Abstract

Since nearly all patients with diabetes mellitus will manifest evidence of dysfunction of their peripheral and autonomic nerves, neuropathy can be considered to be the most common of the so-called "late complications of diabetes." Mononeuropathies are uncommon, but can affect virtually any cranial or nerve and are thought to be due to vascular occlusion. Distal symmetrical polyneuropathy usually begins insidiously with the development of sensory symptoms involving the feet. These symptoms progressively ascend and are accompanied by progressive motor dysfunction as well as cardiac, gastrointestinal, and genitourinary manifestations of autonomic neuropathy. Numerous biochemical abnormalities including impaired neural protein synthesis, abnormal axoplasmic transport, disturbed polyol pathway activity, and abnormal myo-inositol metabolism have been described and have been postulated to underlie the development of diabetic peripheral and autonomic neuropathies. At the present time, the available treatments for diabetic neuropathies are largely palliative and are not curative. In the future, a better understanding of the pathophysiologic basis of diabetic neuropathy will undoubtedly lead to the development of more rational therapeutic approaches.