Precision Prediction & Precision Medicine
Neuronal damage is among the first measurable effects of prolonged hyperglycemia. Nerve conduction velocity can be measured, although this tends only to yield useful results once there has already been substantial damage to multiple neuronal fibers within nerve bundles.
To identify earlier stages of nerve damage, we analyzed compound muscle action potentials (CMAP) as a marker of ‘nerve-health’. This technique measures axonal excitability and axonal loss, to indicate damage to motor nerves. In our study, axonal excitability was already significantly decreased in our youngest patient group compared to the control group. Motor nerve axonal excitability therefore seems to be reduced early in T1DM, even in well-controlled young patients.
No correlation with glucose control was observed, suggesting that other factors are involved in early damage. Overall, the CMAP scan was found to be a promising tool for identifying early neuronal damage.
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Sensory neurons are believed to be most sensitive to hyperglycemia-induced damage. By measuring sensory nerve action potentials (SNAP) in children and youth, we showed that damage to these neurons occurs early in the course of diabetes [link to PubMed abstract]. However, we also found that motor neuron damage coincided with, or even preceded, sensory nerve damage. As with the studies of cIMT and CMAP, glucose control as expressed by HbA1c could not explain the difference between affected and non-affected individuals.