The Diversity of Traction Mechanisms in Myopic Traction Maculopathy

The Diversity of Traction Mechanisms in Myopic Traction Maculopathy

The Diversity of Traction Mechanisms in Myopic Traction Maculopathy BRIAN L. VANDERBEEK AND MARK W. JOHNSON ● PURPOSE: To identify the major traction...

9MB Sizes 11 Downloads 142 Views

The Diversity of Traction Mechanisms in Myopic Traction Maculopathy BRIAN L. VANDERBEEK AND MARK W. JOHNSON ● PURPOSE:

To identify the major traction mechanisms that cause myopic traction maculopathy and to determine whether surgery can be tailored successfully to the specific mechanism involved. ● DESIGN: Nonrandomized, retrospective, interventional case series. ● METHODS: We performed a chart review of consecutive patients who underwent vitreoretinal surgery for myopic traction maculopathy by a single surgeon at a tertiary referral center. Traction mechanisms were identified based on preoperative and intraoperative findings and postoperative response to a tailored surgical approach. ● RESULTS: Six eyes of 6 patients with a minimum follow-up of 6 months were included. Major pathogenic traction mechanisms included perifoveal posterior vitreous detachment with vitreomacular traction in 3 eyes, noncompliance of native internal limiting membrane in 2 eyes, epiretinal membrane in 1 eye, and remnant cortical vitreous layer after posterior vitreous detachment in 1 eye. One eye exhibited 2 traction mechanisms. The surgical approach addressed only the major traction mechanism(s) identified in each eye. After surgery, the visual acuity improved by 2 lines or more in all eyes, and macular thickening resolved completely in 5 (83%) of 6 eyes and partially in the remaining eye. ● CONCLUSIONS: The traction mechanisms causing myopic traction maculopathy are diverse. Vitreoretinal surgical repair for this condition is successful when the major traction mechanisms causing tautness of the inner retina are identified and relieved. (Am J Ophthalmol 2012;153:93–102. © 2012 by Elsevier Inc. All rights reserved.)

T

fore the advent of optical coherence tomography (OCT), this disorder was difficult to diagnose, and surgery typically was performed for presumed foveal detachment or macular hole. As the resolution and the quality of OCT imaging have improved, so has the ability to understand the pathoanatomic features of this condition. As suggested by the name myopic traction maculopathy, it is widely accepted that a pulling or stretching force is the primary pathologic mechanism in this disorder. The precise cause for this traction, however, is still debated. Arguments have been made for each of several preretinal structures as the source of traction, including a partially detached vitreous with vitreomacular adhesion, remnant cortical vitreous plaques after posterior vitreous detachment (PVD), and epiretinal membrane (ERM).1,2,4,6 –9 Other authors, however, have argued that myopic traction maculopathy arises from elements intrinsic to the thinned myopic retina, including a taut internal limiting membrane (ILM) and shortened retinal arterioles, either of which could lead to tangential traction and various pathologic consequences.10 –13 The lack of consensus for a single pathophysiologic mechanism has spawned a similar debate regarding the best surgical approach for treatment of this condition. Major areas of controversy include the role of intravitreal gas after vitrectomy and the need for ILM removal.4,6,7,14 –16 To date, no report has sought to illustrate the multiple tractional elements that can lead to myopic traction maculopathy while demonstrating a similar diversity of successful surgical approaches. Herein, we describe the major traction mechanisms that cause myopic traction maculopathy and demonstrate that surgery can be tailored successfully to the specific pathologic mechanism involved in a given eye.

HE TERM MYOPIC TRACTION MACULOPATHY WAS

used first by Panozzo and Mercanti1 to describe a collection of pathologic changes associated with highly myopic eyes, including macular retinoschisis, foveal detachment, and macular hole. Also known as myopic foveoschisis, these changes occur in approximately 8% to 34% of people diagnosed with pathologic myopia.2–5 Be-

Accepted for publication June 14, 2011. From the Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan (B.L.V., M.W.J.). Inquiries to Mark W. Johnson, Kellogg Eye Center, University of Michigan, 1000 Wall Street, Ann Arbor, MI 48105; e-mail: markwj@ med.umich.edu 0002-9394/$36.00 doi:10.1016/j.ajo.2011.06.016

©

2012 BY

METHODS WE PERFORMED A RETROSPECTIVE REVIEW OF THE MEDICAL

records, OCT images, and color fundus photographs of consecutive patients who underwent vitreoretinal surgery for myopic traction maculopathy by 1 surgeon (M.W.J.). Patients were considered to have myopic traction maculopathy if, in addition to high myopia, they had diffuse schisis-like retinal thickening throughout the macular area confirmed by OCT. All patients were examined, diagnosed, and operated on at a large academic tertiary care

ELSEVIER INC. ALL

RIGHTS RESERVED.

