u0026thinsp;9.43)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;35 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e27 (100%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;35 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e5. LDL-c (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (80.96\u0026thinsp;\u0026plusmn;\u0026thinsp;18.11)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;130 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e27 (100%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;130 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Abnormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0 (0%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003e6. Triglycerides (mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) ( 76.07\u0026thinsp;\u0026plusmn;\u0026thinsp;51.06)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026le;\u0026thinsp;170 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e24 (89%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;170 mg dL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Anormal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c2\" namest=\"c1\"\u003e \u003cp\u003eVitamin D (ng mL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1;) (21.85\u0026thinsp;\u0026plusmn;\u0026thinsp;8.52)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;20 ng mL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (Normal)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14 (52%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e12\u0026ndash;20 ng mL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (insufficiency)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e10 (37%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;12 ng mL\u003cb\u003e⁻\u003c/b\u003e\u0026sup1; (deficiency)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3 (11%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"2\"\u003eHbA1c Hemoglobin A1c or glycated hemoglo 1;HDL High-density;LDL Low-density lipoprotein, BMI body mass index;\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eDuring the summary neurological examination, no abnormalities were found, except in four individuals who exhibited decreased patellar and achilles reflexes. Among these, one reported numbness in the legs. No other complaints were noted.\u003c/p\u003e \u003cp\u003eUltimately, all NCS results were normal. Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e summarises the mean values (\u0026plusmn;\u0026thinsp;SD) for latency, velocity, and amplitude of the peroneal, tibial, median, and ulnar motor nerves. The full dataset is available as supplementary material (see Online Resource 1).\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eNerve conduction study results (latency, amplitude, and velocity) presented as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\"\u0026plusmn;\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\"\u0026plusmn;\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNerve\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLatency (m s)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAmplitude (M v)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eVelocity (m s⁻\u0026sup1;)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLeft Peroneal\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e4.11\u0026thinsp;\u0026plusmn;\u0026thinsp;0.53\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e5.62\u0026thinsp;\u0026plusmn;\u0026thinsp;2.17\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e49.61\u0026thinsp;\u0026plusmn;\u0026thinsp;3.47\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRight Peroneal\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e3.79\u0026thinsp;\u0026plusmn;\u0026thinsp;0.35\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e6.33\u0026thinsp;\u0026plusmn;\u0026thinsp;2.10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e48.69\u0026thinsp;\u0026plusmn;\u0026thinsp;3.26\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLeft Tibial\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e4,11\u0026thinsp;\u0026plusmn;\u0026thinsp;0,54\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e11.39\u0026thinsp;\u0026plusmn;\u0026thinsp;3.65\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRight Tibial\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e4.24\u0026thinsp;\u0026plusmn;\u0026thinsp;0.56\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e11.47\u0026thinsp;\u0026plusmn;\u0026thinsp;3.00\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLeft Medianus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e3.39\u0026thinsp;\u0026plusmn;\u0026thinsp;0.33\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e8.46\u0026thinsp;\u0026plusmn;\u0026thinsp;1.97\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e56.90\u0026thinsp;\u0026plusmn;\u0026thinsp;3.50\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRight Medianus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e3.39\u0026thinsp;\u0026plusmn;\u0026thinsp;0.34\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e9.35\u0026thinsp;\u0026plusmn;\u0026thinsp;1.93\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e58.02\u0026thinsp;\u0026plusmn;\u0026thinsp;2.66\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLeft Ulnaris\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e2.56\u0026thinsp;\u0026plusmn;\u0026thinsp;0.29\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e8.68\u0026thinsp;\u0026plusmn;\u0026thinsp;1.29\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e60.99\u0026thinsp;\u0026plusmn;\u0026thinsp;4.43\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRight Ulnaris\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c2\"\u003e \u003cp\u003e2.66\u0026thinsp;\u0026plusmn;\u0026thinsp;0.30\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\"\u0026plusmn;\" colname=\"c3\"\u003e \u003cp\u003e8.62\u0026thinsp;\u0026plusmn;\u0026thinsp;1.55\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e60.12\u0026thinsp;\u0026plusmn;\u0026thinsp;4.90\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eThe EMG results were also normal, indicating no axonal damage. Additionally, F minimum latency values were within the normal range (below 55 m s) at 45.59\u0026thinsp;\u0026plusmn;\u0026thinsp;3.73 m s in the right tibialis and 45.77\u0026thinsp;\u0026plusmn;\u0026thinsp;3.96 m s in the left tibialis.