Is RRMS misunderstood?

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Is RRMS misunderstood?

Postby NZer1 » Mon Dec 13, 2010 6:41 pm

For some time I have been noticing that the pathology studies done on MS lesions have shown that the immune system is not involved when the lesion is forming. The immune system becomes involved after the lesion is present and the body is attempting to heal the lesion, in essence the immune system comes to clean up the byproducts and scar tissue.
http://www.facebook.com/topic.php?uid=1 ... &topic=257
And I have listed some more info;
http://www.facebook.com/topic.php?uid=1 ... &topic=222
MY THEORY;
The disease form called RRMS is progressive under the cloud of immune system responses which is dependent on the persons immune system having predisposition to 'reacting' at the formation site of MS lesions. The progression is continuing along with/ at the same time as the masking effect of the immune system response at the lesion site.
The DMD drugs are modifying the effect the immune system can have, but it does not change the progression of 'MS' working at the same time.
If the immune system is not involved in such a reactionary way it is because the person has a different or better immune system response to the 'MS' process of damage, and that form of the disease was knick named SPMS or PPMS, or Benign.
Following RRMS people for the past decades has not gotten any closer to the cause of the disease and when the vascular involvement research is spoken about it is shot down with ignorance of the underlying process of 'MS'.
The origin of all forms of MS is not immune system generated it is a process that is caused by blood flow, the immune system has been shown to NOT be present in the early formation of lesions so it cannot be used to study 'MS' causation.
Studying or Modifying immune systems will not get us any closer to the TRUTH about cause of MS!
MS is NOT about faulty immune systems! It lives under that cloud.

Much of the past research on MS supports this opinion, the issue for me is assembling the facts, a challenge for a PwMS.
What do you think?
Regards Nigel
Last edited by NZer1 on Tue Dec 14, 2010 12:44 am, edited 2 times in total.
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Postby CureIous » Mon Dec 13, 2010 8:38 pm

To me, this (in relation to my specific case of RRMS), and more specifically in regards to the heat exhaustion, cog fog and the like, has been about inflow outflow. Fix that, you fix the above, whether I still have this disease known as MS remains to be seen, and likely won't be resolved for many years (once again, just speaking for myself). While the lack of further lesion activity, and definitely not any relapses, this far out would tend to push one towards the "trending positive" end of the spectrum, in the end, there's just no saying either way.

All I am left with is a set of self-reported unscientific anectdotal answers to questions, namely:

1. Is my quality of life better, or worse than before the procedure:
Immensely better. Light years.

2. Has the quality been consistently better on a day to day basis, versus the normal ups and downs and wild swings which are part of the normal RRMS experience?
Without question, in fact it is so reliable, that planning for events and trips and gatherings, whatever they may be, are no longer a cause of consternation whatsoever. (I hope that's not a bad day etc etc). Long range plans are important, vastly important. I went from wondering how in the world I would ever be able to work in my trade again, to actively pursuing and engaging it with gusto.

3. Does heat still bother me, even a little bit, is there an upper limit, does cooling off relieve any negative impact due to heat?
Not-even-remotely.

4. Hows that brainpower doing? What about short term memory, long term memory, memory in general?
Absolutely, 100% beyond a shadow of a doubt, stellar, on a daily basis, I stopped writing directions on paper, even phone numbers sometimes, instant recall is just that, instant. Versus pre-op, when I was constantly stopping people and saying, "would you wait until I got a paper and pencil, or I won't remember a thing you said". This is beyond just remembering appointments or whatever, that can be mitigated, it impacts every facet of one's life, continually, unfortunately it can leave a lot of stuff bouncing around all at once. My recent classroom experience was a good real life "out of the comfort zone" test. Instead of just making it and trying to survive, I was called on to work out complex problems on the board in front of the class to demonstrate that the curriculum had in fact been learned, and did it all from memory, succinctly, with confidence. Then I sat down and wondered who in the heck that was up at the board lol.

The first hour and the last hour of the day are no better/worse than each other, so consistency reigns supreme, and that is a good thing, very good, the best.


All that aside, I'm not surprised in the least that the above transpired in the absence of any DMD's, if the above as part of the complex of MS is strictly an ingress/egress issue, then the DMD's, as they may relate specifically to progression, would have no effect on the above anyways, the symptoms would remain, and worsen steadily, or at a minimum, remain as bad. Should it be discovered in the distant future, that progression indeed is verifiably NOT an issue either, as it relates to nerve/myelin damage or otherwise, then MS, as it exists in my particular world, will be a long gone bad dream.