93

FIGURE 1. Vertical optical coherence tomography images from Patient 1 with myopic traction maculopathy. (Top) Before surgery, there is evidence for vitreomacular traction with diffuse macular thickening and a stage 1B macular hole. The visual acuity is 20/200. (Bottom) Six months after peeling of the posterior hyaloid membrane and fluid– gas exchange, the visual acuity is 20/20, the macular hole is closed, and the diffuse macular thickening is nearly resolved.

center between 2001 and 2009. The minimum period of postoperative follow-up for inclusion in this study was 6 months. No patient meeting these criteria during this period was excluded. OCT was performed through a dilated pupil by a certified ophthalmic photographer using commercially available equipment (Stratus OCT III or Cirrus HD-OCT; Carl Zeiss Meditec, Inc, Dublin, California, USA). The OCT studies comprised scans 6 to 9 mm in length, oriented either as 6 radial lines at intervals of 30 degrees (Stratus OCT) or as 5-line horizontal and vertical raster scans (Cirrus HD-OCT). Each OCT study was centered on the foveola. Preoperative vitreous status was determined by biomicroscopic examination (presence or absence of Weiss ring) combined with OCT images. PVD was staged as described previously.17 Macular traction mechanisms were identified based on preoperative and intraoperative findings and postoperative response to a tailored surgical 94

AMERICAN JOURNAL

approach. Anatomic resolution was defined as the disappearance of schisis-like retinal thickening as observed on OCT images obtained at postoperative follow-up visits. ● CASE 1: A 52-year-old woman with a history of radial keratotomy surgery had an abrupt decrease in vision in her right eye to 20/200. The axial length in the right eye was 25.9 mm and the refractive error before radial keratotomy was unknown. Fundus and OCT examinations showed diffuse thickening of the outer macula and a stage 1 (perifoveal) PVD with a stage 1B macular hole. There was no clinically apparent posterior staphyloma. After core vitrectomy, a PVD was induced, including careful separation of the vitreous from the fovea. Examination of the retina around the fovea with a diamonddusted membrane brush revealed no cortical vitreous remnants or ERM. Fluid– gas exchange was performed using 12% C3F8 gas. The macular hole and macular OF

OPHTHALMOLOGY

JANUARY

2012

FIGURE 2. Horizontal optical coherence tomography images from Patient 3 with myopic traction maculopathy. (Top) Before surgery, there is obvious epiretinal membrane with extensive schisis-like retinal thickening. Visual acuity is 20/70. (Middle) One month and (Bottom) 4 months after epiretinal membrane peeling, there is gradual resolution of macular thickening. The final visual acuity is 20/20.

VOL. 153, NO. 1

TRACTION MECHANISMS

IN

MYOPIC TRACTION MACULOPATHY

95

FIGURE 3. Vertical optical coherence tomography images from Patient 4 with myopic traction maculopathy. (Top) Before surgery, there is extensive macular thickening with traces of a thin preretinal membrane. The visual acuity is 20/80. (Middle) Three and (Bottom) 6 months after peeling of a remnant cortical vitreous layer, there is gradual, partial resolution of schisis-like thickening, with tenting of inner retina at a retinal arteriole (asterisk). The visual acuity returned to its baseline level of 20/60 at 6 months.

96

AMERICAN JOURNAL

OF

OPHTHALMOLOGY

JANUARY

2012

FIGURE 4. Vertical optical coherence tomography images of Patient 5 with myopic traction maculopathy. (Top) Preoperative image showing marked schisis-like macular thickening and a localized vitreous separation over the macular area. Visual acuity is 20/80. (Second row) Three months and (Third row) 6 months after peeling of the internal limiting membrane (ILM), there is gradual resolution of schisis-like thickening, with improvement in visual acuity to 20/25. (Bottom) At 36 months after surgery, there is persistent schisis-like thickening where the ILM was not removed (arrows) and inner retinal tenting at retinal arterioles (asterisks).

