However, just as I prepared to "publish" this, I read a new CCSVI thread "Stem Cell Breakthrough including better CCSVI results." Dr. Dregen explains how introducing a patients own stem cells from their bone marrow into the cerebro spinal fluid overcomes the various complications in angioplasty. I'll just enter his quotes directly.
Fri Sept 14, 2012
"1eye: Yes exactly. When we are infants up to adolesence we have billions of MSCs coursing through our veins ready to locate at the site of any injury or area of inflammation. Healing happens within days after that. MSCs are the body's protector when we are young. They also readily pass through the blood brain barrier (BBB) to protect the central nervous system and they are known to express proteins that turn off over-aggressive immune system activity.
However, by the time we are 25-30 years old they do not exist in enough numbers to make a significant difference and the healing cascade of events in our bodies is different. Hence the dramatic difference in healing times for injuries, and perhaps the ability to heal AT ALL from some diseases such as MS or PD. The introduction of autologous MSCs in a clinical dosage as adults allows us the protection we once had when we were kids.
Yes, with the goal being to prevent restenosis, the evidence for some sort of additional intervention that supports the initial 'liberation' procedure is pretty compelling from the point of view that it not only supports long-term patency, but because of what it can avoid. For example, there is now a new and growing subset of MS patients who have had vein widening venoplasty multiple times, usually to less beneficial effect each time leading to the later discovery of so much intraluminal scar tissue by the second, third or fourth attempt at re-opening the veins that the procedure cannot be performed again. I have noticed that topical amongst this group are vascular grafts, pig veins, etc. The need to remove veins because they are so occluded indicates the possibility that there was 'overtreatment' of the
veins during the initial venoplasty procedure that eventually led to the formation of scar tissue (if they didn't occlude with thrombin build-up immediately post procedure). This further indicates that there may not be recognition of the fragility of the neck vein structure, especially inpatients that already have diagnosed venous disease. The preliminary evidence we are looking at indicates that stromal cells injected through the catheter at the time of the venoplasty prevents the normal healing event cascade and avoids the formation of both thrombin and scar tissue intraluminally. This is well illustrated in the video. It would also be extremely cost-effective to aspirate marrow and separate the patient's own stem cells for injection at the time of the venoplasty. And with a stronger and more durable vein that has been treated for venous disease, it would possibly avoid the need for subsequent vein dilation procedures, with long-term patency as the result. This could be done just about anywhere the liberation procedure is performed because the stromal cells taken from the patients own marrow only have to be separated and purified, not increased in number because they are enough to be considered a clinical dose when super-selectively implanted in the vein directly to the site of injury due to venoplasty."
Next entry: Sept 14, 2012
Cheerleader: That's terrific news for your husband, but I'm addressing the thousands of people for which the 'liberation therapy' has failed as an effective intervention. Not everyone's veins are the same; anatomical structures (including abnormal valves) are different and of course erratic hemodynamic pressures may have existed in the veins for a very long time that have weakened the intraluminal area so that the diseased veins in these
individuals simply cannot be effectively treated in the same way your husband's was.
I have looked at over 300 DU studies in MS patients. Not a huge number in total, but since most demonstrated some retrograde flow, just from a statistical standpoint it's certainly enough to recognize a definite correlation between CCSVI of the neck veins and MS. So I think that the neck veins DO have to be treated to stop the MS trigger from being pulled in those individuals predisposed to the disease. I am simply examining additional therapeutic modalities that will support the optimal flow of blood drainage once the abnormal veins have been corrected. I fear that if the NL study of liberation therapy alone is any indication of the outcome of the Albany trial, there won't be much of a chance of the medical establishment sanctioning neck vein dilation as an effective treatment for MS even though the CCSVI/MS link clearly exists. Long-term patency can't be achieved reliably. All my group is attempting to do is prove a hypothesis in support of/and additional to what Dr. Zamboni has (in my mind) already proven."
End of quote. Sounds good to me.
I wonder how this thinking about stem cells would fit my hypothesis that childhood stress actually "damages" the vascular system in the back, shoulders and neck?
Now for the Dr. Sclafani quotes from ThisIsMs.com.thread "Dr. Sclafani answers some questions". Dr. Sclafani is a pioneering interventional radiologist who treats CCSVI and through experience is learning a great deal about the particular characteristics of vein conditions in MS. (And of course he is a hero for MS patients who seek relief from the sluggish, blocked or reflexed blood flow which injures the Central Nervous System.) His "thread" includes input from patients and other sources so a great deal can be learned.
The "thread" begins March 15, 2010 and is now 479 pages long. I began reading from the beginning but then decided I should begin at the end and read backwards to learn the latest. (I'll never get through all those pages anyway.)
Some info I've picked up.
Dr. Zamboni assesses the blood reflex rather than circulatory obstruction. Dr. Paul Thibault emphasises that CCSVI is an obstructive venous disease.
April 3 2012 quote by Dr. Sclafani
"Firstly, not all resistance to flow is caused by stenosis (narrowing).
