Throughout this text, I needed a non-medical term to refer to the events that I am experiencing. The term could be “condition”, “disease”, “affliction”, or “disorder”, but there is an implied connotation in those terms that does not fit. I have settled on “syndrome” as describing the experience of suffering sudden, randomly occurring intraocular hypertension attacks without clouding the issue with additional negativity.

From my perspective as a long-term glaucoma patient and having received treatment from some of the best ophthalmologists in the world, I have collected and try to expand on the experiences and document what I have learned along the way and posit some scenarios that may be worthy of more attention.
https://www.webmd.com/eye-health/occular-hypertension

INTRODUCTION

I have been suffering from bouts of high IOP since 1987, when it first happened to me, and I have described this experience and all my experience with glaucoma on my website at this link:
https://www.grahamlyleross.net/my-glaucoma

My very first episode (or event or attack) is in the post entitled
GLAUCOMA - My “lucky” diagnosis.

In the posts on my website under My Glaucoma, I have described in a chronological order the diagnosis, what many of the doctors have told me over the years, the many surgeries I have had to go through, and the outcome which is still causing me a lot of difficulty with my vision, pain, lost time, and substantial cost to this day and is ongoing.

All through this experience over the 37 years so far, the treatment approach has been to address elevated IOP events as being the problem. Doctors check and advise me: "You have very high intraocular pressure, you must use these eye drops regularly, and if that doesn't work, there are various surgical procedures that we can apply to control it."

This is an understandable viewpoint for a doctor to take. They see an ailment and look for ways to provide the sufferer with relief based on their medical study, applied knowledge, and experience of all other patients they have seen who have presented with high IOP, and treatments that have been applied and showed positive results.

Not in my case and here is why

My case is very different, and I believe that I am not the only one who has this kind of experience. I now realize that ophthalmologists, while amazingly intelligent and skillful doctors, are not researchers and have neither time nor budget to do so. They have their many diagnostic tools and methods to assess the condition as presented and to use their best judgment based on extensive study and their personal experience for how to deal with and control it to try to preserve the vision of the patient. They also need to use their talents to help as many patients as possible and cannot afford the time to chase down a rabbit hole of questions without answers hoping to make a breakthrough that may never come.

Recently, I had ophthalmologists tell me that they have never seen any patient with a medical condition like the syndrome that I have presented to them. And their experience and their medical training has not prepared them for how to approach it. I have known this to be the case for years, and no doubt their treatment options are the same because there is no choice but to address the high IOP to ensure vision loss is minimized. After that it is only possible to observe the condition and take notes and see is anything anywhere else in the world pops up that may shed some light on how to proceed. So far it has not.

Accordingly, in my search for an origin and a trigger we must enter into speculation, suggesting a hypothesis, and otherwise best guessing using the information gathered. Some of the greatest medical breakthroughs were discovered by accident or by following a hunch, so here is all the information that I can add to the discussion.

Motivation for creating this case study

During the decades that I have been visiting ophthalmologist and receiving a variety of treatments and even differing diagnoses for what they see in their examinations, I have encountered a considerable amount of “nobody knows” or otherwise unsatisfactory answers to my questions that amount to the same thing. I certainly do not fault the doctors for this, it is simply that there has not yet been enough research results available, and not enough feedback from collective experience to answer all the questions. It is just so complex. But we must keep working on it, and so I compile all these notes, examples, anecdotes, and outcomes for the reasons below:

- Distribution of knowledge gained through personal experience. After so many years I now have a wealth of information from experience that I document everything here for the benefit of others who suffer similarly and perhaps stimulate some discussion between researchers to take a new look at this syndrome. Granted that everything here is anecdotal and so not scientific evidence of anything. However, I have been mindful of how exaggeration and “fudging” the figures would distort the picture and so have been very careful to keep the details as factual and “as it really happened” as possible.

- Quest to find the origin. I believe that I was not born pre-disposed to glaucoma nor was I destined to suffer this syndrome, but rather that I have contracted it from an as yet unknown origin. If by careful analysis of the decades of events and (hopefully) discussion with other interested parties we could identify a plausible cause, then diagnosis, preventative measures and treatment options expand considerably.

- Discover the trigger. With the attacks being random in timing and severity, I believe that there must be conditions that I am experiencing that are triggering the mechanism that I have contracted thus initiating an attack. Since I don’t know it until it is happening, the catalyst for an attack is not overt enough that it comes to notice consciously to give warning. It is more subtle, such as a change in immune system strength, ingredients in shampoo or hair conditioner that often can run into the eyes, certain contaminants in food that don’t cause illness but have other effects (thinking MSG here, but others?)

Start of the syndrome: Any hypothesis about an underlying physiological causation for my syndrome must have been present in my body in 1987 at the time of my first attack. Any infections or outside influences on my immune system that happened after the time of my first attack must be ruled out as irrelevant except if such could be shown to exacerbate that existing condition.

DISCLAIMER

I publish all the information below and advise the reader that all this information is just me telling my story and asking my questions that seem to logically come up and where more informed responses would be very helpful. Perhaps someone will read this and follow up on my questioning and use it in applied research to help all patients in the future.