VOL. 153, NO. 1

TRACTION MECHANISMS

IN

MYOPIC TRACTION MACULOPATHY

97

FIGURE 5. Optical coherence tomography images from Patient 6 with myopic traction maculopathy. (Top) Before surgery, vertical scan shows partial posterior vitreous detachment with vitreomacular traction and schisis-like retinal thickening. (Middle) Four months after cortical vitreous peeling, horizontal scan shows persistent retinal thickening and foveal detachment. The visual acuity is 20/80. (Bottom) Horizontal scan obtained 7 months after ILM peeling. The macular thickening has resolved and the visual acuity is 20/20.

● CASE 3: An 81-year-old man sought treatment for a decrease in visual acuity in the left eye to 20/70 with a best correction of ⫺10.00 diopters (D). Fundus examination and OCT of the left eye showed a Weiss ring, an

thickening resolved by 4 months after surgery, and the visual acuity improved to 20/20 by 18 months after surgery. The eye remained stable through 27 months of follow-up (Figure 1). 98

AMERICAN JOURNAL

OF

OPHTHALMOLOGY

JANUARY

2012

TABLE 1. Preoperative Clinical Data for Study Subjects with Myopic Traction Maculopathy

Patient

Age at Surgery (y)

Sex

Eye

MR (D)/Axial Length (mm)

Symptom Duration (mos)

PVD Stage

Staphyloma

Associated Findings

1 2 3 4 5 6

52 60 81 62 46 48

F M M F F F

Right Left Right Left Left Left

NA/25.9 ⫺18.25/NA ⫺10.00/29.19 ⫺22.50/NA ⫺13.50/NA ⫺15.50/27.91

2 6 92 81 36 1

1 1 4 4 2 1

No Yes Yes Yes Yes Yes

Stage IB MH Inner retinal schisis Inner retinal schisis None None 1. Inner retinal schisis 2. Inner retinal schisis and foveal detachmenta

Preoperative VA

20/200 20/100 20/70 20/80 20/80 1. 20/50 2. 20/80a

D ⫽ diopters; F ⫽ female; ILM ⫽ internal limiting membrane; M ⫽ male; MH ⫽ macular hole; MR ⫽ manifest refraction; NA ⫽ not available; PVD ⫽ posterior vitreous detachment; VA ⫽ visual acuity; VMT ⫽ vitreomacular traction; y ⫽ years. a Patient 6 underwent 2 surgical procedures.

obvious ERM, and prominent schisis-like macular thickening throughout a posterior staphyloma. During vitrectomy, a complete PVD was confirmed and the ERM was peeled. Neither ILM peeling nor intravitreal gas were used. The macular thickening resolved by 3 months after surgery, with visual recovery to 20/20 by 8 months. Seventy-two months after surgery, the eye was stable (Figure 2). ● CASE 4:

A 62-year-old woman sought treatment for symptoms of worsening vision, metamorphopsia, and micropsia in the left eye. The past ocular history was notable for high myopia (⫺22.50 D), amblyopia, and esotropia in the affected eye. The visual acuity was 20/80 in the left eye. Fundus examination revealed a Weiss ring and schisis-like thickening within a posterior staphyloma. OCT demonstrated schisis-like macular thickening with traces of a thin preretinal membrane that was invisible clinically. During vitrectomy surgery, triamcinolone was used to identify and to help remove a broad and thin preretinal tissue layer from the macular region and extending into the retinal periphery. The peeled tissue had physical characteristics most consistent with vitreous cortex. Intravitreal gas (10% C3F8) was used. After 6 months, the visual acuity had improved to the baseline of 20/60, and the symptoms of metamorphopsia and micropsia resolved. There was partial resolution of the schisis-like thickening (Figure 3).

