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Neil M. Bressler, MD; Daniel P. Finkelstein, MD; Janet S. Sunness, MD; Albert M. Maguire, MD
Baltimore, Md

David Yarian, MD
Princeton, NJ

Arch Ophthalmol. 1991;109(11):1493.

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

In Reply.

—We appreciate the thoughtful comments of Machemer and Heriot regarding our article.¹ The experimental work they report² demonstrates in rabbit eyes that after removal of the sensory retina and retinal pigment epithelium (RPE), cells (which appear to be pigment epithelial derived) will migrate and proliferate over the defect. We do not know from their experimental studies if the cells within the defect are needed for preservation of visual acuity within the defect (since their animal model involves removal of the sensory retina).

Machemer and Heriot also suggest that their model lends support to the hypothesis that "usually no leakage occurs and only a window defect remains visible" following a tear of the RPE. However, if only a window defect were noted following a tear of the RPE, one would not expect to see the intense hyperfluorescence that is seen in the late angiographic frames showing the . . . [Full Text PDF of this Article]

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