This site is in the middle of a major expansion. It was originally designed as a resource for vision professionals who wanted to better understand how to care for patients with vision impairments. I'm now reworking the site with content for the general public — people with low vision and people who want to know more about low vision. Once that section is complete, I'll rework the section for vision professionals to better integrate with the general public section. Keep checking back to see how it's going, and if you find the content helpful please consider contributing to support the effort.


When I started doing low vision, I didn’t really understand the significance of patchy macular fields. As time has gone on, I’ve realised that understanding them is critical to understanding the apparent paradox of patients who complain of poor vision but still have great VA. This can occur in any posterior pathology, but is particularly common with macular degeneration and glaucoma.

Remember, VA only uses the fovea. Parafoveal vision is critical for ‘integrative’ visual tasks such as recognising faces and facial expressions, and (in particular) reading fluently. If a patient with good VA reports either of these problems, you should strongly suspect parafoveal field loss.

Drusen never sleep

When I started out in optometry, I had the impression that AMD degraded the macula in a fairly even way, and that glaucoma didn’t affect the macular fields until quite late. As it turns out, neither of these things is true.

In fact, in dry AMD the degeneration is quite focal. Drusen often appear around the macula in a roughly circumlinear pattern, creating small dense scotomas that gradually start coalescing to form larger scotomas. Frequently the fovea is spared until the very last, so the patient goes through a period where they have a large horseshoe or ring scotoma.

With wet AMD, the scotoma is much more random, but again if the fovea is not involved the patient can have excellent VA while still having quite complex and dense scotomas right next to fixation.

We’re used to thinking of early glaucomatous field loss as tending to be arcuate, corresponding to the retina just outside of the macula, and only constricting in to the macula later in the disease process. More recent research has shown that’s not the case. Alison McKendrick’s work at the University of Melbourne has shown that typical 24-2 or 30-2 field testing misses macular field loss, since those analyses only include four points in the macular area. Doing a 10-2 will frequently show up scotomas that were missed, but which are functionally significant.

When you think about it, this makes a lot of sense. As optometrists, we’re really aware nowadays of looking for damage to the ganglion cell complexes in our macular OCTs, as an early sign of glaucomatous damage. Those GCCs aren’t just for show, they have a functional job, so it shouldn’t surprise us that there is a measurable functional loss in the macular field if we use the right test to find it. It also fits with my clinical experience in low vision — patients with early-to-moderate glaucoma often report difficulty with reading fluency even when their fields apparently show no macular field loss. They also tend to respond very well to increased illumination on the page, improving in comfort in a way that people with healthy eyes don’t, which implies there is some sort of underlying deficit in the macula.

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