**2. Pathogenesis**

Before the advent of OCT, the anatomic features of MTM were not described and the pathogenesis was poorly understood. Both TD-OCT and SD-OCT studies have provided an invaluable contribution to the characterization and understanding of the underlying pathologic mechanism involved in MTM. There are four major traction mechanisms identified in MTM: (1) Peri foveal vitreomacular traction (2) Cortical vitreous remnants after (PVD) development (3) Epiretinal membrane formation (4) Intrinsic non-compliance of the internal limiting membrane (ILM) and inner retina to conform to the shape of the posterior staphyloma [14, 15]. The first three mechanisms constitute the extrinsic forces (outside the retina) responsible for MTM while the stiff ILM and inner retinal layers constitute the intrinsic force (within the retina) responsible for MTM formation. The ILM itself can cause traction in eyes with posterior staphyloma.

#### **Figure 1.**

*Mechanisms causing MTM. (a) MTM caused by vitreomacular traction with presence of foveal retinal detachment (FRD). (b) Epiretinal membrane causing schisis-like retinal thickening with associated FRD. (c) MTM with no apparent preretinal membranes. (d) Tenting of the inner retina at the retinal arteriole (black arrow) with complete resolution of the retinal thickening following vitrectomy in MTM.*

**111**

**Table 1.**

*OCT Findings in Myopic Traction Maculopathy DOI: http://dx.doi.org/10.5772/intechopen.83766*

surgical approach in these eyes (**Figure 1**).

also be identified with use of OCT.

**4. Staging and classification**

macular involvement (**Table 1**).

**3. Diagnosis**

It appears that in eyes without identifiable preretinal tractional elements, ILM peeling resolves the retinal thickening. There are two possible explanations: One is that the ILM is highly elastic and tough, rendering it taut like a drum. In eyes with posterior staphyloma, the ILM is like the surface of a drum and is relatively resistant to permanent deformation and stretching. The second, more probable, explanation is that microscopic cellular and collagen proliferation develops on the ILM surface after PVD causing the ILM to be less distensible and making it more rigid. This prevents the ILM to conform to the contour of the posterior staphyloma and causes a schisis-like retinal thickening [16]. Understanding the pathogenetic mechanism responsible for MTM formation helps in deciding the

Myopic tractional maculopathy is virtually seen in eyes with posterior staphyloma. In a study using SD-OCT, Henaine-Berra et al. [17] identified MTM in 17 of 116 eyes of pathological myopia, thus reporting a prevalence of approximately 15%. Some of these retinal changes are difficult to appreciate in eyes with high myopia due to the presence of the pathological degenerative changes at the posterior pole. Decreased visual acuity in these eyes is usually attributed to causes other than macular traction. OCT is often used in identifying the different retinal pathologies like vitreomacular traction, retinal thickening, macular retinoschisis, lamellar MH, and FRD. Progression of the myopic tractional detachment to develop a full-thickness MH and macular retinal detachment can

On the basis of OCT, Shimada et al. [4] have classified MTM into five stages from S0 to S4. This staging is based on the location of retinoschisis and its extent of

with S4 MTM progressed to foveal detachment (**Figures 2** and **3**).

3 Both foveal and extrafoveal but not the entire macula

*Staging of myopic tractional maculopathy depending on the extent of involvement.*

**Stage Location and involvement**

0 No retinoschisis 1 Extrafoveal 2 Foveal

4 Entire macula

Shimada et al. [4] 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 MH, FRD, or full-thickness MH. During a mean follow-up of 36.2 months, they reported progression in 11.6% (24/207) eyes, which included 0.9% who progressed to full-thickness MH and 3.4% who progressed to FRD. 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 *OCT Findings in Myopic Traction Maculopathy DOI: http://dx.doi.org/10.5772/intechopen.83766*

It appears that in eyes without identifiable preretinal tractional elements, ILM peeling resolves the retinal thickening. There are two possible explanations: One is that the ILM is highly elastic and tough, rendering it taut like a drum. In eyes with posterior staphyloma, the ILM is like the surface of a drum and is relatively resistant to permanent deformation and stretching. The second, more probable, explanation is that microscopic cellular and collagen proliferation develops on the ILM surface after PVD causing the ILM to be less distensible and making it more rigid. This prevents the ILM to conform to the contour of the posterior staphyloma and causes a schisis-like retinal thickening [16]. Understanding the pathogenetic mechanism responsible for MTM formation helps in deciding the surgical approach in these eyes (**Figure 1**).
