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Year : 2003  |  Volume : 51  |  Issue : 4  |  Page : 353-355

Optical coherence tomographic evaluation of foveal pseudocyst in the formation of macular hole

L V Prasad Eye Institute, Hyderabad, India

Correspondence Address:
N Hussain
L V Prasad Eye Institute, Hyderabad
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Source of Support: None, Conflict of Interest: None

PMID: 14750627

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Optical coherence tomographic documented progression of foveal pseudocyst in a vitrectomised eye to full thickness macular hole is reported. Muller cell alteration and other centrifugal forces are possible pathomechanisms.

Keywords: Pseudocyst, macular hole, optical coherence tomography, Muller cells, vitrectomy

How to cite this article:
Hussain N, Hussain A, Natarajan S. Optical coherence tomographic evaluation of foveal pseudocyst in the formation of macular hole. Indian J Ophthalmol 2003;51:353-5

How to cite this URL:
Hussain N, Hussain A, Natarajan S. Optical coherence tomographic evaluation of foveal pseudocyst in the formation of macular hole. Indian J Ophthalmol [serial online] 2003 [cited 2023 Nov 29];51:353-5. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2003/51/4/353/14646

Early stages of macular hole formation have been variously characterised as macular cyst, foveal thinning, involutional macular thinning or Stage 1 macular hole with posterior elevation of foveal photoreceptors. The use of the scanning laser ophthalmoscope, retinal thickness analyser and optical coherence tomography (OCT) have shown that a foveal cystoid space or pseudocyst is the primary lesion in macular hole formation along with incomplete perifoveal posterior vitreous detachment.[1],[2] Foveal pseudocyst is the preferred nomenclature as this cystoid space has no wall, but seems to result from an intrafoveal splitting.[3] This report describes a prospective evaluation of foveal pseudocyst after vitreous surgery in formation of full thickness macular hole using the OCT.

  Case report Top

A 42-year-old man was seen in the retina clinic, complaining of lack of improvement of vision after cataract surgery in the right eye. On examination, his visual acuity was 6/36 in the right eye and 6/60 in the left eye. There was cataract in the left eye and posterior chamber intraocular lens in the right eye. Dilated fundus examination with indirect ophthalmoscopy showed superior retinal detachment with a large horseshoe tear involving the macula in the right eye. The left eye examination showed attached retina with pigmented lattice in the superotemporal peripheral retina. He underwent scleral buckling, vitrectomy with complete posterior vitreous detachment, perfluoro carbon liquid injection, fluid gas exchange (C3F8) and endolaser in the right eye. Primary vitrectomy was performed, as there was a large horseshoe tear and vitreous haze. Postoperatively, the patient's best-corrected visual acuity was 6/24, N8. Fundus examination at the final follow-up showed an attached macula without any gross macular changes, good buckle effect and reattached retina.

Six months later, the patient complained of metamorphopsia in the right eye. His best-corrected visual acuity at this point was 6/24, N12. Fundus examination showed cystic elevation in the fovea [Figure - 1]. Fundus fluorescein angiography (FFA) showed increasing hyperfluorescence with mild pooling [Figure - 2]. OCT evaluation through the right fovea showed neurosensory cystic elevation with loss of foveal contour [Figure - 3]. He was advised careful observation and self-monitoring with a home Amsler.

Subsequently, when seen again 5 months later, his visual acuity was 6/36, N12 in the right eye. Left eye macula was unremarkable. There was a full thickness macular hole in the right eye [Figure - 4], which was confirmed with OCT [Figure - 5].

  Discussion Top

Although the actual pathomechanism of macular hole is controversial, the sequence of events leading to macular hole formation is well documented. It is postulated that the initial stages of macular hole formation are the result of the process of posterior vitreous detachment. [3],[4],[5] Idiopathic macular holes are caused by tangential contraction of premacular vitreous cortex.

Foveal pseudocyst is a specific entity occurring either as a primary ocular event or in the fellow eye of an eye with macular hole. Foveal pseudocyst formation may be the result of the incomplete separation of the vitreous cortex at the foveal center. This is the first step in the development full thickness macular hole, but it may also evolve into a lamellar macular hole, persist unchanged for months, or resolve completely. Haouchine et al [6] reported serial OCT evaluation of 22 cases of foveal pseudocyst with follow-up period of 3 to 26 months. Three of 22 eyes progressed to macular hole and 4 of 22 developed into a lamellar hole. Seven of 22 eyes resolved completely and eight remained unchanged or exhibited slight enlargement at the end of follow-up.

