A patient, aged 71 years, with−19 spherical equivalent OS and a progressive decrease in visual acuityin the last 16 months from 20/40 to 20/200. A, Color fundus photograph showingabsence of atrophy or Fuchs spot. Media were completely clear. B, Fluoresceinangiogram showing absence of choroidal neovascularization. C, Optical coherencetomography demonstrates retinal traction with schisis and shallow retinaldetachment.
Types of epiretinal traction andmacular damage (myopic traction maculopathy). A, Epiretinal membrane and retinalthickening. B, Vitreomacular traction and retinal thickening and 2 small cystoidspaces. C, Macular retinoschisis. D, Macular retinoschisis and shallow retinaldetachment. E, Lamellar macular hole.
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Panozzo G, Mercanti A. Optical Coherence Tomography Findings in Myopic Traction Maculopathy. Arch Ophthalmol. 2004;122(10):1455–1460. doi:10.1001/archopht.122.10.1455
To describe the features and incidence of epiretinal traction and relatedretinal damage in degenerative myopia.
Consecutive observational case series.
We retrospectively reviewed medical records and optical coherence tomographyfindings of 218 eyes with high myopia of 121 consecutive patients to detectthe incidence and features of epiretinal traction–related macular damage.The degree of myopia ranged from –8 to –26 spherical equivalent(mean ± SD, –16.93 ± 5.74). Mean ± SD axial lengthwas 29.75 ± 2.12 mm. Excluding eyes with possibly confounding features,125 eyes were analyzed.
Main Outcome Measure
Detection of epiretinal traction and related macular damage.
Epiretinal traction was found in 58 (46.4%) of 125 eyes and retinaldamage, in 43 eyes (34.4%). Macular retinoschisis was the most frequent formof macular damage (25 eyes [58%]), followed by retinal thickening, lamellarhole, and shallow retinal detachment.
Epiretinal traction is a frequent finding in degenerative myopia and,particularly if associated with the presence of staphyloma, can generate aform of macular damage unique to eyes with high myopia. This damage can affectup to one third of these eyes and should be considered as a separate causeof visual loss easily detected by optical coherence tomography at its earlystages.
Degenerative myopia, also called pathologic or high myopia, is definedas a myopic refractive error of more than 6 diopters associated with degenerativefundus changes.1 The main feature of degenerativemyopia is a congenital scleral weakness leading to progressive globe enlargement,axial lengthening, and finally the formation of posterior staphyloma. Followingthis scleral stretching, degenerative changes such as progressive atrophyof the choriocapillaris and choroid, linear ruptures of the Bruch membrane(lacquer cracks), and retinal thinning can occur. Other typical features ofdegenerative myopia are vitreous degeneration and high frequency of peripheralretinal lesions such as lattice degeneration and retinal tears. As a resultof all these degenerative processes, eyes with high myopia are at increasedrisk of visual impairment from rhegmatogenous retinal detachment, progressivechorioretinal atrophy, choroidal neovascular membrane, spontaneous fovealhemorrhage, rupture of the Bruch membrane, and macular hole with or withoutposterior retinal detachment.
Apart from these causes of visual loss in eyes with high myopia, theposterior retina can also be damaged by the presence of traction induced bythe epiretinal membrane (ERM) and/or residual focal vitreoretinal adhesion(vitreomacular traction [VMT]), which in these eyes is combined by the distinctivepresence of posterior staphyloma and progressive global scleral stretching.This unique combination of retinal traction generated by ERM and/or VMT mixedwith the complex and distinctive anatomy of degenerative myopia leads to thefrequent presence in these eyes of macular damage such as retinoschisis, lamellarholes, or shallow detachment2 and may alsoplay an important role in the pathogenesis of macular hole formation and posteriorretinal detachment.
We propose to unify all these pathologic features generated by tractionin the myopic environment under the name of myopic tractionmaculopathy (MTM).
Because of the characteristic and confounding features of the choroid,retina, and vitreoretinal interface in degenerative myopia (ie, tigroid fundus,thin retina, areas of choriocapillaris atrophy, retinal pigment epitheliumhypopigmentation and/or hyperpigmentation, posterior staphyloma, etc), theearly stages of traction maculopathy can be easily underestimated by biomicroscopy,angiography, or ultrasonography, and consequently, its presence can remainundiagnosed.
Optical coherence tomography (OCT) with cross-sectional images of retinalstructure greatly facilitates the study of the posterior vitreoretinal anatomyin eyes with high myopia and allows the detection of subtle macular changesthat are otherwise undetectable (Figure 1).
The purpose of this study is to describe the incidence and featuresof macular abnormalities related to traction in a healthy population of 121patients with eyes with high myopia analyzed by OCT.
