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Spontaneous macular hole closure without posterior vitreous detachment in a patient previously treated for diabetic maculopathy

Editor, S pontaneous closure of a fullthickness macular hole (FTMH) in the absence of posterior vitreous detachment (PVD) is a rare event. To date, only one report has described this finding in stage 2 macular holes, in a patient with no coexisting ocular pathology (Abe et al. 2010). Despite this, however, we observed spontaneous closure of a stage 2 FTMH, without release of the vitreofoveal traction, in a patient with diabetes previously treated with macular grid laser photocoagulation. We documented these events using spectral domain optical coherence tomography (OCT), and in this report, we speculate regarding the underlying mechanism for this finding. An 81-year-old patient with type 2 diabetes mellitus was referred with a FTMH in the left eye and a best-corrected visual acuity of 20 ⁄ 80. Of note, he had been treated 7 years previously with laser photocoagulation for diffuse diabetic macular oedema in both eyes (a fluorescein angiogram performed at that time showed macular oedema, greater in the left eye than in the right, and with slightly enlarged foveal avascular zones). Five years later, the patient was diagnosed with vitreomacular traction. At the time of current referral, spectral domain OCT (Topcon 3D OCT-1000) confirmed the presence of a stage 2 FTMH with perifoveolar pseudocysts (Fig. 1A). The hole measured 337 lm in diameter and was partially covered with a retinal flap. The posterior hyaloid was attached and adherent to the edge of the hole. No cuff of subretinal fluid was seen. The patient was bilaterally pseudophakic, with moderate nonproliferative diabetic retinopathy. No previous history of ocular trauma was reported. Prior to any surgical intervention, a repeat OCT, performed 2 months later, showed spontaneous hole closure in the absence of PVD (Fig. 1B) and an improvement of best-corrected visual acuity to 20 ⁄ 63. The OCT appearance was unusual in that the posterior hyaloid remained attached to the retinal flap noted at the previous examination. This was associated with a central foveal detachment and a disrupted photoreceptor inner segment ⁄outer segment junction. Four months later, the visual acuity was unchanged, and OCT examination showed a similar appearance with a stable central foveal thickness at 249 lm. Although the treatment of choice for idiopathic FTMH is surgery, the Moorfields Macular Hole Study Group has shown a 21% rate of spontaneous closure for stage 2 lesions at 24 months’ follow-up. Importantly, this former study was pre-OCT, and spontaneous closure was defined on clinical and angiographic criteria. Nonetheless, this study demonstrated that spontaneous closure was associated with the development of posterior vitreous detachment as assessed clinically (Ezra & Gregor 2004). Gaudric et al. (1999) have proposed a role for anterior–posterior vitreofoveal traction in the initiation of macular hole formation, followed by disruption and opening of the foveal floor to create a FTMH. The mechanism of spontaneous closure by release of anterior–posterior traction does not apply to our patient because there is no PVD. This case is unusual because of the spontaneous closure, and despite the persistent perifoveal hyaloid attachment, it is possible only to speculate as to the reason for this. Pollack et al. (1998) showed that, although the most prominent effects of photocoagulation were in the outer retina, Muller glial cells in some laser spots showed changes in staining intensity throughout their length, including at the vitreoretinal interface. Furthermore, recent studies in mice have suggested that retinal laser injury stimulates a significant glial reaction within the retina with Müller cell activation and targeted Müller cell nuclear migration towards the outer nuclear layer (Tackenberg et al. 2009). Consecutive series have demonstrated that laser photocoagulation to the retinal pigment epithelial (RPE) cells, (A)