Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)-the most common complication of diabetes mellitus. Focal fascicular lesions characterized by reduced density of myelinated axons within fascicles were found predominantly in the specimens from diabetics, mainly in the posterior tibial nerve and lumbosacral trunk. The pathology of diabetic neuropathy is characterized by progressive nerve fiber loss that gives rise to positive and negative clinical signs and symptoms such as pain, paresthesia and loss of sensation. Metabolic changes include high polyol pathway flux, increased advanced glycosylation, elevated oxidative stress, and impaired omega-6 essential fatty acid metabolism. The aim of pathogenetic oriented treatment is to slow down, stop or reverse the progression of neuropathy. Both hyperglycemia and decreased Na/K-ATPase activity are thought to be characteristic features of diabetic neuropathy. Although most of the redundant neurotrophic support is thereby eliminated, IGF-II activity continues to support the nervous system.
Research is focusing on these areas of enquiry in the hope that answers will lead to effective treatments to alleviate pain and reverse pathology for those suffering from painful DPN. Published in 2014.