A new next-big-thing

I recently listened in on the live web forum on chronic cerebrospinal venous insufficiency, or CCSVI, hosted jointly by the American Academy of Neurology and the National Multiple Sclerosis Society at the AAN annual meeting.
 
CCSVI is a narrowing or even blockage of the jugular veins, causing faulty blood drainage from the brain that may contribute to nervous system damage in M.S. This hypothesis has been put forth by Dr. Paulo Zamboni from the University of Ferrara in Italy. [Spectacular name!!!]
 
Based on his report on approximately 65 M.S. patients, published in June 2009 (J Neurol Neurosurg Psychiatry 2009; 80:392-399), venous hypertension treated by the standard endovascular angioplasty, seems to immediately improve the M.S. symptoms of these patients.
 
Angioplasty is where a doctor threads a thin tube through a blood vessel in the arm or groin over to the involved site in the vein. Once the tube is in place, the doctor inflates the tiny balloon at the end of the tube to disturb the plaque build-up and encourage it to move outward against the walls of the vein. This widens it and restores blood flow; it is often even an outpatient procedure.
 
In the U.S., early findings of a high prevalence of venous hypertension in the M.S. population seem to suggest that there is an association, but larger clinical trials are needed to confirm that fact. And if CCSVI plays a role in M.S., it is not yet known whether the condition is a symptom or a trigger.
 
There are other questions as well.
 
For example, since CCSVI occurs in many people who don’t have M.S. as well, does this indicate that the condition is just a false clue, an interesting red herring? (For example, I once heard that M.S. and gout are mutually exclusive: it seems that you can only have one but not both. Interesting but not necessarily relevant.)
 
Also, according to one panelist, the venous system has many redundancies. So does this blockage even need to be corrected?
 
He also reports that the blockages in CCSVI are not plaque but fibrous lesions.
 
Also, some patients who have had the angioplasty procedure subsequently have had the venous obstruction recur. What causes this and are there things patients can do to reduce the incidence?
 
Bottom line: this is one of the next big discoveries in M.S. research and the community is anxious to have larger clinical trials.

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Acupuncture is in my toolbox

I’ve been routinely receiving acupuncture treatments for more than 10 years. I like the Acupuncturist; she has become a friend. I consider her an integral part of my M.S. treatment team.

When people learn of this they inevitably ask “Do you find it makes a difference?  Do you feel better?”  Unfortunately, how can I know?  While an MRI every year can show brain lesion activity over time, researchers haven’t yet discovered whether those lesions even correlate to disease progression and/or current symptoms.

My disease has seemingly progressed in spite of acupuncture treatment. But it also appears to have progressed even with my daily Copaxone® injections too, which are the standard, current recommended medical treatment.   So then, would it have progressed more without the acupuncture? I don’t know. 

Acupuncture has a growing acceptance in western medicine as being good for treating pain. So if I had pain associated with my M.S., as some people do, this might be one way to gauge and easily communicate its effectiveness to others.  As convenient as I might find that, thankfully I do not have pain.

 

At least I get regular check-ins with a healthcare professional who monitors my symptoms so I only have to “bother” my neurologist with any bigger concerns.  I also enjoy 45 minutes of relaxation per session.  Some years it is even partially reimbursed by my health insurance.

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