Unfortunately, this only relates to my particular instance and nobody elses, it proves nothing except that I'm on a really nice long joyride. None of the above can be measured, or scientifically quantified, I know that, and KNEW that before ever setting foot in Stanford. The first group will eventually end up a footnote in the medical books, if that, this was understood also before embarking, and that's okay, really okay.

I went up for myself, my kids, my family, and my quality of life, hoping for improvements. All else is gravy.

I do think though, that my particular flavor of MS, inflow/outflow as I see it, is only part of the MS picture, and fixing that in however it presents in all MS patients is not going to solve the MS puzzle, but it's surely going to make a dent in a lot of people's lives. For now, amoi will take what he can get and be thankful for it, whether I can explain it in molecules and big words or not...

Apologies for the narrative.
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap
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Postby blossom » Mon Dec 13, 2010 9:02 pm

i feel that one thing will not fit all. "i wish" we know some get better with chiro. some with diet, some with liberation still a lot of work to be done there, some were diag. with ms and it was lymes, there have been many testimonies of people getting better from this or that. why not everybody if it is the same disease we all have? so how are these drugs they have peddled gonna help-especially if they are targeting the wrong thing.

ccsvi has proven that there is a connection or why do some get worse and some better. say me, ok, they got the top open but if the veins in the spine are still screwed up for whatever reason could that cause another problem? could that be why i am worse? as far as i know the top is ok. "i hope i think." they dabbled with my agyous vein at the top if the bottom is kinked or has pressure and they have no way of addressing that yet could that be why i am experiencing numbness and getting worse?

so, for sure blood flow is involved. until they figure out why some got worse it leaves a black hole. the ones that improve and then decline when restenosis or clots form get that cleared again and improve again they must have the probem there only. but if you improve some but not enough is the bottom involved? a boat cruises down a river that is all clear but when it runs into a place that is not clear where is it to go? these researching ccsvi have their work cut out for them. we know more now that the risk of clotting and other not so fun things are a real risk and is happening a good bit. they gotta figure out a way that people aren't having to have this done over and over and in time they will.

in the meantime i think we have to stay open minded that anything that could be the culprit causeing our symptoms if you can check it out. myself, i maintain injury started this mess for me. also, there's the fact that my x-husbands first wife had ms. could i have contracted a virus from him and the fall trigured it? adding to a screwed up spine. lymes disease can be sexually transmitted and transmitted from mother to the baby in the womb. could there be a virus or bacteria that weakens or screws up our veins? there is next to no research on if ms can be sexually transmitted but those that have say it may account for parts of the world that was pretty much ms free until frisky little soldiers from areas that ms did exist were in these countries.

then there's the iron deposit issue. this all has to be dealt with and there are those working on it. do i have iron deposits? i should if i have what they call ms and they treated me for ccsvi. is there a way they can check these deposits? i only have 1 lesion all these yrs. that i've been told about. wish they'd figure out a way to get that sucker outta there and see if things cleared up. maybe a shot of stem cells to jump start things.

basically i want to take a screaming fit most of the time because these relentless rotten symptoms have dodged the bullet forever it seems. yep, ms doesn't kill you but the symptoms will and personally i think it is driveing me to the crazy side a lot anymore.
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Postby eric593 » Tue Dec 14, 2010 2:23 am

I thought lesion formation resulted FROM immune system activities, its "cleanup" inadvertently creating scar tissue (lesions). It is what is triggering the immune system to begin with that is the question, be it iron deposition or pathogens or molecular mimicry that Embry argued so forcefully for until CCSVI came along.
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Postby Nasti » Tue Dec 14, 2010 4:51 am

This seems like a plausible explanation, but there also might be other triggers and causes for forming lesions and thus disabilities. CCSVI does not work for everybody all the time.
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Postby Cece » Tue Dec 14, 2010 10:56 am

Nasti wrote:This seems like a plausible explanation, but there also might be other triggers and causes for forming lesions and thus disabilities. CCSVI does not work for everybody all the time.

It might, once the docs work out best practices, including follow-up care! (Ok, "everybody" would be a stretch, but "nearly everybody" would us closer than we are!)