But I am not a doctor, nor do I have any medical qualifications. I advise the reader that you must not take any of my story about symptoms, treatments, medications, or outcomes as medical advice. Always consult medical professionals and strictly do as they tell you.

Where possible, I have included internet links which could be helpful should anyone want to get more information about the various topics.

Features of the Syndrome:

• Occurring over a period of 35 years with some periods of years without any events being noted.

• Generally, in right eye only, although has been noted in left eye on isolated occasions.

• Very rapid onset, going from apparently normal to very high (40+) within a few hours.

• Mostly painless, and mostly evident by the distortion of lights showing rainbow like halos when seen against a dark background.

• Attack is usually stopped with medication (primarily Diamox) and normal pressures are seen again within 24 hours.

• Duration of attack without mediation being applied is not known since each event is considered a medical emergency and treated immediately.

Normal glaucoma vs hypertensive IOP attacks

Here is where I am going to try to document my years of experience over many attacks, what worked, what didn’t work, and generally try to apply some "out of the box" thinking to see what generally overlooked circumstances may become evident and relevant.

"Normal" glaucoma is where a person has higher than normal levels of intraocular pressure, usually in both eyes, and the pressure is relatively constant. Rather like blood pressure, you have it, it generally is the same, and that must be treated before it goes on to cause serious damage. In the eye this damage is called glaucoma, where the nerves and retina are adversely affected by the high pressure of the aqueous humor (the fluid in the front part of the eye).

Reference reading on this is here:
https://my.clevelandclinic.org/health/body/24611-aqueous-humor-vitreous-humor

My syndrome does not follow this pattern.

My IOP is at (generally) normal levels much of the time. In fact, there have been long periods where there were no attacks for years. Admittedly these have followed successful surgical intervention to ensure that a build up in pressure is not possible.

Over time, of course, the trabeculectomy “heals”. The syndrome does not necessarily return right away. But given more time, it always has returned and spectacularly reappears with a very sudden rise in pressure in my eye (right eye only, in all this my left eye has been relatively unaffected. Why - good question, we'll get to that.)

Note that for many years the attacks have been entirely painless. The only indicator I get is very prominent “halos” around lights against a dark background (typically when driving) and sometimes a slight blurring of vision, but not always and not a lot.

As I focus on all the episodes (that I can recall although all are traumatic so do stick in memory) I have always reacted with treatment as quickly as possible. Usually that is a dose of 500mg of Diamox (acetazolamide) which in my case seems to result in a lowering of the IOP almost as fast as it went up. I am warned about just how damaging such high levels of IOP are for my vision that I have never considered NOT medicating and just waiting to see if the attack would subside spontaneously. Most times, I am already using anti-glaucoma drops, Xalatan once a day at night, and sometimes also using Azopt during the day. The attacks occur irrespective of the use of these other anti-glaucoma drops.

Note that Diamox is not a happy medication for me, and I suffer a lot from many of the side effects of this medication, so I use it in emergencies only. https://en.wikipedia.org/wiki/Acetazolamide

Medications that I CANNOT use

Why include what I cannot use: I put in this information about previously tried eye drops that I have had very negative reactions to in case it becomes important later in the discussion. I want to explore deeper health issues that are not only concerned directly with the eye treatments. My immune system is playing a part in this syndrome, there can be no doubt of that, the medications that I react negatively to may be indicators to what else may be happening due to other reactions from my immune system.

Timolol – In very early days of being treated for glaucoma, I was prescribed Timolol drops which I used for some months. One day, I walked only a short distance and was suddenly out of breath and feeling like I had just run a marathon. Fortunately I reported this event to my doctor and he quite hastily had me discontinue use of Timolol. See here: https://www.nhs.uk/medicines/timolol-eye-drops/side-effects-of-timolol-eye-drops/

Alphagan (brimonidine tartrate)– This is a medication that I was asked to use around 2008 and I started using it and was told that it may burn a little when first administered but that over time that would not be such an issue. With this advice, and in spite of the discomfort each application, I persevered with it until by the 3rd day, I was shocked to see how my eye now looked like a bright red party light. It was extremely uncomfortable and constantly watering. I determined for myself that this was an adverse reaction to the Alphagan and stopped using it right away. The inflammation took a week to return to normal. https://www.webmd.com/drugs/2/drug-21714/alphagan-p-ophthalmic-eye/details

Simbrinza (brinzolamide / brimonidine tartrate) More recently I started to use Simbrinza as an alternative to relieve the constant use of other medications and hopefully get a better control of pressure. Note that this drop is half Alphagan but in a lower dose, and combined with brinzolamide which is the active agent in Azopt, a medication that I have used without problems for years and works okay. However, the same issue of inflammation occurred and so this one is off the list of available medications for me.
https://www.webmd.com/drugs/2/drug-164064/simbrinza-ophthalmic-eye/details

MY OTHER ALERGIC REACTIONS: As I believe my attacks are linked to my immune system, then we need to explore what other things my immune system has reacted to so here I record my negative reaction to bites and stings from insects.

