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NEUROLOGY 1985;35:1617
© 1985 American Academy of Neurology

Pyridoxine neuropathy in rats

Specific degeneration of sensory axons

Anthony J. Windebank, MD, Phillip A. Low, MD, Marceil D. Blexrud, James D. Schmelzer, BS and Herbert H. Schaumburg, MD

From the Department of Neurology (Drs. Windebank and Low, Ms. Blexrud, and Mr. Schmelzer), Mayo Clinic and Mayo Foundation, Rochester, MN; and the Department of Neurology (Dr. Schaumburg), Albert Einstein College of Medicine, Bronx, NY.

When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided after the toxin was withdrawn. By using quantitative histologic techniques, we found axonal degeneration of sensory system fibers and that the fibers derived from the ventral root were spared. Although the degeneration approached the dorsal root ganglion, neurons in the ganglion did not degenerate. We found no early decrease in oxygen consumption of nerve, suggesting that impaired oxidative metabolism was not the primary event.

Address correspondence and reprint requests to Dr. Windebank, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905.

Accepted for publication February 6, 1985.




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