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I realize that I posted what I called a "final report" on my TIA, just a few days ago, but it seems to me that the three doctors involved, classified the event as a TIA, by default - IOW, they couldn't rule it out, and they couldn't find a better explanation, even after studying the test results, so they called it a TIA, (to err on the side of caution), even though each of them, individually, initially told me that they didn't believe that it was a TIA.
I've been doing a lot of thinking, and a lot of research, since then, and here's what I think really happened:
It is known that about 13% of the general population of this country, suffers from migraines of various types. At least 30% of migrainers experience auras, and around 3-5% of them experience an aura without headache, known as an acephalgic migraine, (I see these referred to as acephalic migraines, also, in the literature - probably one form is misspelled, but I'm not sure which is correct, because both are widely used). IOW, 4 to 6 people per thousand, in the general population, experience acephalic migraines. Symptoms may include scintillating scotomata, (which most members here will remember me mentioning, on two separate occasions, prior to the "TIA event" on July 19th), or other forms of visual "disturbances".
Then there are hemiplegic migraines, which are a very rare, but well described variant of migraines, during which the person will experience the feeling of numbness, and possibly weakness, on one side of their body, (hemiparesis). This feeling will usually pass within 2-12 hours. Hemiplegic migraines can also be accompanied by temporary hemiplegia, (paralysis of one side of the body), with or without a speech disturbance. In my case, the effect was limited to hemiparesis, (if this is indeed what happened).
If you haven't become bored, and wandered off by now, here's the "qualifying" information, that needs to be considered, before I reveal the key, that I believe makes this fit my case:
A lot of controversy has surrounded the pathophysiology of migraines, and there are still a lot of unanswered questions. However, cortical spreading depression (CSD) is widely accepted as the neuronal process that triggers visual auras. In the simplest of terms, the vascular changes associated with CSD are a large transient increase in blood flow, followed by a prolonged decrease, lasting longer than an hour. The increase in blood flow to the cortex of the brain, can typically be as much as 300% of normal, and when it diminishes, it establishes a state of depression. It amounts to a self-propagating wave of pronounced cellular depolarization of neurons and glia, that spreads slowly across the cortex, followed by a period of depressed electrophysiological activity, that has also been implicated in progressive neuronal injury, following stroke and head trauma, (IOW, secondary damage, that occurs sometime after the initial event).
The cortex is the outer layer of the cerebellum, commonly referred to as "gray matter". Note that the MRI scans of my brain, showed "cerebral cortical atrophy", which may explain why my migraine auras are/were not followed by a headache, as is typically the case with "common" migraines. IOW, the atrophy allows sufficient room in my skull for my brain to expand, (with increased blood flow), and then contract, during the depression phase of the CSD, without undue influence from mechanical constraints.
It has been shown that CSD alters blood-brain barrier, (BBB), permeability, (which, IMO, could make a patient more vulnerable to subsequent problems, if not properly treated).
http://www.jci.org/articles/view/21227/version/1
I believe that the key that unlocks this puzzle, in my case, is monosodium glutamate, (MSG). MSG is known to cross the BBB.
http://www.bluestonechiro.com/pdf/Hdx-M ... 5B1%5D.pdf“Glutamate is a major excitatory neurotransmitter in the central nervous system, widely involved in migraine mechanisms.”
“Glutamate is implicated in cortical spreading depression, trigeminovascular activation, and central sensitization.”
Beginning somewhere about late March or early April of this year, I started regularly eating a flavored tortilla chip snack product, known as "Salsa Verde". It gets it's heat from jalapenos, and a lot of other spices are included in the flavoring, and it's rather "addictive", for some of us who like hot chips. These have been on the market for around 10 years or longer, because I first tried them way back before my reactions to gluten ever surfaced, and I ate a heck of a lot of them, even after my reactions began. I had to stop eating them, of course, when my symptoms became severe enough that it dawned on me that I had a major problem, and I figured out that I needed to modify my diet. Anyway, I tried them again, and they didn't seem to cause any problems, so I began to eat a lot of them, this past spring. Sure, I should have known better, because one of the ingredients is monosodium glutamate, (MSG), but you know how many of us are around food - if something appeals to us, and we think that we can eat it, without having dire consequences, we give it a try, (until something forces us to come to our senses.
)Sooooooooo, I have a hunch, that I brought that whole aura-to-TIA syndrome on myself, by eating something that anyone with half a brain, should have known not to do. I may just happen to be more sensitive to the stuff, than most people, but the problem may have been exacerbated due to the fact that when I eat chips - I EAT CHIPS, so I always got a substantial dose of MSG, on an almost daily basis. I stopped eating those chips, right after the event - not because I came to my senses, but because the Frito-Lay route driver stopped leaving them at my local grocery store.
Is this theory far-fetched? You betcha, but it certainly fits the boundary conditions of the problem. And, as we all know, rare medical conditions are rarely even considered by doctors, in their analyses, and/or diagnoses - they will consider rare possibilities only if no simple explanation is possible. This situation is a medical "zebra", if there ever was one.
I probably won't see my PCP until about April, and I won't see my neuro doc until late February, but when I do, I intend to run this scenario past them. I'll be surprised if they will even consider it, though, but we'll see. In the meantime, I believe the acid test of my theory, will be whether or not I experience any more auras, or any other related neurological, (TIA-like), events. One thing is for sure, I won't be doing any MSG "challenges", just to prove that my theory is correct.
Tex
I think Columbo's is supposed to be kinda "ratty". Go to Goodwill. 