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http://m.ebm.sagepub.com/content/early/ ... 6.abstract

This is an article about ligation of external and internal jugular veins in mice in order to create a mouse model of CCSVI in a recent 2016 study, but as far as I know, it doesn't address the concern that cerebrospinal drainage in mice is not primarily through the jugular veins. I had to look up the name of the vein in mice, it's in this post http://www.thisisms.com/forum/chronic-c ... ml#p189164

It's the retroglenoid vein that would need to be ligated in order to compare mice to men. I think.

Cece wrote:http://m.ebm.sagepub.com/content/early/ ... 6.abstract

This is an article about ligation of external and internal jugular veins in mice in order to create a mouse model of CCSVI in a recent 2016 study, but as far as I know, it doesn't address the concern that cerebrospinal drainage in mice is not primarily through the jugular veins. I had to look up the name of the vein in mice, it's in this post http://www.thisisms.com/forum/chronic-c ... ml#p189164

It's the retroglenoid vein that would need to be ligated in order to compare mice to men. I think.

Anyway mice do not stand up. I remember that jugular veins were contracting and expanding according to the posture. It is probably impossible to reproduce CCSVI in mice.

Humans with jugular vein occlusion as a complication of a central catheter, superior vena cava syndrome, surgical ligation of the jugular veins, dural venous thrombosis, or other causes of venous obstruction do not have an increased risk of developing multiple sclerosis.

You can do the same experiment with ligation of the retroglenoid vein or any other vein, and I assure you the mice will not develop a multiple sclerosis-like disease. They may develop venous infarcts or hemorrhages if the venous hypertension is significant enough (as can occur in humans with dural venous thrombosis for example)

-cent

centenarian100 wrote:Humans with jugular vein occlusion as a complication of a central catheter, superior vena cava syndrome, surgical ligation of the jugular veins, dural venous thrombosis, or other causes of venous obstruction do not have an increased risk of developing multiple sclerosis.

Quite seriously have these studies been done? Please post links, I would be interested, particularly in long-term (20-30 year) neurological sequellae of those conditions. (Thirty years chosen because jugular malformations are believed to be present at birth, with diagnosis of MS at average age of 30, with a likely predisposition to autoimmunity as an additional variable)

Cece wrote:Quite seriously have these studies been done? Please post links, I would be interested, particularly in long-term (20-30 year) neurological sequellae of those conditions. (Thirty years chosen because jugular malformations are believed to be present at birth, with diagnosis of MS at average age of 30, with a likely predisposition to autoimmunity as an additional variable)

You ask a valid question

I don't think anyone would follow up patients with IJ thrombosis for such a long period of time.

Generally, a controlled study would be only 1 year: i.e. here https://www.ncbi.nlm.nih.gov/pubmed/16079942

However, the side effects of poor venous drainage are well known. You can get superior vena cava syndrome for instance: https://www.ncbi.nlm.nih.gov/pubmed/18241760

This can cause facial swelling, difficulty breathing/swallowing, headaches. It is not known to causes brain lesions typical of multiple sclerosis.

I found one study which followed 77 patients with dural venous thrombosis for a mean follow up of 77.8 months (max 204 months), and none developed multiple sclerosis: http://stroke.ahajournals.org/content/27/2/243

These patients had very significantly increased venous pressure, far in excess of what has been reported in CCSVI. It was sufficient to cause seizures, arteriovenous fistulas, and other complications. Don't you think at least one of the 77 patients would develop MS if high venous pressure were such a critical element of the etiology?

There are other follow up studies as well (for instance here: https://www.ncbi.nlm.nih.gov/pubmed/19426890)

This is not something that would likely slip under the radar

I can't find any long term follow up studies on people who had SCV syndrome or had ligated jugular veins for other reasons, but the link between these diseases and multiple sclerosis would be well known if this were truly the culprit.

centenarian100 wrote: You ask a valid question

I don't think anyone would follow up patients with IJ thrombosis for such a long period of time.

Generally, a controlled study would be only 1 year: i.e. here https://www.ncbi.nlm.nih.gov/pubmed/16079942

However, the side effects of poor venous drainage are well known. You can get superior vena cava syndrome for instance: https://www.ncbi.nlm.nih.gov/pubmed/18241760

This can cause facial swelling, difficulty breathing/swallowing, headaches. It is not known to causes brain lesions typical of multiple sclerosis.

