VITREOMACULAR TRACTION SYNDROME

Signs and Symptoms

Vitreomacular traction (VMT) syndrome has no racial or age predilection, though there is a greater incidence in older women than men.1,2 Common symptoms include micropsia, metamorphopsia and vision decrease. These symptoms are often mild and their onset insidious.1-4 In some cases, patients may be asymptomatic and VMT syndrome is discovered on optical coherence tomography (OCT) evaluation being done for other reasons. In other cases, mild symptoms and a subtle ophthalmoscopy appearance leads to performance and subsequent discovery on OCT. Several terms are used to describe this condition, including vitreomacular traction, vitreomacular adhesion (VMA) and vitreomacular traction syndrome (VMTS).

There may exist a discrepancy between signs and symptoms, with some patients demonstrating significant degrees of VMT yet manifesting excellent visual acuity while others with minimal VMT but with significant anterior-posterior vitreal traction having greatly diminished acuity.1

Diagnosis of VMT syndrome is very challenging clinically. Adhesions of the vitreous at the macula may be difficult if not impossible to observe even with high-powered contact or non-contact lens biomicroscopy. More easily observed than the actual vitreal macular traction itself is the surface wrinkling it produces similar to epiretinal membrane (ERM). Other complications that are more observable include actual ERM, cystoid macular edema (CME) and macular pseudohole.1 The definitive diagnosis of VMT syndrome is done through OCT analysis.5-8

Spectral-domain OCT will show a partial posterior vitreous detachment (PVD) with an adherent vitreous attached to the macular region of the retina. The posterior hyaloid space will be hyper-reflective and firmly adherent to the macular region. The adhesion and resultant traction may be focal and not disturb the normal foveal architecture. Alternately, there may be significant anterior traction on this focal adhesion with tenting of the macula, perifoveal macular detachment, tractional CME and lamellar or full-thickness macular hole. These focal adherences are often termed vitreofoveal traction, where VMT syndrome is often reserved for more broad areas of involvement. In these other cases, rather than a focal macular adhesion, the detaching vitreous may be broadly adherent. This type of broad VMT is commonly associated with ERM and diffuse retinal thickening.1,5

Pathophysiology

VMT was first described in 1970 as an incomplete PVD exerting traction on the macula and accompanied by decreased visual acuity.9 Today, VMT can best be described as an anomalous PVD. VMT results from vitreoretinal adhesions at the macula and the onset of a partial PVD. The tractional forces imparted upon the macula have the potential to cause foveal deformation and cavitation, CME, macular detachment, ERM and macular hole formation.10 Indeed, VMT syndrome is within a spectrum of maculopathies caused by vitreoretinal traction.

Posterior vitreous detachment is a normal age-related phenomenon characterized by progressive vitreous liquefaction, resulting in a separation between the posterior vitreous cortex and the internal limiting membrane (ILM) of the retina. Complications of PVD are more likely to arise in eyes where accelerated vitreous liquefaction occurs prior to weakening of vitreoretinal adhesions. An anomalous PVD occurs most likely as a result of premature vitreous liquefaction associated with insufficiently weakened vitreoretinal adhesion. At the posterior pole, vitreoretinal traction may induce VMT syndrome.1

In VMT syndrome, there is a fibrocellular proliferation that accounts for the increased vitreoretinal adhesion at the macula. The most commonly found cells at the vitreoretinal interface in VMT syndrome are astrocytes, myofibroblasts and fibrocytes, though recently it appears that retinal pigment epithelial (RPE) cells may be present as well.10 These cells, especially RPE cells, are commonly found in ERM as well, hence the similarity between the two conditions.

