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Optic nerve head drusen

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Malcolm Gin
BScOptom FVCO

Catherine Cheah
BOptom

 

Optic nerve head drusen (ONHD) is not an uncommon finding with a reported prevalence of between 0.4 and 3.7 per cent of the population.1 Its inheritance is considered autosomal dominant linked with small ONH and a small optic foramen, and the drusen bodies are calcified acellular deposits. They range in size from five to 1,000 microns and are located in the prelaminar portion of the optic nerve head.

ONHD is often buried when young and as the glial tissue overlying the retina thins, the drusen become more obvious and fluoresce (Figures 1 and 2).

OL  023 -Figures -1-and -2
Figures 1 and 2.  Fundus autofluoresence highlights the drusen due to the refractile nature of the calcium, but the definitive test is B scan ultrasonography.

Fundus autofluoresence highlight the drusen due to the refractile nature of the calcium; however, the definitive test is B scan ultrasonography. Differential diagnosis from true papilloedema is essential as the latter signifies raised intracranial pressure that can be life threatening

As the drusen become more visible, visual field defects emerge due to direct pressure on the axons as well as ischaemia as a result of the compromise to the vascular supply. Literature reports the incidence of visual field defects varying from 24 up to 87 per cent,1 typically arcuate and not dissimilar to primary glaucoma.

OCT analysis details a thinning of the retinal nerve fibre layer in accordance with the loss (Figure 3, and normative data details, Figure 4), and the loss can be devastating. All eye-care practitioners should be aware of the greater risk of ischaemic optic neuropathy with ONHD and caution patients on sudden unilateral loss of either field or vision.

OL 023 -Figure -3

Figure 3. OCT analysis shows a thinning of the retinal nerve fibre layer

OL 023 -Figure -4

Figure 4. Normative date details

Treatment options

Treatment for visual field loss with ONHD is controversial. Modalities range from no treatment through to medical therapy and on to surgical options such as ONH decompression and radial optic neurotomy. Success of the modalities seems to be based on anecdotal evidence as in general, the number of cases is small and the changes are slow and occur over a long period.

Grippo and colleagues (2008)2 studied 103 eyes with ONHD and found that in the group of 22 who had coincidental ocular hypertension, 90.9 per cent had visual field loss compared with 66.7 per cent who were normotensive.

It is unclear whether ONHD masks glaucoma or whether ONHD is a risk factor for glaucoma. Certainly, the use of glaucoma medications seems a logical step given this association, and it is intuitive to try to reduce the intraocular pressure and also improve the vascular perfusion of the optic nerve.

Change appears to be the catalyst to begin treatment. Baseline visual fields and OCT is essential, along with careful monitoring of the patient. Loss is generally slow; however, if there are signs of progression then therapy should be considered. Brimonidine has shown neuroprotective characteristics in the rat model3 but it has a greater incidence of allergy. Current theory suggests hypotension should be avoided to preserve vascular perfusion relegating beta blockers to second-tier treatment. Prostaglandins may therefore be first-line course of action.

Prescribing of glaucoma agents for ONHD is considered an ‘off label’ process, so the cost to the patient is not subsidised by the government. This is an important consideration, given that the use of glaucoma medication is speculative in ONHD and the cost may be prohibitive for some. Careful counselling should be undertaken and patients given informed choices—even though no good scientific studies support the benefit, the rationale is solid and if there is a chance of preserving vision and field with a safe and proven medication, then it should be considered.

 

  1. Referrers guide to optic nerve head drusen. Centre for Eye Health 2011 www.cfeh.com.au.
  2. Grippo T, Shihadeh W, Shargus M et al. Optic nerve head drusen and visual field loss in normotensive and hypertensive eyes. J Glaucoma 2008; 17: 2: 100-104.
  3. Galanopoulos A, Goldberg I. Clinical efficacy & neuroprotective effects of brimonidine in the management of glaucoma and ocular hypertension. Clin Ophthalmol 2009; 3: 117-122.


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