My thoughts on the brilliant work done to create CCSVI awareness and the knowledge progression that is unfolding.
What if CCSVI was the primary aspect of what has been nicknamed ‘MS’ (because of its visible later stages of disease damage).
CCSVI primary symptoms are specific to poor drainage of the brain, for example cog fog, heat intolerance, balance issues, cold extremities, vision changes, these symptoms are improved by rectifying the blood flow issues. Drainage improvement from angioplasty treatment can sometimes, in a short time frame, improve the initial symptoms and they can continue to improve over time depending on the flow improvement and amount of nerve conduction damage. These symptoms appear to be related to flow pressure or reflux rather than iron deposition.
CCSVI over time allows iron deposits to build up which then damages and crosses the blood brain barrier which causes direct iron damage to the central nervous system. At this time for some people the disability is more variable and has a relapse remit cycle as the body creates collateral vein flow to bypass the restrictions within main veins (jugular and azygous system).
During this time iron deposits that are crossing the blood brain barrier cause more direct damage to the central nervous system. At this time in the progression the disease course can be classified using the old terminology Begnin, RRMS, SPMS, and PPMS.
The possibilities are:
Benign meaning that the body has developed collaterals that cope with the flow restrictions which has very slow, sometimes stagnant progression of disability, although MRI may show activity of disease.
Relapse remitting form being the process of collaterals improving the flow temporarily, in a repeating fashion, and over time collateral flow will not be able to cope with the deteriorating blood flow that leads to a secondary progression stage that becomes continuous progression because the iron deposition and blood flow issues are getting worse with time.
Primary progressive disability, the growth of collateral and disability are happening at the same time, and disability progresses faster. This is where the stop start nature of the relapse remitting form is balanced out by the timing of collateral flow increases and goes directly to the progressive disease because the blood flow decreases and iron deposition damage increases.
There have been red herrings that have been used as bridge in the lack of research historically with the disease known as MS. Two examples are thinking that inflammation was a primary symptom and using EAE as a research tool have delayed progress in finding the disease origin and treatments for the cause of what became known as ‘MS’.
The signs of inflammation are tertiary symptoms and should not be confused with the primary cause, CCSVI, although one cannot happen without the other.
The mouse model EAE has recently been proven to be a different disease process to the human process.
I think at times the research has to be redirected regularly and reviewed to keep the focus of researchers on track with finding relevant data that will benefit the MS population rather than creating a career in research. Its about us not them!!!!!!!
Enjoy your day!