Sir,

We report a patient with an arcuate scotoma, attributable to traction of neural tissue at the optic disc.

Case report

A 61-year-old woman was referred for evaluation of a standard automated perimetry (SAP) visual field defect OD. Corrected visual acuities were 20/20 OU, and IOPs were 20 mm Hg OD and 22 mm Hg OS. Slit-lamp biomicroscopy was unremarkable OU. Dilated examination OD revealed thick ring-shaped vitreous condensation at the optic disc with no glaucomatous change (Figure 1). Humphrey 24-2 and 10-2 SAP revealed a superior, incomplete paracentral arcuate scotoma OD (Figure 1). Optic disc, retinal nerve fiber layer (RNFL) and SAP were within normal limits OS (Figure 1). Enhanced depth imaging optical coherence tomography revealed prominent vitreous condensation and meniscus tissue of Kuhnt at the optic disc, which were pulling the superficial part of inferotemporal neuroretinal rim in the nasal direction and altering its normal architecture (Figure 2).

Figure 1
figure 1

(a–e) Color optic disc photography, Humphrey 24-2 and 10-2 perimetry pattern deviation probability plots, and RNFL thickness map and profile OD, respectively. (f, g) Color optic disc photography and Humphrey 24-2 perimetry OS, respectively.

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Figure 2
figure 2

(a–e) Infrared optic disc photography and (f–j) enhanced depth imaging optical coherence tomography images OD. (k–o) The same images as in (f–j) without the labels. (a–e, green arrows) The locations of the cross-sectional optical coherence tomography scans. (f–j, red lines, yellow lines, red arrows and blue arrows) Thick, condensed vitreous at Martegiani’s ring and meniscus tissue of Kuhnt, optic disc surface, fibrous tissue filling the optic disc cup (part of meniscus tissue of Kuhnt), and the direction of traction, respectively.

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Comment

Cloquet’s canal is a remnant of the primary vitreous and firmly inserts around the optic disc at Martegiani’s ring.1 The thick ring-shaped vitreous condensation at the optic disc in our case appears to be increased gliosis at Martegiani’s ring, which has been nasally displaced, along with the meniscus tissue of Kuhnt. As vitreous is firmly attached around the optic disc at Martegiani’s ring, its displacement has significantly altered the normal neuroretinal rim architecture (Figure 2).

There are findings that favor traction at the optic disc more than glaucomatous changes, as the cause of the scotoma in our patient. First, no RNFL defect was detected in our case. Second, the inferotemporal rim area that was being dragged by traction spatially corresponded to the superior arcuate scotoma. RNFL bundles arising from peripheral retina lie in the optic disc periphery.2 Therefore, our patient’s arcuate scotoma, which started from the physiologic blind spot and ended in the middle of the arc is consistent with the fact that the superficial part of the neuroretinal rim was affected. Although speculative, a possible mechanism of functional impairment in our case may include impaired axoplasmic flow and/or electrical transmission of visual signals associated with significantly dragged RNFL axons.