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Phillip A. Low, MD; Rose M. Dotson, MD

JAMA. 1998;280:1863-1864.

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

Pain resulting from diffuse and focal neuropathies, such as painful diabetic neuropathy (PDN) and postherpetic neuralgia (PHN), is a relatively common but difficult to manage clinical problem. Neuropathy occurs in more than 50% of patients with diabetes who have been hyperglycemic for more than 15 years,¹ and about 10% of patients with diabetic neuropathy are troubled with persistent dysesthesias or pain. Unfortunately, drug treatment for PDN is often unsatisfactory, as eloquently demonstrated by the large number of drugs that patients will have taken in an attempt to seek relief.

The optimal drug might be one that interrupts the pathophysiology of diabetic neuropathy, simultaneously improving neuropathy and ameliorating the positive symptoms of neuropathy. Potential agents include the aldose reductase inhibitors, neural growth factors, antioxidants, -linolenic acid, and agents that block protein glycation.² However, the efficacy of these experimental drugs is unknown, and for . . . [Full Text of this Article]

From the Department of Neurology, Mayo Clinic, Rochester, Minn.

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