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOur study found no evidence of subclinical motor neuropathy in any of the participants, suggesting that motor nerve function remained preserved in this population. This contrasts with previous studies that reported a higher prevalence of motor involvement.\u003c/p\u003e \u003cp\u003eAbuelwafaa et al. 2019 studied 50 diabetic patients aged 10\u0026ndash;18 years and found that 88% had electrophysiological evidence of peripheral neuropathy, primarily affecting motor function (68.2%) with no cases of pure sensory neuropathy. The most common finding was conduction slowing, particularly in the common peroneal nerve[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. This finding is noted in other studies, highlighting the significance of motor involvement[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]. They used a stricter conduction velocity threshold of 46.7 m s⁻\u0026sup1; compared to our 40 m s⁻\u0026sup1;, which may explain their higher prevalence rates[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. This study was conducted in Sudan, where limited healthcare resources and poor diabetes management may have contributed to the increased prevalence of neuropathy. The mean HbA1c level in their population was 11.28\u0026thinsp;\u0026plusmn;\u0026thinsp;2.75 %, compared toour study's mean of 7.50\u0026thinsp;\u0026plusmn;\u0026thinsp;1.17 %. This indicaes poorer metabolic control, despite a shorter disease duration of 10.21\u0026thinsp;\u0026plusmn;\u0026thinsp;3.93 years[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eSingh et al. 2022 study, out of also 50 children aged 8\u0026ndash;18 years, 56% exhibiting subclinical neuropathy on NCS, with 40% having pure motor, 2% pure sensory, and 14% mixed motor-sensory neuropathy[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. The participants had poorer metabolic control with HbA1c of 9.14\u0026thinsp;\u0026plusmn;\u0026thinsp;2.10 % nd the higher prevalence may also be due to ethnic and genetic differences, limited healthcare infrastructure and environmental factors in India. Glycaemic variability, including the frequency of hypoglycaemia and hyperglycaemia, and different diagnostic criteria may also contribute. The peroneal nerve was also the most affected, with significant risk factors including poor glycaemic control (HbA1c\u0026thinsp;\u0026gt;\u0026thinsp;9 %)and diabetes duration of over five years[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. However, this pattern is not consistently observed in other studies, leading to the belief that the development of neuropathy in childhood is neurophysiologically heterogeneous[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eOn the other hand, Walter-Holiner et al. 2018 conducted a cohort study with a 5-year follow-up, in Austria with a total of 38 patients aged 9\u0026ndash;18 years[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. At baseline, the prevalence of diabetic peripheral neuropathy (DPN) diagnosed through neurological examination was 13.2 %, hile nerve conduction velocity (NCV) testing detected DPN in 31.6 %, ndicating a high prevalence of subclinical cases. After five years, clinically diagnosed DPN increased to 34.2 % (=\u0026thinsp;0.039), while subclinical DPN rose to 63.2 % (=\u0026thinsp;0.002), with the most significant electrophysiological changes observed in the tibial sensory nerve[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Some research indicates that the motor nervous system is more resistant than the sensory nervous system. This difference may be due to anatomy: dorsal root ganglion neurons are outside the blood-brain barrier, while motor neurons are protected within the ventral horn of the spinal cord[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e]. While not the main focus of this study, NCSs were also performed on the median, ulnar, and sural sensory nerves. These revealed no abnormalities, thus providing no evidence of diabetic peripheral neuropathy. In addition, they used reference values like ours for conduction velocity in motor nerves. And so given Austria\u0026rsquo;s advanced healthcare system, the high prevalence cannot be due to limited resources or poor metabolic monitoring, as shown in other studies. Their mean HbA1c was 8.1\u0026thinsp;\u0026plusmn;\u0026thinsp;1.2 %, comparable toours, but with a shorter disease duration of 5.6\u0026thinsp;\u0026plusmn;\u0026thinsp;3.2 years[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThere were one or two individual measurements that were close to the reference range, particularly the common peroneal nerve velocity and F minimum latency. Notably, this phenomenon has been observed in taller individuals with no clinical symptoms and no changes in the physical and neurological exam. Studies indicate that taller people typically exhibit lower nerve conduction velocities and higher F wave latencies, which may represent a physiological variation rather than a pathological one[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e, \u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e]. Secondly, there may also be minor technical factors such as electrode positioning which can introduce small discrepancies in motor nerve assessments. These considerations highlight the need for cautious interpretation of borderline values to avoid overestimating pathological findings.\u003c/p\u003e \u003cp\u003eIn instances of isolated borderline values, it is crucial to consider the broader context, potential concomitant alterations like altered tibial F waves, altered needle electromyography, changes in physical neurological exam and the individual's height. For these individuals, a follow-up evaluation is recommended within a five-year period to determine whether there have been any significant changes in the values compared to the initial assessment. If any changes are observed, it may be appropriate to consider the onset of subclinical motor neuropathy.\u003c/p\u003e \u003cp\u003eConsistent and reliable results were achieved through standardized neurological and electrophysiological assessments, which offered a comprehensive and objective evaluation of neuropathy in patients with T1DM. This also ensured comparability across different settings and populations. It is a relatively underexplored area, especially in our Portuguese population contributing to new knowledge to the field.