[Contemporary views on the pathogenesis of diabetic neuropathy]

The duration of diabetes, age and genetic predispositions are admitted agents of risk in diabetic neuropathy. The reasons of diabetic neuropathy are suspected in cooperation with various factors among which metabolic disturbances and ischaemia are the most important. The abnormal activation of sorbitol tract is very significant agent of development of diabetic neuropathy. The excess of sorbitol which is accumulating also in nervous tissue causes its damage in osmotic way. At the same time decreasing concentration of myoinositol reduces ATP-ase Na+/K+ activity which is important in impulse conduction. The overproduction of free oxygenic radical (oxidative lesion) and nitrogen oxide (vasodilator) deficiency is inducted by hyperglycaemia and the activation of aldolase reductase. Metabolic disturbances cause the decrease of carnitine concentration what deteriorates nerve sensitivity on growth factor. The activation of sorbitol tract leads to nonenzymatic proteins glycation which causes thickening of basement membrane and proliferation of endothelium cells. In this way increased vascular resistance decreases tissue perfusion and induces nerve hypoxia. The impairment of nerve blood supply depends on altered in diabetes rheological properties. They are inconveniently changed through hyperglycaemia, hyperlypidaemia, dysproteinaemia and excessive aggregation and rigidity of morphotic elements of blood.