CCSVI treatment is meant to work as a treatment for CCSVI, i.e. the specific blockages and resulting fatigue, cogfog, weakness, etc. The effect it has on the MS, however, is separate and varied and seems related to how much underlying damage has already occurred. But after that Christmas miracle thread, it seems like there is hope even for the worst cases.
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Postby CCSVIhusband » Tue Dec 14, 2010 11:23 am

... and knowing Barb Farrell's case ...
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Postby Direct-MS » Tue Dec 14, 2010 12:08 pm

There is no doubt that a key question is do people with MS have normal immune systems which simply gain access to the CNS by way of the effects of CCSVI. There is a large data base that indicates that PwMS have dysregulated immune systems (e.g. impaired regulation) and there is also a high association of MS with a specific immune-related gene. In fact that gene is by far the the most obvious one associated with MS. This cannot be chance.
The fact that an EBV infection is mandatory also favours an immune related component to MS
Also other people have CCSVI but no MS. I know there are people with MS but no CCSVI but this can be rationalized by a less than perfect detection rate for CCSVI and a low rate of misdiagnosis for MS. CCSVI may well be mandatory for MS.
With the current data, I still favour a "two to tango" model with persons with a dysregulated immune system and CCSVI (both conditions being caused by genetics and environmental factors) being highly susceptible to MS.
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Postby CCSVIhusband » Tue Dec 14, 2010 12:29 pm

My problem tying EBV into this is:



"In the United States, about half of all five-year-olds and 90–95% of adults have evidence of infection.[4][5][6]"



There's a high association with EBV and EVERY GROUP you'd ever want to say that with, at 90 - 95% of adults having it ... (adults being the most common possible group associated with any disease - 100% of adults with adult diseases are adult, 90-95% of those have EBV already)


What would REALLY be interesting is finding (EDIT: a bunch of someones in each group actually)

someone WITH CCSVI, withOUT EBV, WITH MS.

OR

someone WITH CCSVI, withOUT EBV, withOUT MS
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Postby Cece » Tue Dec 14, 2010 3:55 pm

Direct-MS wrote:With the current data, I still favour a "two to tango" model with persons with a dysregulated immune system and CCSVI (both conditions being caused by genetics and environmental factors) being highly susceptible to MS.

The dysregulated immune system would be part of how the body reacts to the CCSVI and it only makes sense that all of us react differently to some extent. I'd speculate for myself as having bad CCSVI but a reasonably healthy immune system.

CCSVIhusband, I agree about the EBV.
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Postby NZer1 » Tue Dec 14, 2010 4:17 pm

Direct-MS wrote:There is no doubt that a key question is do people with MS have normal immune systems which simply gain access to the CNS by way of the effects of CCSVI. There is a large data base that indicates that PwMS have dysregulated immune systems (e.g. impaired regulation) and there is also a high association of MS with a specific immune-related gene. In fact that gene is by far the the most obvious one associated with MS. This cannot be chance.
The fact that an EBV infection is mandatory also favours an immune related component to MS
Also other people have CCSVI but no MS. I know there are people with MS but no CCSVI but this can be rationalized by a less than perfect detection rate for CCSVI and a low rate of misdiagnosis for MS. CCSVI may well be mandatory for MS.
With the current data, I still favour a "two to tango" model with persons with a dysregulated immune system and CCSVI (both conditions being caused by genetics and environmental factors) being highly susceptible to MS.

Hi Ashton good to see you here.
I believe that BBB breach happens more often than we are aware, and for more reasons we are yet to study and understand.
I think that way to progress MS knowledge is by using the samples taken in the US Forces and the US Nurses study. Searching for people who have MS now and comparing samples before and after for indicators of change in the immune system and compare that with the type of MS dx.
The idea that the immune system has reacted to the formation of MS lesions is what we need to look for. There must be a change that happens in Pw RRMS that is somehow different to SPMS and PPMS.
The samples could be compared in people who have progressed from RRMS to SPMS and see what is the difference here as well.
The immune system has been shown to change in development, with VitD as one modifier, the contact with various viruses will also modify the immune system.
Because the PPMS and SPMS forms of MS are not showing an inflammatory reaction like RRMS, gives reason to believe that the immune system, as shown by the Pathological studies, is a secondary process/aggravation and when the RRMS person is effected by lesions forming after the damage is done to the CNS (which is progressive during the time there are these episodic reactions to some lesions forming), there is then an overt immune reaction and increased disability immediately.
RRMS has progression that is not as noticable during the episodic times before progression to SPMS and the immune system changes its response to the lesions forming.Whereas a person with PPMS or SPMS has slower non-episodic progressive disability from the "cause" of the lesions forming from continuous damage to the CNS. Likely caused by vascular malformations as found in CCSVI and also vascular issues within the brain and spinal cord.
Indications of blood flow and restrictions occur in many other diseases from strokes, transverse myelitis, Parkinson's, Alzheimer's, ON, TN and other diseases listed as "autoimmune" causation.
Lessons from these other disease similarities will help understand the processes involved with blood flow abnormalities.
Keep in mind that the immune system is not involved until after the lesions have formed which is after the damage occurs to the CNS. The immune reaction subsides when a person progresses/ matures to SPMS.
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Postby Direct-MS » Tue Dec 14, 2010 4:27 pm

