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

I'm not sure this is totally accurate based on what I've heard from the various neurologists I have seen and all the medical journal articles I have read. I teach in a university system that has a medical school so I have access to online neuro journals--I've probably read too much of it and given myself a scare. Anyhow, there are still plenty of unknowns with MS and my understanding is that researchers are now making the argument that you can have damage to the brain that is not visible on the MRI. (read some of Dr. Elliot Frohman's research from UT Southwestern Medical School) I'm not sure "transient" really means transient in terms of damage. Just because you can see something or not see something doesn't mean you have a relatively definitive answer as to level of damage or course of disease or even symptoms. Remember there are occasionally people who have no visible lesions on the MRI but seem to have classic MS symptoms. OR you could have lots of lesions and no clinical symptoms (and perhaps no immediate inflammation visible on the MRI) but that doesn't mean your brain is free of any damage. In other words, I don't think that lack of inflammation = lack of damage.

I think we are saying the same thing, Natalie . . . but in that particular paragraph I was only referring to "active" lesions that are apparent on a MRI.

What you are saying is what I was trying to get at with my comments about neurodegeneration causing the damage, vs. inflamation. I believe that they recognize our lesions as the inflamation process that is going on, BUT that this is not the whole story. Some people have considerable disability with few lesions, and vice-versa . . . and some researchers currently suspect that is because there is another process going on too (i.e. neurodegeneration).

http://www.ncbi.nlm.nih.gov/pubmed/17397873

http://www.ingentaconnect.com/conten...00003/art00002

Or did I misunderstand your point?

Cherie

Cherie,

Maybe I misunderstood you! Yes, I was suggesting that some other process is going on that isn't really identifiable on the MRI and they aren't even sure what it is. The research I had read said that it is imperative to get on one of the CRABs because there is always damage going on in the brain that just may not be visible on the MRI. That was a scary proposition. No matter what, the uncertainty of this disease is something that I haven't dealt with yet...maybe it's something you never really adjust to?? I find the whole thing still very frightening-- but I've only been diagnosed for 8 months. It seems that all of the unknowns take a tremendous toll on you psychologically.

Well, they don’t know for sure what our current DMD’s are doing for us, BUT they have proven scientifically that they have the potential to reduce inflammation for some people. What else they might be doing, and/or why, no one really knows.

However, in spite of their effect on a reduction to relapses and/or inflammation, the DMD’s don’t influence ‘disability progression’ to the same degree. For many, they continue to progress with disability at exactly the same pace, even though they appear to be more stable (i.e. less relapses and visible lesions).

So, there is clearly something else to the disease process that the DMD’s aren’t necessarily influencing. The current theory is neurodegeneration, and this is what this Pubmed article is referring to, particularly in the last sentence . . .

"A number of recent magnetic resonance imaging studies have challenged the classical view of multiple sclerosis (MS) as a "two-stage" disease where an early inflammatory demyelinating phase with focal macroscopic lesions formed in the white matter (WM) of the central nervous system is followed by a late neurodegenerative phase, which is believed to be a mere consequence of repeated inflammatory insults and irreversible demyelination. These studies have consistently shown the presence of diffuse normal-appearing WM damage, marked gray matter involvement and significant cortical functional reorganization, as well as the occurrence of the neurodegenerative component of MS from the earliest clinical stages of the disease with only a partial relation to MRI markers of inflammatory demyelination. The present review argues that MS can no longer be viewed as a "two-stage" disease, which suggests that the two pathological components are dissociated in time, but rather as a "simultaneous two-component" disease, where the relative contributions of the various pathological processes of the disease to the development of "fixed" disability, their relationship and their evolution over time need to be clarified. This new view of MS should inform the development of future research protocols to define its actual physiopathology and prompt the institution of early treatment which should ideally target not only inflammatory demyelination, but also the neurodegenerative aspects of the disease, as well as promote neuroprotection and enhance reparative mechanisms and adaptive functional reorganization of the cortex."

Cherie