|Year : 1996 | Volume
| Issue : 4 | Page : 235-239
Optic disc evaluation in glaucoma
G Chandra Sekhar
VST Centre for Glaucoma Care, L.V. Prasad Eye Institute, Hyderabad, India
G Chandra Sekhar
VST Centre for Glaucoma Care, L.V. Prasad Eye Institute, Hyderabad
|How to cite this article:|
Sekhar G C. Optic disc evaluation in glaucoma. Indian J Ophthalmol 1996;44:235-9
| A. INTRODUCTION|| |
The diagnosis of primary open angle glaucoma (POAG) is traditionally based on the triad of increased intraocular pressure(IOP),visual field changes and optic nerve head changes. It is well established that IOP is only a risk factor, albeit, the only risk factor that can be therapeutically manipulated. The fact that upto 50% of POAG patients can present with normal IOP makes it imperative that the diagnosis of POAG be made independent of IOP increase. Occurance of arcuate nerve fibre bundle visual field defects has been taken as the sine qua non for the diagnosis of POAG. Studies by Quigley et al have shown that upto 40% of the axons could be lost before a visual field defect develops on Goldmann perimetry and that 20% of axons are lost before a 5 db loss is detected on standard automated perimetry. The current research efforts in the early "preperimetric glaucoma" diagnosis are aimed either at psychological tests or alterations in the optic nerve head morphology as assesed by scanning laser ophthalmoscope, digital image processing of optic nerve head images or optical coherence tomography., While these advanced technologies are relevant in glaucoma diagnosis and research, they are not practical in routine clinical practice.
With some training it is possible to clinically evaluate the optic nerve head stereoscopically and detect early glaucomatous disc damage.
The aim of this communication is to describe the morphological changes of the optic nerve head in glaucoma, discuss the differential diagnosis and highlight the techniques of clinical evaluation of the optic disc.
| B. FEATURES OF GLAUCOMATOUS DISC DAMAGE|| |
| B. 1 Cup-disc ratio|| |
Cup to disc ratio greater than 0.5:1 is the most often reported sign of glaucomatous disc damage. In a given disc with a cup-disc ratio of more than 0.5:1, it is important to establish if the cup-disc ratio has been large from the onset (large physiological cup) or if it increased over a period of time. Increase in the cup-disc ratio (or enlargement of the cup) over a period of time is diagnostic of glaucomatous disc damage even in the absence of visual field defect. This definitive sign has practical limitation because one time diagnosis is not possible and followup over a period of time is neccesary. The physiological variability of the cup-disc ratio ocurs because of the large variation in the normal optic nerve head size.
Though the normal optic nerve head size is reported to be 1.5 mm in diameter it can vary from 0.96 mm to 2.91 mm. As a result, the physiological cup can be as small as 0.1:1 or as large as 0.8:1.
This is highlighted by [Figure - 1] and [Figure - 2]. The [Figure - 1] shows a small disc with a small pathological cup and [Figure - 2] shows a large disc with a large physiological cup.
Clinical assessment of the optic nerve head size (discussed subsequently) will aid in determining the significance of cup-disc ratio in a given eye.
| B. 2 Neuroretinal Rim Evaluation|| |
Loss of axons in glaucoma is reflected as abnormalities of the neuroretinal rim. Normally the rim is widest in the inferior temporal sector, followed by the superior temporal sector, the nasal and the temporal horizontal sector. Since localised field defects restricted to one hemisphere are an early sign of glaucoma, stereoscopic examination of the neuroretinal rim in the superior and inferior poles comparing carefully their thickness, pallor and notching can aid in the diagnosis of very early glaucomatous damage. [Figure - 1] shows localised notch interiorly with a very small cup. The corresponding small superior paracentral scotoma is shown in [Figure - 3]. [Figure - 4] shows pallor of the inferior neuroretinal rim compared to the superior in a small disc with no apparently discernible cupping. The corresponding field defect in the form of a superior nasal step is shown in [Figure - 5].
| B3. Contour Cupping vs Colour Cupping|| |
To asses the width of the neuroretinal rim, the edge of the cup has to be clearly delineated, the usual temptation is to equate the central pallor of the disc with cup, but atleast in some glaucomatous discs there is a discrepancy between the extent of central pallor (colour cup) and the site at which the vessels change their contour (contour cup). In the evaluation of glaucomatous disc damage it is the contour cup that is of relevance and not the colour cup.
