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Pathologic Myopia

Ohno-Matsui, Kyoko MD, PhD

The Asia-Pacific Journal of Ophthalmology: November/December 2016 - Volume 5 - Issue 6 - p 415–423
doi: 10.1097/APO.0000000000000230
Review Article
Free

Pathologic myopia (PM) is the only myopia that causes the loss of best-corrected visual acuity. The main reason for best-corrected visual acuity loss is complications specific to PM, such as myopic maculopathy, myopic traction maculopathy, and myopic optic neuropathy (or glaucoma). The meta-analyses of the PM study group (META-PM study) made a classification system for myopic maculopathy. On the basis of this study, PM has been defined as eyes having atrophic changes equal to or more severe than diffuse atrophy. Posterior staphyloma and eye deformity are important causes of developing vision-threatening complications. Posterior staphyloma is unique to PM, except for inferior staphyloma due to tilted disc syndrome. It is defined as an outpouching of the wall of the eye that has a radius of curvature that is less than the surrounding curvature of the wall of the eye. The mechanical load onto the important region for central vision (optic nerve and macula) is not comparable between eyes with and without posterior staphyloma. Three-dimensional magnetic resonance imaging is a powerful tool to analyze the entire shape of the eye. When ultra-widefield optical coherence tomography is available, it is expected to be a new tool that will surpass 3-dimensional magnetic resonance imaging. In the future, preventive therapies targeting staphyloma and eye deformity are expected before vision-threatening complications develop and it is too late for patients.

From the Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo, Japan.

Received for publication May 6, 2016; accepted June 26, 2016.

The author has no funding or conflicts of interest to declare.

Reprints: Kyoko Ohno-Matsui, MD, PhD, Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 1138519, Japan. E-mail: k.ohno.oph@tmd.ac.jp.

Pathologic myopia (PM) is different from other types of myopia in the sense that PM causes the loss of best-corrected visual acuity (BCVA), not only the loss of uncorrected visual acuity. It has been reported that PM is a major cause of BCVA loss in the world, especially in east Asian countries.1–5 However, the definition of PM has been inconsistent among studies. In most of the earlier epidemiological studies, refractive error [<−5.0 diopters (D), <−6.0 D, and −8.0 D] or axial length (≥26.0 and ≥26.5 mm) or a combination of both was used to define “pathologic myopia.” However, a definition based on refractive error or increased axial length is considered to show just a “high degree of myopia.” In addition, there has been no clear evidence why these cutoff values were chosen.

In other studies, the presence of myopic maculopathy (sometimes called myopic retinopathy) was used to define PM.6–8 In these studies, myopic retinopathy was defined to include the following specific signs: posterior staphyloma, lacquer cracks, Fuchs spot, and myopic chorioretinal thinning or atrophy. However, the most common type of staphyloma is a wide one beyond the 50 degrees of conventional fundus photos. Thus, it seems difficult to diagnose staphyloma in 50-degree fundus photos. In addition, staphyloma may be a cause of developing maculopathy and is not considered a lesion of myopic maculopathy.

These strongly suggest the necessity of a standardized definition of PM. This could enable a direct comparison between studies and finally could establish a systematic approach to prevent BCVA loss due to PM worldwide.

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DEFINITION OF PM

Pathologic myopia is defined as the presence of myopic maculopathy equal to or more severe than diffuse chorioretinal atrophy. Myopic maculopathy includes diffuse chorioretinal atrophy, patchy chorioretinal atrophy, lacquer cracks, myopic choroidal neovascularization (myopic CNV), and CNV-related macular atrophy (Fig. 1).9 Characteristics of each lesion will be described in detail later.

