NEW: Clinical Trial in Texas w/Dr. Diana

[HappyPoet]

The statistician (uh, that would be me) will be looking at the fundus photos "blindly" and trying to divide them into "normal" and "not normal". Any of the criteria may be enough to put someone in the "not normal" category. Then we'll analyze them from there as to what indicators were most prominent, etc.

Thank you for your explanation, Dr. Diana. Your study will have a total of 30 MS patients; does that equate to a total of 60 MS samples (two eyes/patient) for purposes of statistical significance?

Bilateral ON is one of my most challenging symptoms. I wonder if I would show up as "not normal" in your study with my symptom history of PAIN in eyes, PAIN behind eyes, blurry vision, double vision, tunnel vision, loss of peripheral vision, loss of color vision (much improved post-venoplasty), scotomas (blind spots), and recurrent amaurosis fugax (temporary total blindness, self-inflicted by rubbing eyes while asleep due to PAIN).

I have a theory about that and will present it to everyone for feedback soon. Dr. Dake asked me a similar question, and the only problem I'm running into is how to prove my theory right or wrong WITHOUT using tissue post-mortem. Ewww, and Yikes.

If there's a way to prove/disprove your theory without having to use post-mortem tissue, I do hope you find it!

However, if you do end up needing such tissue samples, I hope you don't run into any problems obtaining them. Do you know of an organization to which a pw'MS' could donate their eyes and/or other organs/tissues to 'MS'-related research?

Also, if it's possible for a person to have Optomap imaging done locally, do you ever look at such images from patients who send them to you?

Thank you again!

[DrDiana]

Whoa! Cece! You are an amazing researcher and a virtual encyclopedia! Great information!! I heartily agree that hypoxia is what dims the colors. BUT, I'm doubtful that is what causes ON (optic neuritis).

Do you think the hypoxia is the "tipping point" for ON?

I will tell you that when I look at the fundi (back part of the eyes) of Ehlers-Danlos patients, the sicker they are and the longer they've been "triggered" (we are actually born with the genetic defect), the worse the vessels look (in a huge sample size of 3, mind you). But the arteries and veins appear too narrow and too far apart. And there are not enough of them! I see that, and I think "there is a stroke waiting to happen". EDS patients have horrible hypoxia. We develop glaucoma fairly often, but NOT O.N.

That's what I'm trying to figure out. Why don't EDS folks develop ON? It must be something beyond hypoxia to cause ON. That's where my hypothesis comes in (and the post-mortem stuff. yikes).

I'm so glad that great minds like YOURS are on this, too,
Cece!

[DrDiana]

Hi HappyPoet,

Almost! We'll have 30 "normal" patients and 30 patients with MS and/or EDS (many have both), but not everyone has 2 eyes (eww again), so it will be 60 participants.

One interesting thing I've noticed in a huge sample (3-4 ha), is that the vascular irregularities tend to be pronounced in only one eye. For ME (it's all about me. ha again), the abnormalities were on the side that HURT -- same thing as you -- eye pain, sinus pain, etc.

I am dying to know what we'll learn with patients like you who have many ocular symptoms. Even though the main thrust of the research is to look for abnormalities that we would expect to see if the venous blood is not draining well, I may find a plethora of other things, too. Or not. Some of these problems may be originating higher up in the brain, as we recently discovered with glaucoma (well, a researcher at Stanford figured out that one!).

GREAT question about tissue donation. I've agreed to donate my body to EDS research, and am still trying to get the correct information as to where to send it! For MS, I hope one of the MS researchers can help us out there. (And this is funny -- I'm leaving a list of instructions of what I want them to check for first! ha. Controlling research even after I'm DEAD. THAT is OCD!).

[DrDiana]

HappyPoet,

I forgot one of your questions. (Whether I can view optomaps 'from afar'). I'm not sure yet, actually. Our equipment is getting the hot off the press latest and greatest software updates, and I'm not sure how many people currently have that (but I'm sure they'll get it soon!). Also, I have to be able to scroll around and magnify the images, use different color filters, etc. to see what I'm looking for. Once I get going (next week!), I'll have a better answer for you.

