Neuropathic pain: multiple mechanisms at multiple sites. (November 2007)

• Record Type: Journal Article
• Authors: Bee, Lucy A; Dickenson, Anthony H
• Is Part Of: Future neurology. Volume 2:Number 6(2007)
• Page Start: 661
• Page End: 671
• Publication Date: 2007-11
• Subjects: allodynia -- antidepressants -- Ca2+ channels -- gabapentin -- Na+ channels -- neuropathic pain -- NMDA receptors -- noradrenaline -- pregabalin -- serotonin -- substance P; Neurology -- Research -- Periodicals; 611.8005
• DOI: 10.2217/14796708.2.6.661
• Languages: English
• ISSNs: 1479-6708

Abstract

Damage to nerves at various levels of the peripheral and central nervous systems will lead to sensory loss, but in a significant number of patients this is accompanied by a series of distressing painful signs and symptoms. Although animal models and clinical studies have shed much needed light on the underlying mechanisms that produce this maladaptive plasticity, the presently available drugs do not always fully control the pain. This review covers some of the important mechanisms that include ion channels, central processing through excitatory amino acid and neuropeptide receptors and, finally, the role of monoamine systems that originate in the brain and descend to alter spinal events. The targets for presently licensed and potential novel drugs are covered in this context, as are perspectives on future research priorities.