Since the earliest descriptions of pain related to injury of the nervous system, it has been recognized that the characteristics of this type of pain differ markedly from those of pain due to nonneural tissue damage. Later as new analgesics were developed, it became clear that neurogenic pain was very often refractory to these drugs. Recently neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system." Inflammatory reaction and neuropathic pain are often considered to be distinct entities. The development of neuropathic pain involves not only neuron but also inflammatory cells, chemokines, and glial cells. Treatment of neuropathic pain is difficult and frequently unrewarding. The basic principles are ① the identification and elimination of the underlying pathologic mechanism that maintains central sensitization; ② the use of nonsteroidal anti-inflammatory drugs to reduce peripheral sensitization and modulate the activity of nociceptors; ③ the use of tricyclic antidepressants to induce sleep and decrease lancinating and burning neuropathic pain; ④ a trial of gabapentin, pregabalin, lamotrigine and topamax; ⑤ the use of lidocaine patch for intractable trigeminal neuralgia; ⑥ sympathetic blockade for complex regional pain syndrome while patients are stick sympathetically maintained; ⑦ dorsal column stimulation; ⑧ intrathecal therapies including morphine, clonidine, and GABA_B agonists when other less invasive therapies have failed. In this article we reviewed the role of peripheral inflammation for development of neuropathic pain, diagnosis, and new opportunities for treatment of neuropathic pain, especially focused on medical treatments with antiepileptics and antidepressants.