ArticlePloS one2017
Uncovering sensory axonal dysfunction in asymptomatic type 2 diabetic neuropathy.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Adaptive Autonomic and Neuroplastic Control in Diabetic Neuropathy: A Narrative Review.Current diabetes reviews · 2024Review
- Theories behind the effect of starch‑ and sucrose‑reduced diets on gastrointestinal symptoms in irritable bowel syndrome (Review).Molecular medicine reports · 2021Review
- Prospects for the application of transcranial magnetic stimulation in diabetic neuropathy.Neural regeneration research · 2021Review
- Evidence of Altered Peripheral Nerve Function in a Rodent Model of Diet-Induced Prediabetes.Biomedicines · 2020Article
- Early sensory neurophysiological changes in prediabetes.Journal of diabetes investigation · 2020Article
- Article
- Peripheral Neuropathy as a Component of Skeletal Disease in Diabetes.Current osteoporosis reports · 2019Review
- Review of Diabetic Polyneuropathy: Pathogenesis, Diagnosis and Management According to the Consensus of Egyptian Experts.Current diabetes reviews · 2019Review
- Article
- A convergence of global epidemics: diabetes as a modulator of neurodegenerative and neuro-inflammatory disorders.Frontiers in neurologyReview
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated sensory and motor nerve excitability properties to elucidate the development of diabetic neuropathy. A total of 109 type 2 diabetes patients were recruited, and 106 were analyzed. According to neuropathy severity, patients were categorized into G0, G1, and G2+3 groups using the total neuropathy score-reduced (TNSr). Patients in the G0 group were asymptomatic and had a TNSr score of 0. Sensory and motor nerve excitability data from diabetic patients were compared with data from 33 healthy controls. Clinical assessment, nerve conduction studies, and sensory and motor nerve excitability testing data were analyzed to determine axonal dysfunction in diabetic neuropathy. In the G0 group, sensory excitability testing revealed increased stimulus for the 50% sensory nerve action potential (P<0.05), shortened strength-duration time constant (P<0.01), increased superexcitability (P<0.01), decreased subexcitability (P<0.05), decreased accommodation to depolarizing current (P<0.01), and a trend of decreased accommodation to hyperpolarizing current in threshold electrotonus. All the changes progressed into G1 (TNSr 1-8) and G2+3 (TNSr 9-24) groups. In contrast, motor excitability only had significantly increased stimulus for the 50% compound motor nerve action potential (P<0.01) in the G0 group. This study revealed that the development of axonal dysfunction in sensory axons occurred prior to and in a different fashion from motor axons. Additionally, sensory nerve excitability tests can detect axonal dysfunction even in asymptomatic patients. These insights further our understanding of diabetic neuropathy and enable the early detection of sensory axonal abnormalities, which may provide a basis for neuroprotective therapeutic approaches.
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