Three-dimensional scanning enhances our knowledge of vitreomacular traction syndrome (Figs. 9.3, 9.4, and 9.5). SS-OCT enables simultaneous high quality three-dimensional visualization of the vitreous, retina, and choroid. Vitreomacular traction should always be regarded as a three-dimensional disease. Many adhesion points between the vitreous and retina exist, besides that seen in the foveola on the central B-scan. The adhesion between retina and vitreous is usually strongest 1500 μm around the fovea [4], at the optic nerve, and along retinal vessels. Three-dimensional imaging might thus facilitate surgical planning, as it reveals multiple traction sites besides the fovea. In the natural course of the disease it is possible that the central traction is relieved, but it persists in the proximity to retinal vessels.

Many morphological changes of the fovea might be observed in SS-OCT. Cystoid spaces in the inner retinal layers are visible in most eyes (Fig. 9.1a [star]). The photoreceptor layer and external limiting membrane might remain intact in the presence of an inner cystoid space despite existing traction. Thus inner cystoid spaces are not always symptomatic. They might progress over time. If multiple cystoid spaces are present in the inner retinal layers, they tend to group into one larger cystoid space (Fig. 9.2c, d). Less frequent, outer retina cystoid spaces may be visible (Fig. 9.6, upper left [star]). If an elevation of the photoreceptor layer coexists with an outer lamellar macular hole, it is highly probable that this appearance will progress to full thickness macular hole (Fig. 9.6) [5]. If vitreomacular traction is released (spontaneously or after treatment), cystoid spaces decrease in size and later disappear (Fig. 9.7).

Epiretinal membranes might coexist with vitreomacular traction syndrome in about 25–83% of eyes (Fig. 9.7) [1, 6, 7]. Spontaneous resolution of eyes with coexisting epiretinal membranes and vitreomacular traction syndrome is less likely, but possible in very rare cases.

Photoreceptor and external limiting membrane defects develop during follow-up of vitreomacular traction syndrome in more than 60% of cases (Fig. 11.​1b) [1]. They are associated with decreased visual acuity and metamorphopsia.

There are only a few studies describing the natural course of vitreomacular traction. In our series of 130 eyes observed for 24 months, only 20 required surgery (Michalewska et al. unpublished data). Most eyes resolve spontaneously with good final visual acuity (Fig. 9.8). In some cases, however, vitreomacular traction may be a very dynamic disease and may lead to development of full thickness macular holes (Figs.9.6 and 11.1), lamellar macular holes or epiretinal membranes.

Earlier spectral domain OCT (SD-OCT) studies reported that spontaneous resolution of vitreomacular traction is more probable in eyes with a smaller adhesion area between the vitreous and retina.

We confirmed with multivariate analysis (Michalewska et al. unpublished data) that two factors are independently associated with progression or resolution of vitreomacular traction syndrome: phacoemulsification (p = 0.02) and observation time (p = 0.03). Unfortunately, it is impossible to predict which vitreomacular traction will progress and which will resolve spontaneously. The only described morphological criterion of progression is the elevation of the photoreceptor layer. If such an elevation exists, it is highly probable that a full-thickness macular hole will develop [5].

Choroidal thickness measurements are possible with SS-OCT. In a group of 27 eyes evaluated for 24 months with SS-OCT we confirmed that choroidal thickness decreases in eyes in which vitreomacular traction is spontaneously relieved (Michalewska et al. unpublished data).

Symptomatic vitreomacular traction may be treated with either intravitreal injection of gas, ocriplasmin, or vitrectomy (Figs. 9.7 and 9.9). Vitreomacular adhesion resolves in about one-quarter of ocriplasmin-treated eyes [8], which makes this technique less efficient than vitrectomy. Even if injections are considered to be less invasive than surgery, about 68% of ocriplasmin-treated patients developed minor adverse events, such as conjunctival hemorrhage or floaters. A small case series reported release of traction in about 55% of cases after intrevitreal gas injection [9]. The lack of randomized studies on this topic make specific treatment recommendations difficult. Earlier SD-OCT studies reported that the outer foveal thickness (the distance between the external limiting membrane and the retinal pigment epithelium) is the sole factor confirmed by multivariate analysis to be correlated with visual acuity 12 months after surgery for vitreomacular traction syndrome [10]. The exact timing for treatment still remains a topic of controversy. It must be taken into consideration that according to recent reports, three years after vitrectomy only about 30% of patients have experienced full restoration of the IS/OS junction [11], whereas just 1 year after vitrectomy for full-thickness macular hole, full restoration occurred in 70% of cases [12]. This is perhaps surprising, as most would assume vitreomacular traction as a less severe disease than an impending macular hole (Figs. 9.7 and 9.9).