In particular, since my syndrome centers around my right eye, I must add this story in detail so that it can be factored into the discussion.

The scrub tick bite. In 1972, while on leave from my National Service in the Australian Army, I visited a National Park and did some bush walking. In the car on the way home, I discovered a scrub tick had somehow latched on in my right eye socket, only about 5mm from my eye beside the bridge of my nose just under my eye brow. I immediately drove to an ambulance station and had the tick expertly removed and the site thoroughly cleaned. For most people, that would have been the end of the issue, perhaps a small wound at the bite site which would heal in a few days. It was far from the end of the issue for me.

At the tick attachment site, a hemorrhagic pool is created. During the prolonged blood-meal, ticks secrete a rich cocktail of bioactive salivary molecules to the host and modulate host defense responses (itch, pain, hemostasis, inflammation, immune reactions) to their benefit. The tick salivary cocktail contains molecules (SAT factors) that facilitate pathogen transmission and infection of the host.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747359/

I had a massive allergic reaction to this tick bite and my entire right eye swelled to the point that it was squeezed closed. It really looked like I had taken a huge hit right in the eye. Back at the Army Base, the medics considered infection or allergy, and settled on unusually severe allergic reaction to the toxins injected by the tick.

Why could this be important in the discussion of my glaucoma syndrome? This bite was very near to my right eye and allergic reactions are part of the immune system functioning. Either I have a big reaction to even a small amount of the mix injected by the tick, or a normal reaction to a large amount of those pathogens. Could the “cocktail” of molecules from this tick bite have gotten inside my eye and started causing problems, or lay dormant for a long time only to cause problems later? This discussion is going to investigate all possibilities, so this event is recorded in this text as well.

This happened some 15 years prior to the first attack of high IOP (that I became aware of). However, prior to my first known attack in 1987 I had no knowledge of glaucoma or IOP or any such bodily mechanism. As mentioned, the attacks are painless and I only get the warning vision anomaly (halos on lights) at night, so it is entirely possible that there were some attacks before that 1987 event so cannot rule out the issue existing long before I finally became aware of it.

MY HYPERACTIVE IMMUNE SYSTEM

It is important to note that I do have much greater reactions to bee stings, wasp stings, ant bites than anyone else that I know. Even the tiny ants encountered in the garden and bite me even briefly, cause a severe itching and a large swelling that remains for about half a day. I watch people around me being stung by bees or wasps and while they get stung, they seem to be fine within only a few minutes – an unpleasant sting but nothing lasting at all.

For me, I react a lot to even a very tiny amount of such venom received by a tiny ant bite for which I show a large swelling at the bite site that is itching for several hours. A bee sting for me means a swelling at the sting site, pain for perhaps an hour, and swelling with severe itching for that lasts well into the next day and would be two days before finally subsiding. Even a mosquito bite for me is a long period of intense itching with swelling at the bite site.

I find that for whatever it is that stings me, if I can apply an antihistamine cream quickly enough, Antergan is my go-to relief for this, the effects will be greatly reduced in severity.

Excessively reactive immune system as factor in causation: I need to highlight this reaction from my immune system to such irritants and venoms as an indicator of how it is working and perhaps how it will react to anomalous foreign activity in my eye that could have the potential to trigger an attack of high IOP. While the actual mechanism of that is yet to be identified, I set up here some parameters for what could be in play when other influences are allowed to dominate or become prevalent.

However, I am NOT ALLERGIC to penicillin or any other medication that I have ever had administered to me throughout my lifetime.

Useful medications for my condition

Azopt - (brinzolamide) eye drops have always been helpful in controlling my IOP but are not greatly effective. This medication is a suspension, so it needs to be shaken before use, and it tends to leave a little bead of white deposit in the corner of my eye. Not a good look but it works without a big reaction so it is useful. It does cause dry eye so that is another issue that requires management using artificial tears.

Xalatan – (latanoprost) By far the most effective and helpful of all the medications used over the years. Xalatan was prescribed early, and I have used it off and on ever since. It is administered one time per day which is convenient. I have also used the others in the prostaglandins group such as Lumigan (bimatoprost) and Travatan (travoprost) with equally good results and no distressing short term side effects although the long term effects have necessitated a cataract procedure in my right eye and there are other structural defects showing up in that eye that are not in my left eye which can only be attributed to the medications and operations over the long time frame of my condition.
https://www.drugs.com/xalatan.html

I have not tried any others (that I can recall now) but knowing the above parameters on how I tolerate the various medications, I have settled to the two listed here as the ongoing anti-glaucoma medications for those times when they are needed.

TOPICS FOR DISCUSSION ABOUT CAUSATION

1. The psudeoexfloiation syndrome theory (originally including pigmentation shedding issue) – my first diagnosis.

2. The traumatic glaucoma theory

3. Possner-Schlossman Syndrome findings - usually unilateral, just like my issue, right eye only. Anything in the PSS studies of value to indicate a causation in my case?

