Sir,

Myopic macular retinoschisis is found in eyes with pathological myopia. It is a precursor to both myopic macular holes and rhegmatogenous retinal detachment.1, 2 This report describes a novel vascular finding in this setting, which offers support to the theory that paravascular anomalies contribute to the pathogenesis of this condition.

Case report

A 45-year-old ethnic-Chinese lady presented with central visual disturbance in the right eye. Her corrected acuity was 6/9 in both eyes and the refraction was −8.0 dioptres in the right eye and −10.0 dioptres in the left eye. The anterior segments were normal in both eyes. Fundoscopy of the right eye revealed fine radial striae at the fovea and subtle cystic spaces. Temporal to the macula there were a number of saccular aneurysm-like structures and a 200° wide-field image of the retina demonstrated that there was no peripheral retinoschisis. (Figure 1) A fluorescein angiogram highlighted these lesions, together with disrupted retinal capillaries. No leakage was demonstrated. (Figure 2) Optical coherence tomography (OCT) confirmed the presence of macular retinoschisis in the right eye (Figure 3).

Figure 1
figure 1

(a) Colour fundus photograph of the right eye demonstrating features of high myopia, abnormal radial foveal striations, and saccular aneurysm-like changes in the temporal macula (black arrow). (b) This wide-field pseudocolour photograph of the right retina demonstrates that there was no peripheral retinoschisis.

Figure 2
figure 2

Early venous, transit phase fluorescein angiogram of the right eye demonstrating the abnormal saccular aneurysm-like dilatations in the retinal capillaries of the right temporal macula (black arrow).

Figure 3
figure 3

Spectral domain optical coherence tomography (OCT) of the right macula demonstrating the vertical inter-bridging strands and cystic degeneration of the outer retina typical of myopic retinoschisis.

Comment

The OCT features of this syndrome can be varied but typically include: columnar bridging structures within the schisis cavity, and a variable degree of vitreo-retinal traction including ILM dehiscence.1, 4 Both of these findings were present in our patient.

Recently, OCT imaging has demonstrated that the contour of larger retinal vessels may also be altered in patients with myopic macular retinoschisis, but to date disruption of the retinal microcirculation has not been described.5 In our patient the blood filled spaces appeared to be dilated capillary terminals and not extravasated blood. This suggests that the vascular anastomoses connecting the superficial and deep retinal capillary networks were physically disrupted as the schisis cavity enlarged. The absence of fluorescein leakage at the vessel terminals together with the increased calibre of the adjacent arterioles and capillaries might further suggest that there was sufficient time for capillary remodelling to occur as the inner and outer retinal leafs separated. Conversely, if the dehiscence progressed more rapidly the risk of bleeding within the schisis cavity would be increased.

This case represents a novel vascular finding in the setting of myopic macular retinoschisis, which may lend support to the theory that paravascular anomalies contribute to the pathogenesis of this condition.