The present patient was diagnosed to have foveal pseudocyst on OCT 6 months after vitreoretinal surgery. Five months later he complained of visual distortion and was confirmed to have full thickness macular hole. Even with the absence of formed vitreous, OCT showed progression of foveal pseudocyst to macular hole. Probably here tangential traction forces were responsible for the formation of macular hole. This is the first case report (Medline search) that was evaluated prospectively in a vitrectomised eye documenting the progression of foveal pseudocyst to a macular hole.

The OCT of both pseudocyst and macular hole show a split of neurosensory retina in our patient [Figure - 3][Figure - 5]. Posterior extension of such aspect probably led to pseudocyst formation. The occurrence of a split in the foveal tissue evolving into a pseudocyst can be explained by particular architecture of the foveola [6],[7] In the foveal center, the outer cone fibres are surrounded and bound together by large Muller cells which have inner processes constituting the foveal floor. It has been shown in monkey fovea that parafoveal Muller cells have long outer trunks in the outer plexiform layer which accompanies and unsheathes the Henle's fibres on their course from the foveal center to the foveal periphery.[8] This anatomical characteristics of the fovea helps in maintaining the cohesion of Henle's layer with the inner retina. Our case did show a neural split on the lateral edge of the macular hole. A serial OCT could have possibly demonstrated these several changes. Haouchine et al [6] have observed initially a split in the foveal center, in the inner part of the foveal tissue and subsequently an outer foveal opening resembling a centrifugal separation of the photoreceptors. They postulated that it might be the result of damage to the foveal and parafoveal Muller cells resulting in dehiscence of the neural tissue from the foveola. Probably, our case developed a pseudocyst and then macular hole due to initial insult to the foveolar Muller cells during vitreous surgery. Since complete PVD was created during primary vitrectomy, the role of posterior vitreous in the formation of macular hole can be ruled out in our case. The various steps of vitreous surgery probably are the inciting factors in stimulating the glial or Mullers cells activation. However, we do not have any other valid explanation for the possible harmful effect of surgery on the macula.

Foveal pseudocyst with progression to full thickness macular hole was not noted earlier in a vitrectomised eye. Since there was no evidence of epiretinal membrane and posterior hyaloid stripping was done in the primary surgery, we hypothesise that Muller cell insult is a probable hypothesis of macular hole formation in a vitrectomised eye. We are aware that a single case report do not confirm the pathomechanism, which is possible only by histopathology.

  References Top

Asrani S, Zeimer R, Goldberg MF, Zou S. Serial optical sectioning of macular holes at different stages of development. Ophthalmology 1998;105:66-77.   Back to cited text no. 1
Kishi S, Kamei Y, Shimuzi K. Tractional elevation of Henle's layer in idiopathic macular holes. Am J Ophthalmol 1995;120:486-96.   Back to cited text no. 2
Avila MP, Jalkh AE, Murakami K, Trempe CL, Schepens CL, Biomicroscopic study of vitreous in macular breaks. Ophthalmolgy 1983;90:1277- 83.  Back to cited text no. 3
Kakehashi A, Schepens CL, Trempe CL. Vitreomacular observations II. Data on the pathogenesis of idiopathic macular breaks. Graefes Arch Clin Exp Ophthalmol 1996;234:425-33.  Back to cited text no. 4
Reese AB, Jones IS, Cooper WC. Macular changes secondary to vitreous traction. Am J Ophthalmol 1967;64:544- 49.   Back to cited text no. 5
Haouchine B, Massin P, Gaudric A. Foveal pseudocyst as the first step in macular hole formation. A prospective study by optical coherence tomography. Ophthalmology 2001;108:15-22.   Back to cited text no. 6
Gass JDM. Muller cell cone, an overlooked part of the anatomy of the fovea centralis: hypotheses concerning its role in the pathogenesis of macular hole and foveamacular retinoschisis. Arch Ophthalmol 1999;117:821-23.  Back to cited text no. 7
Distler C, Dreher Z. Glia cells of the monkey retina. II. Muller cells. Vision Res 1996;36:2381-94.  Back to cited text no. 8


  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]

This article has been cited by
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