FIGURE 1

FIGURE 1

Recently, an international panel of myopia researchers reviewed previously published studies and classifications and proposed a simplified, uniform classification system for PM for use in future studies.10 In this simplified system (META-PM classification), myopic maculopathy lesions are divided into 5 categories: “no myopic retinal lesions” (category 0), “tessellated fundus only” (category 1), “diffuse chorioretinal atrophy” (category 2), “patchy chorioretinal atrophy” (category 3), and “macular atrophy” (category 4). These categories were defined on the basis of long-term clinical observations regarding the progression patterns and risk of myopic CNV development for each stage. Three additional features were added to these categories and were included as “plus signs:” (1) lacquer cracks, (2) myopic CNV, and (3) Fuchs spot. The reason for separately defining these plus signs is that these 3 lesions have been shown to be strongly associated with central vision loss, but they do not fit into any particular category and may develop from, or coexist, in eyes with any of the categories of myopic maculopathy described above. According to the META-PM study, PM is defined as myopic maculopathy category 2 or above, or the presence of staphyloma.10,11

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POSTERIOR STAPHYLOMA: A CAUSE OF PM-RELATED COMPLICATIONS

Posterior Staphyloma and Eye Deformity

A staphyloma is defined as “an outpouching of the wall of the eye that has a radius of curvature that is less than the surrounding curvature of the wall of the eye” (Fig. 2), as reported by Spaide in Pathologic Myopia.12 It is still common for authors to refer to abnormalities in the posterior pole of myopic eyes, even those that do not involve an outpouching, as being staphylomas.

FIGURE 2

FIGURE 2

Posterior staphyloma is unique to PM, except for inferior staphyloma due to tilted disc syndrome. Thus, the presence of posterior staphyloma strongly suggests the presence of PM. Within the area of posterior staphyloma, the sensory retina, retinal pigment epithelium (RPE), choroid, and optic disc are stretched, causing mechanical damage.

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Curtin Classification

In 1977, Curtin13 classified posterior staphylomas in eyes with PM into 10 different types (Fig. 3). Types I to V were considered primary staphylomas, and types VI to X were combined staphylomas. However, this classification was made from the ophthalmoscopic appearances and fundus drawings, which made the classification subjective. In addition, some of the types are rare—especially VI, VIII, and X—and recent studies using optical coherence tomography (OCT) showed that there are more complex irregularities of the scleral curvature14–17 within the area of a staphyloma than Curtin13 noted.

FIGURE 3

FIGURE 3

Interestingly, there is wide variation in axial length in the same type of staphyloma. In type I staphyloma (the most common staphyloma), axial length ranged from 25.1 to 38.0 mm. On the basis of these data, Curtin concluded that refractive error or axial length was not a reliable indicator to define PM, and PM should be defined by the presence of posterior staphyloma. Wang et al18 recently described features of posterior staphyloma seen in eyes with axial length less than 26.5 mm, supporting Curtin’s conclusion.

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Ohno-Matsui Classification

In eyes with deep staphyloma, the curvature of the eye peripheral to staphyloma tends to be flattened. Thus, the formation of staphyloma is not continuous from axial elongation, and a marked change of the shape of the entire globe is considered to occur parallel with staphyloma development.

To analyze the shape of the entire eye, Moriyama et al19,20 established a technique called 3-dimensional magnetic resonance imaging (3D MRI). Volume renderings of the T2-weighted MRI images were done, and the margins of globes were then identified. The 3D MRI technique was found to be well suited to examining eye shape over a wide area that could encompass even a large posterior staphyloma. The presence and types of staphylomas were determined by the entire eye shape on 3D MRI scans. Figure 4 shows representative 3D MRI images of an emmetropic eye and a severely deformed eye with PM. On the basis of 3D MRI images, the eye shapes of PM were classified into 4 types: nasally distorted shape, temporally distorted shape, cylinder shape, and barrel shape.

FIGURE 4

FIGURE 4

Although 3D MRI is a powerful tool to analyze the shape of the eye, it is difficult to perform 3D MRI routinely in a large series of patients. To overcome this issue, Ohno-Matsui21 focused on ultra-widefield fundus imaging and found that pigmentary abnormalities or abnormal reflectance along the staphyloma border in widefield fundus images can predict the presence and types of staphyloma depicted by 3D MRI (Fig. 5). Ohno-Matsui21 simplified the classification into 6 types, renamed according to the extent of staphyloma: wide macular, narrow macular, peripapillary, nasal, inferior, and others (Fig. 6). In an analysis using a combination of 3D MRI and widefield fundus imaging, the most predominant type was wide macular staphyloma, followed by narrow macular staphyloma.