\u003c/p\u003e \u003cp\u003eIn addition, by having a single examiner conduct the neurological exam, inter-observer variability was minimized, enhancing the study's internal validity. However, misinterpretation or subtle variations in reflex evaluations could account for the alterations observed in the four cases. Furthermore, all NCS and EMG assessments were performed by the same highly experienced neurophysiologist, blinded to the patient\u0026acute;s clinical and medical history. This approach minimized, once again, interobserver variability while also reducing observer bias.\u003c/p\u003e \u003cp\u003eSome factors may limit the study\u0026acute;s generalisability. It was conducted in a single centre, CHUSJ, a hospital with experienced physicians and systematic treatment monitoring. This may not fully represent the broader paediatric T1DM population in other hospitals.\u003c/p\u003e \u003cp\u003eThis study may be subject to some healthy user bias, as some children or adolescents who chose not to participate had poorer metabolic control and appeared to be less concerned about their health.\u003c/p\u003e \u003cp\u003eThere are scarce reference values of electrophysiological results in a healthy paediatric population and so incorporating a healthy control group in a cohort study for comparison would improve external validity. However, it would be difficult to get approval from the ethics committee. Although we did not use a control group for reference and comparison, relying instead on fixed reference values, we could possibly say that our individual and mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD values were very similar to those of control groups used as reference in many studies. There could be some doubt regarding the conduction velocity of the common peroneal nerve, which could eventually show statistical significance if analysed with values from control groups in other studies. Nonetheless, we wouldn't consider these individual values to be pathological, given the clinical context, the height of the patients, and additional findings such as normal tibial F waves and needle electromyography, which are more sensitive indicators[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e]. Still, we did not take this approach because no similar study has been conducted in a Portuguese population with comparable characteristics. Using control groups from studies conducted in other countries could introduce bias due to population differences like genetic background, environmental factors, healthcare systems, and lifestyle that could influence the results.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis study indicates that, within our population, where patients receive thorough monitoring and support for their diabetes management, there is no discernible benefit of employing nerve conduction studies, like electromyography, for the purpose of diagnosing or detecting subclinical motor neuropathy. Even children and adolescents with poor metabolic control, altered albumin/creatinine ratios, and a long duration of diabetes exceeding 10 years showed no abnormalities in our study. There is still no consensus on the pattern of nerve involvement and histological abnormalities (demyelination or axonal degeneration), so further research is needed in this area to provide more conclusive information on the possibility of primary and secondary prevention and to improve quality of life. The varying prevalence rates presented are mostly due to the different criteria and lack of standardized characterization of DPN[\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e].\u003c/p\u003e \u003cp\u003e For, now we recommend using the electrophysiological diagnostic method only in accordance with the guidelines established by the American Diabetes Association (ADA). This recommendation applies specifically when clinical features are atypical or when a diagnosis remains uncertain after a comprehensive medical history and basic clinical assessments have been conducted[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e].\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eADA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAmerican Diabetes Association\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBody Mass Index\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCHUSJ\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCentro Hospital Universit\u0026aacute;rio S.Jo\u0026atilde;o\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMAP\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCompound Muscle Action Potential\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eConduction Velocity\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDPN\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDiabetic Peripheral Neuropathy\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDML\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDistal Motor Latency\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDSPN\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDistal Symmetric Polyneuropathy\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEMG\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNeedle Electromyography\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHbA1c\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHaemoglobin A1c\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMNCV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMotor Nerve Conduction Velocity\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNCS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNerve conduction studies\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSD\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eStandard Deviations\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTIR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTime in Range\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 21.6931%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eT1DM\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78.3069%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eType 1 Diabetes Mellitus\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study was approved by the Ethics Committee of Centro Hospitalar Universit\u0026aacute;rio S.Jo\u0026atilde;o. Written informed consent was obtained from children and their parents.