vitrectomy, triamcinolone was used to confirm that no cortical vitreous remnants were present on the retinal surface. The ILM was peeled and 5% C3F8 gas was placed in the eye. The macular thickness resolved slowly over 6 months and acuity improved to 20/25 by 10 months after surgery. The eye remained stable through 35 months after surgery (Figure 4). ● CASE 6: A 48-year-old woman with a ⫺15.50 D spectacle correction sought treatment for gradually progressive vision loss in the left eye. The visual acuity was 20/50. Fundus examination and OCT imaging demonstrated partial PVD with vitreomacular traction causing schisis-like thickening of the macula within a posterior staphyloma. She underwent vitrectomy with peeling of the posterior cortical vitreous. Four months after surgery, the visual acuity measured 20/80, the schisis-like thickening persisted, and a foveal detachment was evident on OCT. During a second vitrectomy, triamcinolone dusting revealed only a few small remnant cortical vitreous plaques on the macula, which were removed easily with a diamond-dusted brush. Because these isolated remnants were not believed to be relevant tractionally, the ILM was peeled and 10% C3F8 gas was placed in the eye. Anatomic recovery occurred within 1 month and the visual acuity improved to 20/20 within 7 months after the second operation. These findings remained unchanged at last follow-up, 32 months after surgery (Figure 5).

● CASE 5:

A 46-year-old woman sought treatment for increased metamorphopsia after slowly progressive vision loss in the left eye for 3 years. The refractive error was ⫺13.50 D and the visual acuity was 20/80 in the left eye. Biomicroscopy demonstrated a posterior staphyloma and diffuse macular thickening. OCT examination showed schisis-like retinal thickening throughout the posterior staphyloma, with a localized vitreous detachment and no ERM. After surgical induction of a complete PVD during

VOL. 153, NO. 1

TRACTION MECHANISMS

IN

RESULTS THE STUDY COHORT INCLUDED 2 MEN AND 4 WOMEN WITH A

mean age of 58.1 years (range, 46 to 81 years) at the time of surgery (Table 1). Features of myopic traction maculopathy were unilateral in all patients. Five of the 6 (83%) study eyes had an obvious posterior staphyloma and high myopia of ⫺10.0 D or more. The remaining eye had an axial length of

MYOPIC TRACTION MACULOPATHY

99

TABLE 2. Traction Mechanisms in Myopic Traction Maculopathy: Surgical and Postoperative Data

Patient

1 2 3 4 5 6

Major Traction Mechanism

Surgical Approach

Intravitreal Gas

VMT VMT ERM Cortical vitreous layer ILM 1. VMT 2. ILMc

Cortical vitreous peeling Cortical vitreous peeling ERM peeling Cortical vitreous peeling ILM peeling 1. Cortical vitreous peeling 2. ILM peelingc

Yes No No Yes Yes 1. No 2. Yesc

Best Postoperative VA

Time to Anatomic Resolution (mos)

Time to Best VA (mos)

Follow-up (mos)

20/20 20/60a 20/20 20/60b 20/25 20/20

4 46 3 Partial resolution 6 1

18 2.5 8 6 10 7

27 90 72 6 35 32

ERM ⫽ epiretinal membrane; ILM ⫽ internal limiting membrane; VA ⫽ visual acuity; VMT ⫽ vitreomacular traction. Final visual acuity was 20/300 because of glaucoma complications. b Amblyopic eye with baseline best-corrected acuity of 20/60. c Patient 6 underwent 2 surgical procedures. a

25.9 mm, no clinically evident posterior staphyloma, and a refractive error that was unknown because of previous radial keratotomy surgery. In addition to diffuse schisis-like thickening in the outer macula, associated findings included inner retinal schisis in 3 (50%) eyes, foveal detachment in 1 (17%) eye, and stage 1B macular hole in 1 (17%) eye. The preoperative vitreous status for each patient is listed in Table 1. The average duration of symptoms before surgery was 36.3 months (range, 1 to 92 months). Symptom progression generally was slow, and surgical intervention was deferred as long as the patient had reading vision in the involved eye. The preoperative visual acuity ranged from 20/50 to 20/200. Each vitrectomy procedure addressed only the presumed major traction element as determined by preoperative and intraoperative findings (Table 2). Thus, the posterior hyaloid was separated from the retina in the 3 eyes with vitreomacular traction associated with stage 1 PVD, ERM was peeled in the 1 eye with clinically evident epiretinal membrane, and a broad layer of cortical vitreous remaining after PVD was identified during surgery and peeled in 1 eye. The ILM was peeled throughout the macular area only in 2 eyes with no other identifiable traction elements (including Patient 6 after a vitreomacular adhesion had been separated during an earlier surgery). Intravitreal gas was used in eyes with foveal detachment or macular hole and also was used in 2 cases without associated features (Table 2). In general, higher concentrations of C3F8 were used in eyes with macular hole or macular detachment. Triamcinolone acetonide was used during surgery as needed to identify cortical vitreous remnants on the retinal surface. No ILM staining agents were used and no intraoperative or postoperative complications developed in any eye, apart from progressive nuclear sclerosis. This tailored surgical approach (which necessitated two procedures in Patient 6) resulted in postoperative visual acuity improvement of at least 2 Snellen lines in all 6 (100%) eyes. The time to best postoperative visual acuity 100