From April 2001 to May 2002, we examined with OCT all the eyes of allpatients with high myopia who came to us for routine examination. Patientsin the study could be asymptomatic or have vision loss. We examined 218 eyesof 121 consecutive patients, 41 men (33.88%) and 80 women (66.12%) with amean ± SD age of 59.24 ± 14.99 years (median, 59 years). Thedegree of myopia ranged from –8 to –26 spherical equivalent (mean± SD, –16.93 ± 5.74; median, −17.5). The mean ±SD axial length was 29.75 ± 2.12 mm.
All eyes had 1 or more chorioretinal features typical of degenerativemyopia (ie, tigroid fundus, stretched vascular arcades, peripapillary andchorioretinal atrophy, posterior staphyloma, and lacquer cracks). Prior toOCT scan, each eye underwent a complete ophthalmic evaluation.
All patients obtained and signed an informed consent prior to examination.Institutional review board approval was not requested for this study.
Because the major goal of this study was to investigate in a healthymyopic population the presence of epiretinal and/or vitreoretinal tractionand related macular damage, we excluded from analysis all eyes with possibleconfounding features such as concomitant ophthalmic pathologic conditionsother than myopia and eyes with Fuchs spots, active choroidal neovascularization(determined by fluorescein angiography), or acute visual loss for posterioror diffuse retinal detachment visible at biomicroscopy. Eyes with pseudophakiathat had or had not undergone Yag laser capsulotomy or eyes that had undergoneperipheral laser or cryopexy treatments were included. A total of 125 (55.5%)of 218 eyes were analyzed.
Among this "healthy" myopic population, we considered patients as symptomaticif they described in 1 or 2 eyes a "worsening" in visual function in the last6 months. We defined this worsening as increased metamorphopsia with a decreasein visual acuity equal to or greater than 2 lines on a Snellen chart, unexplainedby media opacities or changes on fluorescein angiography. Patients were consideredasymptomatic if they described stable vision for at least 2 years or minimalrecent changes. Any previous peripheral laser or cryopexy treatment was recorded.
Optical coherence tomography (Zeiss-Humprey, San Leandro, Calif), basedon the principle of low-coherence interferometry, provides cross-sectionalimages of ocular structures and measurement of retinal thickness with a resolutionof 10 µm. This resolution is superior to other imaging techniques suchas scanning laser ophthalmoscopy (300-µm resolution), B-mode ultrasonography(150-µm resolution), and ultrasound biomicroscopy (20-µm resolution).3
The same observer (A.M.) performed all OCT examinations. We tried tooptimize OCT imaging by obtaining maximal pupil dilation and maintaining agood tear film with frequent blinking or with application of artificial tears.
We used the following OCT scanning techniques:
Two 3-mm "line group" scans, centering the fovea,at 0° and 90°.
Two 7-mm line group scans, one vertical centeredon the fovea and the other starting from the optic disc to the fovea, to explorethe borders of the staphyloma (when present).
Six 6-mm "radial lines" scans centered on the fovea,1 scan every 30°, for complete evaluation of the posterior pole.
The analysis of OCT images was focused on the presence of epiretinaltraction and on changes in retinal structure.
Epiretinal traction was subdivided into 2 groups:
a. Epiretinal membrane: tangential tractionfrom overlying ERM often with multifocal attachments (Figure 2A).
b. Vitreomacular traction: anteroposteriortraction from incomplete vitreomacular separation (Figure 2B).
Retinal damage was classified as follows:
a. Retinal thickening: foveal thickness >200µm (With OCT, the mean ± SD nonmyopic normal adult foveal thicknessis 150 ± 20 µm.4-6)with or without cystoid macular changes (Figure 2A and B).
b. Macular retinoschisis: separation of theneurosensory retina into 2 or more layers (Figure 2C).
c. Retinal detachment: shallow neuroepithelialdetachment (Figure 2D).
d. Lamellar macular hole: partial thicknessmacular hole (Figure 2E).
Each of these categories of epiretinal traction and/or intraretinaldamage could be present in isolation or in combination with others. When appropriate,the data were statistically compared using a χ2 test.
The results of the analyzed sample of 125 eyes are summarized in Table 1. Epiretinal traction was notedin 58 eyes (46.4%). The most frequent form of traction was ERM, found in 31eyes (24.8%), while a mixed form of tangential (ERM) and anteroposterior (VMT)traction was present in 16 eyes (12.8%). Eleven eyes (8.8%) had VMT alone.
Retinal damage was present in 43 eyes (34.4%). Macular retinoschisis,isolated or associated with other lesions, was the most frequent form of damage,identified in 25 eyes (20.0%). Ten eyes (8.0%) had macular thickening, 6 eyes(4.8%) had a lamellar macular hole, and 2 eyes (1.6%) had an isolated shallowretinal detachment. In 53 (42.4%) of 125 eyes a staphyloma was present.
