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An Electron Microscope Study

John Prineas, MB, BS, MRCP

Arch Neurol. 1970;23(6):541-548.

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

THE occurrence of distal degeneration or dying-back of long axons in a symmetrical polyneuropathy is usually interpreted as indicating that the primary metabolic disturbance is located within neurons rather than in myelin or in supporting structures in the nerve. Whether this particular pattern of neuronal degeneration is due to a diminished output from the perikaryon of some essential axonal metabolite or to a disturbance in axonal transport devices, or to some other mechanism is not known. It has recently been shown that the fine structure and the rate of flow of axoplasmic proteins in the peripheral nerves in experimental triortho-cresyl phosphate polyneuropathy and experimental acrylamide polyneuropathy^1-3 are affected in different ways in these two dying-back polyneuropathies, and it would appear that more than one subcellular mechanism can lead to distal axonal degeneration. In the following report, the fine structural changes in the peripheral nervous system in thiamine hydrochloride-deficient . . . [Full Text PDF of this Article]

Author Affiliations
Sydney, Australia

From the Department of Pathology (Neuropathology) and the Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, New York, and the Department of Medicine, University of Sydney, Sydney, Australia.

Footnotes
Accepted for publication Aug 6, 1970.

Reprint requests to Department of Medicine, University of Sydney, Sydney, NSW 2006 Australia (Dr. Prineas).

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