4. The virus causation theory and review of all known viruses, dormant or not that have the potential to do harm.

5. Would a sudden attack also spontaneously subside?

6. Use of steroids and their effect on the immune system.

7. Anti-viral medications and use to prevent attacks

8. Conclusion – Spread the message, doctors can’t do it alone

1. PSUDEOXFOLIATION SYNDROME AS A CAUSE

Note that psudeoxfoliation syndrome encompasses a very complicated set of abnormalities and has a wide range of effects. Since I am not an ophthalmology student I only deal with this is a more simplistic way because I am in the quest for a cause for my sudden very high IOP attacks and once a theory shows that it simply does not fit, I go looking for another rabbit hole to investigate.

During the early evaluation of my condition and the seriousness of my glaucoma, doctors were very concerned that psudeoxfoliation (PEX) was noted in my right eye. Was this at a significant level or something that was discussed because there seemed to be no other cause showing any apparent signs? I do recall asking if this stuff was also present in my left eye, and they said that it was but to a lesser degree. To my question of “why no high pressure attacks in my left eye as well” I could not get any satisfactory answer and likely because this falls into the category of nobody knows.

PEX is characterized by microscopic white or grey granular flakes which are clumps of proteins within the eye which look somewhat like dandruff when seen through a microscope and which are released by cells.

What is puzzling is that PEX tends to happen in only one eye first, which scientists call unilaterality, and in some cases, gradually affects the other eye, which is termed bilaterality. According to this reasoning, if PEX were a systemic disorder, then both eyes should be affected at the same time, but they are not.

So for a few years around the 2007 relapse time, it was considered that I had PEX which was causing drainage problems resulting in elevated IOP. In the absence or any other explanation this had to do but I have always had questions that I hesitated to ask because I was quite sure that there really was no satisfactory answer available.

Here are my questions about psudeoxfoliation as a cause of my syndrome.

I can appreciate how psudeoxfoliation could be considered a cause for elevated IOP, and that seems logical as it is thought to block the drainage of the eye. But in my syndrome of random attack of high IOP in a very short time frame, is it that there is a sudden high volume release of XFM (psudeoxfoliation material) that totally blocks my eye, and even if so, how could the pressure rise so fast? And of course, the corollary to that question, why could the high IOP so suddenly be relieved and pressure return to normal or near normal.

A logical look at the mechanics tells us that PEX doesn’t fit the syndrome

In this scenario, where did all the XFM suddenly come from and where did it also quickly go that allowed the pressure to normalise again? The shortest interval between one attack subsiding and then followed by another attack is around 4 days. If PEX is causing the problems, and that it is still present after the attack, but then somehow not causing drainage problems? But then does again start causing an attack 4 days to 4 weeks later?

You can see my conundrum with this explanation for the events that I was living through if we were going to posit that the psudeoxfoliation material observed in my eye were going to be assigned as the cause of my attacks of sudden high IOP. However, as a theory to explain “normal” elevated levels of IOP that are sustained over time, it does fit and given that the doctors could see PEX in my right eye, it is reasonable for them to assume this is the likely cause. I think that perhaps, in one short examination by an ophthalmologist and the rarity of my cyclic attacks, they simply did not have enough information to warrant much further investigation. Just assign medication and book a follow up visit in a month. This is where I was for many years, knowing that the diagnosis was not correct, but not having the slightest idea what is a better way to address it.
https://www.aao.org/eye-health/diseases/what-is-pseudoexfoliation

2. TRAUMATIC GLAUCOMA RESULTING FROM AN EYE INJURY

In the early days of my treatments, and my inquiring of what could be the cause, I remembered an injury that I suffered to my right eye and asked doctors if it were possible if an earlier eye injury could be a cause for later eye problems such as glaucoma and I was told then that there was no research but thought it would be extremely unlikely to have any bearing on the syndrome now being experienced. I find that now, nearly 20 years later, this opinion is changing and I have read that traumatic glaucoma can occur soon after an injury, particularly an invasive injury, or could surface many years later leaving a mystery of the causation.

The accident I recall happened more than one year prior to my first attack of high IOP. It happened that a tiny fragment of steel ejected from a metal grinding machine and stabbed into the front of my right eye. It would not move because it was lodged in the sclera, the white part in the front of the eyeball, and stayed there for more than a day, going a little rusty before finally being removed in a doctor's office.

Normal traumatic glaucoma is described as being from a blunt force most notably accident injury or sports injury where the eye is impacted and so causing internal damage. This is all very plausible and now recognized as a cause and effect for glaucoma. This kind of traumatic glaucoma does not describe the injury that I suffered in my right eye and I feel that the medical handling of traumatic glaucoma stops well short of the possible effects of the kind of accident damage I experienced.

As a result, my questioning mind and logical thinking takes this to the next level.