AMERICAN JOURNAL

averaged 8.6 months (range, 2.5 to 18 months). Macular thickening and associated findings resolved completely in 5 (83%) patients and partially in the patient with follow-up of only 6 months. Among the 5 eyes with complete anatomic resolution, the average time to resolution was 12.0 months (range, 1 to 46 months). Over the mean postoperative follow-up period of 43.7 months (range, 6 to 90 months), the best postoperative visual acuity and anatomic results remained stable in all patients except Patient 2, whose final visual acuity declined to 20/300 from complications of advanced glaucoma with filtering surgery and hypotony maculopathy.

DISCUSSION OUR CASE SERIES ADDS FURTHER EVIDENCE CONFIRMING

the hypothesis that myopic traction maculopathy is caused by a relative tautness or noncompliance involving the inner retina as compared with the outer retina, typically within the concavity of a posterior staphyloma. In our patients, and in previously reported case series,6–8,12–16,18–21 schisis-like macular thickening and other pathologic features of myopic traction maculopathy resolved after surgical procedures that removed anatomic structures causing reduced compliance or distensibility of the inner retina. This strongly suggests that tautness of preretinal structures or the ILM is responsible for the gradual stretching of the inner retina away from the outer retina that characterizes the pathoanatomic features in these eyes. It is likely that the anatomic feature predisposing eyes to this condition is the posterior staphyloma.3 That is, in eyes in which the outer retina conforms to the concavity of a posterior staphyloma but relative tautness prevents the inner retina from doing so, the retinal layers would be expected to stretch apart gradually over time, resulting in schisis-like retinal thickening. As suggested by previous authors,1,2,22 other nontractional factors related to high myopia, such as decreased pumping capacity of the retinal pigment epithelium or alterOF

OPHTHALMOLOGY

JANUARY

2012

ations of retinal cell adhesion properties, may play contributing pathogenic roles in this disorder. However, such factors are unlikely to be necessary or sufficient to cause myopic traction maculopathy, because complete resolution of this condition is seen routinely with surgical relief of tangential traction, anteroposterior traction, or both. An important objective of this report is to illustrate that the traction mechanisms responsible for the relative tautness of the inner retina in eyes with myopic traction maculopathy are diverse and vary from one eye to another. We retrospectively determined major traction mechanisms based upon preoperative and intraoperative findings and response to a tailored surgical approach. Within our small case series, we identified the following major traction mechanisms, each of which has been suggested independently by other authors: vitreomacular traction associated with perifoveal PVD,6,18,22 relative noncompliance or nondistensibility of native ILM,13,15,19 –21 ERM,4,14,18,23,24 and remnant cortical vitreous layer after PVD.7 Inner retinal traction from retinal blood vessels is a minor mechanism identified on postoperative OCT images in our series and by other authors.11,12,15 It is evident from the results of our tailored surgical approach and from previous reports that myopic traction maculopathy can be treated successfully by relieving the major traction mechanism identified in a given eye. Thus, removal of obvious preretinal structures such as vitreomacular adhesion associated with perifoveal PVD,6,14, 25,26 ERM,26 or a remnant layer of cortical vitreous after PVD,7 can lead to resolution of macular abnormalities without peeling the ILM. However, our experience and that of other investigators1,2,6,8,19 demonstrates that in certain eyes, no preretinal structures can be identified before or during surgery. In such eyes, relative noncompliance of the inner retina is likely the result of the highly elastic nature of native ILM, which renders it relatively taut (like a drum) and resistant to permanent stretching and deformation.19 Alternatively, it may be the result of microscopic cellular and collagen proliferation on the surface of the ILM that develops after PVD and is not detectable

