Diabetic neuropathy is one of the most common and serious complications of diabetes both type I and type II. In type I diabetes mellitus neuropathy usually assumes form of a distal symmetric polyneuropathy (DPN) and/or a diabetic autonomic neuropathy (DAN). Other forms as acute sensory neuropathy, cranial neuropathy, truncal radiculoneuropathy or proximal motor neuropathy are present sporadically in patients with type I diabetes. Damage to nerves in the abnormal environment of diabetes mellitus leads to diabetic neuropathy. There are three hypotheses that explain the pathogenetic mechanism of polyneuropathy: metabolic, vascular and immunological. Many diabetic patients have demonstrable abnormalities of autonomic function without any evidence of clinical disease. Tests of autonomic function and tests of conduction velocity in peripheral nerves are assumed to be a measure of neurological state and may be important methods of assessing therapy of diabetic complications. Control of hyperglycaemia is the basis of the adequate management. α-liponic acid is used due to some evidences suggesting the role of free radicals in pathogenesis diabetic neuropathy. Antiepileptics and antidepressants inhibiting selective norepinephrine and serotonin reuptake are administered for pain control in symptomatic management.