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ANDREW de ROETTH, JR., MD; YEN FEN PEI, MD

Arch Ophthalmol. 1964;71(1):73-76.

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

Introduction

The investigations of Ballantyne,¹ Friedenwald,² and Ashton³ have shown that the earliest recognizable (ie, recognizable by ophthalmoscopy or by various histological methods) lesions of diabetic retinopathy are the microaneurysms. While these microaneurysms are universally accepted as the characteristic feature of diabetic retinopathy, no one has been able to explain satisfactorily how and why these microaneurysms develop with such regularity in this disease. Since the pioneering work of Ballantyne, there have been many attempts, in both the clinical and the experimental field, to find the cause for the development of these microaneurysms or at least offer reasonable postulates. More recently Ashton⁴ and Bloodworth⁵ have offered interesting theories along these lines; they believe that there is an accumulation of metabolic waste products in the diabetic retina; ie, there is an incomplete or defective metabolism in the diabetic retina.

Postulating that the basic lesion before the development . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Ophthalmology, Columbia University, College of Physicians and Surgeons, and the Institute of Ophthalmology, Presbyterian Hospital.

Footnotes
Submitted for publication June 14, 1963.

This investigation was supported by Research Grant B-1521 from the National Institute of Neurological Diseases and Blindness, National Institutes of Health, US Public Health Service.

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