Stimulus-Evoked Pain

Stimulus-evoked pain appears to result in part from central sensitization of the dorsal horn neurons resulting from continuous input from spontaneously firing C-fibers postinjury. This is mediated by N-methyl-D-aspartate (NMDA) receptor sensitization through a biochemical signal cascade involving Substance P and activated protein kinase C [5]. In addition to hyperalgesia, hyperpathia, allodynia, and the universal sensory loss, central sensitization results in a spreading localization of pain from the site of the initial injury [6]. This is commonly noted in the neuroma, the swelling found at the proximal end of the injured nerve which contains the regenerative terminal nerve fibers.

In patients who exhibit only allodynia, the pathophysiologic process may be related to different processes: A-fiber sprouting and peripheral disinhibition. A-fiber sprouting represents a physiologic response to injury of C-fibers that induces growth of A-fiber terminals in the dorsal horn, which includes the anatomic areas of the dorsal horn where A-fibers are not normally found (Lamina II). These areas are primarily related to pain processing which can induce allodynia. Peripheral disinhi- bition represents a decreased inhibitory signaling of the dorsal horn neuron by the injured peripheral neuron [7].

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