[Cellular mechanisms in diabetic neuropathy].

Although the pathogenesis of distal diabetic neuropathy is still uncertain, a possible mechanism might be postulated on the basis of results of several experimental studies. Differences between animal and human models are obvious--especially with regard to the time factor, but in attempts at elucidating basic mechanisms use can be made of the close resemblance between animal and human nerve fibres at the cellular and molecular level. A decrease in sodium potassium ATPase activity, causing intracellular accumulation of oxidised sodium, cellular oedema, and myelin detachment around the nodes of Ranvier, would seem to be the central component in the pathogenesis.