Could my earlier eye accident have introduced a contaminant which, while it did not have an immediate reaction, leave some pathogen that lay dormant for years before becoming active and causing the ciliary body (the part of the eye that produces the fluid in the eye called aqueous humor) to become hyperactive thus over supplying the eye and overwhelming the eye's ability to drain quickly enough. But when the pathogen is again quelled by the body’s natural immune system, the ciliary body with the help of the medications that I take, quickly returns to normal, and so the condition is relieved.

The unanswered questions with the above hypothesis are…

- Is this a realistic scenario to warrant investigation and if so, how can it be investigated given that having an active case to examine is almost impossible to have in the hospital with medical staff at the ready at that very moment?

- What known pathogens are there that could be introduced in this way and then to function in this way, that is to lay dormant and activate when (unknown) conditions were suitable for it? Sounds a lot like a virus? I will get to virus theory shortly, but what else could fit?

EYE COLOR

Note that in the early years of my syndrome, I showed an acquired heterochromia (differing iris color in my eyes) which is usually due to injury, inflammation, the use of certain eyedrops that damage the iris. Originally it seemed to me logical that it was Siderosis – iron deposition within ocular tissues due to a penetrating injury and a retained iron-containing, intraocular foreign body due to the 1987 accident described above. For a long time I had thought this to be a viable theory to explain this color difference in my eyes. My logical thinking then takes this another step and asks that if it is possible that a penetrating injury can leave iron deposition, what else could also have been admitted to my inner eye in that event?

From my research, I also find that one major ocular adverse effect of latanoprost (Xalatan which by this time I had used every day for years) is that it can cause darkening of the iris. During first year of treatment, about 20% of eyes treated with latanoprost darken to a noticeable extent. Uniformly brown and blue irises darken rarely, but hazel eyes darken frequently. I have hazel eyes and cannot factor out that the Xalatan was the cause, but the earlier invasive injury with rusty metal object is certainly intriguing and worth keeping in the notes for reference in case it becomes relevant again.

3. POSNER-SCHLOSSMAN SYNDROME

During research, I found information about this syndrome which seems to fit my syndrome very well in many of the major aspects. The description is:

Posner-Schlossman Syndrome (PSS), also known as glaucomatocyclitic crisis, is a disease typified by acute, unilateral, recurrent attacks of elevated intraocular pressure (IOP) accompanied by mild anterior chamber inflammation. The pathophysiology is still unknown, although there are several theories proposed, ranging from autoimmune to infectious. Treatment management is focused on controlling the intraocular pressure and decreasing inflammation. While an attack usually resolves without sequelae, repeated attacks over time may lead to long-term glaucomatous damage (a secondary glaucoma).
https://eyewiki.aao.org/Glaucomatocyclitic_Crisis_(Posner-Schlossman_Syndrome)

Critical indicators noted for PSS that fit my experience are worth noting:
- Acute onset
- Unilateral
- Recurrent attacks
- Inflammation
- Pathophysiology unknown
- Symptoms of elevated IOP last from hours to weeks and may be recurrent.
- PSS has been postulated to be linked to autoimmune conditions.

What is not indicative of my syndrome is “In general, the frequency of attacks decreases with increasing age. There is usually no inciting event or precursor to attacks.”

So this research would suggest that my syndrome is not a typical PSS showing.

I have not researched this any further since the treatment for PSS, assuming a confirmed diagnosis which seems less than certain, would be no different to the approach that I have been advised by my doctors. Since nothing would change in what we needed to do to attend to the syndrome, I add no more on this but I put my notes and a lot more relevant links about PSS on my website here:
https://www.grahamlyleross.net/blog/posner-schlossman-syndrome

4. VIRUSES AND GLAUCOMA

There are evolving theories of how viruses play a part in the causation of glaucoma. The following text is intended as a case study of my personal experience with the syndrome of sudden, randomly occurring attacks of high intraocular pressure.

WHAT IS KNOWN: Viruses are predominant ocular pathogens and can impose both acute and chronic pathological insults to the human eye.

WHAT IS INCLUDED IN THIS CASE STUDY: There are many candidate viruses in the research work that is ongoing. However, for this discussion of my personal experience as a case study, we need to limit the scope to only those viruses that may have been present (and/or dormant) in my body at the time of my first attack in 1987.

This list must include:
- herpes simplex virus,
- varicella-zoster virus (chicken pox),
- Human Papilloma Virus (which caused occasional warts on hands as a child)
- Mumps (caused by a paramyxovirus, a member of the Rubulavirus family),
- measles virus,
- possible unknown others (ebstein barr virus),

All of these have been associated with the development of either primary or secondary glaucoma. For each one of these viruses, I will explain my exposure to the virus, my presumed immunity or lack of immunity as the medical institutions may advise, and what perceived danger they may pose to my overall health. It is presumed that chicken pox, mumps, and measles are fully dealt with my immune system because once infected with these viruses we are said to then have an immunity for life. We know that HSV and HPV can be dormant but become active when certain conditions favorable for the virus prevail. We are looking for the link to the glaucoma episodes for both causation and if a virus may be acting as a trigger for the attacks and all of the viruses in this list must be looked at and assigned a probability value for causation of the syndrome or as a trigger for the syndrome events.

