MS: a chronic infective cerebrospinal venulitis?

[Cece]

http://phleb.rsmjournals.com/content/ea ... 8.abstract

Abstract:

The aetiology proposed for the development of chronic cerebrospinal venous insufficiency (CCSVI) associated with multiple sclerosis (MS) has been the presence of congenital truncular venous malformations. However, this hypothesis is not consistent with the epidemiology or geographical incidence of MS and is not consistent with many of the ultrasonographic or radiographical findings of the venous disturbances found in MS patients. However, the probability of a venous aetiology of MS remains strong based on evidence accumulated from the time the disorder was first described.

The method used in this review was to search PubMed for all past medical publications related to vascular, venous, haematological, epidemiological, biochemical, and genetic investigations and treatments of MS.

Epidemiological and geographical findings of prevalence of MS indicate the involvement of an infective agent. This review of the venous pathology associated with MS describes a hypothesis that the pathogenesis of the venous disease could be initiated by a respiratory infective agent such as Chlamydophila pneumonia, which causes a specific chronic persistent venulitis affecting the cerebrospinal venous system. Secondary spread of the agent would initially be via the lymphatic system to specifically involve the azygos, internal jugular and vertebral veins. The hypothesis proposes mechanisms by which an infective venous vasculitis could result in the specific neural damage, metabolic, immunological and vascular effects observed in MS. The hypothesis described is consistent with many of the known facts of MS pathogenesis and therefore provides a framework for further research into a venous aetiology for the disease.

If MS does result from a chronic infective venulitis rather than a syndrome involving congenital truncular venous malformations, then additional therapies to the currently used angioplasties will be required to optimize results.

[tzootsi]

This may be totally out in left field, but if it's a valid hypothesis it could be a major breakthru.

[NZer1]

http://freepdfhosting.com/e843c163b1.pdf
A link to Dr Thibualt's paper
Enjoy,
Nigel

[cheerleader]

We're discussing this with Dr. Thibault on Facebook. He says that the venous malformations he's seeeing in CCSVI don't look like truncular venous malformations.

Here's his quote:

Regarding the nature of the venous lesions, I have observed venous diseases closely with ultrasound for the past 24 years and have frequently noted that infalmmation (phlebitis) of the veins will results in localised thrombosis along the wall of the vein, this thrombosis resolves by fibrosis and recanalisation of the vein leaving intraluminal membranes, septa, webs, and fixed and distorted valves. You do not require congenital venous malformations to produce these lesions. I have been looking at these abnormalities in MS patients for the past 2 years, and I personally don't believe that they resemble congenital truncular malformations in any way. This is a very nasty venous vasculitis that we are dealing with, hence the serious consequences.

I'm not completely convinced that it's all about Cpn. I still believe it's more global, and related to endothelial dysfunction. I know a few people who were on the Stratton/Wheldon antibiotic protocol who continued to progress, and one person who was on it and still had stenotic veins. Cpn may be part of the puzzle for some however. I know that Anecdote (Dr. Wheldon's wife who writes in the antibiotic forum here) has recovered from her MS with the antibiotic protocol for Cpn, and she is doing quite well. Obviously, Cpn was involved in her disease process.

I wish it was easier to know what these malformations are...I was pretty sure the autopsy study from Dr. Fox described the valves as something never seen before....really not sure how inflammation could make more leaflets or invert them, but I'm not a phlebologist

But the big picture is that another phelbologist is finding severe venous vasculitis in MS--as Dr. Dake said to Jeff, "I've never seen veins like yours before." This is a serious problem, and we need to get these guys together to figure it out. Inflamed and narrowed veins draining the brain is a dangerous situation....
onward--
cheer

[NZer1]

I hear there is a second paper coming with research results so we will have some more insight to Dr Thibaults experiences.
I do believe that autopsy results are going to be the way to understand this chicken and or egg dilemma.
There is allot of work to be done, the good news is that the treatment availability is becoming real!
I hope that IVUS is going to be used!
Regards Nigel

[ikulo]

Thanks for the full link Nigel!

An infectious agent causing change in the vascular system makes more sense to me than a congenital cause.

[ikulo]

Third, according to the venulitis theory, the stenoses are an end result of the progressive persistent venulitis caused by the chronic infection rather than the primary cause of the neurological damage. . . . Reversal of the decreased cerebral perfusion may be the mechanism for virtually immediate improvement in symptoms such as fatigue, brain fog and cognition reported by patients following successful angioplasty of stenoses. However, the stenoses and occlusions are not the cause of the MS, they are, along with myelin damage, a result of the infective venulitis.

interesting.

[CuriousRobot]

I'm not completely convinced that it's all about Cpn. I still believe it's more global, and related to endothelial dysfunction. I know a few people who were on the Stratton/Wheldon antibiotic protocol who continued to progress, and one person who was on it and still had stenotic veins. Cpn may be part of the puzzle for some however. I know that Anecdote (Dr. Wheldon's wife who writes in the antibiotic forum here) has recovered from her MS with the antibiotic protocol for Cpn, and she is doing quite well. Obviously, Cpn was involved in her disease process.

cheer

Can you elaborate on that a bit?

[se1956]

Infection ALONE must be wrong.

Because the probability that MS parents transfer the disease to their children is close to 10%.

http://www.neurology.org/content/69/12/1208.abstract

So there must be a congenital part (a metabolism dysfunction?).

But may be it's an/the important trigger.

R.

[NZer1]

Infection ALONE must be wrong.

Because the probability that MS parents transfer the disease to their children is close to 10%.

http://www.neurology.org/content/69/12/1208.abstract

So there must be a congenital part (a metabolism dysfunction?).

