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Abstract and Introduction
Abstract
Neuropathic pain is a common problem in clinical practice and one that adversely affects patients' quality of life. Converging evidence from animal and human studies demonstrates that neuropathic pain arises from a lesion in the somatosensory system. Injured peripheral nerve fibers give rise to an intense and prolonged ectopic input to the CNS and, in some cases, also to secondary changes in dorsal horn neuronal excitability. Convincing evidence now suggests that classifying neuropathic pain according to a mechanism-based rather than an etiology-based approach might help in targeting therapy to the individual patient and would be useful in testing new drugs. This article summarizes our current understanding of the peripheral and central pathophysiological mechanisms underlying neuropathic pain and focuses on how symptoms translate into mechanisms.
Introduction
The widely accepted definition of neuropathic pain is 'pain arising as a direct consequence of a lesion or disease affecting the somatosensory system'.
Neuropathic pain is a frequent problem in many peripheral and CNS diseases. The peripheral nerve diseases that most commonly cause neuropathic pain are distal symmetric peripheral neuropathies (e.g., diabetic neuropathy) and focal neuropathies related to trauma (e.g., traumatic brachial plexus injuries), as well as surgical interventions (e.g., breast surgery). Exemplary CNS diseases causing neuropathic pain include multiple sclerosis, spinal cord injury and stroke. The widely ranging etiologies suggest a high prevalence of neuropathic pain in the general population. Postal surveys designed to investigate chronic pain with neuropathic characteristics in large community samples have reported a 7–8% prevalence of neuropathic pain in the general population.
Neuropathic pain arises through multiple and complex pathophysiological mechanisms. Convincing evidence on the relationship between the underlying pathophysiological mechanisms and neuropathic pain symptoms now suggests that classifying neuropathic pain according to a mechanism-based rather than an etiology-based approach might help in targeting therapy to the individual patient and would also be useful in testing new drugs. In this article we summarize our current understanding of the peripheral and central pathophysiological mechanisms underlying neuropathic pain and focus on how symptoms translate into mechanisms.
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