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Editors Selection IGR 13-4

Anatomical Structures: Lamina Cribrosa and Disc Hemorrhage

Comment by Franz Grehn on:

65998 Lamina cribrosa defects in eyes with glaucomatous disc haemorrhage, Kim YK; Park KH, Acta Ophthalmologica, 2016; 94: e468-e473

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Recent developments in OCT technology such as SS-OCT (swept-source optic coherence tomography) and enhanced depth imaging provide more information on morphology of the various changes of the lamina cribrosa (LC) in glaucomatous eyes during the process of progressive damage. Optic disc haemorrhages (ODH) are typical in glaucoma, in particular in normal tension glaucoma, as frequently present in the authors' country, South Korea.

This paper describes the spatial correlation of LC defects, retinal nerve fiber layer (RNLF) defects and optic disc haemorrhages (ODH). SS-OCT was used for quantifying LC defects. ODH were documented by stereo photography, and RNFL were visualized by SD-OCT. Photographs were electronically superimposed and adjusted to the LC images which allowed to investigate the spatial correlation of DH to LC and RNFL defects.

The two authors were masked to previous information and a consensus was needed to define presence/absence and clock hour (in 1/4 hour steps) position of ODH, RNFL and LC defect. The minimal size of a LC defect was defined as > 100 µm diameter and > 30 µm depth.

Two thirds of disc haemorrhages were infero-temporal, less than 1/3 supero-temporal, a few infero-nasal. Eighty percent of eyes with ODH showed LC defect versus 40% of eyes without ODH. Two thirds (50/75) of the LC defects were located in the infero-nasal quadrant of the optic disc. Eighty-one percent of the eyes with ODH showed a spatial correlation to the RNFL defect, and 60% of the eyes with ODH showed a spatial correlation to the LC defect.

The paper shows that twice as many focal LC defects exist in eyes with ODH than in eyes without ODH. There was a high spatial correlation between ODH and RNFL defects and a clear spatial correlation between ODH and LC defects.

This paper also discussed whether DH is a cause or a consequence of LC defects or RNFL defects. If the focal LC defect and DH are spatially correlated, the LC defect can directly trigger ODH by mechanical stress to the capillaries. If focal defect and DH are not correlated the following sequence of events could be assumed: (1) LC focal defect; (2) RNFL defect; (3) ODH.

However, we have to consider that the appearance of ODH may follow a dynamic process of increased distensibility of the weakened LC beams and this process cannot be visualized by a cross sectional study. In so far ODH could also be an event before the LC defect becomes visible while the mechanic stress of the LC beams has been already active (such as distensibility, shear stress, etc.) and the build-up of a visible LC defect (as seen as a hole) may only follow during the subsequent period. This sequence would then explain why some LC defects are not correlated to the present event of ODH, as they date back to an earlier, previously occurring process at a different location while the ODH is a sign of a presently ongoing damage.

In summary, this paper adds very valuable information on the spatial correlation of DH, RNFL defects and LC defects in glaucoma and allows more insight into the mechanism of damage of the RNFL at the optic disc.

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