Narrowing can be secondary to
1.hypoplasia,or failure to grow to proper size
2. extrinsic compression by a duplicated vein
3.transverse webs of tissue acting like a lid on the vein
4. or septum that divides the tube (jugular) into two smaller tubes
5. A diverticulum that compresses the vein
6. by valves that are stiff and do not open and close properly
7 valves made of several leaflets that end up fused together
8 valves that are located in abnormal locations
Almost all of these narrowings occur near the confluens of the jugular vein with the subcclavian where valves are seen normally in about 85 per cent of patients. Problem is these valves are highly dysfunctionally developed in patients with MS. I think the IVUS really shows this really well.The venogram shows narrowing but the IVUS
shows that the narrowing is valvular.
These narrowings are not inflammatory strictures and they are not "buildup of tissue on the wall of the
vein (sort of like plaque).
Quotes from the thread continue.
"There are other malformations of veins that are well known. They include problems with the veins of the liver as they join the inferior vena cava. This well known entity is called Budd Chiari syndrome and results in major problems of the liver.
"The SPINAL CORD has an interesting venous drainage. There are small veins that exit the spinal cord and enter venous plexuses that surround the spine and vertebrae. (A venous plexus is a tangle of very small venous channels
and lakes. )These plexuses connect up and down the spine. Some then drain out into larger more defined veins. These veins can drain upward into the brain and then back down the venous sinues to the jugular vein. There are also veins that connect the cervical plexuses to the upper jugular vein itself. The cervical venous plexus also drains into the vertebral veins and they connect to the subclavian or innominate veins. lower down in the thoracic spine these plexuses drain into veins that connect to intercostal veins and hemiazygous and azygous veins. Lower down still there are veins that connect the vertebral veinous plexuses to lumbar veins, ascending lumbar veins, and the inferior vena cava and lots of other veins."
WOW. Me again. Dr Zamboni began by treating the Jugular Veins, the Vertebral Veins and the Azygous vein. However, many other veins lead from the brain and in particular the spinal cord (Renal, Ileac etc) so it appears that treatment of the "Zamboni" veins may not suffice if other veins are involved. If one's condition doesn't improve after angioplasty it may be because other veins than those treated were compromised, OR the nerve damage is too old to heal.
Dr Sclafani states that the valves are implicated in 85% of cases. This is alot. But what if these valves can be opened and treated "manually"?
It is understood in scientific research that the position of the observer can distort perception of what is being observed. Maybe the mere act of threading a catheter in the vein is enough to stress and "close" the valves that otherwise could be kept open.
Dr. Sclafani states elsewhere that a restenosis may simply be a case of inadequate vein dilation.
Quote by Dr. Sclafani.
"In my experience narrowing of the venogram is caused in decreasing order of frequency by
1. Valve immobility at least 85%
2. muscular compression
5. C2 bony compression
6. prior occlusion
#1, 3, 4, and 6 would require an IR or vascular surgeon to treat, if treatable. #5 bony compression gets a lot of discussion here at TiMS but I see you ranked #2 muscular compression as being more frequent. Solutions previously brainstormed were using botox to completely relax the muscle or trying neck stretching/massage/heat. Would you term these compressions to be secondary CCSVI'?"
Aug 29, 2012
"Stylocervical compression is something that is more apparent on MRV than on catheter venography. when i look at these narrowings with IVUS many of them seem to be phasic. In other words rotation, flexion or extension of the
neck allows the vein to take on a larger diameter with better flow. Is this a normal physiological situation? Does relieving this narrowing result in sustained clinical improvements? Do they need treatment? Tough questions with
unclear answers so far."
Page 474 Aug 15 2012
"Thanks for your response Dr. Sclafani, when my azygos was first treated I had large improvements, in saying this my right IJV was also ballooned, this was in August last year, I had been fine for the year up until the last month. I had a Doppler indicating restenosis of my right IJV and it wasn't until yesterday that I found out that the azygos had occluded. I wouldn't even be too sure regarding how long it's been like that. My recent symptoms already seem to be improving from yesterday's ballooning of the right IJV.
Do you believe occlusion is being caused by a blood clot in most cases or scarring of the vein? I also would love to know your thoughts on using drug eluting balloons if scarring may be the cause of restenosis and/or occlusions? Do you think they have any benefit?
Thanks for your time, it is very much appreciated.
To Dr. Sclafani, have you seen an occluded azygous vein in any of your CCSVI patients? Or have any other IRs shared images of an occluded azygous vein?"
Yes, I have seen this complication. It is mostly likely caused by thrombosis rather than scarring.
From Dr. Sclafani. "Drug eluding stents and balloons show promise in reducing intimal hyperplasia, but intimal hyperplasia is not common after jugular angioplasty.
There are no drug eluding balloons in the sizes currently used to treat jugular stenoses."
Thanks once again for your response Dr Sclafani. I discussed your thoughts regarding this type of complication with my surgeon although he does not believe that my case is caused by thrombosis. He also advised that he would be very open to discuss with you the details of my recent procedure and complications regarding the occlusion, for your thoughts and comments. Would it be ok if I included you in an email to him via your
firstname.lastname@example.org email address in order to initiate this contact?"
End of quoted entries.
At one point Dr. Sclafani states "My guess is that this is maldevelopment of the valves in the fetus." Needless to say, I don't agree with this last statement. Given the various factors such as geography, culture and gender revealed in the epidemiological studies on MS I would say the following:
"My guess is that this is maldevelopment of the valves in the fetus" OR GROWING CHILD. I wonder how this hypothesis would fit into Stem cell theory?