Diabetic neuropathy (DN) is chronic complication which occurs in 50% of long standing diabetes mellitus. DN is a consequence of hyperglycemia probably through the following mechanisms: a) activation of aldose-reductase, intracellular sorbitol accumulation and myoinositol depletion, reduced activity of Na+/K+ATPase, loss of Na+ channels and demyelination; b) proteins glycation; c) microangiopathy; the first mechanism being the best known and the most reliable. DN may be subclinical or clinical. The main clinical picture is a peripheral, bilateral, symmetric polyneuropathy with a "socks and gloves" sensory impairment, muscular weakness, hyporeflexia, plantar ulcers and arthropathy. Less frequent syndromes are proximal motor neuropathy and mononeuropathy of cranial nerves or thoraco-abdominal roots. Diagnosis is based on clinical data, and may be sustained on impaired nerve conduction velocity, abnormal evoked somatosensory potentials, or sural nerve biopsy. These methods are highly sensitive but unspecific. Etiopathogenic treatment is based on glycemic control and aldose reductase inhibitors. Improvement in clinical, electrophysiologic and histopathologic data have been obtained with the latter. Symptomatic treatment includes carbamazepin, phenytoin, tricyclic antidepressives and a phenotiazin. Mononeuropathies tend to complete recovery in less than 6 months. Polyneuropathy is thought to be irreversible and progressive; however, with excellent glycemic control or with aldose reductase inhibitors nerve damage may be stabilized or even reversed.