But may be it's an/the important trigger.

R.

The question that comes to mind is does this vascular disease theory cover disease transmission from parents??
Seems a better possibly than a hereditary theory. And would also give some insight to the twins theories where each have different forms of MS or only twin has MS?
Also;
The development of the disease per 15-17 years crosses over to other development stages and theories such as the sutures of the skull (Dr. Flanagan) and skull shape/deformities.

[CureOrBust]

We're discussing this with Dr. Thibault on Facebook. He says that the venous malformations he's seeing in CCSVI don't look like truncular venous malformations.

This guy was the referring dr for my first CCSVI procedure in Sydney, and was recently on an Australia news story regarding CCSVI. I remember when I saw him after my second procedure and told him neither procedures had produced any real tangible difference, he implied to me that he did not believe CCSVI would be the answer for everyone's MS, and believed there was most likely some infective agent (either bacteria OR virus). He said (something like) that he would love access to a scrape or slice of the venous tissue at the point of a stenosis to examine it for this agent.

I hope that IVUS is going to be used!

This was probably over a year ago, and when I asked him about IVUS, he had never heard of it before! but that was over a year ago.

Infection ALONE must be wrong.
Because the probability that MS parents transfer the disease to their children is close to 10%.

Maybe they are transferring an immune system that cannot handle a type of infection well?

We're discussing this with Dr. Thibault on Facebook. He says that the venous malformations he's seeing in CCSVI don't look like truncular venous malformations.

He did not have access to IVUS last time I saw him. Maybe let him know one of his patients has been to see Dr Sclafani and has the disk from the IVUS. The US is not performed by him, and last time I went, they could not find any issues (ie cross any of their US criteria). However, at Dr Sclafani's clinic using Dr Zamboni's US they found more than 2.

[cheerleader]

He's had further dialogue with Nigel on the Facebook thread for those on there who are interested. He's been treating patients with venoplasty and a modified Wheldon protocol.
https://www.facebook.com/pages/CCSVI-in ... 297?ref=ts


Robot--The reason I believe MS must be more "global" and not about a single infection is because of the other, scientifically proven environmental and infective associations with MS:
EBV type 1 and 2, smoking,low vitamin D, processed foods, lack of exercise, shift work, obesity, northern European populations, etc.

The only thing I could find that united all of these factors was the endothelium, or lining of the blood vessels. Each of the factors I mentioned above changes the nitric oxide balance in our body, and could potentially make a vascular malformation worse, make blood more hypercoaguable and make inflammation worse. This would decrease cerebral perfusion and increase the inflammation in an already inflamed vein. It was because of my husband's high c reactive protein, high coagulation numbers and high liver enzymes at his very first flare that I went down this path. It takes two to tango....blood and vessels. The researchers need to consider both.
Here's the research I put together for Jeff and sent to Stanford--
http://www.ccsvi.org/index.php/helping- ... ial-health

cheer

[CuriousRobot]

Robot--The reason I believe MS must be more "global" and not about a single infection is because of the other, scientifically proven environmental and infective associations with MS:
EBV type 1 and 2, smoking,low vitamin D, processed foods, lack of exercise, shift work, obesity, northern European populations, etc.
cheer

I'm still not sure what you mean by "global." Smoking, processed foods, lack of exercise, shift work and obesity can all be factored similarly as an increase of oxidative stress in the human body. I understand the potential with EBV, but I feel it is still ambiguous. Other pathogens have been implicated: various herpes, endogenous retros, varicella, etc. Northern European populations still escapes me as to what you are alluding. The lack of MS despite being so far from the equator? It's definitely possible that your husband was an anecdotal case who exhibited stellar progress post-CCSVI and that a pathogen wasn't really something affecting his disease progression. I might also add that there is definite, studied interaction between C. pneumoniae, the vasculature and nitric oxide.

[cheerleader]

This is how BNAC explains the links of MS/CCSVI with bacterial and viral infections and susceptibility-

...it could be hypothesized that venous stasis in the superior saggital sinus due to extracranial outflow impairment could affect the drainage of bridging veins that pass through the subarachnoid space (near the meninges and EBV-infected B-cell follicles) and contribute to EBV activation. The venous stasis hypothesis in the SSS may contribute to understanding why so many different viruses and bacteria [3,111] have been linked to increased MS susceptibility risk over the last 50 years.

http://www.expert-reviews.com/doi/abs/1 ... ern.11.117

I agree, Cpn affects nitric oxide, and I have written about that. There is not just one factor linked to MS susceptibility, Robot. That is what I mean by global--not the planetary definition, but the definition of global as thorough, or all-encompassing. We need to look at MS susceptibility from ALL that we know about the risk factors. And the link to EBV is far from ambiguous. Just go to pubmed and search EBV and MS.

The venous stasis and endothelial understanding considers the big picture-
cheer

[CuriousRobot]

There are quite a number of studies related to Epstein-Barr virus and multiple sclerosis in a PubMed search, most likely only accessible after a $35 (+/-) fee (your link case in point). However, don't you think you are being a little hypocritical? Wouldn't it be MORE global to research "viral DNA and multiple sclerosis" in PubMed, rather than "ebv and ms" alone?

I haven't seen anything as fastidious as the Vanderbilt work with C. pneumoniae and multiple sclerosis. If you find something comparable with EBV, then please send me the link, I would like to read it, fee notwithstanding.

I think a statement like "the venous stasis and endothelial understanding considers the big picture-" sounds a tad Kool-aid-y.