HUMAN AND EXPERIMENTAL DIABETIC NEUROPATHY
1978; Elsevier BV; Linguagem: Inglês
10.1016/b978-0-444-80079-4.50026-0
Autores Tópico(s)Parkinson's Disease Mechanisms and Treatments
ResumoThe wide range of the clinical manifestations displayed by diabetic neuropathy suggests that its causation is multifactorial. Clinically a subdivision may be made into symmetrical polyneuropathies, and mononeuropathies or multiple mononeuropathies. A metabolic basis seems the likely explanation for the former but its nature remains obscure. Osmotic damage secondary to sorbitol accumulation has been suggested but has not been substantiated and it is not known what role abnormalities of lipid metabolism may play. Vascular features are probably unlikely to be important in the origin of symmetrical polyneuropathies but may be involved in the causation of localized lesions, as may the so far unexplained heightened vulnerability to pressure. The cause of the reduced nerve conduction velocity in experimentally induced diabetes remains in dispute. Structural changes may develop after prolonged diabetes but have been disputed in the early stages. Electrophysiological observations have suggested that this may depend upon alterations in the electrical properties of myelin but require substantiation. There is a reduced myoinositol content in diabetic peripheral nerve, but claims that dietary supplementation with myoinositol correct the reduced nerve conduction velocity have not be validated. The neuropathy that may develop in genetic diabetes in animals offers an additional experimental model.
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