Mechanisms of pain sensitization and the treatments

Hyperalgesia and allodynia, major symptoms of neuropathic pain can results after nerve injury or chronic inflammation. Trigeminal neuropathic pain resulting from alterations in peripheral and central noxious transmission systems often produced after nerve injury by pulpectomy or tooth-extraction or from temporomandibular joint inflammation. Neuropathic also occurs in some disease state, diabetic peripheral neuropathy, post-herpetic neuropathy and trigeminal neuralgia. Allodynia is characterized by long lasting pain evoked by essentially non-painful stimuli such as just light touch and tolerance to medication with conventional analgesics.Neuropathic pain is probably not a result of a single pathological mechanism, but the final product of an altered peripheral and central processing. Recent advances in pain research revealed that many factors derived from neurons and also non-neuronal neighboring residents participate in the initiation, development and maintenance. Among them, lipid mediators such as prostaglandins, lysophosphatidic acid and platelet-activating factor are recently found to play conspicuous roles for development of allodynia and hyperalgesia in spinal cord. Further advance by using cellular biological and molecular techniques would dig into the mechanisms underlying neuropathic pain and illustrate the new strategy and target candidate for drug development.There are also needs for tools and methods to assess neuropathic pain, common guidelines on classification, diagnosis and management, and evidence-based approach to the treatment of neuropathic pain