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Editorial Views  |   March 2004
One Thing Leads to Another
Author Notes
  • Simon Gelman Professor of Anesthesi-ology, University of Alabama at Birmingham, Birmingham, Alabama.
Article Information
Editorial Views
Editorial Views   |   March 2004
One Thing Leads to Another
Anesthesiology 3 2004, Vol.100, 472-473. doi:
Anesthesiology 3 2004, Vol.100, 472-473. doi:
MS. Smith comes to clinic and reports having diffuse lower abdominal pain ever since her hysterectomy. When she voids, her bladder hurts. When she evacuates, her bowels hurt. She has aching in her back and legs. The gynecologists, urologists, and gastroenterologists have no answers. Her pain seems visceral in nature with poor localization and extreme sensitivity to activities of her internal organs, but no visceral disease is identified. What is going on? The basic science article by Shin and Eisenach 1 in this issue of the Journal suggests a potential cause for such a visceral pain: nerve injury. It has been long accepted that nerve injury can lead to back pain, leg pain, skin pain, almost any pain, but for some reason a link with visceral pain has not been commonplace. This article forms such a link. It demonstrates that peripheral nerve injury can result in both cutaneous and visceral hypersensitivity (a.k.a. possible pain states). At the same time, it demonstrates that the pharmacology of cutaneous hypersensitivity may not necessarily be extrapolated to visceral hypersensitivity. These observations are important for both intellectual and pragmatic reasons.
Intellectually, these results allow a sense of unity in the cognitive realm where similarities and dissimilarities must somehow be integrated. The authors’ results suggest underlying principles associated with nerve dysfunction that are similar for all nociceptors. As a consequence, we do not have to invoke unique “protective” processes associated with one subtype of pain, and we must recognize the potential negative consequences of nerve injury in all sensory modalities. At the same time, neurochemical differences in the modulation of differing inputs seem to exist, which allows us to explain why all pain is not perceived as the same.
Now for the pragmatic issues. If we accept that peripheral nerve injury may result in visceral hypersensitivity, then we must widen our differential diagnosis regarding visceral pain complaints and  we must consider the potential consequences of visceral nerve neurolysis as a therapeutic intervention. The first of these, a wider differential diagnosis, is not really a new consideration: nerve injury has long been proposed as a source of bowel and bladder dysfunction (outflow effects) and more recently proposed as an etiology of neurogenic pelvic pain. 2 Others have gone so far as to propose that the painful bladder syndrome, interstitial cystitis, is a neuropathic, visceral, complex regional pain syndrome. 3 The more ominous issue is whether the practice of visceral nerve neurolysis for noncancer-related pain may create iatrogenic problems while trying to solve others. I have had a patient utter the frightening words “phantom pancreas” to me after a surgical splanchnectomy for chronic pancreatitis and at the time, I felt justified in discounting the idea as the whining of a chronic pain patient. Now I may need to reconsider.
Before agonizing over the harm I may have done, I will remember that this article is a first, basic science report. It relates to partial nerve injury—not total neurolysis—and there are other explanations for some of the data. Nerve-injured rats were compared with unoperated controls, so the deep-tissue-non-neural effects of the surgery could have contributed to effects on visceral sensitivity. Likewise, the cutaneous and visceral pharmacologic data cannot be directly compared, because one set of measures uses a threshold stimulus of ascending intensity and the other uses a fixed suprathreshold stimulus. Those interpretative issues aside, this information demonstrates an important relation between neural injury and the possibility of clinical pain. As more information becomes available, this may result in altered clinical practice.
References
Shin S-W, Eisenach JC: Peripheral nerve injury sensitizes the response to visceral distension, but not its inhibition by the antidepressant milnacipran. A nesthesiology 2004; 100: 671–5Shin, S-W Eisenach, JC
Zermann DH, Ishigooka M, Doggweiler R, Schmidt RA: Postoperative chronic pain and bladder dysfunction: Windup and neuronal plasticity—do we need a more neurological approach in pelvic surgery? J Urol 1998; 160: 102–5Zermann, DH Ishigooka, M Doggweiler, R Schmidt, RA
Galloway NT, Gabale DR, Irwin PP: Interstitial cystitis or reflex sympathetic dystrophy of the bladder? Semin Urol 1991; 9: 148–53Galloway, NT Gabale, DR Irwin, PP