LOL, Jack. I don't seem to follow your hypothisis, so far...thank God.

And I hope you stay that way, too, Sally!

MS is such an individual disease. If the researchers know enough to state so emphatically what it definitely is and isn't......then why can't they find a cure or at least a DMD that works well for everyone? Just sayin'...........

MS is more than a demyelinating disease! It also involves massive death of axons and neurons as the disease progresses beyond the myelin damage stage resulting in irreversible neurologic impairment.

jackD

N Engl J Med. 1998 Jan 29;338(5):278-85.

Axonal transection in the lesions of multiple sclerosis.

Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mörk S, Bö L.

Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.

Comment in:

N Engl J Med. 1998 Jan 29;338(5):323-5.

BACKGROUND: Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults.

Despite antiinflammatory or immunosuppressive therapy, most patients have progressive neurologic deterioration that may reflect axonal loss.

We conducted pathological studies of brain tissues to define the changes in axons in patients with multiple sclerosis.

METHODS: Brain tissue was obtained at autopsy from 11 patients with multiple sclerosis and 4 subjects without brain disease. Fourteen active multiple-sclerosis lesions, 33 chronic active lesions, and samples of normal-appearing white matter were examined for demyelination, inflammation, and axonal pathologic changes by immunohistochemistry and confocal microscopy.

Axonal transection, identified by the presence of terminal axonal ovoids, was detected in all 47 lesions and quantified in 18 lesions.

RESULTS: Transected axons were a consistent feature of the lesions of multiple sclerosis, and their frequency was related to the degree of inflammation within the lesion.

The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains.

CONCLUSIONS: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

PMID: 9445407 [PubMed - indexed for MEDLIN

In about 85% of MS folks the 10 year rule applies (taking a Disease Modifying Medication may extend this for many years)

And what's that percentage for people ON DMD's?


So cheer up things WILL get worse.

Well aren't we a ray of sunshine!!!

I have been dx in 2006, but can trace back my first huge flair to 2001. that makes 9 years for me.

The big girl hospital told me that SPMS has an inflammatory component to it, and they do keep trying steroids as long as the patient shows improvement with the infusion (which I am) and that they will even continue some RRMS treatments such as copaxone. They just really hesistate to move someone to that catagory, unless they are kinda forced to.

One website said inflammatory follows all the way through, and one says NOPE, its only in RRMS, and yet another give a mixed view. If nothing else, this disease has confused me thoroughly.

Thanks for the spiffy drawing!

My first BIG flare was in 2003. Both of my legs were numb and I assumed I had a pinched nerve. No other sx....jut the numbness. So I guess I've actively had MS for about 7 years.

It was two years after that first big flare that I had my second (even bigger) flare. Double vision, numbness, balance, etc.

I tend to think I'm probably SPMS, too. But, my neuro hasn't changed my dx status.

Right now it seems that the visual sx are what I predominately have. If I had to choose, I would have something be numb (besides my right hand/arm. It already is.). Visual sx are awful.....they affect every aspect of your life. Not saying the numbness is any fun.....but at least I can see where I'm going.

There are exceptions to every rule, including Jack's favorite 10 yr rule.....and after all, most of us are exceptional, aren't we?

I had my first big exacerbation in 1975 with SX back to 1964. I didn't become SPMS until around 1998. I'm not in a WC, although, I use my scooter most of the time.

I think my age is now in the SP stage, too, though.

I've had just one truly massive, disabling flare and that was in 1995. It got me diagnosed, although I had dealt with symptoms coming and going for 4 or 5 years prior.

The primary area of attack for me has always been my legs. Some time in 2003, without any noticeable flareup, my walking and balance just started getting worse. In my opinion, that increase in disability without a distinct flare was the hallmark of becoming SPMS.

However, I have had flares since then, too. But also a gradual progression of disability. This could be because the attacks keep hitting the same areas and I end up with axonal damage. Or that glutamate thing that I don't quite comprehend yet (must read more).

At any rate, I think it stands to reason that repeated myelin destruction in the same areas along a nerve axon will result in permanent effects. All the more reason to battle inflammation and modify disease activity as we are able.

The big MS center is now having a huge debate over me. Since they have figured out that my "MS hug" or "flipped intestine" or whatever this is that keeps happening is actually pancreatitis, it may have been keeping those exascerbations going, and there fore, may not be a "true SPMS" so, for now, I sit and wait for this latest event to settle itself, and get over the latest insult, before they re evaluate what is truly happening.

Just like any infections, colds, stress, or whatever can keep MS stirred up, I bet this whole thing has been stirred from the pancrease thing.