Pathologic Myopia: Complications and Visual Rehabilitation

*Enzo Maria Vingolo, Giuseppe Napolitano and Lorenzo Casillo*

## **Abstract**

High myopia, defined as refractive error of at least −6.00D or an axial length of 26.5 mm or more, can induce many modifications in eye's anatomy that can lead to complications. When high myopia is able to decrease best corrected visual acuity (BCVA) due to its complications, it is called pathologic myopia. Pathologic myopia is one of the major causes of blindness, and it represents a serious issue, since incidence of myopia and high myopia is constantly rising. For educational purposes, in this chapter, complications of pathologic myopia will be divided into anterior (when structures external to the globe or anterior to the ora serrata are involved, such as motility disturbances and cataract) and posterior (when structures posterior to the ora serrata are involved, such as lacquer cracks, chorioretinal atrophy, Fuchs maculopathy, myopic choroidal neovascularization, and retinal detachment). Many treatments are available for pathologic myopia complications depending on their type, such as vascular endothelial growth factor (anti-VEGF) injections and surgery. We will focus on visual rehabilitation interventions, such as visual biofeedback and visual aids that in many cases are the only chance that the ophthalmologist has in order to help patients suffering from pathologic myopia to use at their maximum their residual vision.

**Keywords:** visual rehabilitation, low-vision aids, microperimetry, high myopia, pathologic myopia complications

### **1. Introduction**

Many modifications in normal eye anatomy and structure occur in high myopic patients. Sclera is the most external layer of the eye. In normal nonelongated eyes, scleral thickness decreases from the limbus to the equator, then increasing again to the posterior part of the eye. Normal sclera has also well-known tensile and elastic properties. In highly myopic eyes, these properties are altered with tensile strength reduced and augmented elasticity especially at the posterior pole of the globe. The reason can be searched in the alteration of its ultrastructure (which is more layered and lamellar compared to the normal sclera), in thinning and decreased diameter of the collagen fibers, and also in configuration and conformation of the collagen fibrils. In highly myopic eyes, also a remodeling of the extracellular matrix is observed during the extension of the eyeball, even if its mechanisms are not fully understood. These modifications lead to the fact that in highly myopic eyes, sclera is thinner in the part that goes posterior to the equator, while the anterior part does not show any significative difference with normal eyes. This kind of modification can contribute to the development of many

complications that will be discussed in this chapter. Corneal modifications in high myopic patients are still under debate; some studies reported modifications in corneal biomechanical properties in high myopic patients, such as lower hysteresis. According to some studies [1], highly myopic patients had flatter curvature, modifications in corneal thickness, and decreased endothelial density, while other studies did not report any statistical difference in central corneal thickness (CCT) in various ranges of myopia [2]. Choroid's thickness is significantly reduced in highly elongated eyes; its thickness in foveal and parafoveal portions showed to be inversely proportional to parameters such as patient's age, myopic sferic equivalent, and axial length of the globe, with this last parameter showing to be the most consistently related. Also, distribution of choroidal thickness is altered in these eyes, with temporal and superior regions far from the fovea that show to be thicker than foveal region. Another strong predictor for choroidal thinning in high myopic patients is the presence of a posterior scleral staphyloma [3]. Furthermore, this thinning in choroidal tissue has a negative impact on retinal trophism. With regard to choroidal flow in highly myopic eyes, studies are controversial; for some of them, blood flow in choriocapillaris is augmented, while for others not. It is possible to find differences between high myopic patients and emmetropic ones even in retinal blood flow. Density of the superficial and deep plexus is significatively reduced in high myopic subjects, and the magnitude of this phenomenon is negatively related to axial length and myopic refraction. It is possible to postulate that increasing of the axial length on this eyes can lead to mechanical stretching of ocular structures, leading to damage to retinal pigmented epithelium (RPE), retinal microvascular network, and endothelial cells. Furthermore, in highly myopic eyes, excessive elongation of the globe and tilting of the optic disc can lead to posterior staphylomas formation and the tilting of the optic disc could lead to alterations in macular and foveal morphology, leading to a change in foveal position that can be found moved mainly in the vertical direction. High axial length is associated with many morphologic changes in the optic nerve and peripapillary region. The axial elongation is associated with the enlargement of the optic nerve head and of the peripapillary scleral tissue. The scleral flange is strongly adherent to the lamina cribrosa and axial-elongation-induced scleral enlargement during eye movements. This condition may lead to thinning of the lamina cribrosa, and it may also be associated with the formation of peripapillary choroidal cavitation. Thinning of lamina cribrosa leads to an alteration between intraocular pressure (optic nerve tissue pressure and cerebrospinal fluid pressure) with a steepening of the translamina cribrosa pressure gradient; this may play a role in the development of the glaucomatous optic neuropathy.