clinically.21,23,27 In either case, peeling of the ILM in such cases typically results in resolution of the maculopathy.4,10,13,15,16,19 –21,28 This is not unexpected in light of observations that the biomechanical rigidity of the ILM increases with age and that ILM peeling increases retinal compliance by 53.6%.29 Based on the above considerations, a surgeon has 2 options when approaching a patient with visually significant myopic traction maculopathy. A minimalist approach seeks to identify and resolve surgically only the major traction mechanism, leaving the ILM intact in eyes with preretinal traction elements such as vitreomacular adhesion or ERM. This approach avoids the risk of operative complications associated with ILM peeling,7,30 but is unlikely to be successful in every case. Alternatively, a comprehensive approach addresses any apparent preretinal traction elements and also includes ILM peeling in every case. This approach is likely to have the highest singlesurgery success rate, given that native ILM itself may be a significant cause of inner retinal noncompliance in some eyes. ILM peeling also ensures complete removal of all vitreous, cellular, and collagen components that may contribute to current or future tangential traction.23,27 Indeed, our report and others26,28,31 document cases of persistent or recurrent myopic traction maculopathy after vitrectomy without ILM peeling that resolve when reoperation includes ILM peeling. Our impression is that intravitreal gas is a critical component of surgery for myopic traction maculopathy with macular hole, foveal detachment, or both; however, our small series does not permit conclusions regarding its role in cases with retinal thickening alone.15 In summary, our results suggest that myopic traction maculopathy is caused by a relative tautness of the inner retina overlying a posterior staphyloma. The traction mechanisms responsible for noncompliance of the inner retina in this disorder are diverse and vary from one eye to another. Surgical repair of myopic traction maculopathy typically is successful both anatomically and visually when major traction mechanisms are identified and relieved.

THE AUTHORS INDICATE NO FINANCIAL SUPPORT OR PROPRIETARY INTEREST IN THE MATERIAL PRESENTED. DR JOHNSON IS an Independent Data Monitoring Committee member at Oraya and Ophthotech and receives grant support from Regeneron and Thrombogenics. Involved in Design and conduct of study (M.W.J.); Data collection and management (B.V.B.); data analysis and interpretation (M.W.J., B.V.B.); and manuscript preparation and approval (B.V.B., M.W.J.). This study was in compliance with and approved by the University of Michigan Institutional Review Board.

REFERENCES 1. Panozzo G, Mercanti A. Optical coherence tomography findings in myopic traction maculopathy. Arch Ophthalmol 2004;122(10):1455–1460. 2. Wu PC, Chen YJ, Chen YH, et al. Factors associated with foveoschisis and foveal detachment without macular hole in high myopia. Eye 2009;23(2):356 –361. 3. Baba T, Ohno-Matsui K, Futagami, S, et al. Prevalence and characteristics of foveal retinal detachment without macular

VOL. 153, NO. 1

TRACTION MECHANISMS

IN

hole in high myopia. Am J Ophthalmol 2003;135(3): 338 –342. 4. Fang X, Weng Y, Xu S. Optical coherence tomographic characteristics and surgical outcome of eyes with myopic foveoschisis. Eye 2009;23(6):1336 –1342. 5. Takano M, Kishi S. Foveal retinoschisis and retinal detachment in severely myopic eyes with posterior staphyloma. Am J Ophthalmol 1999;128(4):472– 476. 6. Gaucher D, Haouchine B, Tadayoni R, et al. Long-term follow-up of high myopic foveoschisis: natural course and

MYOPIC TRACTION MACULOPATHY

101

7.

8.

9.

10.

11.

12.

13.

14.

15. 16.

17.

18.

19.

