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Highlights potential mechanism in inflammatory pain; leaves open clinical relevance and therapeutic implications pending further evidence.
In recent years, fine sensory nerve fibres have been detected that are not excited by physiological stimuli, even at potentially tissue damaging intensities. These silent afferents are known to supply knee joint, skin and viscera; in the last case, silent afferents seem to be particularly numerous. 2. When an artificial inflammation is induced, many silent afferents develop spike activity, others remain quiescent. Silent afferents that do respond probably have a nociceptive sensory function. Under inflammatory conditions some silent afferents are sensitized to physiological stimuli, others are probably chemospecific. 3. Orthodromic activity in silent afferents may sum spatially and temporally in second order neurons with other nociceptive information and may thereby contribute to different pain states. Furthermore, there is evidence that the activation of chemospecific silent afferents may lead to sensitization of nociceptive dorsal horn neurons. 4. Some silent afferents probably contain neuropeptides that may be liberated under pathophysiological conditions, such as inflammation. 5. Whether certain pathological states can be exclusively attributed to the activation of silent afferents or whether silent afferents sustain the functions of 'conventional' nociceptors remains to be clarified.
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Michaelis et al. (1996) studied this question.
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