FIGURE 5

FIGURE 5

FIGURE 6

FIGURE 6

Unfortunately, the scan length of currently available OCT machines is not long enough to cover the extent of wide macular staphyloma. However, because of advances in OCT technology, ultra-widefield OCT could become a powerful tool to determine the presence and type of posterior staphyloma in the near future.

Because posterior staphyloma is an important feature and the ideal treatment strategies to prevent BCVA loss should target staphyloma, defining PM based on the presence of staphyloma by using ultra-widefield OCT would be expected.

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DETAILED CHARACTERISTICS OF MYOPIC MACULOPATHY LESIONS

Diffuse Chorioretinal Atrophy

Because PM is defined by the presence of atrophy equal to or more severe than diffuse atrophy, the proper diagnosis of diffuse atrophy is clinically important. Diffuse chorioretinal atrophy (Fig. 7) can be identified by the yellowish-white appearance of the posterior pole. The extent of the diffuse atrophy may vary from a restricted area around the optic disc and part of the macula to the entire posterior pole. The area of atrophy generally first appears around the optic disc, often increasing with age, and finally covers the entire area within the staphyloma. Both age and axial length have been described as risk factors for the development of diffuse atrophy.22 Yokoi et al recently found that peripapillary diffuse atrophy was an important indicator in children to predict eventual PM in adults.

FIGURE 7

FIGURE 7

Marked thinning of the choroid in the area of diffuse atrophy can be appreciated on OCT, with occasional sporadic large choroidal vessels remaining (Fig. 7). The choroid is disproportionally thinned compared with the thinning of retina and sclera. This extreme thinning of the choroid is a fundamental characteristic for diffuse atrophy (and also for PM).

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Patchy Chorioretinal Atrophy

Patchy chorioretinal atrophy (Fig. 8) appears as a well-defined, grayish-white lesion(s) in the macular area. Patchy chorioretinal atrophy is characterized by a complete loss of choriocapillaris and can progress to the absence of outer retina and RPE. Recent analyses using the most updated swept-source OCT showed that patchy atrophy was not simply chorioretinal atrophy but was Bruch membrane hole, as shown for the peripapillary gamma zone23 and for myopic CNV-related macular atrophy.24 Because of the inherent elasticity of the Bruch membrane, once a defect is created, it would be expected to increase over time.

FIGURE 8

FIGURE 8

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Lacquer Cracks

Lacquer cracks (Fig. 9) appear as yellowish linear lesions in the macula. They can often be seen to crisscross over the underlying choroidal vessels. Lacquer cracks are believed to represent mechanical breaks of the Bruch membrane.7,22,25,26 They may appear as linear horizontal or vertical cracks or exhibit a crisscrossing pattern.27 Lacquer cracks show clear hyperfluorescence on fluorescein angiogram and show hypofluorescence in the late phase of indocyanine green angiography. It is difficult to detect this lesion with OCT, mainly because the lesion is too narrow. Thus, it is not clear whether ophthalmoscopically observed lacquer cracks truly represent Bruch membrane rupture. When lacquer cracks are newly formed, simple macular bleeding is observed. This hemorrhage is spontaneously absorbed, and lacquer cracks are observed later.

FIGURE 9

FIGURE 9

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Myopic CNV

Myopic CNV (Fig. 10) is a common cause of the loss of central vision in patients with PM. On the basis of published studies, it has been estimated that the prevalence of myopic CNV ranges from 5% to 11% among individuals with high myopia.22,28–30

FIGURE 10

FIGURE 10

Optical coherence tomography is useful for the detection of myopic CNV. Exudative changes around the CNV tend to be milder than CNV due to age-related macular degeneration.

On clinical examination, myopic CNV typically appears as a flat, small, grayish subretinal lesion beneath or near the fovea with or without hemorrhage. There are usually minimal subretinal fluid or exudative changes associated with myopic CNV. The diagnosis of myopic CNV can be confirmed by fluorescein angiogram and spectral domain OCT. Fluorescein angiogram findings in myopic CNV usually demonstrate well-defined hyperfluorescence in the early phase, with a classic CNV pattern of leakage in the late phase. Spectral domain OCT has the advantage of being noninvasive and fast to perform.

