This Is MS Multiple Sclerosis Knowledge & Support Community

My question on the list above Cece, from Dr S, is why is the valve immobility the commonality for PwMS ( and other diseases) and not the general population?

Infections? Are some infections only common to Latitude?

Vascular disease? What starts the disease and spreads it to the CNS veins or CNS drainage veins?

PTA first time around has the best hope of positive outcomes? What damage happens every time and is the area damaged already and the infection or diseased area grows and worsens if the cause of the infection or disease is not addressed?

From Birth? Is there any visual proof of malformations in young persons?

Diet, lifestyle, western way of life? The data on vascular diseases is growing does it correspond?

Genetic? There is commonality in some gene pools, and is that a side effect of Latitude settlement of cultural grouping? Why is MS now more common in other countries, change of diet to western or technology used to modify food shelf life?

Deficiency of minerals eg Zinc related to Latitude/food sources/farming methods?

Decades of drug use in modern society, everything from birth control to food preserving?

There is a commonality, it is going to take some thinking, (Fararoe Islands experience with MS?)

Science does not 'as yet' understand the cause of the symptoms in MS, it is not able to define what is causing each symptom from origin to effect, not being able to trace from feeling to cause is stopping movement forward in understanding MS, CCSVI or any of the other diseases associated with current knowledge or current technology.
Management of symptoms is the best that we can expect at this time, even PTA is symptom management or hope of it, at this time!

Regards,
Nigel

In Multiple Sclerosis blood vessels "deformed" by childhood
stress cannot accommodate the blood flow. The auto-immune response is secondary to the true cause of MS, a blood reflux which injures the brain and spinal cord. The origin of the reflux may be structural (CCSVI stenosis) as proposed by Professor Zamboni or it may be a "temporary" stress reaction to a toxic substance.

Let's re-think first causes. And then move on to real solutions.

Epidemiological studies on MS show that those who grow up close to the equator have less chance to develop MS than those living in latitudes closer to the poles. It is the latitude where one lives before age 15 that counts, not where one lives subsequently. It is therefore thought that the lack of sunlight – hence Vit D – is a factor in susceptibility to MS. Vit D is recommended for M.S. patients.

But perhaps a better explanation of the geographical factor is Winter Cold.

The shoulders and neck typically tense up under stress thus restricting circulation to and from the brain. Cold weather stiffens the muscles. Winters bring the body aches of colds and flus.

It is also said that MS patients tend to be high powered, ambitious people. Tensed up in other words. MS cases cluster in northern Europe and North Amerca. Let’s say growing up in a culturally demanding family environment (or in any case stressful) while subject to Cold weather and frequent colds and flus actually compresses and deforms the circulatory system in the child’s developing body. By the time he/she reaches age 15, the stunted blood vessels can no longer accommodate the blood flow. MS first appears in adolescents, seldom in children. Let’s compare the deformity to ancient Chinese footbinding where the tiny child’s foot cannot support the adult woman.

Food intolerances, especially to wheat and dairy products, can further compound the stress. The Neolithic agricultural revolution dates back not much more than 10,000 years, a blink of the eye in terms of biological evolution. Bowel problems are a sure sign of food “stress”.

And the disadvantage of being female. Between puberty and menopause at least two-thirds of MS patients are women. This implies that gynecological problems (including menstrual cramps) both stress and require "poisoning" treatment which impact negatively the vascular system. Perhaps monthly menstrual cramps in a growing girl actually "stunt" the circulatory system. Stress.

Maybe the real story behind MS is the damage to the blood vessels caused by growing up in a 1) driven, ambitious or otherwise stressful family environment compounded by 2) a climate of Cold winters which contribute to 3) frequent viral illnesses compounded by 4) an intolerance to the wheat and lactose of a Neolithic diet.

Self treatment ideas in MS Cure Enigmas.net. Also more about geography and culture under "Success Stress" blog.
My hypothesis is plausible, but even if you think it nonsense I do have some lived healing tips and the Zamboni idea has transformed my life, coupled with Chinese Acupuncture theory. Vesta

Dr. Sclafani,

Paul Healy here, you placed a stent in my right Jugular vein before Christmas. Just wanted to let you know things are going great. My annual MRI reports show no new lesions. Looking forward to seeing you around December/January for my third follow up Ultrasound.

Thanks again for everything!

Paul

I've been thinking that the Placebo effect and Fight or flee fits in this paradym. Intracellular infection is the most probable likelihood of feeling ok when things are not. Drugs, spinal alignments, vascular improvements because of PTA cannot make this difference in a 'moment'! Hope does!
http://www.abc.net.au/catalyst/stories/3572695.htm
Regards,
Nigel

Dear Professor Sclafani,

I am relieved to report that my ultrasound scans of both jugulars and the left renal vein showed no signs of thrombosis and flow seemed good everywhere except the left jugular where the bony transverse process is likely causing compression of the stent and reducing flow significantly. The radiologist also said that he could see no evidence of valves in either jugular vein. Should I be worried that the valves have disappeared?

