**3. Diagnosis**

*A Practical Guide to Clinical Application of OCT in Ophthalmology*

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.

*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.*

**2. Pathogenesis**

**110**

**Figure 1.**

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 also be identified with use of OCT.

### **4. Staging and classification**

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 macular involvement (**Table 1**).

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


**Table 1.**

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

**Figure 2.** *(a–d) Progression of MTM leading to FRD over a period of 5 years.*

#### **Figure 3.**

*(a–c) Progression of MTM in the fellow eye of a patient who had undergone vitrectomy for MTM with foveal detachment in the other eye.*

**113**

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

The indications of surgery in MTM are:

thickness MH or FRD.

cessful in each and every case.

3.Vision <20/50.

**5.1 Surgical techniques**

approaches:

The goal of treatment in MTM is to relieve the tractional forces responsible for the formation of MTM [18]. This can be achieved primarily with the help of internal procedure with vitrectomy and external procedure with macular buckle. Pharmacologic vitreolysis can be considered a useful treatment option if vitreomacular traction from the perifoveal PVD or traction associated with a remnant cortical

1.Recent onset reduction in visual acuity secondary to development of full-

2.Progression in the extent of the schisis-like thickening documented by OCT.

Most surgeons while dealing with myopic traction maculopathy have two

1.Minimalist approach—This involves identifying and resolving only the major traction mechanism visible on OCT. In this approach, only vitrectomy with PVD induction is carried out. ILM peeling is not done in these cases. This avoids complications of ILM peeling in select eyes, but it is unlikely to be suc-

2.Comprehensive approach—In this approach, all the preretinal tractional elements are removed along with ILM peeling in every case. This approach has the highest single-operation success rate and ensures complete removal of all cellular and vitreous components that might cause current or future traction [14].

Taniuchi et al. [19] evaluated the effect of vitrectomy with and without ILM peeling in 71 eyes of 64 patients with myopic traction maculopathy. They studied the effects on visual acuity and post-operative complications. The results indicated that vitrectomy with ILM peeling can lead to improvement in vision in patients with macular retinoschisis or foveal detachment. Recurrences of tractional macular

Basically, vitrectomy with removal of the posterior cortical vitreous is what is minimally required in relieving the tractional forces responsible for MTM formation. The role of additional procedures like peeling of internal limiting membrane and use of gas tamponade in MTM is debatable. In eyes with MTM secondary to vitreomacular traction from the perifoveal PVD and traction associated with a remnant cortical vitreous layer after PVD, vitrectomy alone with removal of posterior cortical vitreous is sufficient in relieving the traction and achieves a normal retinal anatomy. In eyes with MTM secondary to epiretinal membrane formation, additional removal of epiretinal membrane is required. MTM caused by intrinsic stiffening of the ILM requires peeling of ILM with or without the placement of macular buckle [20, 21]. Few studies have shown that sparing a small island of ILM over the fovea in eyes with MTM can prevent the development of post-operative

detachment were also more frequent in eyes without ILM peeling.

MHs which are usually difficult to fix [22, 23] (**Table 2**).

vitreous layer after PVD is responsible for the MTM formation.

**5. Treatment**
