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Normal tension glaucoma


Alice Hall
BMedSci(VisionSci) MOptom Flinders University



A 79-year-old Caucasian female presented for annual review in July 2015. Since her initial presentation in 2009, she had been monitored annually as a suspect for normal tension glaucoma (NTG) due to cup-to-disc ratios of 0.70 and 0.75, and IOPs of 12 mmHg and 14 mmHg, right and left, respectively.

These readings had remained unchanged between 2009 and 2014. OCT had been performed at each visit and showed no evidence of thinning of the retinal nerve fibre layer (RNFL). The patient was not taking any medications but she was symptomatic of Raynaud’s phenomenon. In addition to peripheral vasospasm, her rural location and advancing age are relevant risk factors to her development of NTG.1

Examination July 2015

Best corrected visual acuity (BCVA), OD: 6/7.5-, OS: 6/7.5+.
IOP Perkins 9:30 am, OD: 13 mmHg, OS: 14 mmHg.
Central corneal thickness (CCT), OD: 520 µm, OS: 522 µm.
Pupils PERRL, no RAPD.

Slitlamp examination revealed a clear and quiet anterior chamber with open angles. No pigment, inflammatory cells, pseudoexfoliative material, neovascularisation or other signs of secondary glaucoma were present OU.

Mild nuclear and cortical cataract was present in each eye (graded LOCS III NO2 NC3 C2 P0.1 OU). A dilated fundus examination revealed OD C/D 0.70, OS C/D 0.75 with an inferior temporal disc haemorrhage in the left eye.

The patient had no known history of disc haemorrhages. No abnormalities were present at the macula or peripheral retina OU. The OCT showed no decrease in RNFL thickness compared with previous scans; it was in the normal range circumferentially, and showed acceptable symmetry (Figures 1 and 2).



Figure 1. Disc circle (Nidek RS-3000 OCT)



Figure 2. Disc map (Nidek RS-3000 OCT)


Examination August 2015

The patient returned for repeated IOP measurement and automated perimetry. IOP was 14 mmHg OU (Perkins 11:20 am). The right eye had an inferior nasal step (Figure 3), though given the extended nasal field area measured by Matrix automated perimetry, it is possible that this was caused by a nose defect and thus repeated perimetry to establish consistency would be useful. The left VF was full (Figure 4), with no evidence of glaucomatous defects or otherwise. The reliability indices were excellent bilaterally.



Figure 3. Visual field test, right eye (Medmont M700 Automated Perimeter)



Figure 4. Visual field test, left eye (Medmont M700 Automated Perimeter)



A diagnosis of NTG was made, based on the appearance of the optic nerves; in particular, the left disc haemorrhage.

Reasonable differential diagnoses include POAG, pseudo-glaucoma (that is, large physiological cup) and pigmentary glaucoma. Pachymetry is crucial in the diagnosis of NTG, as underestimation of IOP due to low CCT may cause POAG to be incorrectly diagnosed as NTG.

Low CCT is also a risk factor for NTG, with CCT being lower in NTG than in POAG.2 Similarly, repeated baseline tonometry is essential to differentiate POAG from NTG. Establishing a comprehensive baseline range of diurnal IOP measurements is required to form an accurate baseline that accounts for diurnal variation.

Other causes of optic disc haemorrhages must also be considered. These include diabetic papillopathy, ischaemic optic neuropathies and localised retinal branch vein occlusion.3 However, in the absence of disc oedema, retinal abnormalities and retinal vascular changes, these causes were unlikely.

Disc haemorrhages can also occur in association with posterior vitreous detachment, but dilated fundus examination revealed no sign of this, and the patient had not experienced any flash or floater symptoms. Given her five-year history as a NTG suspect and in the absence of other ocular signs, the disc haemorrhage seems most likely to be associated with glaucoma.


The patient was initiated on latanoprost 0.005% (Xalatan) nocte OU with the aim of achieving 30 per cent reduction in IOP and therefore, target pressures were set at 9.8 mmHg OU.

At the four-week review, IOP was measured as 8 mmHg OU (Perkins 10:00 am). The medical therapy was deemed to be successful.