Regards,

Alex

CureOrBust wrote:

NZer1 wrote:

CureOrBust wrote:I have had two treatments in Australia. After these two, I went and saw Dr Thibault and his sonographer for a follow up, and they could not find any evidence of CCSVI. I was then treated by Dr S in Brooklyn, and he did find evidence using the ultrasound, and also more than one location to treat. NB I am a non responder.

When I go to see Paul this is the sort of info I need to be telling him. He is in favour of IVUS and there isn't interest from the IR's, so its a problem for us all at the end of the day.
The areas that Sal found may not have been detectable with Doppler, eg azygos. Where were the areas Sal found using ultrasound Cure?

Sal are you able to help in this, I want to give Paul the benefit of your experience, even if he doesn't contact you for what ever reason to ask for help!

If Paul doesn't get this feed back nothing will change!

Dr Sclafani, please feel free to provide Nigel the information regarding the locations found by Ultrasound and those identified by IVUS. Its good to hear he is now interested in IVUS, in my treatment. I remember the last time I saw him I explained to him what it was. He hadn't heard of it, at least not as IVUS. I should really set up another appointment for a scan.

From memory, I had no treatments of the Azygos. I do remember the ballooning in my Jugulars. It hurt!

So sorry for the long delay in responding. I have been on vacation and then it felt so good to not stay up writing answers that i continued the hiatus. I always feel badly about not responding in a timely fashion. I guess sometimes I really need more of a break than I usually admit to.


The patient has given me permission to discuss his case here. My recollection was that he had severe spasticity and that is not one of the most favored symptoms when it is very profound.

It was quite clear that there were abnormalities of the valves on venography and IVUS and they were treated quite well. unfortunately, the procedure was a success but the patient did not improve.

Nigel, cure or bust may indeed be a non-responder. That does not discount CCSVI. ccsvi may not be the cause of his symptoms.

Lety wrote:hello to everyone here in the forum and in particular to Prof. Sclafani, I am new here but read you for a long time (I'm sorry my English is not so good, I'm from Germany, hope you understand me anyway).

Prof. Sclafani, as you know I'm interested in a treatment, I am plagued by uncertainties, unfortunately, that's why I could not decide yet.

Can you please tell me how high the risk of complications from a stent is (you had cases in which stents were used and it still came to restenosis?)

Then you have to take blood thinners for life?

Is it according to your experience that problems with legs, bladder, bowel are associated with Problem to the Azygosvein?

Thank you in advance for your answer.

Best Regards

Lety

I do not put many stents in. I think that IVUS directed large balloon high pressure dilatation is usually sufficient to open these veins for more than six months. the stents I have put in have been to bale out vein wall dissections that put the vein at risk for thrombosis. Approximately 1/3 of the stents I have placed (not many) in such circumstances have developed intimal hyperplasia that has persisted up to one year. Most of the intimal hyperplasia has stabilized or partially or completely subsided.
However other stents have been placed for restoration of occlusions, mostly resulting from treatments by other physicians. These do not do as well, with some developing severe intimal hyperplasia and at least one going on to complete occlusion. That was frustrating case, as it was a very long very heroic technical tour de force requiring rendevous procedure stenting, etc. in a patient who had bilateral occlusion after prior angioplasty in another country.

I continue blood thinners after stenting for a minimum of six months. I Decide subsequently based upon ultrasound whether to continue anticoagulation.

I believe that the jugular veins, the azygous vein, the ascending lumbar vein, the dural sinuses and the vertebral veins all contribute to the cerebrospinal venous circulation. Treatment of any and all of these veins can impact on patient clinical outcomes

S

CureOrBust wrote:A little off topic, but have you been in contact with anyone (or yourself?) performing CCSVI treatments for Lyme? This web page says that they present with 3-4 of Zamboni's criteria; compared to our measly 2.
http://betterhealthguy.com/joomla/blog/ ... eyond-lyme

COB
i have treated a couple of patients with lymes. The appearance is totally different. I still plan to show a comparison of the two when i get some time

DrS

Cece wrote:

CureOrBust wrote:A little off topic, but have you been in contact with anyone (or yourself?) performing CCSVI treatments for Lyme? This web page says that they present with 3-4 of Zamboni's criteria; compared to our measly 2.

•There are 5 parameters that are looked at during a CCSVI evaluation. In MS, 2 of 5 are often observed. In Lyme, it has been closer to 4 of 5 and in autism, it is often 5 of 5. The best Lyme patient thus far was 3 of 5. Lyme patients, on average, test worse than MS patients.