WHY DON’T WE ALREADY KNOW?

The association of viruses with glaucoma is considered relatively uncommon in part due to underreporting and/or lack of long-term follow-up studies.
https://pubmed.ncbi.nlm.nih.gov/37966199/

In discussion with my ophthalmologist, I was told that in order to verify if a virus is present in my aqueous humor and so verify if a virus is playing a part in the attack, they would need to withdraw from my eye a sample of the fluid at the time that the attack was happening. Given the description of the attacks from earlier in this document in that they occur with random timing, onset is very rapid, and IOP goes to dangerously high levels within hours and is critical that it is dealt with as a medical emergency. For me to report to a medical facility capable of extracting the sample and the medical professionals were available at that moment to do it is mission impossible – unfortunately, but this shows why there is a lack of research into this linking. Hopefully the information I supply here will shed just a little light on it.

MY PERSONAL VIRUS EXPOSURE BACKGROUND

I was born in the 1950s and at that time, children would become infected with the big three - mumps, measles, and chicken pox, as a normal part of growing up. Vaccines were unheard of, not even for polio, so it was a dangerous virus filled world we grew up in. To get their children immunity, parents would send their children to visit other family or friends if they heard that someone with one of these in their house so that they could get infected, recover, and then no need to worry because they would have the lifelong immunity that is the silver lining of those illnesses (excluding polio of course). I will briefly put some background to each one along with the current research findings linking the viruses with glaucoma (as much as I can find) for each one.

This list must include:
- herpes simplex virus,
- varicella-zoster virus (chicken pox),
- Human Papilloma Virus (which caused occasional warts on hands as a child)
- Mumps (caused by a paramyxovirus, a member of the Rubulavirus family),
- measles virus,
- possible unknown others (ebstein barr virus),

HSV Herpes Simplex Virus

Herpes simplex virus (HSV), known as herpes, is a common infection that can cause painful blisters or ulcers. It primarily spreads by skin-to-skin contact. It is treatable but not curable.

HSV-1 seemed so common when I was growing up and even into middle age, I don't recall anyone claiming not to have suffered from cold sores. The virus is mostly spread by oral contact and causes infections in or around the mouth (oral herpes or cold sores). The HSV-2 virus, the one responsible for genital herpes was talked about, but I did not encounter anyone who would admit to having been infected such is the stigma associated with it.

My experience was that I would get a cold sore somewhere on my lips a couple of times a year, and usually when I was not in great health otherwise, indicating that my immune system would be at a low level and the HSV was allowed to become ative. They seem to have stopped as I get older although they say that you always have the virus dormant waiting for opportunities to assert.

However, I did get a "sign" just before my most recent attack, the one that followed my recent trabeculectomy on 15 March 2024, then two weeks of recovery and suddenly a huge attach. I recounted the story here:
https://www.grahamlyleross.net/blog/it-is-happening-again-is-this-a-glaucomatocyclitic-crisis?categoryId=394403

I was in recovery from the glaucoma surgery, things finally progressing well following some earlier complications with hypotony and choroidal detachment but I was on track and doing well. I then became aware of a couple of very small blisters on the corner of my mouth. I knew instantly what they were, and I applied ice to them for about 15 minutes which does seem to make them go away faster. This was without doubt a resurfacing of the HSV-1 virus that I had not seen for years.

As stated, I was in recovery from hypotony and CD, and part of the required medication is Prednisone tablets. Prednisone is a glucocorticoid medication mostly used to suppress the immune system and decrease inflammation. I also used Pred Forte eye drops, more of this steroid directly to the affected eye to control inflamation and to raise the IOP to help avoid further hypotony.

Is it then a coincidence that 2 days later I had a massive attack as described in the blog on my website? I will further deal with this issue in the summary on viruses, immune system, steroids medications, and possible causation for the syndrome at the core of this paper.

There is substantial amount of information and observations linking HSV and below are some links and relevant information.

Each year, about 50,000 new and recurring cases of Ocular HSV (predominantly type 1) are diagnosed in the United States. HSV can cause disease in any layer of the eye, and common manifestations include blepharitis, follicular conjunctivitis, keratitis, and keratouveitis.

Managing Glaucoma in the Patient With Herpetic Disease
https://glaucomatoday.com/articles/2017-may-june/managing-glaucoma-in-the-patient-with-herpetic-disease

Glaucoma Associated With Herpes Simplex Virus
https://glaucomatoday.com/articles/2013-may-june/glaucoma-associated-with-herpes-simplex-virus

Understanding the pathways to herpes simplex virus reactivation
https://www.sciencedirect.com/science/article/pii/S0042682218302137

Herpes Simplex Virus: An Important Etiology for Secondary Glaucoma
https://www.ophed.com/system/files/2012/07/herpessimplexvirus-3407-3407.pdf

HSV-1 in a case of intractable glaucoma with rapid progress of cataract after transscleral cyclophotocoagulation
https://www.sciencedirect.com/science/article/pii/S221150561100007X

UVEITIS – At some of the above links about HSV and possible links to glaucoma, uveitis is mentioned as being present and a major contributing factor. However, after consulting with my ophthalmologist who has examined my eyes many times and performed several surgeries for me, I am informed that uveitis is NOT present in my eye even when the pressure is abnormally high.

