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Nerve Conduction Abnormalities in Untreated Maturity-Onset Diabetes: Relation to Levels of Fasting Plasma Glucose and Glycosylated Hemoglobin

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Grant support: in part by the Medical Research Service of the Veterans Administration, Rehabilitation Medicine Grant #16-P-56818, and National Institutes of Health Grants AM20754, AM05498, and AM12829.

This paper was presented in part at the 38th Annual Meeting of the American Diabetes Association, 11-13 June 1978, Boston, Massachusetts.

▸Requests for reprints should be addressed to Ronald J. Graf, M.D.; Division of Metabolism, Veterans Administration Medical Center, 4435 Beacon Avenue South; Seattle, WA 98108.

Seattle, Washington

Ann Intern Med. 1979;90(3):298-303. doi:10.7326/0003-4819-90-3-298
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The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the influence of hyperglycemia on nerve conduction, we studied 20 untreated maturity-onset diabetic patients and 23 normal control subjects of similar age. Nerve conduction velocity of motor (median, peroneal, and tibial) and sensory (median and sural) nerves in diabetic patients was significantly slowed and H-reflex latency time prolonged. Levels of fasting plasma glucose in diabetic subjects were correlated with slowed motor conduction velocity of the median, peroneal, and tibial nerves but not with sensory nerve conduction velocities. Levels of glycosylated hemoglobin, an index of long-term glycemia, were correlated with slowing of peroneal motor conduction velocity in diabetic patients. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of untreated maturity-onset diabetes contributes to the motor nerve conduction abnormalities in this disease.





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