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James F. Toole, MD; John A. Gergen, MD; Donald M. Hayes, MD; John H. Felts, MD; Winston-Salem, NC

Arch Neurol. 1968;18(6):680-687.

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

SINCE its introduction in 1952¹ the hydantoin compound, nitrofurantoin (Furadantin), has proved to be an effective agent for the treatment of many types of organism causing urinary tract infection. Unfortunately, its use has occasionally been associated with sensorimotor neuropathy^2-11 which usually has developed in patients with impaired renal function. Some investigators have suggested that this complication is a direct neurotoxic effect of the drug⁹ or the result of impaired renal excretion of toxic metabolic products.^12-15 Others have considered that preexisting systemic disease such as diabetes mellitus has caused subclinical neural damage which is aggravated by nitrofurantoin. A fourth hypothesis, also unproved, is that nitrofurantoin might cause neuropathy by acting as a folic-acid antagonist. Supporting this point of view are reports that neural as well as hematopoietic effects may be produced by depleting the body's stores of folic acid.^16-21 Furthermore, megaloblastosis similar to that occurring . . . [Full Text PDF of this Article]

Author Affiliations
From the departments of neurology (Dr. Toole), physiology (Dr. Gergen), and medicine (Drs. Hayes and Felts), the Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC.

Footnotes
Submitted for publication Jan 6, 1968; accepted Feb 5.

Reprint requests to Dept of Neurology, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC 27103 (Dr. Toole).

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