Painful Eye Muscles, Disorientation and Vertigo: Brief Discussion of MG/ACh, OP Toxicity, and MAO Dysfunction

Along with the dry eyes, it felt like the muscles/tendons/ligaments around my eyes were extremely painful as well.  Moving my eyes up, down, left, and right could be extremely painful at times.  Another horrific symptom that occurs as a result of this or along with it is this feeling of “disorientation” with my vision.  The only way to describe it is that if I move my eyes, or even head, to the left or right to look at something, it feels like either my brain or my eyes/vision is “delayed” or “behind”.  This is extremely disorienting all around, and again, left me non-functional.  During Year 4, when I was flaring wildly, this symptom progressed to all out vertigo, with eventual nystagmus.  I was diagnosed with BPPV (Benign Paroxysmal Positional Vertigo), and dealt with this on a daily basis for about 6-8 months.  During this time, I was literally forced to titrate off all TH, as that plus the flaring left me feeling like I was dying with all the accompanying symptoms of vertigo.

There’s no way I can say with any certainty what the painful muscles and tendons around my eyes were due to.  I do know that when I would take too much iodine at once (rapid increase in iodine), that this symptom would get worse.    It also got worse when I was too “low” on thyroid hormone.   In other words, my eyes were best in the “sweet spot”, and painful when I was on either side of that.    I also strongly suspected a few other culprits though, other than just thyroid hormone.

One of these would be acetylcholine (ACh) – related.  In this case, a diagnosis of Ocular Myasthenia Gravis (MG) would be the closest traditional diagnosis.  However, in my opinion, other forms of MG would also be strong contenders:  MuSK MG, LEMS, and Generalized MG.  So looking for these antibodies seemed like a reasonable approach to me (but not to my physicians, unfortunately).  The tests for these are simple blood tests, but they are expensive, so perhaps that was one problem.  The other is that I had a negative ANA, which many physicians unfortunately use as a “gateway” test for other autoimmune conditions.  The problem with ANA, is that it is very fluid, and waxes and wanes not only based on actual disease pathology, but on drugs and other toxins as well.  Most people who are finally diagnosed with MG, on average 5-7 years after symptoms start, are already on polypharmacy with a ton of drugs, and not surprisingly, their ANA is finally elevated.

When I say I wanted to test for MG, it’s not because I thought that having a diagnosis would make me feel better, or that there was a treatment I would do.  Treatments for some forms of MG exists, and in the most severe cases, people must take the medications or risk death.  In my case, I probably would not have done the treatments.  The reason I so desperately continued my search for a diagnosis was simply to try and help delineate possible FQ mechanisms of action.  This is the first step in looking for a biomarker for FQ-induced pathology, and only by comparison of symptoms, other diseases or conditions, and even primary and adverse effects of other drugs, can some logical guesses be used as a start.

Another big ACh-related possibility in my mind is basically an organophosphate (OP) toxicity or “nerve gas toxicity” due to irreversible inhibition of acetylcholinesterase (AChE).  I often felt like my symptoms overall fluctuated between a nerve gas toxicity and a good shot of Atropine (the antidote to OP toxicity).  And I felt like literally all of my symptoms, including these eye symptoms, could quite easily be muscarinic in nature, as well as nicotinic.  Not only that, but remember that one of the Black Box Warnings for FQ literally states that “Fluoroquinolones have neuromuscular blocking activity”.  This is a big clue in itself from pharma about a potential mechanism of action here.  As an aside, non-neuronal ACh is implicated in tendon pathologies, and ACh pathology could easily be implicated in every other organ system as well.  This includes cholinergic innervations of the thyroid gland and axis.

Lastly, I also suspected some form of Serotonin Syndrome (SS) or monoamine oxidase inhibition (MOAi).  This was for several reasons.  One of them was that I had once tried Prozac in 1990, after the death of a family member, but only lasted a day or two on it.  This was because I always remembered this very characteristic pain around my eyes, along with disorientation and a bit of nausea – which is exactly what I’m experiencing now with my eyes (except now it’s permanent).  Fluoxetine (Prozac) not only acts as a Selective Serotonin Reuptake Inhibitor (SSRI), but also has substantial binding to all five muscarinic (acetylcholine) receptors.  So once again, I suppose this effect could be due to the muscarinic actions of Prozac (the side effects) rather than the serotonin effects.  But I also had noticed that with the major massive flares I had experienced, the day before I would actually feel really good – as if I were passing through some sort of “sweet spot” while “on the way up”.  I started questioning if this feeling was a sudden burst or surge of serotonin, which initially made me feel good.   (Update:  this is another reason I started suspecting Mast Cell Activation Syndrome as well).    By the next day though, I was “too high” (or maybe too low, I have no way of knowing exactly what was going on within me) — and the resultant flaring could have possibly included this component as well.  I also felt I suffered from the “cheese effect” – if FQ’s somehow irreversibly inhibit monoamine oxidases, a build up of tyramine from tyrosine could occur, essentially leading to an adrenergic crisis.  I already suspected a tyrosine metabolism dysfunction.  And monoamine oxidases, by the way, are a family of enzymes bound to the outer membrane of mitochondria in most cell types in the body.   So if mitochondria are being damaged or depleted by FQ’s, it’s reasonable to assume that monoamine oxidases will be in short supply as well.    And MOA’s are necessary for a number of important neurotransmitter reactions.

I know I’ve mentioned a lot of potential mechanisms here.  Wiki is always a good place to start for basic information on any of the phrases or words I’ve mentioned.  From there, go on to PubMed to learn more.

 

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