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INTRODUCTION
Welcome to our internationally operating startup non-profit organization’s website for NAAION – also called NAION or eye stroke – (non-arteritic anterior ischemic optic neuropathy) patients and family, as well as for physicians and researchers involved, that is under construction.

We have started this to help put a stop to this life disturbing always unexpectedly sudden disease that is getting so many fully or partially blind in one or both eyes. Even better, we plan to stimulate finding a cure for NAAION (also called NAION). Here starts the road to better outcomes for NAAION patients and their family.

Meanwhile you will find here already:

1. Our closed (members only) NAAION (NAION or eye stroke) support group for patients and family at

http://www.facebook.com/groups/naaion/

2. Our Twitter page @naaion at

https://www.twitter.com/naaion/

 

 

What is NAAION

NAME: NAAION (or NAAION) or non-arteritic anterior ischemic neuropathy, is the sister disease of AAION, and forms with it the group of two AION’s. Popularly it is also called an ‘eye stroke’.

EFFECT: The effect of NAAION is a partial or full blindness in one or both eyes, often through a sudden nighttime NAAION event, where one wakes up in the morning and discovers the disturbing fact that one cannot see or see much in one eye (followed by both eyes in about 20% of cases). About 35% of NAAION patients may see a partial recovery over a few weeks or months, but most do not. The disease is still incurable.
So NAAION will impact not only one’s health.  It will also force patients (and families) to make life style changes. to change work or jobs, to close down one’s business, to handle lower income and higher costs and even to resolve or end strained stressful relationships.

Patients will especially have to act like the above to try prevent a second attack that will blind them entirely. Yes, it is a constant, so lifelong ‘sword of Damocles’ hanging over pone’s head.

Such an second NAAION event in the fellow eye that would blind one entirely, would mean a NAAION patient would become strongly dependent on the goodwill and help of others, often of many who do not understand the impact of the disease. This is foreseeable, since it is hard to imagine partial or total blindness for oneself if one is a healthy person. NAAION patients will benefit from educating their environment, so the impact of their (partial) blindness does not get trivialized or underestimated. It is major even if often quite ‘invisible’.

Often the underestimation by one’s environment and one’s physicians comes due to the medical industry not yet being capable of qualifying and quantifying the effect of NAAION on one’s ‘functional vision’. Especially the field of ophthalmology is still too much focused on identifying solely refractory issues or taking refraction related measurements not on mainly neurological issues like this (and their functional consequences). That is visible in the still dogmatically used ancient (over 160 years old) Snellen test determining visual acuity of patients with vision loss, while that is a test mainly once invented for refractory issues, and not even for all. Use of the Snellen visual acuity test (or more modern sister – the Logmar visual acuity test) trivializes what NAAION patients have and deal with. Those visual acuity tests actually misrepresent the NAAION condition for the most part since many NAAION patients can show a relatively good visual acuity test following the Snellen method (or its modernized Logmar version) and still have a terrible remaining functional vision.

Imagine also  how insulting it is to have an eye doctor do a pinhole test to establish if you are not ‘inventing’ your disease. Like most patients have nothing better to do.

Imagine how even more so disturbing it is for an NAAION patient to see his disease, his blindness trivialized, as if he is imagining:
– being exhausted already halfway the day,
– seeing only blurred images in his eye,
– having varied quality of vision through the day,
– seeing letters merge into each other, 
– making numerous typos due to insufficient distance between letters,
– bumping into persons, (car) doors, bed edges, open windows, cupboards, chairs, pets, or stumbling int objects unexpectedly put in one’s path by others,
– dropping glass and porcelain ware due to putting it in the wrong spot due to poor visual navigation,
– spilling food over one’s clothes and on the table for wrongly estimating speed and distance of one’s movement,
– losing entirely the ability to drive due to losing overview, reacting slower, lacking correct estimation of speed and distance of oneself and others, blinding glare at night and during rain, or being forced to only drive at day time an in rural quiet areas, without being able to cover great distances so long trips due to quick exhaustion from the more frequent head movements and difficulty of brain adapting to quick  and more burdensome image input changes,
– worrying about structural stress as it may trigger another attack due to teh adrenaline impacting the blood pressure,
– being constantly on and off blinded by glare both in daytime condition outside and inside as well as even going into a dark room,
–  having the sword of Damocles hang over him every minute of the day that the other eye may also go blind,
– losing access to insurance as one’s insurability is diminished since underwriters are not so much interested in heavily handicapped people with incurable diseases given that they greatly increase their risk to have to pay out claims,
– always second guessing what to eat, drink and how much and what drugs to take or not and when, whether to fly or not, whether to exercise or not and how much, whether to give up one’s stressful job or abandon other stressers to try prevent that second attack.

