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Hi folks

Saw on Pub Med today a new review article on CCSVI that's also open access.

Endovascular Therapy for CCSVI in MS

My initial take is that it's fair and balanced, presenting both supportive and non-supportive information with lots of info on the anatomy.

It definitely recommends clinical trials and concludes in part:

The incomplete understanding of the pathophysiology and effective treatment in a chronic and debilitating disease that affects up to 2.5 million people worldwide is the foundation of the enthusiasm for a proposed treatable vascular model such as CCSVI.

If confirmed, the vascular model would change understanding of the pathophysiology of MS considerably.

That certainly echoes some of my thoughts.

Take care all and enjoy

--sharon

Thank you.

The review is one of the most informative, comprehensive articles about CCSVI that I've ever read.

Interesting. Froedtert Hospital is where I used to go to see a neurologist, and I notice that Dr. Woo is one of the authors.

The last time I saw him in 2010 he was 100% convinced that MS was an autoimmune disease.

Donnchadh

Furthermore, interest has emerged for endovascular therapies including angioplasty and stent implantation for venous stenosis. However, rigorous data demonstrating safety and efficacy are lacking and considerable controversy remains.

Can we agree with this statement? We have seen studies showing that the procedure is very safe in the short term (Simka's study, Siskin's study). I think we may need more long-term data on safety and short- and long-term data on efficacy, but I am satisfied with the short-term safety profile.

And here they include the vertebral veins as an area of interest in CCSVI, but since the verts can't be treated (and since they are tiny in comparison to the jugulars and the azygous), are they of interest?
http://c431376.r76.cf2.rackcdn.com/1152 ... 4-g001.jpg

Integration of the vascular model into the pathogenesis of MS will likely be as an adjunctive role in patients who have an underlying autoimmune susceptibility that could be enabled by venous congestion. The current understanding of the pathophysiology of MS has been an autoimmune process, however the etiology remains poorly understood. It is plausible that the vascular model offers an additional explanation to the heterogeneity of the disease and compliments the well-established role of autoimmunity.

I disagree, I think it is too early to know what role immunity or autoimmunity play. Autoimmunity assumes an otherwise healthy system in which the immune system becomes sensitized to myelin and attacks it. CCSVI describes an unhealthy brain environment where the immune system may play a clean-up role or a secondary inflammatory response (as in ischemia). I would agree with the authors that there is a well-established role of the immune system in MS; however I would not agree one way or the other if autoimmunity is involved. The lack of an antigen would put some weight on the side of no autoimmunity being involved. It could go either way, frankly, and it might be that autoimmunity is a factor for some MS patients and not for others and that this helps describe the heterogenous course of MS which is a point the authors were making as well.

continuing to work through this article....

Grants for research investigating CCSVI have thus far been awarded for seven projects by the National MS Society and the MS Society of Canada (FAQs About New CCSVI Grants, 2011). Intentional cerebral venous obstruction in an animal model of MS could also further elucidate the role of a vascular model in MS by testing the hypothesis that venous congestion leads to BBB disruption and enables the autoimmune response. Additionally, review of MS registries for an association between IIH and severity of MS disease may also be helpful in better understanding the role of venous obstruction.

For the animal model, there has been the mouse model of CCSVI which results in minor gait impairment and there is a marmoset model of CCSVI in development, which is great, because they are more similar that mice to humans in their cerebrospinal drainage.

Would having idiopathic intracranial hypertension cause MS to be more severe, in the CCSVI model? If a person with MS also has IIH, would the IIH even be diagnosed? I know our symptoms are often ascribed as being due to our MS, with no further testing or investigation necessary, so it would be easy for an additional condition such as IIH to go unrecognised.

Endovascular therapy for MS remains investigational and should remain limited to multicenter, blinded, randomized, controlled clinical trials.

Ok, endovascular therapy for MS can remain limited to such trials.
Endovascular therapy for central venous stenosis resulting from jugular valvular malformations, however, can be widely available.
It has done me a world of good.
My jugulars had a combined functioning CSA of 33 mm prior to the procedure and a combined CSA of approximately 210 mm after the procedure. Healthy controls have an approximate combined CSA between 200 - 250 mm from a few reports that I have read.

Really great article overall.

thanks for the rundown , Ceci . I can't seem to find the time to read
every CCSVI article , and therefore I rely on you and a handful of other trustworthy , bright TIMS members ...... to bring me up to speed.

I'm also willing to read the other side of any coin .......... provided that is presented as a scientific point of view ....... not just " I don't think this works " ...... as one multiple personality regularly posts .

I will view the article later ...... but for now ..... I'll accept your good judgement.




Mr.Success

tx cece
i go cross-eyed as soon as it gets technical, you're a godsend

There is so much in the article, I only touched on a little of it. Glad it was of help.

They talked about the genetics study. It had a small number of subjects but found abnormalities in the markers for vein abnormalities in the HLA genes which are already known to be associated with MS. That may not be a fully accurate explanation but suffice it to say there is reason to explore the genetics of CCSVI and MS further.