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.