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

**Authors:** Joana Helena Bourbon Lopes, Jacinta Fonseca, Fernando Silveira, Cíntia Castro-Correia

PMC · DOI: 10.1007/s40200-026-01865-z · Journal of Diabetes and Metabolic Disorders · 2026-02-26

## TL;DR

This study found no evidence of motor neuropathy in teenagers with type 1 diabetes, even in those with long disease duration or poor blood sugar control.

## Contribution

The study provides new evidence that motor neuropathy is not prevalent in this specific pediatric type 1 diabetes population.

## Key findings

- No cases of motor neuropathy were detected in 29 participants using nerve conduction studies.
- Even participants with poor metabolic control showed no signs of subclinical neuropathy.
- The study suggests nerve conduction studies may not be beneficial for early detection in this group.

## Abstract

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.

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.

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.

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).

The online version contains supplementary material available at 10.1007/s40200-026-01865-z.

## Linked entities

- **Diseases:** type 1 diabetes mellitus (MONDO:0005147), peripheral neuropathy (MONDO:0003620)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** axonal degeneration (MESH:D009410), nephropathy (MESH:D007674), tingling (MESH:D010292), DPN (MESH:D010523), T1DM (MESH:D003922), diabetic ketoacidosis (MESH:D016883), neuromuscular disorders (MESH:D009468), allodynia (MESH:D006930), gait instability (MESH:D043171), cognitive disorder (MESH:D003072), autonomic neuropathy (MESH:D009422), axonal damage (MESH:D001480), chronic (MESH:D002908), Charcot-Marie-Tooth syndrome (MESH:D002607), motor (MESH:D000068079), long-term diabetes (MESH:D000088562), nerve deterioration (MESH:D005155), cramps (MESH:D009120), albuminuria (MESH:D000419), nerve function abnormalities (MESH:D000014), Primary demyelination (MESH:D003711), nutritional deficiencies (MESH:D044342), Diabetic neuropathies (MESH:D003929), infections (MESH:D007239), Chronic sensorimotor distal symmetric polyneuropathy (MESH:C565773), foot deformities (MESH:D005530), endocrine disease (MESH:D004700), polydipsia (MESH:D059606), numbness (MESH:D006987), vascular and neuronal damage (MESH:D057772), nodal dysfunction (MESH:D013611), weight loss (MESH:D015431), ulceration (MESH:D014456), insulin deficiency (MESH:D007333), hammer toes (MESH:D037801), sensory neuropathy (MESH:D009477), autoimmune disorder (MESH:D001327), fatigue (MESH:D005221), retinopathy (MESH:D058437), NCS (MESH:C537568), shock (MESH:D012769), inflammatory lesion (MESH:D007249), hyperglycemia (MESH:D006943), Pain (MESH:D010146), hereditary neuropathy (MESH:D009386), arteriosclerosis (MESH:D001161), irritation (MESH:D001523), sensory dysfunction (MESH:D012678), Diabetes (MESH:D003920), DSPN (MESH:D011115), polyuria (MESH:D011141), axonal swelling (MESH:D004487), axonal atrophy (MESH:D001284)
- **Chemicals:** lipid (MESH:D008055), hexamine (MESH:D008709), glucose (MESH:D005947), Creatinine (MESH:D003404), ADA (-), Urea (MESH:D014508), advanced glycation end products (MESH:D017127), cholesterol (MESH:D002784), vitamin D (MESH:D014807), polyol (MESH:C024617), Triglycerides (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

5 references — full list in the complete paper: https://tomesphere.com/paper/PMC12946334/full.md

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Source: https://tomesphere.com/paper/PMC12946334