Retinal damage was most often associated with the presence of epiretinaltraction as summarized in Table 2.Of 43 eyes with a form of retinal damage, 36 eyes (83.7%) had an associatedepiretinal traction, isolated (16 eyes [37.2%]) or combined with staphyloma(20 eyes [46.5%]). Only 7 eyes (16.2%) with retinal damage had a posteriorstaphyloma without epiretinal traction. Table 2 also presents the relationship between each form of retinaldamage and the presence of epiretinal traction and/or staphyloma.
In our series, 9 eyes had previous peripheral treatment for latticedegeneration or atrophic breaks (7 laser, 2 cryopexy). Four of these eyes(3 laser, 1 cryopexy) had macular retinoschisis.
Of 121 patients (125 eyes) included in the study, 23 (19%) were judgedto be symptomatic (see earlier description) in one eye. Only 6 (26.1%) ofthese 23 eyes had no abnormalities on OCT, while 17 (73.9%) had some macularanomalies; 14 had a form of retinal abnormality, mostly retinoschisis, and3 had an epiretinal traction not associated with other macular lesions. Onthe contrary, of 43 eyes with retinal abnormalities, only 14 (32.5%) werejudged symptomatic. The relationship between macular abnormalities and symptomsare summarized in Table 3.
It is well known that myopic macular holes can be complicated by developmentof extensive retinal detachment.7-9 Thisunusual natural history for macular holes is probably determined by the combinationof epiretinal and/or anteroposterior traction with the unique presence ofposterior staphyloma7,10-12 andprobably also a weak retinal pigment epithelium–photoreceptor adherence.13 The clinical anatomy preceding and leading to thispathologic event has not been studied extensively.
In 1985, Green1 reported in histopathologicstudies of eyes with high myopia the presence of so-called stretch schisisin the peripheral retina. These studies did not identify internal membranesor focal inner retinal traction in these areas, and this retinal splittingwas related to low elasticity of some retinal components, mainly blood vesselsand internal limiting membrane, that cannot follow the progressive scleralstretching and elongation so pronounced in some of these eyes.
Although back in 1938, Rochon-Duvigneaud14 reportedsimilar findings in the posterior pole, it is only recently that Takano andKishi,2 using OCT, demonstrated in vivo thefrequent presence of posterior retinoschisis and shallow macular detachmentin eyes with degenerative myopia. Their findings were confirmed in 21 eyesby Benhamou et al.15 Takano and Kishi relatedthese findings with the formation of macular hole and hypothesized that inthese eyes, posterior retinal detachment precedes the formation of the hole,without speculating about the relative importance of "internal" traction combinedwith posterior staphyloma in the determination of posterior macular detachmentin the presence of macular hole in eyes with high myopia.
In this study, we analyzed a sample of 125 eyes of 121 consecutive patientswith degenerative myopia on routine examination with no symptoms or with onlymild visual impairment in the last months (see earlier definition of symptomatic). This sample could therefore well representa "healthy" myopic population. Using the high resolution of OCT and excludingactive or fibrotic choroidal neovascularization or other possibly confoundingpathologic conditions, we looked in these eyes for the presence of early andotherwise undetectable epiretinal traction or retinal abnormalities.
The results of our study were partially unexpected; almost half of thispopulation (58 eyes [46.4%]) revealed at OCT examination an epiretinal tractiondetermined by ERM or VMT, and one third of eyes (43 [34.4%]) had a form ofretinal damage (Table 1).
In the presence of epiretinal traction, the posterior retina in degenerativemyopia lies in a peculiar and unstable condition determined by 2 oppositeforces: (1) epiretinal membranes and vitreomacular adhesions generate a centripetaland/or internal traction, while (2) staphyloma and progressive scleral stretching,although not being an active form of traction, generate an external forcethat greatly enhances the internal traction. The retinal damage produced bythis unique combination is therefore much more profound compared with thedamage caused by epiretinal membranes or vitreomacular traction in eyes withoutmyopia.
Because of the distinct features and clinically significant effect onretinal tissue and visual function, we have to consider this condition separatelyfrom the epiretinal traction syndromes found in eyes without myopia. Withthe purpose of unifying all the possible features of myopic macular damagefrom traction under a single name, we propose to call this syndrome myopic traction maculopathy (MTM).
Identification of the early stages of MTM is difficult with commonlyavailable diagnostic techniques and tools. With biomicroscopy, a clear viewof the vitreoretinal interface usually is precluded by the absence of a uniformretinal pigment epithelial background. The image is distorted by the posteriorstaphyloma and media opacities. There often are zones of chorioretinal atrophy,retinal pigment epithelial hyperplasia, or subretinal fibrosis, and the retinacan be thinner than normal.