This is tricky stuff. On some of the images, especially on young folks, the reflection from the nerve fiber layer (normal) interferes with the ability to see how smooth the vessels are on their edges. The new software should really help with that. Some of the abnormalities are VERY subtle and only jumped out at me because 1) I'm OCD and 2) I was a highly motivated patient! So reading the images "blindly" (so to speak -- not knowing who is healthy and who is not) will be fascinating.

Oh, another thing that came up in preparation for this study -- while I was viewing some "normals" that were already in our system, I came across a patient who had an area that did not look normal. Some patients don't tell us everything about their health, for whatever reason, and I was tempted to call him to see how he was feeling. Perhaps he had symptoms and didn't say anything, or -- this is the big one -- could he be ABOUT TO HAVE SYMPTOMS? Could it be possible that we could pick up the poor drainage through tests like this before the patient becomes symptomatic?

Wow, wouldn't that be something? Then you treat them (CCSVI) and they avoid the whole MS thing altogether? Some studies are showing that the MS CAUSES the CCSVI. BUT I don't have MS and neither does my son, but we both have CCSVI, hypoxia to the brain, and Ehlers-Danlos. The mystery deepens.

Maybe I'm hoping for too much, but the eye is SO revealing.

[Cece]

Your excitement is contagious, DrDiana.
I will have to think about some of what you raised here. I've seen the hypoxia-color connection as separate from optic neuritis. I also had red 'dimming' from my optic neuritis in one eye on two separate occasions (separated by five years or so) but that was very different from the all-over brightening of all colors after venoplasty.

In EDS, when you say that there is severe hypoxia, is it that the carotid artery is affected too? Where is the hypoxia coming from in EDS?

[DrDiana]

Oh boy, Cece,

We need your mind in the EDS world, too.

With Ehlers-Danlos, the hypoxia is so bad that we feel as though we are suffocating. I kid you not. We tend to develop left ventricular diastolic dysfunction (the heart can't push enough blood into our brains) AND I THINK I KNOW WHY! It's an incredibly long explanation, but half of it is coming out on the website "Prettyill" next week. And world renowned geneticist (in connective tissue disorders) Dr. Clair Francomano also thinks we're onto something big here... I am incredibly humbled just to be able to speak to someone with her credentials. So, yea, I'm kind of excited!

One reason I'm enjoying being with you all (besides the fact that EDS folks often develop MS - from hypoxia? maybe so! AND besides the fact I feel a sense of family that I've really missed the last few years AND of course the fact that you guys are smart, funny and kind), is that the overlap can help us rule some things out and some things in, if that makes any sense.

If I am right (I hope and pray that I am), I may have a potential treatment for all of us, whether successful with angioplasty or not. We MUST increase the circulation of CSF and blood in our brains. (We'll duct tape the rest of us together for now. The brain gets priority.) It is definitely making a difference with most EDS patients (yea), so I am hopeful.

[newlywed4ever]

I just subscribed! www.prettyill.com

[DrDiana]

Hi newlywed4ever!

Sweet! I wasn't even sure that button was working yet. ha. (I have a love/hate relationship with technology).

Thanks for subscribing -- this will be fun!

[Laurellynne]

Hello Dr. Diana. Can you not enlist the usage of cadaver dog eyes with known animal model EAE??

Laurel

[DrDiana]

Hi LaurelLynne,

That would be tremendous if I was associated with a large research institution. But it is just lil ol' me...

I need to get the interest of a larger facility who doesn't want to just take the theory as their own and leave me in the dust. Amazingly, it is dog-eat-dog out there!

Thanks so much,

[Cece]

EAE would not be a good animal model for this, since EAE addresses a theoretical purely autoimmune disease. If the lesions caused the vascular abnormalities, then it would work, but it seems more likely that it's other way around and the vascular abnormalities cause the lesions. No vascular abnormalities in EAE.

[Cece]

Oh boy, Cece,

We need your mind in the EDS world, too.

