our understanding is that glaucoma IS high eye pressure
Maybe that is the source of some confusion. Glaucoma is not equal to elevated eye pressure (intraocular pressure). Technically, elevated intraocular pressure is just a risk factor for glaucoma.
Elevated intraocular pressure (IOP) is the most important risk factor because it is the only medically treatable risk factor at this time.
Many years ago, Dr. Robert Ritch shared this important understanding of glaucoma with the FitEyes community:
All glaucomas have a final common pathway of retinal ganglion cell death involving low-grade inflammation, oxidative damage, mitochondrial dysfunction, and glial hyperactivation.
You could say that is "glaucoma in one sentence."
Notice that elevated eye pressure is not part of that sentence. That's as it should be because glaucoma does not equal elevated eye pressure, as I said above. Elevated eye pressure is just one risk factor.
Therefore, it is not an oxymoron to speak about normal tension glaucoma (or even low tension glaucoma).
That probably answers the question for many readers. Stop reading here if you feel satisfied. However, a deeper exploration of the question continues below the fold.
Today, medical science does not know exactly what causes glaucoma. We know that there are many factors that contribute to it, and that some of these factors are more important for some individuals. Without understanding the root cause, and by virtue of the fact that there are many variants of the optic neuropathy we call glaucoma, defining glaucoma is difficult. Therefore, defining normal tension glaucoma will entail challenges.
There are around thirty factors that contribute to glaucoma, from genes to systemic inflammation to mitochondrial dysfunction. Elevated IOP is the most important factor for many people living with glaucoma, but others have glaucoma without elevated IOP -- which is the point of this question.
I need to say that IOP remains the most important treatable risk factor even for people with normal- or low-tension glaucoma. Many people with NTG rightly feel dissatisfied with that state of affairs, but our best science hasn't yet given us better treatment options. However, many patients with NTG want to see more research attention focused on other factors, and they often focus their own lifestyle approaches on factors such as inflammation, blood flow to the eye, etc.
In this spirit, I want to mention one other major theory about a fundamental cause of glaucoma -- mechanical stress on the optic nerve where it exits the back of the eye. That topic is highly relevant to NTG.
The optic nerve exits the back of the eye through a structure called the lamina cribrosa. It is the boundary between two systems. There are two opposing pressures pushing on each side of it.
On one side of the lamina cribrosa is IOP (what we commonly call eye pressure). On the other is the cerebral spinal fluid pressure ("CSFP" or "CSF pressure"). The difference between those two pressures is more important than the absolute value of either one (except possibly in extremes). This is a key factor in understanding normal tension glaucoma.
If a person has an elevated IOP of 30 and a similarly elevated CSFP they would have balanced pressures at the lamina cribrosa and may not experience glaucoma -- even with elevated IOP.
Likewise, a person with normal IOP but below normal CSFP would have a pressure imbalance at the lamina cribrosa and may experience glaucoma -- even with normal or low IOP.
CSFP measured at the base of the spine and with the patient lying on the side is normally 8-15 mmHg. That rises to 16–24 mmHg when we sit up. As you see, CSFP is in the physiological range of IOP.
The pressure imbalance (between IOP and CSFP) puts mechanical stress on the optic nerve. That's bad for the nerve.
Some studies have confirmed that glaucoma patients with normal intraocular pressure glaucoma have significantly lower CSFP and a higher trans-lamina-cribrosa pressure difference when compared to normal subjects.
But this topic gets a bit complicated. For example, CSFP behind the eye may not be equal to CFSP at the base of the spine due to compartmentalization. Measuring absolute CSFP directly behind the eye is not easy. It is also not routinely done.