[Figure - 6] shows a cup disc ratio of about 0.6:1 by colour, however, the inferior temporal vessels are exiting from the edge of the disc. Further, on comparison to the superior neuroretinal rim there is significant pallor of the inferior neuroretinal rim. The corresponding visual field defect is shown in [Figure - 7].
| B. 4 Myopic Changes vs Glaucoma|| |
Myopic disc can cause difficulties in glaucomatous disc evaluation either because of the oblique entry resulting in tilted disc or because of the peripapillary changes. [Figure - 8] shows a myopic disc in which the glaucomatous damage is not obvious. The inferior peripapillary atrophy results in a wrong estimation of the extent of the cup as this is mistaken for a part of the disc.
Careful evaluation reveals the edge of the disc to be more central with a change in vessel contour at the edge of the disc revealing the inferior notch. The corresponding superior field defect is shown in [Figure - 9].
| B. 5 Peripapillary Changes|| |
Acquired peripapillary atrophy has been described to be secondary to glaucomatous disc damage. Some authorities feel such changes may predispose to glaucomatous damage.
The zone closer to the optic nerve head with retinal pigment epithelial (RPE) and choroidal atrophy with sclera showing through is called zone-α. The more peripheral zone with only RPE atrophy is called zone-β. Since these changes could be seen in myopia also [Figure - 8] appearance of these changes de-novo or their occurrence in small discs or non myopic eyes [Figure - 1], [Figure - 3] is more suggestive of glaucomatous disc damage. A correlation between the location of disc haemorrhage and location of peripapillary atrophy has been reported. If this is so, peripapillary atrophy could be a more reliable and permanent marker for progression than disc hemorrhages.
| B. 6 Nerve Fibre Layer (NFL) Changes|| |
NFL atrophy is associated with a high risk for field loss. Localised defects are the easiest to detect and may be very specific to differentiate early glaucoma from normal eyes [Figure - 10]. While they occur in 10 to 20% of ocular hypertensive eyes they must be looked for in every glaucoma suspect as the high specificity is clinically useful in identifying patients with impending or established perimetric loss.
| C. DIFFERENTIAL DIAGNOSIS|| |
A large physiological cup has already been addressed [Figure - 3]. If one takes care to asses the neuroretinal rim carefully and measures the optic nerve head size, one can be reasonably sure of a large physiological cup in a large disc.
Congenital colobomas of the optic nerve head are some times easy to diagnose because of the morning glory appearance or other associated colobomas. Optic nerve pit and conus of the disc can some times cause diagnostic difficulties.
Pallor disproportionate to cupping, normal intraocular pressure or unusual history of onset, progression and age should arouse suspicion of a neurological cause for the disc changes and appropriate investigations should be carried out. [Figure - 11] shows cupping and pallor secondary to pituitary tumour which was mistaken for glaucoma. The correspoding temporal hemianopia is shown in [Figure - 12].
| D. EVALUATION TECHNIQUES|| |
The most important points in clinical evaluation of the Optic nerve head are a stereoscopic view with magnification for proper evaluation of the neuroretinal rim changes and an estimation of the optic nerve head size.
Stereoscopic view of the optic nerve head is possible by indirect ophthalmoscopy, central part of goniolens, Hruby lens and Volk 90, 78 and 60 D lenses. Indirect ophthalmoscopy is inappropriate for assesement of the optic disc in glaucoma. I prefer the Volk lens systems. While the 78D lens provides a good balance between the field of view and magnification, the 60D lens can make measurement of optic nerve head size simple.
