Few medical problems are more complex in nature and perplexing to effectively manage than pain. Pain, in its acute form, is necessary for survival and serves an important role in the way an organism interfaces with its environment by signaling real or impending harm. Occasionally, circumstances lead to activity in the pain-signaling pathway that is not beneficial to the organism and has no survival value. Injury to nerve fibers or their projections may cause conditions that are not usually perceived as painful to become excessively painful. Although most nerve injuries do not lead to clinically important and sustained pain, in some cases, even small degrees of insult can precipitate severe and unremitting pain. Neuropathic pain exists when a nerve responds to an injury in a typical fashion and then continues to respond and signal pain long after the injurious stimulus is removed.
KeywordsSpinal Cord Injury Neuropathic Pain Carpal Tunnel Syndrome Trigeminal Neuralgia Complex Regional Pain Syndrome
- Bouhassira D, Lanteri-Minet M, Attal N, Laurent B, Touboul C. Prevalence of chronic pain with neuropathic characteristics in the general population. Pain 2008;136(3):380–7.Google Scholar
- Campbell CM, Edwards RR, Carmona C, et al. Polymorphisms in the GTP cyclohydrolase gene (GCH1) are associated with ratings of capsaicin pain. Pain 2009;141(1–2):114–8.Google Scholar
- Challapalli V, Tremont-Lukats IW, McNicol ED, Lau J, Carr DB. Systemic administration of local anesthetic agents to relieve neuropathic pain. Cochrane Database Syst Rev. 2005(4):CD003345.Google Scholar
- Gagnon B, Almahrezi A, Schreier G. Methadone in the treatment of neuropathic pain. Pain Res Manage. 2003;8(3):149–54.Google Scholar
- Mersky H, Bogduk N. ed. Classification of chronic pain. Seattle, WA: IASP Press; 1994. pp. 209–14.Google Scholar
- Wilson JA, Garry EM, Anderson HA, et al. NMDA receptor antagonist treatment at the time of nerve injury prevents injury-induced changes in spinal NR1 and NR2B subunit expression and increases the sensitivity of residual pain behaviours to subsequently administered NMDA receptor antagonists. Pain 2005;117(3):421–32.PubMedCrossRefGoogle Scholar