The subtle and early retinal changes generated by traction can be alsoinvisible by stereoangiography (Figure 1)because they do not create vascular abnormalities and are also under the resolvingpower of ultrasonography.
With these tools, only the most advanced stages of MTM can be diagnosed,when retinoschisis cavities or neuroepithelial detachment are wide and elevatedor when a macular hole with or without retinal detachment has already developed.As demonstrated by Gallemore et al,16 OCT ismuch more sensitive than biomicroscopy in detecting subtle internal retinalchanges, and especially in the unusual and often variegate fundus photographsof eyes with degenerative myopia, OCT can greatly contribute to the fine analysisof the retinal structure through cross-sectional images with a resolutionof about 10 µm.
In our series, we found a form of retinal damage in one third of cases(43 eyes [34.4%]). The most frequent abnormality was macular retinoschisis(25 eyes), alone or associated with other lesions (Table 1). Such a high frequency of retinal damage in a myopic populationcorresponds to the 34% reported by Takano and Kishi2 ina smaller sample (32 eyes).
In their recent report, Baba et al17 divided134 eyes with high myopia into 2 groups according with the presence or absenceof staphyloma. They reported 7 cases of foveal detachment (prevalence of 9%)only in the group with staphyloma. Two of these eyes had the contemporarypresence of foveal detachment and retinoschisis. In our sample of 125 eyes,we found an even smaller percentage of isolated shallow detachment, only 2cases (1.6%), and even in our sample, both of these eyes had a posterior staphyloma.On the contrary, we report a much higher presence of retinoschisis (25 eyes[20%]), isolated or often combined with focal and shallow detachment (Table 1). Of these 25 eyes, 17 (68%) hada posterior staphyloma, and 7 (32%) had only a form of epiretinal traction.This difference may be partially related to some differences in judgment regardingthe presence or absence of staphyloma, sometimes arbitrary in these very longeyes, or to the interpretation of the OCT scan. In our sample, retinoschisishad a much higher prevalence, and we have no explanation for this difference.
Only about one third of macular abnormalities found in our sample wereassociated with symptoms (Table 3),probably because visual impairment in eyes with myopia is multifactorial andthese lesions may represent a chronic condition. In almost all the patientswho had a progressive decrease in visual function unexplained by media opacitiesor changes in fluorescein angiography, we found a form of macular damage orepiretinal traction (Table 3).
Although it is possible other factors contributed to the cause of visualimpairment in addition to MTM (amblyopia, chorioretinal atrophy, lacquer cracks,etc), the results of this study suggest that MTM should be considered a frequentabnormality in degenerative myopia and a possible cause of decreasing visualfunction.
Almost half the eyes in this study (58 [46.4%]) revealed at OCT a formof epiretinal traction in the macular area, tangential (ERM) and/or anteroposterior(VMT) to the inner retinal surface. This unexpected high frequency of epiretinaltraction is higher than in eyes without myopia. Although in our series a posteriorstaphyloma was present in 53 eyes, just 7 (16.2%) of the 43 eyes with retinaldamage were only associated with staphyloma, and 36 of these eyes (83.7%)were associated with the presence of epiretinal traction, isolated or in combinationwith a staphyloma. These findings suggest that this form of retinal damageis mainly related to epiretinal tractional forces and then enhanced by thepresence of staphyloma and retinal stretching due to progressive scleral elongation.
Polito et al18 in their recent case reportsupport this hypothesis, describing the resolution of retinoschisis in aneye with myopia following spontaneous vitreofoveal separation.
This study does not give information about the natural history of MTM,but from observation of some patients with bilateral myopia who had a stablemacular retinoschisis in one eye and a macular hole with posterior retinaldetachment in the fellow eye, we can speculate that in degenerative myopia,macular holes and MTM could represent 2 possible evolutions of the same tractionaldisorder, depending on depth, width, and shape of staphyloma and degree oftangential or anteroposterior traction.
The results of our study and the relationships between retinal damageand epiretinal traction seem to indicate that in the case of symptomatic patients,vitrectomy may have a positive effect on vision by releasing this traction,stopping the progression of macular damage such as retinoschisis, and possiblyreducing or eliminating shallow posterior retinal detachment.
In summary, in this large case series, we demonstrated that retinalabnormalities in the macular area can be a frequent finding in eyes with degenerativemyopia. Epiretinal traction probably plays a major role in this condition,especially if combined with staphyloma. Optical coherence tomography can greatlycontribute in the examination of eyes with high myopia and may even show abnormalitiesin asymptomatic cases.
Correspondence: Giacomo Panozzo, MD, Via del Perlar 2, 37135 Verona,Italy (firstname.lastname@example.org).
Accepted for publication May 27, 2004.
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