For those intersted in EBV and MS see http://nro.sagepub.com/content/early/20 ... 81531.long
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Postby NZer1 » Tue Dec 14, 2010 4:48 pm

For those following the Vascular Involvement;
Slowed blood flow thru MS brains....it's a scientific fact.
by CCSVI in Multiple Sclerosis on Sunday, September 26, 2010 at 9:12am
Please read this note I posted last January about hypoperfusion (slow blood flow) and the MS brain. Many researchers had noted this phenomena before Dr. Zamboni came forward with his discovery of CCSVI. Slow blood can create an hypoxic (low oxygen) situation in the brain, and this in itself can damage brain tissue, causing axonal death and activating the immune system. Here is the note:
http://www.facebook.com/note.php?note_id=229656952210

Remember, the autoimmune theory of MS is still just a theory. Doctors have never proven that MS is started by the immune system.
Here is a wonderful editorial on this topic by Dr. Peter Behan, called
"The Futility of the autoimmune orthodoxy in multiple sclerosis research"
"...a false orthodoxy claiming that multiple sclerosis is an autoimmune disorder has developed and formed the present basis of treatment, drug trials and research. The outcome of this misplaced creed has been truly catastrophic.”
http://www.expert-reviews.com/doi/pdf/10.1586/ern.10.69

If you are curious as to how CCSVI could cause lesions and brain and spinal damage in MS, please, read this note and the paper I have linked. Yes, it is very technical, but I break it down into chunks, and explain what the researchers found.

Again, Here's the Note
http://www.facebook.com/note.php?note_id=229656952210

No matter what neurologists may claim, they have never proven that MS is a purely autoimmune driven disease. Researchers have noted that in the beginning the lesions look like ischemic (low oxygen) events, even before the immune system is activated. Here is a link to Lassmann's paper on this: http://www.ncbi.nlm.nih.gov/pubmed/12559509

Here is a paper by Prineas and Barnett--where they study fresh lesions upon autopsy, and discover that there is axonal death without ANY immune activation: This discovery makes them question EAE as a model for MS.
Relapsing and Remitting Multiple Sclerosis: Pathology of the Newly Forming Lesion
Michael H. Barnett, MBBS and John W. Prineas, MBBS
The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis,
who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases, namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.
http://www.CPn Help.org/files/Ref1_Annals04.pdf

It is vitally important that we understand the science behind Dr. Zamboni's discovery, in order to be informed patients and caregivers. Slowed venous drainage can create slowed perfusion....just like all those researchers noted in MS brains. There will continue to be much push back from the status quo. They need to maintain the current dogma on MS, in order to keep their jobs and pharmaceutical ties. But we need to ask, How do you KNOW MS is initiated by the immune system? Have you read the other research??

Be informed. Read the research. It's not snake oil. It's scientific fact.
http://www.facebook.com/note.php?note_i ... 0796282297
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Postby NZer1 » Tue Dec 14, 2010 4:58 pm

Direct-MS wrote:For those intersted in EBV and MS see http://nro.sagepub.com/content/early/20 ... 81531.long

Thanks Ashton, I like the way there is room in his hypothesis for the maturing of the individual and the maturing of the immune system response, giving understanding to the disease change from RRMS to SPMS.
The genetic link helps to link to European decent.

The question, what causes the activation of the immune response after the damage has occurred in the CNS and the healing fails and the lesion forms?

Blood flow issues as the primary cause of MS, some we are identifying as CCSVI?
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Postby NZer1 » Tue Dec 14, 2010 9:52 pm

Another factor in this is the bodies ability with neuro plasticity. In PPMS and SPMS the changes can be mapped as the brain enlists new areas for functions as the disease progresses. In RRMS because the immune system flares the body has to catch up after the inflammatory event with the transferring of functions to areas in the brain that are not effected by CNS damage caused prior or happening in conjunction with the current episode. Hence the waiting period after an episode when recovery is attempted through neuro plasticity.
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