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Glycemic Control and Nerve Conduction Abnormalities in Non-Insulin-Dependent Diabetic Subjects

RONALD J. GRAF, M.D.; JEFFREY B. HALTER, M.D.; MICHAEL A. PFEIFER, M.D.; EUGEN HALAR, M.D.; FRANK BROZOVICH, B.S.E.; and DANIEL PORTE Jr., M.D.
[+] Article and Author Information

Grant support: in part by the Medical Research Service of the Veterans Administration, Rehabilitation Medicine Grant 16-P-56818; grants AM 20754, AM 05498, and AM 12829 from the National Institutes of Health; and Special Emphasis Research Career Award AM 00738 from the U.S. Department of Health and Human Services.

This paper was presented in part at the 10th Congress of the International Diabetes Federation, 9-14 September 1979, Vienna, Austria.

▸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. 1981;94(3):307-311. doi:10.7326/0003-4819-94-3-307
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The influence of therapy of hyperglycemia on the progression of diabetic neuropathy is unclear. We studied variables of glycemia and motor and sensory nerve conduction velocity in a group of 18 non-insulin-dependent diabetic subjects before and after institution of diabetes therapy. Diabetes therapy significantly reduced variables of glycemia after 1, 3, 6, and 12 months. Conduction velocity of the median motor nerve was improved from baseline at each time tested during treatment. In addition, peroneal and tibial motor nerve conduction velocities improved in patients whose levels of hyperglycemia were lowered. Moreover, extent of improvement of conduction velocity of some motor nerves was related to the degree of reduction of hyperglycemia. Sensory nerve conduction velocity was not altered by diabetes therapy. These findings support the hypothesis of a metabolic component to diabetic neuropathy and suggest that optimal glycemic control may be beneficial to patients with this disorder.

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