ow that we've established a diagnosis — and a presumptive one at that — what do we do to treat the condition? Strangely enough the answer is: nothing. The operative word in the title of this section is ‘for'. Treatment ‘for’ glaucoma — not ‘of'. Frankly, we can't treat the condition for the simple reason that — as I detailed earlier (see What in Blazes is Glaucoma?) — we don't know what causes the condition.

I can hear the wheels whirring now; I can even feel some temperatures rising; faces getting red, that sort of thing. And the question forming on many people's lips:

‘Then what's with all the expensive drops that Auntie Claire, my mother, and … I are taking? Eh!? Answer me that you charlatan!’

The answer is easy enough: we're treating a symptom. It's as if we only gave you a pill for the chest pain while you were having a heart attack. It eases the pain perhaps but doesn't address the underlying cause of the pain — not the real cause in any event — granted that a vasodilator given at that time would be a better idea and also relieve the symptom of pain. In point of fact, much of the medication that we all take for one condition or another treats only the symptom(s) and/or sign(s) and except for antibiotics and a few others, few medications actually attack the underlying cause of the problem and effect a cure. Which is why many surgeons say (and not altogether tongue-in-cheek) ‘to cut is to cure'. So in a sense, all those folks who decry modern medicine, label physicians charlatan's, et cetera, et cetera, are correct — in a way.

I'll let you in on a little secret — if you haven't figured it out already: The sad truth is that modern medicine, despite all its ‘whistles and bells’ and its ability to prolong life, doesn't really ‘cure’ anything. All we as physicians can do is try to restore something called homeostasis long enough so that the body — the ultimate ‘physician’ — can heal itself and perhaps ‘cure’ the problem. But that's all we physicians have ever been able to do since the dawn of history — tales of Atlantis aside; granted that we're somewhat better at it now. If that upsets you — I apologize — but that doesn't make physicians charlatans because despite what I've just said, physicians are working to the best of their ability with the tools at hand and are making a difference despite all. And I'll wager that all those folks who decry modern medicine will not hesitate to call 911 when they're having a heart attack!

So what has this to do with glaucoma and its ‘treatment'? Everything in point of fact. Because despite the fact that IOP per se is not glaucoma per se, it is the IOP to which most treatment addresses itself despite all the hue and cry about the latest buzzword: ‘neuroprotection’. And if it's true that elevated IOP is merely a symptom of an underlying defect, it is also true that lowering the IOP through various means seems to slow down the rate at which the vision in a patient with this condition deteriorates over time. Hence beta-blockers — such as timolol — lower IOP by increasing the outflow of aqueous. There is no credible evidence, however, that timolol (or betoxalol) is somehow ‘neuroprotective’ in any direct sense. And so it goes.

To illustrate that the 150 year-old paradigm — Elevated IOP Equals Glaucoma — is alive and well, I offer the following reference: Kass, M.A., et al., The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol, 120(6): p. 701-13; discussion 829-30; 2002. Of the patients studied — 10% of the untreated control group developed glaucoma. Whereas, only 5% of the treated group developed glaucoma. Wowser! A 50% response! Sounds great! Until you are acquainted with the facts. And these are that it was not possible to predict which of the patients would benefit ahead of time. That means treating 100% of the patients for a 5% result. I'll have more to say on this.

Face it — if it is a fact that all patients who have glaucoma (whatever it may be) lose vision over time — then anything we can do to slow that process down is a good thing. Because it is equally true that not one of us gets off this planet alive. Nonetheless we go to great lengths to prolong this terminal condition we call life. So in the final analysis, it may be sad that we don't know what causes glaucoma but it would be sadder still if we allowed it to proceed without interference of whatever stripe.

Mark Twain once said: “There are lies, damned lies and then there are statistics.” But often statistics are all we have. If we look at groups of patients with IOP's at various levels, it appears to be true that if the IOP can be kept down around 15 mm Hg (some would say 13), the number and rate in progression of field changes over time is significantly less. There is a profound paradox here. We've said that there is no absolute correlation between IOP per se and field loss. That is — it cannot be said that in a given eye, an IOP of a certain degree is more or less likely to show progressive changes. To put it another way: no IOP is absolutely safe. It's just that some IOP's are safer than others. Get it?

Well fine. But if what we've said is true, why is it that treated IOP's of 15 or less statistically show slower progression of field loss? ‘Haven't a clue’ is the honest answer except that it may be that the medication is somehow affecting the underlying disease mechanism and that the IOP level is reflective of that effect. There is danger in getting into a tail-spin here but we can avoiding crashing and burning as long as we maintain a specific paradigm. That is:

lowering IOP statistically results in less visual field loss over time.

Don't get too worked up about this. For many years we treated heart failure with digitalis despite our not knowing how digitalis ‘did its thing’. Eventually we found out. T'was ever thus because man is a curious beastie.

Philosophy aside ...

... what do we do to ‘treat’ the condition?