I found one study which followed 77 patients with dural venous thrombosis for a mean follow up of 77.8 months (max 204 months), and none developed multiple sclerosis: http://stroke.ahajournals.org/content/27/2/243

These patients had very significantly increased venous pressure, far in excess of what has been reported in CCSVI. It was sufficient to cause seizures, arteriovenous fistulas, and other complications. Don't you think at least one of the 77 patients would develop MS if high venous pressure were such a critical element of the etiology?

There are other follow up studies as well (for instance here: https://www.ncbi.nlm.nih.gov/pubmed/19426890)

This is not something that would likely slip under the radar

I can't find any long term follow up studies on people who had SCV syndrome or had ligated jugular veins for other reasons, but the link between these diseases and multiple sclerosis would be well known if this were truly the culprit.

Here are some thoughts on jugular vein ligation.

http://www.thisisms.com/forum/chronic-c ... ml#p128070

http://www.thisisms.com/forum/chronic-c ... ml#p159495

NHE wrote:Here are some thoughts on jugular vein ligation.

http://www.thisisms.com/forum/chronic-c ... ml#p128070

http://www.thisisms.com/forum/chronic-c ... ml#p159495

As I said, there are enough causes of acquired venous hypertension that there would be an obvious link to multiple sclerosis if this were the cause. There are many teenagers and some children with multiple sclerosis, so it's silly to say that you would need at least 30 years of follow up. venous hypertension causes a distinct pathology that does not resemble demyelinating disease.

Also, other diseases which are clearly autoimmune and monophasic can be perivenular

for instance, ADEM (acute disseminated encephalomyelitis) is perivenular

"The pathological hallmark of ADEM is perivenular inflammation with limited ‘‘sleeves of demyelination.
24–28 In some cases, larger areas of demyelination occur secondary to coalescence of many perivenous
demyelinating lesions.26–29"

Source: https://www.orpha.net/data/patho/Pro/en ... 590v01.pdf

Would you dispute that ADEM has an autoimmune pathology? Is ADEM related to CCSVI?

-cent

centenarian100 wrote:

NHE wrote:Here are some thoughts on jugular vein ligation.

http://www.thisisms.com/forum/chronic-c ... ml#p128070

http://www.thisisms.com/forum/chronic-c ... ml#p159495

As I said, there are enough causes of acquired venous hypertension that there would be an obvious link to multiple sclerosis if this were the cause. There are many teenagers and some children with multiple sclerosis, so it's silly to say that you would need at least 30 years of follow up. venous hypertension causes a distinct pathology that does not resemble demyelinating disease.

Also, other diseases which are clearly autoimmune and monophasic can be perivenular

for instance, ADEM (acute disseminated encephalomyelitis) is perivenular

"The pathological hallmark of ADEM is perivenular inflammation with limited ‘‘sleeves of demyelination.
24–28 In some cases, larger areas of demyelination occur secondary to coalescence of many perivenous
demyelinating lesions.26–29"

Source: https://www.orpha.net/data/patho/Pro/en ... 590v01.pdf

Would you dispute that ADEM has an autoimmune pathology? Is ADEM related to CCSVI?

-cent

A long time ago Dr. Zamboni said he was not a mouse doctor. Cece has said that the jugular is not the correct vein to model CCSVI in a mouse. It has been pointed out that there are significant differences in physiology and posture which (aside from the use of EAE which, by itself, makes them irrelevant) mean that mouse models of MS are mostly useless to CCSVI research. It is generally agreed that treatment of CCSVI causes at least a temporary (sometimes permanent) improvement in MS symptoms, leading toward the conclusion that some symptoms are attributable to CCSVI and not MS. MS is a problematic diagnosis given the frequency people are misdiagnosed with it. There is a large contingent of knowledgeable people who do not even believe MS as commonly thought, is auto-immune in origin. Given it is not known what its origin is, that is reasonable. It seems you are trying to stir things up, which have been settled long ago. I suggest anyone who wants to continue this madness should take it off-line. Since you are so sure that the mice will not develop a multiple sclerosis-like disease, I suggest you apply for a grant and prove it.

It has been shown that MS-like disease appears in mice treated with CSF from humans with MS. It would be useful if you could reproduce those findings using vein ligation in other mice. But your assurances prove nothing.

There was research being done on marmosets, did that ever come to anything?