Antiangiogenesis treatment with intravitreal antivascular endothelial growth factor (anti-VEGF) therapy has become the standard-of-care first-line treatment for myopic CNV.31 Two large multicenter, double-masked, randomized, controlled clinical trials have been performed to evaluate the use of anti-VEGF therapy for myopic CNV.32,33 The RADIANCE [the ranibizumab and photodynamic therapy (verteporfin) evaluation in myopic CNV] study was a 12-month clinical trial that randomized 275 patients to 2 regimens of intravitreal 0.5 mg ranibizumab versus verteporfin photodynamic therapy for the treatment of myopic CNV.32 In the MYRROR study, the use of intravitreal 2 mg aflibercept was compared with a sham control group for the treatment of myopic CNV.33 Both studies showed the effectiveness of anti-VEGF therapy for myopic CNV.

Several studies have evaluated the long-term outcomes of anti-VEGF therapy for myopic CNV. In a retrospective study by Lai et al,34 37 treatment-naive eyes of 37 patients with subfoveal myopic CNV were treated with intravitreal bevacizumab or ranibizumab and were observed for at least 2 years. Mean logMAR visual acuity improved significantly from 0.86 to 0.48. The mean visual improvement at 2 years was 2.8 lines for the bevacizumab group and 5.1 lines for the ranibizumab group, but the difference was not statistically significant. Oishi et al35 further evaluated the use of intravitreal bevacizumab in 22 eyes with myopic CNV, and patients were observed for at least 4 years. After intravitreal bevacizumab treatment for myopic CNV, significant visual improvements were observed at 1, 2, and 3 years. The improvement in visual acuity became marginally nonsignificant at 4 years after treatment. The main reason for the slight decline in visual improvement at 4 years might be related to CNV-related macular atrophy. A recent study by Ruiz-Moreno et al,36 which evaluated the 6-year outcome of anti-VEGF therapy in 97 patients with myopic CNV, showed that visual acuity improvement after bevacizumab or ranibizumab treatment was no longer significant after 4, 5, and 6 years. Further studies are necessary to examine whether anti-VEGF therapy is effective in the long-term.

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Choroidal Neovascularization–Related Macular Atrophy

After the regression of myopic CNV with or without anti-VEGF therapy, well-defined macular atrophy gradually develops around the scarred CNV. This is known as myopic CNV-related macular atrophy (Fig. 11) and is the main cause of long-term decreased vision in patients with myopic CNV. A recent study using swept-source OCT showed that myopic CNV-related macular atrophy was also a Bruch membrane hole,37 like patchy atrophy. These suggest that Bruch membrane holes might be a common hallmark of lesions of myopic maculopathy.

FIGURE 11

FIGURE 11

The site where myopic CNV penetrates into the retina is originally a Bruch membrane hole. In eyes with PM, consistent mechanical tension is loaded on the area within staphyloma. When the penetrating site is not fully regenerated, the Bruch membrane hole continues to enlarge and ends up becoming CNV-related macular atrophy. Thus, approaches to prevent the enlargement of the Bruch membrane hole are necessary to truly improve long-term vision for patients with myopic CNV.

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OTHER COMPLICATIONS

Myopic Traction Maculopathy

Takano and Kishi38 first demonstrated foveal retinal detachment and retinoschisis in severely myopic eyes with posterior staphyloma using OCT. Panozzo and Mercanti39 proposed the term myopic traction maculopathy (MTM; Fig. 12) to encompass various findings with traction on OCT in highly myopic eyes. Myopic traction maculopathy includes retinoschisis, foveal retinal detachment, lamellar or full-thickness macular hole, and/or macular detachment.40 Optical coherence tomography is an indispensable tool for diagnosing MTM.

