الفهرس 
ANATOMY OF PAINOnly 14 pages are availabe for public view
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Abstract
Neuropathic pain is caused by functional abnormalities of structural lesions in the peripheral or central nervous system, and occurs without peripheral nociceptor stimulation. Many common diseases, such as postherpetic neuralgia, trigeminal neuralgia, diabetic neuropathy, phantom pain, complex regional pain syndrome, spinal cord injury, cancer, stroke, and degenerative neurological diseases may produce neuropathic pain. Recently, theories have been proposed that state there are specific cellular and molecular changes that affect membrane excitability and induce new gene expression after nerve injury, thereby allowing for enhanced responses to future stimulation. In addition, the ectopic impulses of neuroma, changes of sodium and calcium channels in injured nerves, sympathetic activation, and deficient central sympathetic activation, and inhibitory pathway contribute to the mechanisms of neuropathic pain.
Currently, treatment of neuropathic pain is still a challenge. Pharmacotherapies (antidepressants, antiepileptics) remain the basis of neuropathic pain management. However, patient satisfaction in the results of the treatment of neuropathic pain is still disappointing. Since it has been established that intense noxious stimulation produces a sensitization of central nervous neurons, it may be possible to direct treatments not only at the site of peripheral nerve injury, but also at the target of central changes. In order to provide better pain control, the mechanism-based approach in treating neuropathic pain should be familiar to physicians. In the future, it is hoped that a combination of new pharmacotherapeutic develop-ments, careful clinical trials, and an increased under-standing of the contribution and mechanisms of neuroplasticity will lead to an improvement in the results of clinical treatments and prevention of neuropathic pain.