Of course, as part of my PhD, I’ve been doing a lot of reading about glaucoma and visual field loss.  I’m still working in practice at the weekends and I find my approach to managing patients has changed based on the papers I’ve read.

I know not everyone has a spare three four months to read up on the latest research in glaucoma so I’ve chosen five interesting facts that may help my fellow optoms, pre-regs and students with their decision making.  For those who want to read more, I’ve added references*.

1) Early glaucoma affects central vision.  Usually we think of glaucoma as a disease that causes loss of peripheral vision.  Most example field plots will show a baring of the blind spot, arcuate defects and nasal steps but only the most severe will show macular involvement.  There’s actually a reason for this – we’ve been using the wrong test.

In practice, the standard field test we use is a 24-2 which covers the central 48 degrees with a 6 degree spacing between the test points.  Only four of the points tested fall within the macular region (central 8 degrees) .  If you can imagine, the little fixation spot the patient is looking at is located at 0 degrees, then the four points checked by the 24-2 are all just over 4 degrees from fixation.  Here’s a napkin drawing to help you visualise (and to show off my mad geometry skills):


Considering 30% of all retinal ganglion cells originate from the macula, it makes sense that this area is affected by glaucoma, a disease that causes ganglion cell death.  Several papers have been published recently showing that, despite previous wisdom that the macula was only affected in severe, end stage glaucoma, it can actually be one of the first areas affected.  Using a 10-2 visual field pattern may pick up macular defects that are too small or not in the correct location to be detected by the 24-2 pattern.  The 10-2 test covers the central 20 degrees (10 degrees either side of fixation) with a 2 degree spacing between test points.

Optical coherence tomography (OCT) shows thinning of the retinal nerve fibre layer (RNFL) in glaucoma.  Usually, if you suspected glaucoma, you would check the disc scan but, again, the macula with its abundance of ganglion cells is a better place to look for thinning.

Further reading: Grillo L. M., Wang D. L., Ramachandran R., Ehrlich A. C., De Moraes C. G., Ritch R. & Hood D. C. The 24-2 Visual Field Test Misses Central Macular Damage Confirmed by the 10-2 Visual Field Test and Optical Coherence Tomography. Translational Vision Science & Technology, 2016, 5(2): 15.


2) Certain areas of the disc are more likely to be damaged first.  As clinicians, we all know the ISNT rule and anyone lucky enough to have an OCT at their disposal will see that there is a “double hump” in the retinal nerve fibre layer profile around the disc.  The two humps are the inferior and superior regions of the disc:


Anyway, these two humps (the thickest parts of the optic nerve head) are the most prone to damage.  Any lady with a large chest will confirm this**.

If you think the optic disc of a right eye in terms of a clock face (superior is 12 o’clock, inferior 9 o’clock, nasal 6 o’clock and temporal 9 o’clock) then the areas corresponding to 6, 7, 11 and 12 on the clock are the most likely to be damaged by glaucoma.  For a left eye, it would be 5, 6, 12 and 1.  Interestingly enough, disc haemorrhages are usually seen in the inferior temporal portion of the disc (around 7 o’clock in right eyes and 5 o’clock in left eyes).

Further reading: Hood, D. C. Improving our understanding, and detection, of glaucomatous damage: an approach based upon optical coherence tomography (OCT). Progress in Retinal and Eye Research, 2017, 57: 46-75.


3) Normal tension glaucoma is a bit different.  Obviously it’s different in terms of intraocular pressure but let’s think about what causes glaucoma.  Well, there are two main theories: 1) the raised IOP squeezes the nerves until they die (the mechanical theory) and 2) there are issues with the blood supply, starving the nerves until they die (the vascular theory).  In normal tension glaucoma (NTG), the IOP is within normal limits (there’s nothing smooshing the nerves to death) so we can assume that the vascular theory is probably more applicable to NTG.

It’s been found that NTG patients tend to present with deep, well defined visual field defects that tend to be closer to fixation than those found in high tension glaucomas.

Normal tension glaucoma is probably one of the most challenging diseases to diagnose in practice.  If someone comes in with IOPs around 30mmHg, we are immediately on alert.  But, and I came across this a few weeks ago, what if your patient has IOPs around 15mmHg, moderate cup to disc ratio, deep cupping, no sign of focal neuroretinal rim (NRR) loss, normal central corneal thickness and a family history of glaucoma? Well, you do a 24-2 (as I did) and you find no defects.  Case closed?

My optom-sense was tingling from the moment I saw a photo of the patient’s discs – even before I heard that his father was registered blind as a result of glaucoma.  So I did a 10-2 test and, yes, there was a deep defect relatively close to fixation.

Research has been done into visual field defect location and those with a defect within 5 degrees of fixation are at a greater risk of losing their visual acuity – this makes NTG even scarier! It’s certainly worth taking an extra five minutes and doing a 10-2 test if the 24-2 is unremarkable but your gut instinct tells you something is amiss.

Further reading: Cho H.-K., Lee J., Lee M. & Kee C. Initial central scotomas vs peripheral scotomas in normal-tension glaucoma: clinical characteristics and progression rates. Eye, 2014, 28: 303-311.


4) Glaucoma doesn’t just affect the eye.  This is something I’d never really thought about until recently but what happens when those ganglion cells die? It creates dead space in the visual cortex.

You know that glaucoma is a disease which causes a negative scotoma (as opposed to the positive scotoma that results from advanced AMD) – why? Because the brain fills in the missing areas with information from around the scotoma.  When we talk about glaucoma, we may imagine tunnel vision but that’s not actually what patients say they experience.  They have blurred bits and missing bits.  It’s like that trick we do where we draw a small cross on a piece of paper then move it across our visual field until it disappears – that’s the cortex producing a negative scotoma so we aren’t aware we actually have a blind spot.

Of course, the cortex isn’t really doing us any favours when it comes to glaucoma – it’s hiding the disease from the patient and even when diagnosed, it’s sometimes difficult to convince a patient that they have an issue with their vision (especially when it comes to something as important as driving).

So, please don’t tell your patients that they have brain damage as well as glaucoma, but maybe be more aware that the visual experience of someone with the disease is different from what you may believe.  When those patients (and I’ve had my share) come in and say “something just isn’t right” then maybe think of glaucoma as a possibility – especially if they have normal IOPs.

Further reading: Crabb, D.P. A view on glaucoma – are we seeing it clearly? Eye, 2016, 30: 304–313.


5) Over 111 million people will be living with glaucoma by 2040.  I’ll just leave that there.

Further reading: Tham, Y.-C., Li, X., Wong, T.Y., Quigley, H.A., Aung, T., Cheng, C.-Y. Global prevalence of glaucoma and projections of glaucoma burden through 2040. Ophthalmology, 2014, 121, 2081–2090.


* If you are a Scottish optometrist, you can get access to Athens through your health board so you can read these papers for free.  If anyone in Wales, England or NI knows if this is also the case, please comment.

** Or men, I’m not being sexist here.