FIGURE 12

FIGURE 12

Shimada et al41 have classified MTM according to its location and extent from S0 through S4: S0, no retinoschisis; S1, extrafoveal; S2, foveal; S3, both foveal and extrafoveal but not the entire macula; and S4, the entire macula. Shimada et al further defined the progression as an increase of the extent or height of retinoschisis (more than 100 μm) or the development of an inner lamellar macular hole, foveal detachment, or full-thickness macular hole.41 They reported progression during a mean follow-up of 36.2 months in 24 (11.6%) of 207 eyes, which included 0.9% who progressed to full-thickness macular hole and 3.4% who progressed to foveal detachment. The eyes with extensive macular retinoschisis (S4) showed progression significantly more (42.9%) than eyes having less extensive macular retinoschisis areas (6.7%). Six (21.4%) of 28 eyes with S4 MTM progressed to foveal detachment.

The formation of full-thickness macular hole is a serious complication during and after vitrectomy for MTM. A foveolar internal limiting membrane–sparing technique was used in an attempt to reduce the development of macular hole after vitrectomy, which is a severe complication that results in poor visual recovery. Several studies showed good visual and anatomic outcomes with this technique.42–44

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Myopic Optic Neuropathy or Glaucoma

The papillary and peripapillary regions of eyes with PM are distorted by the mechanical stretching of the globe. After marked mechanical stretching and distortion of the papillary and peripapillary regions, structural abnormalities occur. Using swept-source OCT, Ohno-Matsui et al45 found pit-like clefts at the outer border of the optic disc or within the adjacent scleral crescent in 32 (16.2%) of 198 highly myopic eyes but none in emmetropic eyes. The pits were located either in the optic disc area, in the optic disc pits, or in the conus area and conus pits, outside the optic disc. The optic disc pits were associated with discontinuities of the lamina cribrosa, whereas the conus pits seemed to develop from a scleral stretch-associated schisis or emissary openings for the short posterior ciliary arteries in the sclera. The nerve fiber tissue overlying the pits was discontinuous at the site of the pits, and this might explain the cause of visual field (VF) defects in highly myopic eyes in some cases. The location of the conus pits might partly explain why the papillomacular bundles tend to be damaged in highly myopic eyes. Peripapillary intrachoroidal cavitation was observed as yellowish-orange lesions located most typically inferior to the optic disc in highly myopic eyes.46,47

Visual field findings are difficult to interpret in eyes with PM. They usually have a large conus together with various extents of myopic maculopathy, which make the analyses and interpretations of automated VF examinations difficult. To overcome the disadvantage of the Humphrey 30-2 automated VF test, Ohno-Matsui et al17 used Goldmann kinetic perimetry and reported that the incidence of significant VF defects in myopic eyes was significantly higher in eyes with an oval optic disc than that in eyes with a round optic disc. During a mean follow-up of 10.2 ± 3.4 years, 73.8% of eyes had significant progression of VF defects.

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Dome-Shaped Macula

Dome-shaped macula (DSM; Fig. 13) was first described by Gaucher et al14 in eyes with myopic posterior staphyloma. A characteristic inward bulge inside the chorioretinal posterior concavity of the eye in the macular area was noted in 15 eyes. Subsequent imaging studies by Imamura et al48 demonstrated that the bulge is associated with a local thickening of the subfoveal sclera.

FIGURE 13

FIGURE 13

Liang et al15 reported the prevalence of DSM was 20.1% in a cohort of 1118 eyes in Japanese patients with high myopia. Recently, the prevalence of DSM was evaluated in the RADIANCE study, which recruited 277 eyes with myopic CNV, and DSM was present in 18% of patients.49 Ellabban et al50 reported the macular complications occurring in eyes with DSM, such as CNV and serous retinal detachment.

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CONCLUSIONS

According to the definition by the META-PM study, PM is easily identified in fundus photos by the presence of diffuse atrophy. This standardized definition enables the direct comparison of the prevalence of PM between races in epidemiological studies. Peripapillary diffuse atrophy is an important indicator to show whether children will eventually develop PM as adults. In the near future, ultra-widefield OCT is expected to become a powerful tool to analyze eye deformities, surpassing 3D MRI techniques. Preventive therapies targeting staphyloma and eye deformities are expected before vision-threatening complications occur.

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Try to be a rainbow in someone’s cloud.

— Maya Angelon

Figure

Figure

Keywords:

pathologic myopia; posterior staphyloma; myopic maculopathy; myopic optic neuropathy; 3D MRI

© 2016 by Asia Pacific Academy of Ophthalmology