Testing Peripheral Sources of Secondary Hyperalgesia in Irritable Bowel Syndrome Patients

A test of the role of tonic peripheral impulse input is suggested by a model of neuropathic pain, in which ongoing afferent input from a peripheral source maintains altered central processing that accounts for spontaneous pain, allodynia, hyperalgesia, and other motor abnormalities (21). In their study, the potential role of ongoing afferent input was demonstrated in CRPS patients. Peripheral anesthetic blockade of nociceptive input from a few critical foci effectively abolished both spontaneous and elicited pain and cold/mechanoallodynia within widespread body regions in these patients, including regions that were remote from these critical foci. A similar reversal occurs with sympathetic blocks in some CRPS patients (37,61). Given the presence of widespread zones of hyperalgesia in neuropathic pain, fibro-myalgia, and IBS patients, it is possible that hyperalgesia of these of patients is maintained to some extent by tonic impulse input from nociceptive and/or non-nociceptive primary afferent neurons.

Thus, the results of studies just described suggest that a similar experiment could be carried out in the case of IBS patients. If visceral hyperalgesia and secondary cutaneous hyper-algesia are dynamically maintained by tonic input from the rectum and/or colon, then local anesthesia of one or more of these visceral structures should reduce these forms of hyperalge-sia. Our recent study tested the hypothesis that local anesthetic blockade of peripheral visceral nociceptive input reduces both visceral and cutaneous secondary hyperalgesia in IBS patients (51). This hypothesis was tested by administering controlled rectal distension and cutaneous heat stimuli before and after rectal administration of either lidocaine jelly or saline jelly in a double-blind crossover basis in IBS patients. The comparison was ideal because subjects cannot subjectively distinguish the two agents.

In comparison to saline placebo, lidocaine jelly completely normalized not only rectal hyperalgesia, as shown in Figure 4 (left panel), but also hyperalgesia to heat stimuli applied to the foot. This was not the result of systemic absorption of lidocaine, because significant blood levels were not detected during the 50-minute experimental session and most of the effects were present five minutes after treatment. Thus, tonic impulse input from the rectum appears to dynamically maintain not only primary hyperalgesia from the rectum/colon but also the secondary hyperalgesia that is spatially remote from the peripheral source of impulse input. One likely mechanism is that tonic input from the rectum/colon sensitizes spinal cord neurons that have viscerosomatic convergence, a mechanism additionally supported by animal studies described above.

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