Neuropathic pain: mechanisms and treatments.
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, 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 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 Dr. Long-Sun Ro 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 developments, careful clinical trials, and an increased understanding of the contribution and mechanisms of neuroplasticity will lead to an improvement in the results of clinical treatments and prevention of neuropathic pain.
Ro
Long-Sun
LS
Section of Neuromuscular Disorders, Department of Neurology, Chang Gung Memorial Hospital, Taipei, Taiwan, ROC. cgrols@adm.cgmh.org.tw
Chang
Kuo-Hsuan
KH
D015220:Calcium Channels / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D009437:Neuralgia / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D009473:Neuronal Plasticity; D010146:Pain / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D015222:Sodium Channels / Q000502:physiology; D004561:Transcutaneous Electric Nerve Stimulation
D015220:Calcium Channels; D016207:Cytokines; D015222:Sodium Channels