With Ehlers-Danlos, the hypoxia is so bad that we feel as though we are suffocating. I kid you not. We tend to develop left ventricular diastolic dysfunction (the heart can't push enough blood into our brains) AND I THINK I KNOW WHY! It's an incredibly long explanation, but half of it is coming out on the website "Prettyill" next week. And world renowned geneticist (in connective tissue disorders) Dr. Clair Francomano also thinks we're onto something big here... I am incredibly humbled just to be able to speak to someone with her credentials. So, yea, I'm kind of excited!

One reason I'm enjoying being with you all (besides the fact that EDS folks often develop MS - from hypoxia? maybe so! AND besides the fact I feel a sense of family that I've really missed the last few years AND of course the fact that you guys are smart, funny and kind), is that the overlap can help us rule some things out and some things in, if that makes any sense.

If I am right (I hope and pray that I am), I may have a potential treatment for all of us, whether successful with angioplasty or not. We MUST increase the circulation of CSF and blood in our brains. (We'll duct tape the rest of us together for now. The brain gets priority.) It is definitely making a difference with most EDS patients (yea), so I am hopeful.

It's really interesting that EDS folks often develop MS. I had first thought the connective tissue disorder might mean that the valves in the jugulars were abnormal in EDS folks but it seems such a pervasive problem in EDS with connective abnormalities throughout the cerebrovasculature, and even the heart! But it would seem that the end result is the same: a poor environment for the neurons (with hypoxia and low glucose).

Do you know if there is known reduced cerebral perfusion in EDS? And if so, it's believed to be due to the left ventricular diastolic dysfunction? Feeling like one is suffocating has got to be awful. I have often felt faint, like I might pass out (but without passing out), over the course of the day, it might be similiar?

[DrDiana]

Hi Cece,

Well, if I can claim to be an expert in anything (besides collecting dust bunnies on those bad days), LIGHTHEADEDNESS would be it.

I personally believe that the diastolic dysfunction is a RESULT of the hypoxia (we can't get oxygenated blood INTO our brain because we can't get the old nasty stuff OUT, which is what may be happening in MS, too, hence the CCSVI interest...).

Autonomic dysfunction is fairly common with MS. You can test for "POTS" - postural orthostatic tachycardia syndrome at home, usually. Lay on the floor quietly for about 10 minutes, check your heart rate. Then stand up for 10 minutes. You must stand perfectly still, no shifting, talking, laughing, etc. Check your heart rate again (it's easiest to use heart rate monitors like many of us use for exercise). If your rate has gone up 30 beats or more in that 10 minutes - BINGO, you have POTS. If not, then you need to find a tilt table and let a doc test you (usually a cardiologist). Silly me! I have a VIDEO on POTS! Here it is:
http://prettyill.com/videos/watch/pots_and_dysautonomia

This is the site that will go live any day now! Certainly by Friday. Yea.

It should have LOTS of info for you...

The feeling of suffocation is horrible, as you can imagine. We all go through it and fortunately, it comes in waves, so we know it will end. I usually end up on all fours trying to breath. Yikes. The air is going in and out, but NOTHING is getting to our brains. Try explaining that to most doctors and they give you "that look".

Party on,

[blossom]

dr. diana, for those of us that have no brain lesions but like me i have a lesion on the cervical and the spine is a mess. but i have most of the so called ms symptoms from the neck down. i had stenosis and was treated but was no help only got worse.

what i'm trying to ask i guess is that if mine and some others symptoms aren't so much like cece's or happy poet's - eyes, brain fog, balance etc.
will the things you are researching and possible treatments be able to help us too. or are we a different species? since i did have ccsvi i'm hopeing the answer is yes.

thank you again for being a part of trying to figure this out. now in hopes that the other med. fields join ranks and put their heads together jointly so to for once be in the interest of the sick instead of it seems at times their own interest.

[DrDiana]

Hi Sweet Blossom,

As I love to say, BRAIN FOG IS REAL. I can't remember the specifics of your condition, but I remember that your spine was involved...

I only have 1 brain lesion (do you celebrate that or not?), but am responding to my own treatment!

So am I right, you have no brain fog, fatigue, autonomic dysfunction?

Thanks for the reminders!