20. Ikuno Y, Sayanagi K, Ohji M, et al. Vitrectomy and internal limiting membrane peeling for myopic foveoschisis. Am J Ophthalmol 2004;137(4):719 –724. 21. Kumagai K, Furukawa M, Ogino N, Larson E. Factors correlated with postoperative visual acuity after vitrectomy and internal limiting membrane peeling for myopic foveoschisis. Retina 2010;30(6):874 – 880. 22. Smiddy WE, Kim SS, Lujan BJ, Gregori G. Myopic traction maculopathy: spectral domain optical coherence tomographic imaging and a hypothesized mechanism. Ophthalmic Surg Lasers Imaging 2009;40(2):169 –173. 23. Tang J, Rivers MB, Moshfeghi AA, Flynn HW, Chan CC. Pathology of macular foveoschisis associated with degenerative myopia. J Ophthalmol 2010. Forthcoming. 24. Sayanagi K, Morimoto Y, Ikuno Y, Tano Y. Spectral-domain optical coherence tomographic findings in myopic foveoschisis. Retina 2010;30(4):623– 628. 25. Hirakata A, Hida T. Vitrectomy for myopic posterior retinoschisis or foveal detachment. Jpn J Ophthalmol 2006; 50(1):53– 61. 26. Ratiglia R, Osnaghi S, Bindella A, Pirondini C. Posterior traction retinal detachment in highly myopic eyes: clinical features and surgical outcome as evaluated by optical coherence tomography. Retina 2005;25(4):473– 478. 27. Bando H, Ikuno Y, Choi JS, Tano Y, Yamanaka I, Ishibashi T. Ultrastructure of internal limiting membrane in myopic foveoschisis. Am J Ophthalmol 2005;139(1): 197–199. 28. Futagami S, Inoue M, Hirakata A. Removal of internal limiting membrane for recurrent myopic traction maculopathy. Clin Experiment Ophthalmol 2008;36(8):782– 785. 29. Wollensak G, Spoerl E, Grosse G, Wirbelauer C. Biomechanical significance of the human internal limiting lamina. Retina 2006;26(8):965–968. 30. Gandorfer A, Haritoglou C, Kampik A. Toxicity of indocyanine green in vitreoretinal surgery. Dev Ophthalmol 2008; 42:69 – 81. 31. Sayanagi K, Ikuno Y, Tano Y. Reoperation for persistent myopic foveoschisis after primary vitrectomy. Am J Ophthalmol 2006;141(2):414 – 417.

surgical outcome. Am J Ophthalmol 2007;143(3):455– 462. Spaide RF, Fisher Y. Removal of adherent cortical vitreous plaques without removing the internal limiting membrane in the repair of macular detachments in highly myopic eyes. Retina 2005;25(3):290 –295. Benhamou N, Massin P, Haouchine B, Erginay A, Gaudric A. Macular retinoschisis in highly myopic eyes. Am J Ophthalmol 2002;133(6):794 – 800. Polito A, Lanzetta P, Del Borrello M, Bandello F. Spontaneous resolution of a shallow detachment of the macula in a highly myopic eye. Am J Ophthalmol 2003;135(4):546 –547. Sayanagi K, Ikuno Y, Tano Y. Tractional internal limiting membrane detachment in highly myopic eyes. Am J Ophthalmol 2006;142(5):850 – 852. Ikuno Y, Gomi F, Tano Y. Potent retinal arteriolar traction as a possible cause of myopic foveoschisis. Am J Ophthalmol 2005;139(3):462– 467. Sayanagi K, Ikuno Y, Gomi F, Tano Y. Retinal vascular microfolds in highly myopic eyes. Am J Ophthalmol 2005; 139(4):658 – 663. Ikuno Y, Sayanagi K, Soga K, Oshima Y, Ohji M, Tano Y. Foveal anatomical status and surgical results in vitrectomy for myopic foveoschisis. Jpn J Ophthalmol 2008;52(4):269 –276. Kwok AK, Lai TY, Yip WW. Vitrectomy and gas tamponade without internal limiting membrane peeling for myopic foveoschisis. Br J Ophthalmol 2005;89(9):1180 –1183. Panozzo G, Mercanti A. Vitrectomy for myopic traction maculopathy. Arch Ophthalmol 2007;125(6):767–772. Ikuno Y, Sayanagi K, Ohji M, et al. Vitrectomy and internal limiting membrane peeling for myopic foveoschisis. Am J Ophthalmol 2004;137(4):719 –724. Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages. Am J Ophthalmol 2010; 149(3):371–382. Yeh SI, Chang WC, Chen LJ. Vitrectomy without internal limiting membrane peeling for macular retinoschisis and foveal detachment in highly myopic eyes. Acta Ophthalmol 2008;86(2):219 –224. Kuhn F. Internal limiting membrane removal for macular detachment in highly myopic eyes. Am J Ophthalmol 2003; 135(4):547–549.

102

AMERICAN JOURNAL

OF

OPHTHALMOLOGY

JANUARY

2012