Asymmetry and Nasalisation of Retinal Nerve Fiber Layer in Glaucoma
Dr. Donamol Cyriac, Mr. Samuel Premkumar, Dr. Rashmi Nagar, Dr. Prabhat Nangia, Dr. Sarang Lambat and Dr. Vinay Nangia
Suraj Eye Institute, 559 New Colony, Nagpur
A female, 58 year old presented to us with complaints of blurring of vision in both eyes associated with flashes since 6 months which was gradual and worsening. There was no significant past ocular or medical history. Her best corrected visual acuity was 6/12, N10 in the right eye and 6/9, N8 in the left eye. Her anterior segment examination showed the presence of immature cataract in both eyes. Intraocular pressure recorded by Goldman applanation tonometer was 20mmHg in both eyes. Gonioscopy showed open angles in both eyes. Fundus examination showed 0.55 vertical CDR with inferior notch and a wedge defect inferiorly in right eye and 0.3 vertical CDR in left eye. She was diagnosed to have primary open angle glaucoma in right eye. She was advised to use timolol maleate drops in the right eye and she underwent cataract surgery and trabeculectomy with MMC in the right eye.
Our patient presented with initial loss of the most vulnerable zone of retinal nerve fiber involving the inferior part of the macular segment and the superior part of the inferior temporal segment. This manifested with a significant loss of retinal nerve fiber layer (Fig. 1- yellow arrows), (Fig. 3 B and C red arrows). This also resulted in significant infero-foveal loss of ganglion cells. (Fig. 5, A,B,C red arrows). The left eye does not show any significant glaucomatous changes clinically and on imaging. There is significant asymmetry between the two eyes, which is known to occur. However, we do need to watch the left eye for development of early signs of glaucoma. There is a suspicious early wedge in the ganglion cell layer of the outer circle temporally but not sufficient to say that glaucomatous damage has started.
The patient also shows that the superotemporal and inferotemporal peaks of RNFL are located nasally (Fig. 3 and 4, B, and C, blue arrows) compared to the expected location of the standard peaks seen in figure 3C and 4C, green arrows.
Let us call this ‘nasalization of the RNFL’. This so called shift is associated with the location of the vascular temporal arcades. As we know the greatest thickness of the RNFL correlates with the path of the temporal retinal vessels. When these vessels change their path to either come close temporally to the fovea or to move away from the fovea, they carry the main segments of RNFL thickness with them. This leads to nasalization of the RNFL as in this patient. It is also interesting to note that the RNFL thickness in both eyes is significantly greater in the inferotemporal quadrants compared to the superotemporal quadrants. There is therefore an asymmetry of RNFL thickness in the same eye. The exact clinical implication of this asymmetry is not known in normal or in glaucoma subjects. In the left eye the nasalization of the RNFL superiorly and inferiorly may have caused the appearance of RNFL thinning superotemporally and infero temporally. Therefore, one is unsure that this relative thinning of RNFL is normal or indicative of early glaucoma. The global values of RNFL are within normal limits. This patient therefore needs follow up for early signs of definitive development of glaucoma in the LE. In the RE also the nasal shift of the peaks of RNFL in the superior and inferior quadrants is evident. (Fig. 3, C blue arrows). The general implications are to recognize these shifts and take them into account when assessing the RNFL loss in patients of glaucoma.
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Dr Vinay Nangia
MS, FRCS, FRCOphth
Suraj Eye Institute