We present review of pathophysiological mechanisms of development of polyneuropathy with the painful syndrome in patients with diabetes mellitus. We consider the leading pathogenetic role of hyperglycemia in the formation of neuropathies due to glycosylation of protein structures and excessive accumulation of sorbitol (product of polyol shunt in glucose metabolism) in the nerve cells against a background of deficiency of thiamine. Administration of Milgamma (high doses of B vitamins) and Milgamma compositum (combination of benfotiamine with pyridoxine) has pronounced trophic and analgesic effects in the treatment of diabetic polyneuropathy.

Keywords: sorbitol, diabetic polyneuropathy, benfotiamine, thiamine, hyperglycemia