The rate of progression in cases of untreated NTG is highly variable.4,5 Some cases progress within a few months; however, about half show no progression within five years. About one-third of patients with untreated NTG will show localised progression (defined by a VF loss of at least 10 dB deterioration from baseline) within three years.4

Some cases never progress, while others demonstrate episodic failure.6 For this reason and given that the average rate of deterioration is slow, clinicians may not need to initiate treatment immediately.4 The urgency and aggressiveness of therapeutic management in NTG should be decided on an individual basis, with consideration of the stage of the disease at presentation and the expected untreated trajectory for the individual.5

Risk factors that can act as prognostic indicators for progression of NTG are migraine, female gender and disc haemorrhage at diagnosis.5 An optic disc haemorrhage is one of the most important risk factors for development and progression of glaucomatous VF deterioration.7

Optic disc haemorrhages are reported more frequently in NTG but are also observed in uncontrolled POAG, as they represent an active disease process.7,8 Despite this, one study reported that of 23 patients with disc haemorrhages observed at the time of initial presentation, the course of the 11 subjects treated to lower the IOP was not statistically better than that of the 12 patients who were left untreated.5,7 Evidence also suggests that recurrent disc haemorrhages show significantly more progressive VF loss compared with disc haemorrhages that were not observed to be recurrent.7

Although the presence of a disc haemorrhage suggests active glaucomatous disease, the appearance of the OCT and VF and a five-year history of annual monitoring without progression suggests that this particular individual has a slow rate of progression. This provides the managing clinician with the latitude to closely monitor the patient for evidence of progression without necessitating immediate treatment.

This is especially valid, given that this patient is 79 years old. A younger patient typically requires more aggressive treatment, as glaucomatous visual loss is more likely to occur in their lifetime.1 Conversely, for an elderly patient, the decline in quality of life associated with use of medical therapy may outweigh the decline in quality of life associated with gradual visual deterioration, considering the financial expense of medications, the need to use them every day, physical ability to administer the drops and the adverse effects associated with their use.9

The need to preserve vision and the urgency to commence medical therapy may be more vital in patients with co-morbidity. For example, it may be reasonable to commence treatment sooner in a patient with macular degeneration, which is likely to impact central vision and therefore, preserving peripheral vision may be of higher importance. This patient did not have any relevant co-morbidity that would skew the risk-to-benefit analysis towards earlier or more aggressive treatment.

Given that this patient has not demonstrated progression throughout years of monitoring, and in light of the individual factors discussed above, a period of observation would have been a reasonable alternative management protocol.8 If progression were observed, initiation of topical latanoprost would be sensible. A uniocular trial to determine if the treated eye fares better than the untreated eye should also be considered.1,8

As this patient has been diagnosed with NTG and initiated on medical therapy, she should be monitored every four to six months for the first two years to establish if the VF loss is progressing; stabilisation would warrant reduced review frequency.1

1. NHMRC Guidelines for the screening, prognosis, diagnosis, management and prevention of glaucoma 2010. Australian Government, National Health and Medical Research Council. Commonwealth of Australia 2010.

2. Bowling B, Kanski JJ. Kanski’s Clinical Ophthalmology. Edinburgh: Elsevier, 2015.

3. Kanski J, Nischal K, Milewski S. Ophthalmology. London: Mosby, 1999.

4. Collaborative Normal-Tension Glaucoma Study Group. Natural history of normal-tension glaucoma. Ophthalmology 2001; 108: 2: 247-253.

5. Anderson D, Drance S, Schulzer M. Factors that predict the benefit of lowering intraocular pressure in normal tension glaucoma. Am J Ophthalmol 2003; 136: 5: 820-829.

6. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol 1998; 126: 4: 487-497.

7. Suh M, Park K. Pathogenesis and clinical implications of optic disk hemorrhage in glaucoma. Surv Ophthalmol 2014; 59: 1: 19-29.

8. Anderson D. Normal-tension glaucoma (low-tension glaucoma). Indian J Ophthalmol 2011; 59: 7: 97.

9. Guedes R. Quality of life and glaucoma. Revista Brasileira de Oftalmologia 2015; 74: 3.

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