Neuropathic pain: multiple mechanisms at multiple sites

Authors: Bee, Lucy A; Dickenson, Anthony H

Source: Future Neurology, Volume 2, Number 6, November 2007 , pp. 661-671(11)

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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.

Keywords: allodynia; antidepressants; Ca2+ channels; gabapentin; Na+ channels; neuropathic pain; NMDA receptors; noradrenaline; pregabalin; serotonin; substance P

Document Type: Research article

DOI: http://dx.doi.org/10.2217/14796708.2.6.661

Publication date: 2007-11-01

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Future Neurology provides a forum to address the most important challenges and advances in our understanding of neurological disease, and highlights emerging trends and prospects for effective treatments in common but very serious disorders such as stroke, epilepsy, multiple sclerosis and Parkinson's disease.
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