The vitreous cortex adherent to the ILM provides the scaffolding for this fibrocellular proliferation and the development of firm vitreoretinal adhesion seen in VMT syndrome. The proliferating cells and their accompanying extracellular matrix fortify the attachment of the vitreous to the retina. Small defects in the ILM, possibly as a result of a slowly detaching posterior vitreous, have been proposed as the nidus for the proliferating cells to gain access to the ILM surface, although this does not seem to explain the presence of RPE cells.10

As the vitreous continues to detach, the fibrocellular proliferation forming a tight adhesion between the retinal surface and the posterior hyaloid allows for both lateral and anterior vitreoretinal traction. This results in VMT syndrome with possible subsequent macular tenting, foveal cyst formation, tractional CME, ERM, foveal detachment and macular hole formation.1,5,10

Management

In cases where the patient is asymptomatic or minimally symptomatic with good visual acuity (>20/30), observation should be the first consideration as there may be no functional deficits induced by VMT.6 There exists the possibility that complete vitreous separation may spontaneously ensue, with relief of the vitreomacular traction, restoration of normal macular architecture, and an excellent visual outcome.11-14

In cases with reasonable acuity, observation is the preferred management. Here, the patient should be instructed on the use of Amsler grid for home monitoring and to report any visual changes immediately. Repeat OCT is recommended every three to six months. Any documented progression of the condition or loss of function should precipitate a discussion considering more invasive therapy.

Eyes with focal VMT syndrome (vitreofoveal traction) are more likely to progress to macular hole formation with worse visual outcomes than those eyes with broad VMT. These cases should be considered for surgical intervention earlier.

Vitrectomy has long been the procedure of choice to resolve VMT syndrome and prevent other macular complications.15-19 Vitrectomy will relieve vitreomacular traction and often prevents progression to more serious maculopathies such as macular hole. It has been demonstrated that vitrectomy can impart a significant improvement in visual acuity and central foveal thickness postoperatively. Eyes with lamellar separation of the inner and outer foveal layers preoperatively tend to have worse prognoses, whereas eyes with cystoid macular edema or broad VMT have better postoperative visual results.17 Preoperative foveal structure, macular thickness, and duration of symptoms are also correlated with post-operative visual outcome.18

A new method to relive traction in VMT is the advent of pharmacologic vitreolysis using ocriplasmin (Jetrea, Thrombogenics).20-25 Ocriplasmin is a genetically engineered version of a plasmin proteolytic enzyme. Fibronectin and laminin are clinically relevant plasmin receptors located at the vitreoretinal interface which are cleaved by ocriplasmin. Ocriplasmin has been shown in clinical trials to safely release vitreomacular adhesion and close Stage 2 macular holes in a significant number of patients.25 A single intravitreal ocriplasmin injection can induce separation of the vitreous from the macular surface and thereby relieve the tractional changes that contribute to vision loss from VMT syndrome and macular hole. Due to the recent FDA approval and only recent clinical availability (January 2013), it is unclear where this new modality will fall in the treatment of VMT syndrome and whether or not it will replace vitrectomy.

Clinical Pearls

Focal vitreofoveal traction more commonly leads to CME, foveal cyst formation, and macular hole development. Broad VMT will typically lead to ERM formation, tractional CME and increased foveal thickness, but is less likely to result in macular hole formation, thus a better overall visual prognosis.

VMT is more common than expected, as many patients are either asymptomatic or minimally symptomatic and the condition is found surreptitiously on OCT scanning.

In mild cases, it is difficult to separate the degree of vision loss due to VMT from that caused by co-existing cataract.

1. Bottós J, Elizalde J, Arevalo JF, et al. Vitreomacular traction syndrome. J Ophthalmic Vis Res. 2012;7(2):148-61.

2. Yonemoto J, Ideta H, Sasaki K, Tanaka S, Hirose A, Oka C. The age of onset of posterior vitreous detachment. Graefes Arch Clin Exp Ophthalmol. 1994;232(2):67–70.

3. Bottós JM, Elizalde J, Rodrigues EB, Maia M. Current concepts in vitreomacular traction syndrome. Curr Opin Ophthalmol. 2012;23(3):195-201.

4. Shechtman DL, Dunbar MT. The expanding spectrum of vitreomacular traction. Optometry. 2009;80(12):681-7.

5. Barak Y, Ihnen MA, Schaal S. Spectral domain optical coherence tomography in the diagnosis and management of vitreoretinal interface pathologies. J Ophthalmol. 2012;2012:876472. Epub 2012 Jun 4.

