Biology of Neuropathic Pain − a Brief Review

Tony L. Yaksh, Ph.D.
Department of Anesthesiology
University of California, San Diego

Introduction - TOP

Following soft tissue injury and inflammation, pain is a common symptom, the disappearance of which is considered to be a consequence of the healing process. In contrast, over time after a variety of injuries to the peripheral nerve, the animal and human will often reflect the appearance of a constellation of pain events. Frequent components of this evolving syndrome are i) ongoing incidences of sharp-shooting sensations referred to the peripheral distribution of the injured nerve and ii) abnormal painful sensations in response to light tactile stimulation of the peripheral body surface. This latter phenomenon is referred to as tactile allodynia. The psychophysics of this state clearly emphasize that the pain is evoked by the activation of low threshold mechano-receptors (Aß afferents). This ability of light touch evoking this anomalous pain state is de facto evidence that the peripheral nerve injury has led to a reorganization of central processing, i.e. it is not a simple case of a peripheral sensitization of otherwise high threshold afferents.

In addition to these behavioral changes, the neuropathic pain condition may display other contrasting anomalies, including on occasion, an ameliorating effect of sympathectomy of the afflicted limb and an attenuated responsiveness to analgesics such as opiates. What are the mechanisms which underlie this nerve injury pain phenotype? This review addresses the principal changes that occur in connectivity and processing after peripheral nerve injury.

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