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William E. Smiddy, MD

Arch Ophthalmol. 2008;126(5):737-738.

Macular hole formation has been postulated to occur due to vitreofoveal traction based on sequential clinical examination features, inferences from histopathological studies, and imaging studies. Some reported cases seem to have occurred outside of the context of such traction, raising the possibility that traction is not the only precipitating factor in macular hole formation. This article demonstrates such a case with the clarity of optical coherence tomography (OCT).

Report of a Case
A 70-year-old woman had decreased vision in her left eye for several weeks. Visual acuity was 20/50. Funduscopic examination (Figure 1) showed a yellow spot in the central fovea, which correlated with a focal area of vitreofoveal traction as demonstrated by OCT (Figure 2A). There was no change 3 months later, but 6 months after the initial visit visual acuity had improved to 20/40; OCT imaging demonstrated release of the vitreofoveal traction (Figure 2B). The foveal contour had further improved 18 months later and visual acuity had increased to 20/30 (Figure 2C). The patient returned 6 months later (2 years after the spontaneous vitreofoveal release) with visual loss to 20/60 and a small central full-thickness macular hole (Figure 2D). Macular hole surgery was performed with successful closure and a return of visual acuity to 20/30.

View larger version (55K): [in this window] [in a new window] [as a PowerPoint slide]   Figure 1. Fundus photograph at the initial visit showing a yellow spot at the fovea. Visual acuity was 20/50.

View larger version (108K): [in this window] [in a new window] [as a PowerPoint slide]   Figure 2. Optical coherence tomographic images. A, Corresponding vitreofoveal attachment and foveal elevation. B, Six months later, the image shows spontaneous vitreofoveal traction release. Visual acuity was 20/40. C, Improved foveal contour 18 months after vitreous traction release corresponds to further visual acuity improvement to 20/30. D, Macular hole formation 2 years after vitreofoveal release. Visual acuity is 20/60.

Comment
Gass¹ systematized the stages of macular hole formation based on clinical examination features, deducing that vitreofoveal traction at the time of posterior vitreous detachment appeared to mediate the formation. These observations were corroborated by ultrasonography² and OCT studies.³

However, certain cases seemed not to be consistent with these observations, such as eyes with macular hole formation at least several months after definitive posterior vitreous separation, scleral buckling surgery (implying a well-established posterior vitreous detachment), and vitrectomy for unrelated disorders.⁴ These exceptional cases seem to indicate that something in addition to a mechanical, tractional relationship participates in macular hole formation, at least in some instances. The OCT images in the case reported here depict this apparently tractionless sequence more clearly than previously described.

An alternative explanation is that the traction component is below the resolution of OCT. A possible mediator might be the outer wall of vitreoschisis as has been proposed by Sebag,⁵ and this may be depicted on the left side of Figure 2A and B as focal areas of minimal separation of what might alternatively be interpreted as the internal limiting membrane. Degenerative factors such as subtle defects or breaks in the internal limiting membrane (tractionally or senescently induced) may allow hydration of the fovea and distort tissue enough to form a full-thickness macular hole.⁶ This may explain why surgical removal of vitreofoveal traction does not uniformly prevent macular hole formation.

The mechanisms of macular hole formation are still incompletely understood but may involve degenerative and tractional factors. A full understanding of pathogenetic mechanisms would likely optimize treatment and prevention of full-thickness macular holes.

AUTHOR INFORMATION
Correspondence: Dr Smiddy, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, 900 NW 17th St, Miami, FL 33136(wsmiddy{at}med.miami.edu).

Financial Disclosure: None reported.

REFERENCES
1. Gass JDM. Idiopathic senile macular hole: its early stages and pathogenesis. Arch Ophthalmol. 1988;106(5):629-639. FREE FULL TEXT 2. Johnson MW, Van Newkirk MR, Meyer KA. Perifoveal vitreous detachment is the primary pathogenic event in idiopathic macular hole formation. Arch Ophthalmol. 2001;119(2):215-222. FREE FULL TEXT 3. Gaudric A, Haouchine B, Massin P; et al. Macular hole formation: new data provided by optical coherence tomography. Arch Ophthalmol. 1999;117(6):744-751. FREE FULL TEXT 4. Smiddy WE. Atypical presentations of macular holes. Arch Ophthalmol. 1993;111(5):626-631. FREE FULL TEXT 5. Sebag J. Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease. Graefes Arch Clin Exp Ophthalmol. 2004;242(8):690-698. FULL TEXT | WEB OF SCIENCE | PUBMED 6. Lipham WJ, Smiddy WE. Idiopathic macular hole following vitrectomy: implications for pathogenesis. Ophthalmic Surg Lasers. 1997;28(8):633-639. WEB OF SCIENCE | PUBMED

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