Thanks Beauty. You are right about "borrowing trouble." I am swearing off of MS research readings for awhile. No worries about asking your doc. the questions. You had plenty on your mind!!

I am too much of an advocate -- I think I drove some of the doctors crazy. The college I teach at is part of a system with a medical school. So I have online access to thousands of medical journal articles through my library. I went on an MS research binge right after the diagnosis and practically made myself an obsessive compulsive. I knew so much that I think the most recent neuro was rather surprised -- but thought it was cool that I could have a more detailed conversation about treatment, symptoms etc. But I am at a point in my life where maybe I don't need any more info....I just need to stop worrying and take it day by day.

I am like that right now. I have read 4 books, and have about 5 more to read. I have a notebook full of questions for the Specialist, and have faxed him all my info so we can spend QUALITY time instead of him reviewing the info while I am there...LOL

But, then we reach a point where we can't answer our own questions, and research tuns scarey. Sounds like that is where you are!! Hope you get all the answers you need, and it isn't as bad as you think.

Quite honestly, they do not know for sure the significance of T2 lesions to the disease process yet (believe it or not), but what they do know is that people with this certain type of lesion in their brain or spinal cord will likely be dx with MS at some point. That is the main significance of a MRI; to DIAGNOSE the disease.

The more you research and think you understand about this disease, the more you realize "they" don't know a lot either yet. They are not even absolutely sure that repressing the inflammation that goes on in the lesions (causing them to appear less hyperintense in a MRI) is necessarily a good thing . . . but at this point they are approaching them on the premise that the inflammation is bad.

That is the reason that they treat us with steroids and the CRABs, to hopefully reduce the "flare-ups" of T2 lesions . . . in an effort to try to affect the disease process in the longer run. However, other researchers are of the opinion that we should let our bodies "run the course" of inflammation rather then try to suppress it with meds . . .

The way I understand it, the T2 lesions are the more transient type, that inflame and then most often disappear at will. The drugs we use tend to manage the flare-ups of these lesions, but the fact that they are flared does not mean anything absolute either. That's why you will hear people say that they are very disabled with few lesions, and others have no obvious problems with 100+.

Besides, a person could take a MRI every week and get a different outcome of the number of visible lesions.

T1 lesions are the destructive ones, that imply more "axonal loss and matrix destruction." Having them correlates more closely with clinical disability then the number of T2 lesions (which tend to be more transient). T1 lesions are the more permanent (black holes), and are found more commonly in those with SPMS (and possibly PPMS). These lesions generally indicate a longer duration of the disease process, and people with RRMS will generally have a lower ratio of T1/T2 lesions then those with SPMS.

Cherie

Thanks for the info Cherie. I'm not sure if the above information makes me feel any better as I was told I have a significant amount of T1 lesions. It really kind of scares me. I don't have any disability though. Why? I just one mild case of O.N. (clinically isolated syndrome) and occasionally dizziness -- but who knows, that could have been from the psuedo-panic attacks I was having in the months after I was diagnosed because I was so freaked out. It has been almost a year since the O.N. began and nothing new has cropped up.

Beauty, great idea on faxing the questions ahead of time!

I think what makes this disease so infuriating is that it is a slippery little critter. There are never really any definitive answers. Knowledge and information always make me feel better but most of the time I can't find the answers to my questions in all of the MS research I read. So that leaves me feeling not only frustrated but scared to death. I am practicing taking Vic's advice about recognizing that MS just IS. Just trying to learn how to be zen. I'm about to sign up for a yoga class.

Natalie, do you have access to your MRI report, as deciphered by the technician? I would get a copy, if you don't already have one.

I mixed up a lot of things that were said to me in those early days, so with any luck, you may find they said T2 lesions instead.

On the other hand, if it is T1 lesions . . . like I said, nothing really seems to make sense with this disease. I had only 3 small lesions in my brain, even after 12 yrs with this disease, yet they told me I had a significant chance of being bedridden from the get-go with the first and second attack because the attack was from severe spinal ones (lesions); transverse myelitis. I am still walking, 17 yrs later.

There are no absolutes. Even if there are trends, it doesn't mean that is what is going to happen to any one of us.

Cherie

Thanks Cherie. Yes I have access to the 3 MRI's I had in Sept. 2007, Oct. 2007, and Dec. 2007 and every other report written by every doc. I saw The first two MRI's were in my home city. The reports didn't talk much about T1 lesions. But the Mayo Clinic doctor who interpreted them said I had multiple T1 hyperintensities (and black holes) which is why I should go on high dose interferon immediately. I only lasted 2 weeks on Rebif--severe depression and bedridden the entire time from sickness. And I only made it to the lowest titrated dose. I'm on copaxone now, for 3 weeks, and it is making me feel REALLY crappy. My body does not like meds at all. I don't know how long I can last on it. Anyhow, I have an appointment with my city's MS clinic and the famous doc and his cohorts on June 5. So I will be anxious to see what they say. The neuro I have now pointed out some black holes and white lesions but didn't say much--she certainly wasn't alarmist like that hideous mayo clinic doctor. It's just the more I read the more freaked out I get. Which is why I need to cut back on the reading!