6. Reibaldi M, Avitabile T, Uva MG, et al. Ten Years of Severe Vitreomacular Traction Syndrome without Functional Damage Demonstrated by Optical Coherence Tomography. Case Rep Ophthalmol Med. 2011;2011:931038. Epub 2011 Sep 8.

7. Zhang ZQ, Dong FT, Yu WH, et al. Features of vitreomacular traction syndrome assessed with three-dimensional spectral-domain optical coherence tomography. Zhonghua Yan Ke Za Zhi. 2010;46(2):106-12.

8. Brasseur G. Vitreomacular traction. J Fr Ophtalmol. 2008;31(2):208-13.

9. Reese AB, Jones IS, Cooper WC. Vitreomacular traction syndrome confirmed histologically. Am J Ophthalmol. 1970;69(6):975–977.

10. Chang LK, Fine HF, Spaide RF, et al. Ultrastructural correlation of spectral-domain optical coherence tomographic findings in vitreomacular traction syndrome. Am J Ophthalmol. 2008;146(1):121-7.

11. Selver OB, Parlak M, Soylemezoglu ZO, Saatci AO. Spontaneous resolution of vitreomacular traction: a case series. Clin Exp Optom. 2013 Jan 24. [Epub ahead of print].

12. Hung KH, Yang CS, Lin TC, et al. Optical coherence tomography in spontaneous resolution of vitreomacular traction syndrome. J Chin Med Assoc. 2010;73(6):334-7.

13. Weinand F, Jung A, Becker R, Pavlovic S. Spontaneous resolution of vitreomacular traction syndrome. Ophthalmologe. 2009;106(1):44-6.

14. Levy J, Klemperer I, Belfair N, et al. Rapid spontaneous resolution of vitreomacular traction syndrome documented by optical coherence tomography. Int Ophthalmol. 2004;25(4):247-51.

15. Suárez Leoz M, Vidal Fernández P, Baeza Autillo A, et al. Vitrectomy for vitreomacular traction syndrome. Arch Soc Esp Oftalmol. 2001;76(1):37-41.

16. Toklu Y, Demirel S, Sarac O, et al. Anatomic and functional outcome of triamcinolone-assisted 23-gauge vitrectomy in vitreomacular traction syndrome. Semin Ophthalmol. 2012;27(3-4):73-7.

17. Witkin AJ, Patron ME, Castro LC, et al. Anatomic and visual outcomes of vitrectomy for vitreomacular traction syndrome. Ophthalmic Surg Lasers Imaging. 2010;41(4):425-31.

18. Sonmez K, Capone A Jr, Trese MT, Williams GA. Vitreomacular traction syndrome: impact of anatomical configuration on anatomical and visual outcomes. Retina. 2008;28(9):1207-14.

19. Jiang YR, Ma Y, Li XX. Analysis of the effect of surgical management on vitreomacular traction syndrome. Zhonghua Yan Ke Za Zhi. 2004;40(10):670-3.

20. Mitchell MD, Miller DM. Looking at ocriplasmin as a new option in eye disease. Drugs Today (Barc). 2012;48(8):519-24.

21. Stalmans P, Benz MS, Gandorfer A, et al. Enzymatic vitreolysis with ocriplasmin for vitreomacular traction and macular holes. N Engl J Med. 2012;367(7):606-15.

22. Tsui I, Pan CK, Rahimy E, Schwartz SD. Ocriplasmin for vitreoretinal diseases. J Biomed Biotechnol. 2012;2012:354979. Epub 2012 Oct 14.

23. de Smet MD, Jonckx B, Vanhove M, et al. Pharmacokinetics of ocriplasmin in vitreous. Invest Ophthalmol Vis Sci. 2012;53(13):8208-13.

24. Wong SC, Capone A Jr. Microplasmin (ocriplasmin) in pediatric vitreoretinal surgery: Update and Review. Retina. 2013;33(2):339-48.

25. Kuppermann BD. Ocriplasmin for pharmacologic vitreolysis. Retina. 2012;32 Suppl 2:S225-8.