Written by Tyson Xu BOptom (Hons) BSc, Specsavers Nowra NSW

Tyson graduated from UNSW in 2017 and was the recipient of the Andrew Whatham Centre for Eye Health prize, the Leonard Fine Therapeutics prize and a UNSW Summer Research Scholarship. He has had work experience at the Centre for Eye Health, Omni Eye Services in Atlanta and with Lion’s Outback Vision as part of the Judy Glover Memorial Scholarship. Since graduating, he has moved to regional NSW to practise and is currently co-chair of the ECONA Rural and Regional Committee.

This case study appeared in the July issue of Optometry Connection.

Glaucoma has historically been a challenging disease to detect and diagnose as demonstrated by the Blue Mountains Eye Study, where 50% of the estimated 300,000 Australians over the age of 40 with glaucoma were undiagnosed 1.

Normal tension glaucoma is one of the most common forms of glaucoma in Australia, Japan, Western Europe and the US 2,3. In addition to other forms of detection such as fundoscopy, enhanced visibility of the retinal architecture enabled by OCT has been hugely beneficial in supporting optometrists to detect early nerve fibre layer and ganglion cell loss. Equipped with this information, optometrists have been more able to make consistent patient management decisions to perform clinically indicated visual field assessment, interpret structural and functional correlations and then refer for ophthalmological intervention appropriately, as recommended in the RANZCO Referral Pathways for Glaucoma Management and Optometry Australia Clinical Practice Guide for the Management of Open Angle Glaucoma.

Case study and examination

An 82-year-old Caucasian female presented for a routine eye test. She had no initial complaints but on questioning mentioned that vision in her right eye wasn’t as clear as her left eye, even with optical correction from a year prior. Her medical history included controlled hypertension and migraine headaches, and she was taking multiple medications, but no steroidal medication. Previous ocular history included successful cataract surgery in both eyes six years prior.

Clinical assessment

The patient’s best corrected visual acuity was 6/7.5-1 in the right eye and 6/6 in the left, with mild astigmatic correction (R pl/-0.75 x 100, L +0.25/-1.00 x 80). IOP measured with Perkins tonometry at 11:10am, was 11 mmHg in both eyes. Corneal thickness was 474 µm in the right eye and 495 µm in the left.

The patient’s angles were open on Van Herick, and there were no signs of pigment dispersion or pseudoexfoliation syndrome. The patient’s IOLs were clear and well centred.

The patient was dilated with 0.5% Tropicamide. Internal examination showed flat maculae with no evidence of epiretinal membrane or vitreomacular traction. The right optic nerve showed focal rim thinning inferiorly, with correlating retinal nerve fibre layer (RNFL) wedge defect and thinning of ganglion cell layer (GCL) inferiorly noted in the OCT scan (Figure 1). The left optic nerve appeared normal (Figure 2). Comparison of the two OCT scans showed marked disc asymmetry (Figure 3)

On the basis of the optic nerve findings, a full threshold visual field test was conducted (Medmont M600 Glaucoma module). A repeatable paracentral visual field defect was found in the right eye, in the superior nasal quadrant – this correlated to the inferior temporal thinning of the ganglion cell layer (Figure 4).

Diagnosis and management

Several differential diagnoses were considered. With no evidence of pseudoexfoliation or pigment dispersion, secondary causes of open angle glaucoma were ruled out. Physiological disc asymmetry was ruled out by the visual field defect in the right eye, which correlated with the structural changes seen. A diagnosis of normal-tension glaucoma was made, and the patient was referred to a local glaucoma specialist for management.

Figure 1. 3D wide report of RE showing RNFL wedge defect (yellow arrow)
and GCL thinning (yellow circle)
Figure 2. 3D wide report of LE showing RNFL and GCL within normal limit

The patient was also counselled that her right eye vision was affected by the absolute paracentral scotoma, and she was referred to Glaucoma Australia to help facilitate her understanding of her disease. She was also advised to encourage her family members to have their eyes tested.


The patient outlined was a classic case of normal tension glaucoma. Compared to other forms of glaucoma, normal tension glaucoma has a relatively slower average rate of progression with reported mean deviation visual field loss of 0.36 dB-0.41 dB/ year as opposed to 3.13 dB/year in pseudoexfoliative glaucoma and 1.31 dB/year in high-tension glaucoma 4,5. However, normal tension glaucoma visual field defects tend to be more localised, dense and closer to fixation 6-9. In this patient’s case, it had resulted in a central visual field defect in her right eye.

Since ophthalmological assessment, the patient’s intraocular pressure has been controlled with selective laser trabeculoplasty (SLT) and prostaglandin analogue eyedrops (Xalatan, latanoprost 0.005%) and she is being reviewed on a six-monthly basis.

When we last saw her six months ago, all findings were relatively stable and she was still able to have great quality of life by being able to drive, read and crochet. However, she was still noticing that her right vision was worse than her left and this would sometimes affect her ability to perceive detail. From our discussions and her communications with Glaucoma Australia, she understood that the vision loss was irreversible and whilst it is a shame that we can never grant her that vision back or go back in time to make the diagnosis and referral earlier, we can be thankful that her level of vision has been preserved and with that her quality of life.

Successful glaucoma management is a collaborative effort between optometrist, ophthalmologist and patient advocacy groups such as Glaucoma Australia. Managing the disease is important, but so is managing the patient.

Figure 3. 3D disc report showing disc asymmetry
Figure 4. Visual field from most recent presentation showing a repeatable
paracentral defect in the right eye


  1. Mitchell P, Smith W, Attebo K et al. Prevalence of open-angle glaucoma in Australia: The Blue Mountains eye study. Ophthalmology 1996; 103: 1661-1669.
  2. Weinreb R, Leung C, Crowston J et al. Primary open-angle glaucoma. Nat Rev Dis Primers 2016; 2: 16067.
  3. Iwase A, Suzuki Y, Araie M et al. The prevalence of primary open-angle glaucoma in Japanese The Tajimi Study. Ophthalmology 2004; 111: 1641-1648
  4. Heijl A, Bengtsson B, Hyman L et al. Natural History of Open-Angle Glaucoma. Ophthalmology 2009; 116: 2271-2276.
  5. Anderson D, Drance S, Schulzer M. Natural history of normal-tension glaucoma. Ophthalmology 2001; 108: 247-253.
  6. Caprioli J, Spaeth G. Comparison of the Optic Nerve Head in High- and Low-Tension Glaucoma. Arch Ophthalmol 1985; 103: 1145-1149.
  7. Thonginnetra O, Greenstein V, Chu D et al. Normal Versus High Tension Glaucoma. J Glaucoma 2010; 19: 151-157.
  8. Caprioli J, Spaeth G. Comparison of Visual Field Defects in the Low-Tension Glaucomas with Those in the High-Tension Glaucomas. Am J Ophthalmol 1984; 97: 730-737.
  9. Araie M. Pattern of visual field defects in normal-tension and high-tension glaucoma. Curr Opin Ophthalmol 1995; 6: 36-45