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Carl J. Belber, MD
University of Illinois School of Clinical Medicine Burnham Hospital Champaign. Ill

JAMA. 1982;247(2):175.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

The development of postoperative compressive neuropathies—ulnar, radial, and peroneal—in our series was related not only to prolonged compression of several hours, but also, in every instance, to a chronic, dense neuroma in continuity. There is no doubt that the short-term compression was the proximate cause of the neuropathy but, from the operative evidence, the preexisting chronic neuroma would appear to be an essential cofactor; in other words, an already partly anatomically compromised—but fully functional— nerve was pushed "over the edge" by a compressive stress, causing an acute neuropathy.

Therefore, in contrast to the outlook promoted by John F. Aita, MD (1981;245:2295), stating that these patients have a "poor prognosis... whether treated medically or surgically with transposition or decompression" and suggesting that treatment is "limited to counseling the patient," I would urge physicians to look at this lesion in a more positive way.

In my experience, during a . . . [Full Text PDF of this Article]

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