I am aware that it is accepted by researchers that oculotropic viruses cause immune cell-mediated ocular inflammation, called uveitis, that results into elevated IOP, and I have just stated that uveitis is not noted in my eye, or at least has not been noted, so if present, apparently not severe.

I do not think that non presence of this uveitis in relation to virus impact on the eye disqualifies the hypothesis that a virus is the cause of my attacks, or at least contributes to the attacks in combination with other coinciding but as yet unidentified circumstances. By following logic, I would posit the theory that a virus (HSV 1 seems most likely) becomes active at a time when my immune system is compromised by sickness, fatigue, or emotional stress. However, it is most noted for me when using prescribed steroid medications administered to address other issues notably and ironically, with inflammation (of other types than uveitis).

VZV - Varicella zoster virus

VZV is a human alphaherpesvirus that causes varicella (chickenpox) as the primary infection and establishes latency in sensory ganglia. Shingles is also caused by varicella-zoster virus (VZV). Once a person has chickenpox, the virus stays in their body. The virus can reactivate later in life and cause shingles.

VZV causes two different illnesses: Varicella, or chickenpox, develops after an individual is exposed to VZV for the first time. Herpes zoster, or shingles, develops from reactivation of the virus later in life, usually many decades after chickenpox.

Shingles can cause serious harm to the eyes. The inflammation can cause swelling in all parts of the eye. This can alter your vision and potentially increase the pressure of your eye, which can cause glaucoma if it isn't successfully controlled.

I cannot say if this virus, which definitely is in my body, and does have the ability to reactivate if conditions are such that it is allowed, is the cause of my random high IOP attacks. But if the virus causation theory it to be researched, then VZV must be a serious candidate for being the culprit.

What You Need to Know About Shingles of the Eye
https://www.drbeeve.com/blog/what-you-need-to-know-about-shingles-of-the-eye

The ocular manifestations of herpes zoster
https://pubmed.ncbi.nlm.nih.gov/185734/

Mumps virus

The mumps virus is an RNA virus in the family of Paramyxoviridae. The virus is primarily transmitted by respiratory secretions such as droplets and saliva, as well as via direct contact with an infected person. Mumps is highly contagious and spreads easily. The average incubation period for mumps is 16 to 18 days, with a range of 12 to 25 days.

I had mumps as a child, quite young, I don’t remember it, but it was one of those very common childhood illnesses during the 1950s that were considered almost trivial and parents welcomed when their child got it, and gave it to siblings, because that meant that it was done with forever once they all got over it.

Given that mumps virus is another that stays in the body but reportedly can do no damage due to the immunity resulting from the first infection, I have gone looking for more information to see if it may be possible that it could in some way have an influence on my eye pressures and random attacks of high IPO.

In short, I didn’t find very much, and conclude that it is either unheard of ever happening or it does happen but has not been studied due to the rarity of it. Perhaps also due to the the considered impossibility of it becoming virulent enough despite the immunity to do any damage.

An intriguing coincidence with mumps and start of the syndrome

Turn the clock back to the time in 1987 before my first ever attack. I lived in the country and my wife was working at the local high school. She became quite ill suffering from pain around her neck and lower face. Finally, it was diagnosed that she had contracted a mumps infection. I was not concerned for myself given that I had mumps as a child and have immunity, was able to be in close contact with her to care for her, and never thought any more about it. She recovered in the usual time frame given a little longer due to adult mumps infection being a more severe and painful than it is for a child.

My first ever episode of an attack of very high IOP occurred about a month or so after this exposure to an active mumps virus although I was not infected or more correctly, all viruses that I ingested were dealt with by my immunity. This of course proves nothing toward the theory that mumps or any other virus is the cause or part of the cause of my attacks.

But it certainly is an intriguing coincidence and worth noting in this article as it may be important to researchers to know about in the future.

A case of transient glaucoma as a manifestation of mumps
https://pubmed.ncbi.nlm.nih.gov/990027/

NHS website for causes and treatments of mumps
https://www.nhs.uk/conditions/mumps/causes/

Measles virus

Measles infects the respiratory tract and then spreads throughout the body. It causes high fever, cough, runny nose and a rash all over the body. The virus is related to several viruses that infect animals, including the Canine Distemper Virus.

As with chicken pox and mumps, catching measles was just another part of growing up in the 1950s and because there was no vaccine available till mid 1960s, we were on our own getting our immunity by suffering through infection and rehabilitation. I still have a measles scar on my forehead now, roughly 70 years after my infection with this virus. We never really appreciated just how dangerous this virus was, and again parents were not upset when their child contracted measles because that meant that they would get sick, get treated and helped through the tough days, and after that, bask in the fact that they had achieved immunity through their baptism of fire.

