T he current global prevalence of diabetes mellitus (DM) among adults (aged 20-70 years) is 537 million (one in every ten adults) that is expected to raise to 643 million by the year 2030, and 783 million by the year 2045. [1] The increasing prevalence of DM has led to a rise in chronic diabetic complications. Diabetic peripheral neuropathies (DPNs) are the most common chronic complications of diabetes. [2] Among these, the distal symmetric polyneuropa-thy (DSPN) is the most prevalent form which may affect up to 50% of patients with type 2 DM (T2DM) after 10 years of the disease, and at least 20% with type 1 DM (T1DM) after 20 years of the disease. [3] Furthermore, nearly 10-15% of newly diagnosed T2DM may have DSPN.Although a vast majority of patients with DPN may remain pain-free, painful DPN (PDPN) is estimated to affect 6-34% of all patients with DM. [4] The disease burden from PDPN The rising prevalence of diabetes mellitus (DM) leads on to an increase in chronic diabetic complications. Diabetic peripheral neuropathies (DPNs) are common chronic complications of diabetes. Distal symmetric polyneuropathy is the most prevalent form. Most patients with DPN will remain pain-free; however, painful DPN (PDPN) occurs in 6-34% of all DM patients and is associated with reduced health-related-quality-of-life and substantial economic burden. Symptomatic treatment of PDPN and diabetic autonomic neuropathy is the key treatment goals. Using certain patient related characteristics, subjects with PDPN can be stratified and assigned targeted therapies to produce better pain outcomes. The aim of this review is to discuss the various pathogenetic mechanisms of DPN with special reference to the mechanisms leading to PDPN and the various pharmacological and non-pharmacological therapies available for its management. Recommended pharmacological therapies include anticonvulsants, antidepressants, opioid analgesics, and topical medications.