I'm glad you are still walking!

What's the saying, "we only use 1/10th of our brain" . . .??

Location, location, location . . . that's what we all used to say on the forums, when it comes to lesions. Yours must be in good places, or perhaps very small.

Ask lots of questions next time you see him/her . . . for what it's worth.

Cherie

Someone sent me a PM expressing concern over my previous comment, "they told me I had a significant chance of being bedridden from the get-go". I thought I should try to explain what I meant because it was specific to my situation with this disease . . .

We can have lesions in our brains or our spine, and although many of us apparently have spinal lesions (something like 75%), for some unknown reason it seems that most people don't seem to EVER have ANY significant problems from the spinal ones. (I don't know the % that does, but after being on the forums for many years, it seems a relatively small number . . .).

The reason the doctors mentioned "bedridden from the get-go, etc.", for me, was because I tend to have considerable inflammation with my spinal lesions, and the attacks are severe when they occur. The odds are not that great of full recovery from a severe spinal lesion attack . . . but I have been reasonably lucky that the lesions have healed fully, or at least somewhat, each time after the attack.

Spinal damage, from whatever cause (a fall, lesions, etc.), is not good. It's kinda' like when someone breaks their neck (think Christopher Reeves), as far as the "threat" to our eventual outcome. In our case (with MS lesions), the amount of "permanent damage" from flare-ups is dependant on how high up the inflamed lesion is (C-spine), how severe the inflammation is when it occurs (how much of the spinal cord is damaged), and then how much recovery there is after healing.

So . . . it's my understanding that inflamed spinal lesions are the biggest IMMEDIATE threat some of us might have from with this disease, no matter how progressive the disease appears (or doesn’t appear) to be in our brain.

As far as T2 brain lesions, the inflammation tends to be more transient in that they inflame and disappear sometimes very regularly . . . but fortunately our brains can usually re-route/compensate for this. Transient inflammation of brain lesions often leaves no damage what-so-ever either, and it may take several years before we even notice disability from them (except perhaps temporary effects during an attack). That's why we can have "dozens" of lesions (and not even necessarily be in an attack) . . . yet not feel a thing or have any damage.

The theory is that the drugs we use might reduce the amount of inflammation/potential attacks, hopefully resulting in less T2 lesion activity. Theoretically, this might ultimately reduce the number/size of T1 lesions (the more permanent kind) too, hopefully leading to less “permanent” disability. The process for this cycle (from T2 to T1 lesions & disability) is usually fairly long-term, unless any one lesion is in a critical part of the brain.

The problem with the current approach to managing this disease, i.e. reduced inflammation hopefully leading to reduced disability, is that things don’t always work out that way. Even if our drug of choice might lead to a 100% reduction in relapses/acute disease activity (as measured by a MRI) . . . this doesn’t necessarily amount to a reduction in disease progression or disability. There is some correlation, but it is not entirely convincing, IMHO.

The current research seems to point to inflammation as being the initial phase of the disease, but that it is neurodegeneration that ultimately leads to disability. The inflammation process might play a part in neurodegeneration, and they suspect it does, but it is actually the neurodegeneration process that leads to disability. That is perhaps the reason that PwPPMS and SPMS have very little inflammation activity, yet they quickly or continuously decline.

This is how I understand things anyway.

Anyway, I really just wanted to clarify the role of spinal lesions, and why they had told me I might be bedridden from the get-go, even though I only have 3 brain lesions. Spinal lesions are my biggest obstacle/immediate threat with this disease.

Cherie

I shouldnt have read the last few messages in this thread. I have spinal lesions (C4 and T12), and only two little "white dots" in my left frontal lobe that "are not indicative of MS".

Now I'm going to be worried about those spinal lesions. I have to resist the urge to dig out my MRI reports and see if they're T1's or T2's.

But Erin, like I said earlier:



After all these years on the forums, I can only list off a handful of people that have had spinal lesion attacks like the ones I've had; THEY ARE THAT UNCOMMON! And, even though I've had them . . . here I am 17yrs later and still walking.

Some people are exceptionally curious about sourcing this information, and they ask the hard questions (about T1 vs. T2 vs. spinal vs. brainstem lesions, etc.) Other people find it frightening, but still want to know. Then there are those that find it stressful to know. I struggle with what to say to satisfy the questions, and of course it is only my interpretation of the way things are too (to be taken with a grain of salt). . .

The thing to keep in mind though is that there are no absolutes with this disease. We all know this isn't a great disease to have (without being subject to the nitty gritty details), but it is one disease where they are very motivated to find the answers too. As my doctor said a few months ago, there couldn't be a better time to have it then right now, with all the new technology and treatments on the horizon. There was nothing to help us back in 1991 (when I was dx), and we've come a long way since then . . .

Don't worry about something you can do nothing about, especially if it's never caused you any significant problem in the past. There are a few people who have bigger challenges, or perhaps somewhat worse odds then the majority, but these complications are highly unlikely. It's the same with anything in life; bad things happen to a few people. . . but we can't let that fear rule OUR lives.

Cherie