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Progressive visual field loss from optic nerve head drusen


Dr Mark Chiang
Queensland Eye Institute, City Eye Centre, Brisbane


Visual field loss is one of the hallmarks of glaucoma. In general or glaucoma clinics, we often encounter patients with visual field loss that may or may not be progressive.

In assessing a patient with visual field loss, it is important to obtain a thorough history, followed by a complete ophthalmic examination, a central nervous system (CNS) examination, as well as other systemic examination as indicated. Investigations are then performed to provide further support or to confirm the diagnosis.


A 60-year-old male was referred for symptomatic progressive visual field loss. The patient had been aware of gradual constriction of his peripheral field over several years. There were no other associated symptoms such as headache or transient visual loss. He was otherwise well, without any medical problems. He works as a company executive, which requires extensive driving.

On examination, pupils were equal and reactive and there was no relative afferent pupillary defect. Ishihara colour plates were full in each eye. He had full ductions and versions as well as a normal CNS examination. His BCVAs were 6/6 in each eye. Anterior segment examination was normal and gonioscopy revealed open drainage angles. Presenting IOPs were 19 mmHg in each eye. Dilated fundal examination showed bilateral optic nerve head (ONH) drusen and attenuated retinal vasculature (Figures 1A and 1B).


32 OL ONH drusen Figures 1A and 1B

Figures 1A and 1B. Optos imaging showing bilateral ONH drusen with attenuated retinal vasculature


OCT performed on presentation showed grossly reduced retinal nerve fibre layer (RNFL) thickness in both eyes and illustrated well the readily-visible ONH drusen (Figure 2).


32 OL ONH drusen Figure 2

Figure 2. OCT of the ONH and RNFL analysis


Visual fields were also performed and confirmed the constricted fields (Figures 3A and 3B). Surprisingly, his performance on the binocular Esterman field test fulfilled the requirements for the driving standard.


32 OL ONH drusen Figures 3A and 3B

Figures 3A and 3B. Visual fields on presentation


A diagnosis of bilateral progressive field loss secondary to extensive ONH drusen was made and the patient was commenced on brimonidine bd OU and aspirin 100 mg daily. At the same time, a gadolinium-enhanced MRI of the visual pathway was performed, which did not show any other intracranial lesion that could have caused the patient’s field loss.

On review two months later, vision and visual fields remained stable and the IOPs were 17 mmHg in each eye. Latanoprost nocte OU was then added in an attempt to lower further his IOPs. On subsequent reviews over the next 18 months, his vision and fields remained stable with IOPs at around 13 mmHg OU.

About two years after initial presentation, he noticed a fairly rapid worsening of both the BCVA and fields. His BCVAs had reduced to 6/12 OD and 6/9 OS with worsening of visual fields (Figures 4A, 4B, 5A and 5B). Clinical examination did not reveal any additional pathologies such as central artery or vein occlusion, or choroidal neovascular membrane (CNVM) which can be associated with ONH drusen. The patient needed to cease his current employment as he could no longer drive.


32 OL ONH drusen Figures 4A and 4B

Figures 4A and 4B. Latest 24-2 fields showing significant progression


32 OL ONH drusen Figures 5A and 5B

Figures 5A and 5B. Latest 10-2 visual field with extensive central vision involvement



This case represents the severe end of the spectrum of visual field loss secondary to ONH drusen. The exact aetiology of ONH drusen is not well understood but it is thought to be congenital. Some suggested an abnormal axonal metabolism leading to calcium deposition. Others postulated reduced anterograde and retrograde axoplasmic flow leading to axoplasmic stasis and subsequent mitochondrial calcium deposition.

ONH drusen may be buried or readily visible and can be confused with optic disc swelling. In buried drusen, investigations such as B-scan ultrasonography, autofluorescence or even CT scans can aid in the visualisation. It is associated with central retinal vein occlusion, central retinal artery occlusion, anterior ischaemic optic neuropathy, choroidal neovascular membranes, and glaucoma. Patients may range from being totally asymptomatic to having transient visual obscurations, or having visual field loss.

While there is no proven treatment for ONH drusen, some patients are treated with IOP-lowering medications to relieve ONH mechanical stress and improve blood flow. Hopefully, with future research, we can better understand this condition and perhaps offer an effective treatment for this infrequent but sometimes debilitating condition.


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2 comments for “Progressive visual field loss from optic nerve head drusen”

  1. Gravatar of AliceAlice
    Posted Sunday, March 6, 2016 at 7:08:36 PM

    Fascinating article. Just wondering why brimonidine was used as initial therapy instead of latanoprost?

  2. Gravatar of Jeff MegahanJeff Megahan
    Posted Friday, March 11, 2016 at 8:06:27 AM

    The author Mark Chiang has responded: "Brimonidine was used initially instead of prostaglandin analogues for the presumed neuroprotective effect in addition to its IOP lowering effect."

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