Also, one flare or lesion post hicy doesn't necessarily mean its failed.
For just under the majority the effect is fleeting.
I'd love to see an RRMS study with copaxone follow up, I guess we'll see that in a couple of years and Mel will be part of it.
Pretty cool really.
Fingers crossed she is a complete responder. No flares other than old symptoms coming back for heat or stress, no enhancing lesions, two black holes disappeared and shrinking lesion load. MRI next week, Hopkins on 16th, I'll update everyone as I get news.
HiCy except for getting sick is no biggy. You are on a cocktail of drugs to prevent any infections. You are only without an immune system for about 14 days. The neutropenic fever wasn't even that bad for me. Keri didn't even puke.
I don't know about NW program but I know JH is getting good at this.
Intentional or not, that's quite a snarky comment. Not to be argumentative, but I really want to understand how intelligent people could not have significant doubts as to whether PPMS and RRMS/SPMS are actually two expressions of the same disease.Lyon wrote: Not to be argumentative but I really want to understand how intelligent people can come to that conclusion. Please explain your reasoning.
To start with, the patient populations of these maladies differ significantly. PPMS strikes males in equal number to females, while the female to male ratio of RRMS is at least two to one, with recent evidence suggesting the gap is widening. Furthermore, the onset of PPMS is typically seen at least 10 years later than the average onset of RRMS.
There are also striking differences in the pathologies of the two populations. MRIs show that PPMS patients generally have far lesser lesion loads than RRMS patients, and a much greater likelihood of having spinal lesions. In fact, PPMS has sometimes been referred to as "spinal MS".
The wide majority of PPMS patients show no gadolinium enhancement in their nervous system lesions, indicating that inflammation (a sign of active immune system involvement) plays a very limited role in the disease process. Despite the lesser lesion loads seen in PPMS patients, their physical disability is usually greater, and proceeds more rapidly, then those afflicted with RRMS.
CFS analysis reveals that PPMS patients are much less likely to have O-bands in their spinal fluid than their RRMS cousins, so much so that the updated McDonald diagnostic criteria removed the presence of O-bands from the PPMS equation. Again, this points to a different pathogenesis between the two symptom sets.
The Lesion Project has found that the lesions of MS patients fall into one of four categories, and that each patient only displays one type of lesion. This highlights the heterogeneity of MS, and points to the possibility that what we call Multiple Sclerosis is more a syndrome than the disease, and may very well turn out to be a number of different diseases sharing a common set of symptoms.
The work of The Lesion Project has shown that the nervous systems of PPMS patients are damaged exclusively by only one of the four types of lesions. PPMS patients were found to be afflicted only with lesion type IV, while none of the RRMS patients sampled displayed this type of lesion.
Each of the four type lesions types displays different levels of immunologic related damage and damage due to other mechanisms. The PPMS lesions show very little immunologic involvement, and are marked more by neural degeneration, again distinguishing PPMS from the other forms of multiple sclerosis.
None of the treatment options now available, or even under study, has shown any effectiveness in treating PPMS. Even Novantrone, which has been approved for the treatment of SPMS, does not benefit PPMS patients. Rituxan recently failed its stage III trial for the treatment of PPMS, though there is some evidence that a small cohort of patients might have benefited from the drug. This actually should not come as much of a surprise, since all of the MS treatments either modulate or suppress the immune system, which doesn't seem to play much of a part in the PPMS disease process.
On more personal terms, my own experience with this disease differs greatly from the many RRMS patients I've been in contact with. In discussing our diseases, it's often apples vs. oranges. While the disease histories of RRMS patients can differ significantly, when you throw in the experiences of PPMS folks, the differences are stark.
In my case, I was diagnosed in 2003, with a grand total of two lesions (one small lesion in the brain, and in other much more significant plaque at the cervicomedullary junction). Comparing the many MRI scans I've undergone since my diagnosis reveals that the visible damage to my nervous system has remained virtually unchanged.
