Short Communication - (2025) Volume 10, Issue 1
Received: 23-Jan-2025, Manuscript No. jdcm-25-168165;
Editor assigned: 25-Jan-2025, Pre QC No. P-168165;
Reviewed: 08-Feb-2025, QC No. Q-168165;
Revised: 13-Feb-2025, Manuscript No. R-168165;
Published:
20-Feb-2025
Citation: Geneium, Hamila. "Early Detection of Diabetic Peripheral Neuropathy through Sural Nerve Conduction Testing." J Diabetic Complications Med 10 (2025): 296.
Copyright: © 2025 Geneium H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
DPN develops gradually due to prolonged exposure to hyperglycemia, which causes both metabolic and vascular damage to peripheral nerves. Key mechanisms include, oxidative stress from excess glucose metabolism, Advanced Glycation End-Products (AGEs) damaging nerve proteins and microvasculature, Inflammation and impaired blood supply to nerves, Mitochondrial dysfunction and apoptosis in nerve cells. These processes lead to axon loss and demyelination, particularly in long peripheral nerves. The sural nerve, being distal and purely sensory, is highly vulnerable and often among the first to exhibit dysfunction in diabetic patients [2].
Nerve Conduction Studies (NCS) measure the speed and strength of electrical signals traveling through peripheral nerves. For diabetic neuropathy, sensory nervesâ??especially in the lower extremitiesâ??are tested first, as they tend to be affected before motor nerves. Sensory Nerve Action Potential (SNAP) Amplitude, reflects the number of functioning sensory fibers. Decreased amplitude suggests axonal loss. Conduction Velocity (CV), reflects the integrity of myelin sheaths. Slowing indicates demyelination. These parameters help distinguish between normal, subclinical, and established neuropathy [3].
The pancreatic islets are highly integrated micro-organs where cells communicate closely through paracrine signaling. β-cells secrete insulin, which diffuses locally to suppress glucagon release from α-cells. This intra-islet communication is essential for tight regulation of glucose levels. Chronic hyperglycemia may disrupt this local crosstalk by impairing insulin signaling at the α-cell membrane. Studies show that insulin receptors are present on α-cells, and activation of these receptors under normal conditions reduces glucagon secretion. When hyperglycemia is sustained, this signaling pathway may be downregulated due to receptor desensitization or post-receptor defects. As a result, insulin's paracrine inhibition on α-cells is weakened, and glucagon secretion becomes dysregulated. Traditionally, NCS required referral to neurophysiology labs. However, newer portable devices (e.g., NC-stat DPNCheck) now enable point-of-care sural nerve testing in primary care and endocrinology settings. These devices offer fast, reproducible measurements, minimal training requirements, Immediate results.
Despite its usefulness, sural NCS is not without limitations: Small fiber neuropathy (affecting pain and temperature) may go undetected in early stages.Results can be influenced by age, skin temperature, and technical variability. Not all clinics have access to trained personnel or devices.Patient discomfort from electrical stimuli, though minimal, can occur. For comprehensive assessment, sural NCS can be combined with quantitative sensory testing, skin biopsies, or corneal confocal microscopy in research settings.
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