Do you think he's likely to publish on this? I'm not familiar with who Dr. Klinghardt is.

sorry i do not

NZer1 wrote:Dr S I am not sure if I have suggested this before,
I think with the talk on CPn and Lyme and the coincidence of CCSVI that having bloods done as part of your work up, pre PTA, may be a way to confront the restenosis/vascular infections that is found in some people and also to get a balanced picture on 'issues' that may get across the BBB, due to reflux, that will need attending to in order to address the symptoms of those invaders, as well as dealing with the standard IVUS findings at PTA?
There is also the issue of some Labs consistently coming back with negatives to contend with, quote from Dr Paul Thibault;

• "Why there is so much variance in Cpn serology results is probably due to sourcing of the reagents, but I haven't enquired into that at this stage."

Thoughts?

Regards
Nigel

NNIgel, i have limiited experience with imaging lymes patients. However in those cases i have seen, the difference in appearance is dramatic.

dlynn wrote:Dr. Sclafani,
When stenting the renal vein, does the patient receive "conscious sedation" as in CCSVI procedure?
And do you enter the femoral vein?
If I recall correctly, you addressed this topic several pages back, but I can't find it.
thank you!

I use narcotics but i do not use conscious sedation unless the patient is very anxious as i find it detracts from optimizing the examination. Patients usually cannot follow instructions as well when they are sedated. Recovery time is much longer.

Cece wrote:

CureOrBust wrote:A certain Australian female singer was played and Dr S let us all in a small crush he had on her. At the time I didn't know it, but by unfortunate chance, she also has MS now. And only a few months ago a TV programme they showed here a story of her travelling to Brooklyn for CCSVI treatment.

Lol! She was also in attendance at the CCSVI Patient Day last year. Rock stars, Montel, Dr. Sclafani, Wheelchair Kamikaze...rather a celebrity-packed event!

I found bilateral stenosis of the J1 segment of each internal jugular vein. My records show that there were immobile valves causing about 60-70% stenosis. There was also hypoplasia of the ascending lumbar vein. 18 and 20mm balloons were used requiring 13-15 atmospheres.

non-responder? perhaps. but perhaps the valves just will not stay open. perhaps surgery or stenting would have a better chance.

Have you seen any association between the percentage of stenosis and whether or not the stenosis stays open in the long-term?
Previously another doctor suggested that the best chance at success is on the first procedure. (Obviously this would not hold true for any stenoses that were missed on that first procedure.) But that made me wonder if the stenosis is at its highest grade or most resistant on that first procedure, and if that would mean the localized pressure on the stenosis would be higher?
Conversely a higher-grade stenosis would mean more residual valve material and more of a chance to restenose due to that. It would be nice to be able to predict restenosis, even roughly.

in my experience narrowing of the venogram is caused in decreasing order of frequency by

1. Valve immobility at least 85%
2. muscular compression
3. hypoplasia
4. septum
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'?

cece
i do not think that muscular compression is really ccsvi unless there is also obstructions at the valves. until someone proves that treatment of muscular compression improves symptoms, i would no longer treat it.

Welcome back Dr. .
Happens to be best and the worst of us, haha!

Paul Thibault may have some insight to the CPn and CCSVI appearances, I'll ask him.

**Can you explain what is dramatic or definite when 'you' see Lyme or CPn?

**Is there a difference between these two?

There may be a situation where the Aust and NZ CCSVI PwMS have a percentage of CPn and Lyme cases that the Northern Latitude doesn't?

NZer1 wrote:I've been thinking that the Placebo effect and Fight or flee fits in this paradym. Intracellular infection is the most probable likelihood of feeling ok when things are not. Drugs, spinal alignments, vascular improvements because of PTA cannot make this difference in a 'moment'! Hope does!
http://www.abc.net.au/catalyst/stories/3572695.htm
Regards,
Nigel

nigel, there are some pretty nasty intracellular infections. why do you say patient is likely to feel ok when things are not



i have seen some pretty amazing rapid responses

gibbledygook wrote:Dear Professor Sclafani,

I am relieved to report that my ultrasound scans of both jugulars and the left renal vein showed no signs of thrombosis and flow seemed good everywhere except the left jugular where the bony transverse process is likely causing compression of the stent and reducing flow significantly. The radiologist also said that he could see no evidence of valves in either jugular vein. Should I be worried that the valves have disappeared?

Regards,

Alex

alex, thanks for the followup, but please provide followup via ccsviliberation@gmail.com because it enables me to readily access records. in this overly long forum, searching for results does not come as easily.

the valve is visible when it is thickened. otherwise the valve is just a layer of endothelium and some collagen matrix. It is "gossamer". on ultrasound of normal veins we rarely see such thickening except at the annulus. I think that angioplasty may stretch the vein enough to make it very thin and "gossamer" .

unless some of my patients are willing to donate their bodies, which i hope is not the case, then speculation remains the ansswer.

i do not worry about loss of the vein unless their are symptoms. I have read that as many as 15% of humans do not have valves discovered in the jugular vein.