My original two lesions have never been joined by any others and have never enhanced, nor have they changed in any other discernible way. Yet my level of disability over those six years have increased dramatically. At diagnosis, I had a slight limp in my right leg. Today, my right arm and leg are entirely useless, and my left side is weakening by the month. I require a wheelchair to travel any significant of distances, though I can still shuffle clumsily around my apartment with the help of a cane. The path of my disease is clearly heading to a very unhappy place.
My CFS has remained clear of O-bands as well.
In my quest for answers, I've been examined by and spoken to some of the most prominent MS specialists in the United States. They have all openly entertained the idea that PPMS is a disease entirely separate from RRMS. This is not to say that they consider this a proven hypothesis, but the starkly different pathology and incredible difficulty in treating PPMS certainly has them open to the idea.
I hope this explanation has been reasonably intelligent enough to at least partially satisfy your lofty standards...
Please excuse any typos or misplaced words. I use voice recognition software, which is far from perfect...
Also, sorry for the thread hijack...
Bob, reviewing your post, and my reaction to it, I think I just happened to come across your words while in a bit of a grumpy mood. I'm sure you didn't mean to tweak anybody.Lyon wrote:I suppose my mistake was in not PM'ing the question directly to Jamie rather than addressing him in the open forum. I suppose it would seem "snarky" (snotty??) to anyone else.marcstck wrote:Intentional or not, that's quite a snarky comment. Not to be argumentative, but I really want to understand how intelligent people could not have significant doubts as to whether PPMS and RRMS/SPMS are actually two expressions of the same disease.
Truth is, I said it exactly as I meant it, meaning that I have no doubt of Jamie's intelligence and I honestly do wonder how he came to the conclusions that he has when I used the same information to draw an entirely separate conclusion.
While someone like Jamie using the same information to arrive at a different conclusion doesn't instantly cause me to doubt my opinion, it does make me want to determine whether or not there was something I missed along the way.
I'll PM Jamie instead.
I would like to know what your take is on my reasons for believing that PPMS could very well be a different entity than RRMS, if you feel like explaining it. I do respect your intelligence, and thus your opinion...
I've also read with interest some of the evidence suggesting that PPMS is simply SPMS that has skipped the RRMS phase, or in which the RRMS phase was so mild that it was overlooked.
This may be true in some cases labeled PPMS, but in general, SPMS and PPMS do not look anything alike in regards to MRI studies and spinal fluid analysis. Likewise, the female to male ratio of SPMS matches that of RRMS, whereas PPMS strikes men and women in equal numbers.
PPMS patients generally display a far lesser lesion load than their SPMS compatriots, and their spinal fluid is much more often free of O-bands. The assertion that PPMS and SPMS are identical is flawed, in my opinion.
Thanks for kicking this around with me, Bob. It's always interesting to get the well considered viewpoints of others.
I also admit to being an "MS is caused by a pathogen" fanatic (I was also kissed on the lips by the Phillies Phanatic once--so maybe that's why )
Not that anyone cares, but my take on the Revimmune research is that no one really knows anything about what is going on with MS (or other so-called autoimmune diseases). Not our doctors, researchers, or patients. My husband's doctor (who is treating my husband for chronic, bacterial infection fully admits that he knows very little----reassuring, I know!). In every treatment there are countless modes of action that might not be fully elucidated given our admittedly rudimentary current state. Carrying flowers in one's pocket did nothing to prevent the plague--but the poor b-stards kept trying.
I do want to share this paper that kind of blew me away........this really is only a paper for someone who has done a good amount of research on a bacterial cause of MS (and a plethora of other diseases) because if one hasn't, it will kind of leave the person scratching their head saying, "huh, what does that have to do with MS?"
So for those who are interested, take a look.
For those who I have stolen away their Revimmune thread and RRMS v. SPMS v. PPMS info I apologize.
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