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data generated or analysed during this study are included in this published article [and its supplementary information files].\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo financial support was received for our study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eJL was deeply involved in all stages of the study, including the conception and design, data acquisition, analysis and interpretation. Took the lead in drafting the manuscript. Conducted all neurological examinations for all participants during their semestral appointments.\u003c/p\u003e\n\u003cp\u003eJF made significant contributions to the conception and design of the study, data acquisition, and overall interpretation of the results. Played a major role in critically revising the manuscript for important intellectual content\u003c/p\u003e\n\u003cp\u003eFS made significant contributions to the conception of the study and the interpretation of data. Was actively involved in critically revising the manuscript for important intellectual content. Also played a key role in performing nerve conduction studies and needle electromyography for all participants, as well as in analysing the results.\u003c/p\u003e\n\u003cp\u003eCC made significant contributions to the conception and design of the study, data acquisition and interpretation of data. Was involved in critically revising it for important intellectual content.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAll authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflicts of interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll other authors state no conflict of interest.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eDiMeglio LA, Evans-Molina C, Oram RA. Type 1 diabetes. Lancet. 2018;391:2449\u0026ndash;62. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/S0140-6736(18)31320-5\u003c/span\u003e\u003cspan address=\"10.1016/S0140-6736(18)31320-5\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStoian A, Muntean C, Babă DF, et al. Update on biomarkers of chronic inflammatory processes underlying diabetic neuropathy. 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Lond J Pediatr Endocrinol Metabolism. 2005;18:1087\u0026ndash;94.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZochodne DW, Verge VMK, Cheng C, et al. Does diabetes target ganglion neurones? Progressive sensory neurone involvement in long-term experimental diabetes. Brain. 2001;124:2319\u0026ndash;34.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRamji N, Toth C, Kennedy J, et al. Does diabetes mellitus target motor neurons? Neurobiol Dis. 2007;26:301\u0026ndash;11. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.nbd.2006.11.016\u003c/span\u003e\u003cspan address=\"10.1016/j.nbd.2006.11.016\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSoudmand R, Ward LC, Swift TR. Effect of height on nerve conduction velocity. Neurology. 1989;32:407\u0026ndash;10.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRota E, Quadri R, Fanti E et al. Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus. J Peripheral Nerv Syst 2005:348\u0026ndash;53.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Motor neuropathy, nerve conduction studies, type I diabetes mellitus, paediatrics","lastPublishedDoi":"10.21203/rs.3.rs-6514477/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6514477/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003ePurpose\u003c/h2\u003e \u003cp\u003eOur objective is to conduct a screening for motor neuropathy in children and adolescents with type 1 diabetes to assess its point prevalence and to analyse potential risk factors associated with any positive motor neuropathy diagnosis.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis is a cross-sectional study involving children aged 12 to 18 years who have been diagnosed with diabetes for five or more years and are receiving treatment with an insulin pump. All participants underwent a neurological examination and were questioned about symptoms of neuropathy. A nerve conduction study was conducted to evaluate the median, ulnar, common peroneal, and tibial motor nerves. Sensory nerves were also examined. The F-wave response of the tibial nerve was analysed, and needle electromyography was performed on a proximal and distal muscle of the lower limb.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eA total of 29 children completed the study (mean age: 15.34\u0026thinsp;\u0026plusmn;\u0026thinsp;1.56 years; mean duration of diabetes: 11.93\u0026thinsp;\u0026plusmn;\u0026thinsp;2.84 years; HbA1c levels: 7.50\u0026thinsp;\u0026plusmn;\u0026thinsp;1.17%). Results were normal, indicating adequate motor nerve integration and excluding the presence of motor neuropathy as well as peripheral neuropathy, even at subclinical level.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eIn our studied population, which receives tight monitoring and support for diabetes management, using nerve conduction studies to detect early subclinical motor neuropathy shows no clear benefit. This finding was consistent even among individuals with poor metabolic control, altered albumin/creatinine ratio, and diabetes duration over 10 years, with no abnormalities observed. We recommend following the latest guidelines provided by the American Diabetes Association (ADA).\u003c/p\u003e","manuscriptTitle":"Point prevalence of motor neuropathy in children and adolescents with type 1 diabetes mellitus ","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-13 06:48:54","doi":"10.21203/rs.3.rs-6514477/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"401a13c3-acda-4830-b590-84bed7040550","owner":[],"postedDate":"May 13th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-03-02T16:02:38+00:00","versionOfRecord":{"articleIdentity":"rs-6514477","link":"https://doi.org/10.1007/s40200-026-01865-z","journal":{"identity":"journal-of-diabetes-and-metabolic-disorders","isVorOnly":false,"title":"Journal of Diabetes \u0026 Metabolic Disorders"},"publishedOn":"2026-02-26 15:59:09","publishedOnDateReadable":"February 26th, 2026"},"versionCreatedAt":"2025-05-13 06:48:54","video":"","vorDoi":"10.1007/s40200-026-01865-z","vorDoiUrl":"https://doi.org/10.1007/s40200-026-01865-z","workflowStages":[]},"version":"v1","identity":"rs-6514477","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6514477","identity":"rs-6514477","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}