Apart from the information given for the VZV virus, the predominant threat of the group of three, mumps, measles, and chicken pox, there is not a lot that research shows that can be added to in respect of measles virus specifically. It does seem that if a person has survived the full process of infection and immune system initiated recovery and subsequent immunity, there is no ongoing threat from this virus, so I leave it here.

Virus (or other pathogens) from the Tick bite?

This is impossible to measure or demonstrate one way or another. It is important to keep this event in the text for future reference should any later research uncover a link, vague that it may be at first, requiring evidence, even anecdotal as this event is in nature.

5. Would a sudden attack also suddenly subside spontaneously

This question remains unanswered due to the risk of allowing very high IOP to persist with the potential to cause irreversible nerve damage. I am intrigued by the prospect because it seems plausible that it would do so. But in what time frame would that happen is the critical factor that I have not been brave enough, or reckless enough, to find out.

A test to find the pathogen.

Suggested to me is to try to find an opportunity to have the sample of the fluid in my eye examined at the time of an attack by withdrawing a sample of it through a surgical procedure at the time. This is simply so impractical that it is not going to happen.

However, in the event that such a process was achieved, and during an actual attack, an sample of the fluid in my eye were able to be harvested without complications, what would it prove? Can be only yes or no to the presence of a virus but that would not necessarily be conclusive anyway and it seems to me not worth the huge effort and expense for me and the medical staff to make it happen. The ongoing treatment either way would not be changed that much so benefits to be had for me in preserving what is left of my sight seem to be minimal at best.

6. USE OF STEROIDS AND EFFECT ON THE IMMUNE SYSTEM

Steroids reduce the activity of the immune system, which is the body's natural defense against illness and infection. A weakened immune system provides an opportunity for latent or dormant viruses to activate causing numerous issues. For HSV this manifests itself in cold sores... and possibly other deeper issues.

I have had many surgical procedures on my eyes, mostly my right eye, and each time I have been prescribed prednisone steroid tablets to help with recover in two ways. First the steroid treats the inflammation from the surgery to assist with healing processes. Second, in relation to a trabeculectomy to control attacks of high IOP, there is a risk of hypotony (IOP way too low) and the Pred Forte steroid eye drops can cause the IOP to elevate to help avoid this.

I have now had 4 trabeculectomy procedures on my right eye, and every time taken prednisone tablets and Pred Forte eye drops in the immediate recovery phase. At the follow up in each one of these cases, I have had numerous attacks that would cause high IOP but the surgery procedure vented the pressure away. Such was the severity of the attacks that they became evident also in my left eye, a serious escalation of the syndrome.

Once off the steroids, the rate of attacks dropped down and have even disappeared for several years a couple of times over the decades of dealing with this syndrome. This seems to demonstrate that while the steroid medications inhibited my immune system latent or dormant viruses in my system were able to become active in the most opportunistic way, which the experience seems to show is triggering an attack of high IOP in my right eye. Note that at the time of all attacks, I do not experience any other signs or symptoms of viral activity.

Too much prednisone can weaken immune system: a You Docs column.
https://www.cleveland.com/healthfit/2010/03/too_much_prednisone_can_weaken.html

Prednisone: What are 12 Things You Should Know?
https://www.drugs.com/medical-answers/prednisone-12-things-you-3573757

7. ANTI-VIRAL MEDICATIONS AND USE TO PREVENT ATTACKS

I would consider it useful experimentation for me to initiate a process to ensure that any virus present in my system is repressed to the point that even if I had a period of low immune system help, the virus could not become active enough to initiate an attack.

That would entail that I simply took some antiviral medications on an ongoing basis and wait to see if/when another attack turned up. My research shows that the anti-viral medication Acyclovir 400 mg twice daily could reduce the risk of recurrent HSV and other viruses.

SHINGLES VACCINE - If the virus reactivation theory is given credibility, and it is thought that VZV is likely, then I should get the shingles vaccine. The vaccine has been shown to help prevent herpes zoster from re-activating. In the instances where it does, the symptoms are typically less severe.

Further reading about anti-viral medication therapies for maintenance. https://my.clevelandclinic.org/health/drugs/21531-antivirals
https://www.drugoffice.gov.hk/eps/do/en/consumer/news_informations/dm_17.html

Treatment and prevention of herpes simplex virus type 1 in immunocompetent adolescents and adults
https://www.uptodate.com/contents/treatment-and-prevention-of-herpes-simplex-virus-type-1-in-immunocompetent-adolescents-and-adults
https://www.cdc.gov/std/treatment-guidelines/herpes.htm

8. CONCLUSION

As I have stated, I am not a doctor and I have a little knowledge only which may well be dangerous. But I do believe that research depends on real world patients reporting accurately and concisely their experiences. All those brilliant and dedicated doctors and researchers working on finding new ways to treat these conditions can’t do it on their own. Perhaps if my case study is published it may encourage many others to similarly participate in the quest for effective treatments and preventative measures.

I welcome any and all criticisms, feedback, suggestions and support for this work. I am contactable at grahambkk@yahoo.com and I continue to post on my website (link in the footer) in the My Glaucoma section with update and further events.