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