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A Sweet Smell of Success?

Arch Neurol. 2006;63:1055-1056.

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

Even after extensive diagnostic evaluation, the cause of peripheral neuropathy remains uncertain in as many as 40% of patients who present to tertiary care referral centers. The management of these patients with so-called chronic idiopathic axonal polyneuropathy (CIAP), especially those with predominantly sensory symptoms and pain, is a difficult and frustrating clinical problem faced by neurologists.¹ Patients usually find this nondiagnosis of idiopathic neuropathy difficult to accept, especially when they learn that treatment often involves only symptomatic pain management, a process that is often unsatisfactory.

In this context, it is easy to understand the excitement and enthusiasm generated by recent observations that many nondiabetic patients with CIAP have disturbed glucose metabolism as evidenced by impaired fasting glucose (IFG) (defined as a fasting venous glucose level >100 mg/dL [>5.55 mmol/L] and <126 mg/dL [<6.99 mmol/L]) or impaired glucose tolerance (IGT) defined as a 2-hour plasma glucose level between 140 mg/dL [7.77 . . . [Full Text of this Article]

AUTHOR INFORMATION

John T. Kissel, MD

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