[Physiopathology of diabetic neuropathies. Functional exploration of peripheral involvement]

Neuropathy is a common complication of Type 1 and Type 2 diabetes. In the peripheral nerve, persistent hyperglycaemia leads to metabolic and vascular disorders responsible for nerve fibre abnormalities. Genetic predisposition has been mentioned more recently. Among metabolic factors, an increase of the polyol pathway, a linoleic acid metabolism abnormality, a decrease of carnitine level, an increase of protein glycation, nerve growth factor abnormalities, and high production of oxygen free radicals can be involved. These factors could account for nerve membrane phospholipid pattern disorder, a decrease of Na/K ATPase activity and disequilibrium in prostaglandin production. Vascular factors involve a decrease in nitric oxide production, an abnormality of eicosanoid production, and an increase in the oxidative pathway, inducing vasoconstriction of endoneural microvascularisation and nerve hypoxia. Strong interactions exist between metabolic and vascular factors, making it difficult to distinguish between them. Moreover, a restriction polymorphism in the first intron of the Na/K ATPase ATP1 A1 gene is associated with low enzymatic activity and a relative risk of neuropathy of 6.5. Electromyography determines the myelinisation state of large nerve fibres and the number of functional axons. However, it cannot detect damage to small fibres, and the study of sensitive nerves is difficult. Electromyography is not a systematic examination and should be preceded by a clinical examination of sensitivity.