With one of these lenses and slitlamp with redfree light source, it is possible to asses the NFL abnormalities also, though specialised NFL photography systems are more sensitive. Use of direct ophthalmoscope in serious glaucomatous disc evaluation is to be discouraged.
Clinical estimation of optic nerve head size is possible with a Welsch Allen Ophthalmoscope or with Volk 60D lens. The smallest white round spot of the Welsch Allen ophthalmoscope usually illuminates a cone angle of 5° and casts a light of 1.5 mm in diameter on the retina. This retinal spot size remains constant in phakic eyes with refractive errors between -5.00 D and + 4.00 D.
The location of the originating point of the light cone does not significantly affect the retinal spot size as long as it is ± 3mm from the anterior focal point of the patient's eye. Since 1.5 mm is the usual size of the optic nerve head, this can be used as a yard stick for measuring disc size. Simplistically, in eyes with large physiological cups due to large discs the area illuminated is less than the area occupied by the cup.
Disc diameter can be measured by adjusting the slitlamp beam height to the edges of the disc while viewing the disc with a 60 D lens. This measurement is roughly equal to the measurement obtained by planimetry of disc photos with Littmann's correction.
A similar measurement of the vertical and horizontal disc diameter can be obtained with other lenses by multiplying the measured value with the appropriate magnification factor: Goldmann contact lens (1.26) and Volk superfield lens (1.5).
It is useful to get habituated to a routine pattern of examination of the disc and look sequentially for findings as follows:
- 1. Overall impression of the disc
- 2. Size and shape of the disc
- 3. Evaluation of the neuroretinal rim keeping in mind the variability of its thickness in various zones mentioned in the text and also look for notch and neuroretinal rim haemorrhage.
- 4. Peripappillary atrophy
- 5. Nerve fibre layer abnormalities
- 6. Vertical cup-disc ratio and asymmetry.
| E. CONCLUSION|| |
Stereoscopic evaluation of the optic nerve head with emphasis on changes of the neuro retinal rim and not estimation of cup-disc ratio will aid in early diagnosis of glaucoma.
| References|| |
|1.||Leibowitz HM, Kruger DE, Maunder LR, et al. The Framingham Eye Study monograph: An ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration and visual acuity in general population. Surv Ophthalmol 24 (suppl):335-610, 1980. |
|2.||Quigley HA, Dunkelbarger GR, Green WR. Retinal ganglion cell atrophy correlated with automated perimetry in human eyes with glaucoma. Am J Ophthalmol 107: 453-464, 1989. |
|3.||Weinreb RN. Diagnosing and monitoring glaucoma with confocal scanning laser ophthalmoscopy. J Glaucoma 4:225-227, 1995. |
|4.||Schuman JS, Hee MR, Puliafito CA. et al. Quantification of nerve fibre layer thickness in normal and glaucomatous eyes using optical coherence tomography. Arch Ophthalmol 113:586-596, 1995. |
|5.||Jonas JB, Gusek GC, Naumann GOH. Optic disc, cup and neuroretinal rim size, configuration and correlations in normal eyes. Invest Ophthalmol Vis Sci 29:1151-1158, 1988. |
|6.||Jonas JB,Dichtl A. Advances in assessment of the optic disc changes in early glaucoma. Cur Opi Ophthalmol 6:61-66, 1995. |
|7.||Geijssen HC,Greve EL. Disc haemorrhages and peripapillary atrophy. Invest Ophthalmol Vis Sci 32:1017, 1991. |
|8.||Gross PG, Drance SM. Comparison of a simple ophthalmoscopic and planimetric measurement of glaucomatous neuroretinal rim areas. J Glaucoma 4:314-316, 1995. |
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11], [Figure - 12]