This article was originally published in French in Diabete et Metabolisme (vol. 3: 97–107, 173–182, 245–256; 1977). The Editors of DIABETES CARE thank the author, and the editors and publisher of Diabete et Metabolisme for granting permission for us to print this English translation. The paper was translated by Marjorie Levin of Miami, Florida.
Part 2 of this translation will appear in the July–August issue of DIABETES CARE.
A group of 1,175 unselected diabetics was examined and the degenerative lesions were correlated with each other and with other clinical data. Diabetic neuropathy was found in 21 per cent of the patients. It is closely related to diabetic retinopathy and nephropathy and to peripheral artery disease, but not to blood cholesterol or to coronary sclerosis, aortic sclerosis and myocardial degenerative disease not related to proved coronary disease. It is related to severity, poor control and duration of the diabetes.
A group of 235 cases of asymptomatic diabetic neuropathy (asymptomatic loss of a deep reflex) was compared with a selected group of fifty-eight cases of symptomatic diabetic neuropathy (symptomatic with often severe motor, sensory, autonomic and/or trophic disturbances). The correlations previously found were still more striking in the group of symptomatic diabetic neuropathy.
The clinical picture of fifty-eight cases of symptomatic diabetic neuropathy shows such a close association between acute and chronic, between symmetrical and asymmetrical, and between motor, sensory, autonomic and trophic defects that any classification of diabetic neuropathies seems artificial. Only paralysis of extra-ocular muscles might be classified in a separate group. Attention is drawn to the acute course (weeks) of some cases of paralysis and, on the other hand, to the very slow evolution of some cases of trophic lesions of the feet (up to twenty-five years).
Certain cases are briefly reported to show that the vascular pathogenetic theory of diabetic neuropathy is not in agreement with several clinical observations.
Regulation of glucose uptake by muscle. 5. Effects of anoxia, insulin, adrenalin and prolonged starving on concentrations of hexose phosphates in isolated rat diaphragms and perfused isolated rat heart.
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