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Author(s): Costigan M; Scholz J; Woolf CJ
Title: Neuropathic Pain: A Maladaptive Response of the Nervous System to Damage
Source: ANNUAL REVIEW OF NEUROSCIENCE 32: 1-32
Date: 2009
Document Type: Journal : Review
DOI:
Language: English
Comment:
Address: Massachusetts Gen Hosp, Neural Plast Res Grp, Dept Anesthesia & Crit Care, Boston, MA 02129 USA.
Harvard Univ, Sch Med, Boston, MA 02129 USA. Reprint: Costigan, M, Massachusetts Gen Hosp, Neural Plast Res Grp, Dept
Anesthesia & Crit Care, Boston, MA 02129 USA. E-mail: mcostigan@partners.org
scholz.joachim@mgh.harvard.edu cwoolf@partners.org Author Keywords: neural plasticity; synaptic facilitation; disinhibition; neuroimmune
interaction; pain phenotype
KeyWords Plus: SPINAL DORSAL-HORN; CHRONIC CONSTRICTION INJURY; PRIMARY SENSORY
NEURONS; GATED SODIUM-CHANNELS; ROOT GANGLION NEURONS; SUBSTANTIA-
GELATINOSA NEURONS; PERIPHERAL-NERVE; CENTRAL SENSITIZATION; SCIATIC-
NERVE; UP-REGULATION
Abstract: Neuropathic pain is triggered by lesions to the somatosensory, nervous system that alter its structure and function so that pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. The pain is an expression of maladaptive plasticity within the nociceptive system, a series of changes that constitute a neural disease state. Multiple alterations distributed widely across the nervous system contribute to complex pain phenotypes. These alterations include ectopic generation of action potentials, facilitation and disinhibition of synaptic transmission, loss of synaptic connectivity and formation of new synaptic circuits, and neuroimmune interactions. Although neural lesions are necessary, they are not sufficient to generate neuropathic pain; genetic polymorphisms, gender, and age all influence the risk of developing persistent pain. Treatment needs to move from merely Suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk.
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