Imagine also what it means financially and emotionally for a NAAION patient claiming a disability benefit, when all the deciding authority uses as a standard to determine whether one qualifies is the subjective, ancient Snellen (or its newer Logmar) visual acuity test that in no way is an accurate reflection on what remains of functional vision with a NAAION patient. One then gets denied the benefit as if one is not severely handicapped, but one is if one cannot function by far like one used to. There is no functional vision test though to provide an objective decision. Again this is also a form of trivialization beyond ignoring that one is often half as productive (with one eye affected and even far less or little with two affected.

Try then as an NAAION patient feel comfortable knowing that. Or try stick your head in the sand ignoring that.

Either way, NAAION is initially an unavoidably big presence. The battle is really to reduce its importance by getting more knowledgeable and getting more acceptance and understanding as well as consideration by one’s surroundings and by oneself. That way one  can reduce its impact on one’s life and move on to being as productive and happy as is still possible within the new NAAION limitations.

NAAION never goes away, but one can work on making its effect more manageable, less dominant up to the limit of one’s capacities. It requires being creative and being much more a champion for oneself than before.

CAUSE: It is not clear why NAAION happens. The main theory and partially proven, is that it is caused by a sudden hypotensive (drop in blood pressure) event, most often at night (when blood pressure already decreases naturally) resulting in  poor perfusion, so poor blood flow  around the optic nerve head (=optic disc), which is followed by optic nerve fiber cells (axons) and retinal ganglion cells (RGC’s) that connect the optic nerve with the retina, dying off.  In the first 14 days, unless treated, usually 80% of RGC’s die off.
The acute NAAION event phase is visible as a swelling of the optic nerve head (disc edema).

No, it is absolutely NO blood clot, so no thromboembolism, no obstruction of arteries, no occlusion (technical term (neuro-)ophthalmologists and optometrists often use.

Several risk factors make NAAION more likely, such as a ‘disc-at-risk’ shown in a small cup-to-disc ratio and/or drusen (deposit of fat and protein, often seen in their ‘hard’ version with calcification) at the optic nerve head.
Other factors that increase the risk for NAAION are for example: hypertension (high blood pressure), sleep apnea, vascular and heart problems,  stress, excessive weight, certain blood pressure lowering (over the counter or prescription) medications (also certain eye drops), overexertion, dehydration, flying in non-pressurized planes, climbing/hiking at high altitudes and more. Some of these factors are entirely proven in clinical studies, some are proven and contradicted in some studies or there are researchers who do not like the methods used by their colleagues, so they are then considered debatable. Or there are even lots of anecdotal causes that really have no evidence to back up their identification as cause, except MAYBE sometimes with tiny studies of a mere couple of patients that are hard or impossible to reproduce.

 

 

How do NAAION eyes look like

<under construction>

Treatments

Despite that many doctors and clinics are not aware of this, treating NAAION is an emergency situation, at least for those approximately 60% of patients who will not see improvements or stabilization of the vision loss occur without intervention.

The two sole existing and potentially working (not with all NAAION patients) treatments available to try stop loss of vision – even possible blindness in one eye or both – by reducing the disc edema faster than occurs naturally, must be started at the latest within 14 days of the NAAION event, preferably a week or more earlier, when optic disc swelling is still present. The earlier the better.

These two potentially working treatments are:

a) Oral steroids following the protocol advised by neuro-ophthalmologist and the ‘father’ of NAAION, Prof. Sohan Hayreh.

For the details of the oral steroids treatment, please consult the section Management of NA-AION of Prof. Hayreh’s excellent online article for clinicians on AION’s.  The orals steroids course (not IV!) starts with 2 weeks of 80 mg daily followed by tapering off in weekly steps). The purpose is to speed up the resolution of the optic disc edema to break the cycle of destruction of axons and retinal ganglion cells faster than with letting it run its course without treatment..

b) Join the worldwide clinical trials in 89 locations of the neuroprotectant intravitreal QPI-1007  (by Quark Pharmaceuticals) injections (has a 20% placebo component). Minimum age is 50, maximum age is 80. A previously treated eye disqualifies that eye for this trial. Disclaimer: There is still too little evidence from the preceding phase 1 trial to say that this would work. Neuroprotectants have been used with humans before and failed. Until now (end of July 2018)there have been no intermediary reports about this trial. Thepro ject presupposes 12 months of follow up of a patient and it started in October 2017. In April 2018 the project was redesigned for unknown reasons and its length extended. We point out though that any damage reduced by this drug should already show in the first months, since the all important axons and retinal ganglion cells will incur most of their permanent damage in the first few weeks after an NAAION attack. It will not take a year to see the impact on functioning vision

The NCT02341560 clinical trial information and the full contact details of the 89 clinics offering the  trial treatment, can be found here at Phase 2/3, Randomized, Double-Masked, Sham-Controlled Trial of QPI-1007 in Subjects With Acute Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)

So remember: Time is of the essence! This is an emergency treatment disease, not one to be gradually diagnosed and treated via appointments.

Note: There are presently no other treatments that have a chance of working. Many treatments have been experimented with and failed. Some are outright scams.

 

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