DrSclafani answers some questions

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drsclafani
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Re: DrSclafani answers some questions

Post by drsclafani »

gibbledygook wrote:Dear Professor Sclafani,

It's now been 2 months since my operation which involved stenting the left renal vein and ballooning both jugular valves and the azygous vein. I deteriorated immediately after the operation and have remained worse than I was before the operation in terms of walking ability, bladder control, eyesight and twitchiness. Both the left renal vein and the jugular veins were scanned for thrombosis and were found to be free of clots. What probability do you assign to a restenosis of the azygous vein?

Best regards,

Alex
Alex, because you mentioned it here, i will answer it here.

please recall that you had a stent placed at stanford that is compressed at the C-2 level. I performed angioplasty but it sounded from your recent ultrasound that the stent is compressed again. That suggests to me that you have "restenosis" of the left internal jugular vein.

I have found that restenosis of the azygous vein is pretty uncommon. Thrombosis is more common that restenosis but both are uncommon.

We shall see soon

DrS
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Re: DrSclafani answers some questions

Post by dlynn »

Dr. Sclafani,
Could a compressed Renal Vien, inadvertently, affect the blood flow in the Azygous Vein?
Thank you
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Re: DrSclafani answers some questions

Post by Cece »

For a jugular stent compressed at the c-2 level, is this a possible solution?
CONCLUSION: Intracranial venous hypertension may result from extrinsic osseous compression of the jugular veins at the skull base. Although rare, this phenomenon is important to recognize because primary stenting not only is ineffective but also may actually exacerbate the outflow obstruction. The osseous impingement of the dominant jugular vein can be relieved via a decompressive styloidectomy, and the clinical results can be excellent.
http://www.ncbi.nlm.nih.gov/pubmed/21866063

Or is the styloid not involved?
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Re: DrSclafani answers some questions

Post by drsclafani »

dlynn wrote:Dr. Sclafani,
Could a compressed Renal Vien, inadvertently, affect the blood flow in the Azygous Vein?
Thank you
When the renal vein is compressed significantly, the vast volume of blood draining from the kidney must be drained elsewhere. There are three major routes for that blood to exit the kidney when the left renal vein is obstructed
1. the gonadal (ovarian or testicular) vein
2. the hemiazygo-renal connection. From there into the azygous vein
3. The ascending lumbar vein

As you can see, two of the three veins impact on the flow within the cerebrospinal venous circulation.

Renal blood flow is 4-5 times as much as azygous flow, so this can be a very significant problem
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Re: DrSclafani answers some questions

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Cece wrote:For a jugular stent compressed at the c-2 level, is this a possible solution?
CONCLUSION: Intracranial venous hypertension may result from extrinsic osseous compression of the jugular veins at the skull base. Although rare, this phenomenon is important to recognize because primary stenting not only is ineffective but also may actually exacerbate the outflow obstruction. The osseous impingement of the dominant jugular vein can be relieved via a decompressive styloidectomy, and the clinical results can be excellent.
http://www.ncbi.nlm.nih.gov/pubmed/21866063

Or is the styloid not involved?
i think that many of these compressions are indeed due to muscular compression between the styloid or its attachmed musculature and the the C1 or C2 vertebrae. They are other compressions as well.

I am intrigued by this treatment since I agree that stenting and angioplasty seem to have little value at this level in the cases that have been treated elsewhere and seek consultation with me afterwards. I have stented with little value and do not routinely do this. However often the obstruction is relieved by rotating or flexing the neck, not a practical solution.

However, there are fixed noncompression stenoses that occur here as well. my approach to this problem remains fluid and this article helps me move toward resolution of a treatment algorithm I feel comfortable with.

now i just have to find a surgeon willing to participate.
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Re: DrSclafani answers some questions

Post by tzootsi »

Hi Dr. S,
A question about the C2 compression issue - am I correct in assuming this is not the area of the IJVs where the valves (and most stenosis issues) are located? This problem is a totally different animal than the more common stenosis in the caudal or valve area?

ps: does the acquisition of American Access by Fresenius have any impact on CCSVI treatments? I see no mention of CCSVI on Fresenius' web site.
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Re: DrSclafani answers some questions

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tzootsi wrote:Hi Dr. S,
A question about the C2 compression issue - am I correct in assuming this is not the area of the IJVs where the valves (and most stenosis issues) are located? This problem is a totally different animal than the more common stenosis in the caudal or valve area?

ps: does the acquisition of American Access by Fresenius have any impact on CCSVI treatments? I see no mention of CCSVI on Fresenius' web site.
you are correct about that. the usual location of obstructions is the area of the valves near the chest. This C2 compression occurs near the inlet into the neck from the head.

If one accepts Dr schelling's theory regarding venous obstructions causing backflowing jets that damage the deep white matter, these upper lesions cannot cause backjets: they are located above the area of venous distension. However it appears that they can increase intracranial venous pressures and may be a cause of symptoms of ccsvi, even in the absence of MS.

While Fresnius does not want to advertise regarding CCSVI, i am allowed to continue treatments. They also chose not to continue the annual symposium in New York City each summer. This does make it slightly more difficult for me to keep a high profile but patients seem to be finding me and I continue to spend the majority of my time caring for patients with CCSVI.

.
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Re: DrSclafani answers some questions A CASE OF CHRONIC FATI

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Many patients with CCSVI associated with multiple sclerosis complain of chronic fatigue. Indeed, many carry a diagnosis of chronic fatigue before they are finally diagnosed with multiple sclerosis. I became interested in chronic fatigue both from my dealings with patients with MS as well as with patients who have Nutcracker syndrome, ie, compression obstruction of the left renal vein. In fact, Nutcracker syndrome has been stated to be the most common cause of chronic fatigue in children.

Recently, I consulted with a 69 year old man who has had a diagnosis of chronic fatigue syndrome for the past 35 years. He has various medical complaints but seemed generally in good health for his age. His chief complaints besides his fatigue were memory loss, predominanly short term in nature, inability to complete his thoughts, numbness in his legs and hands, and a generalized weakness that he could not clarify as fatigue or weakness. His exam revealed a thin healthy looking man, looking younger than his stated age. On exam, he had memory disturbance, weakness in the left hip, decrease sensation to vibration and sharp touch. He weaved during his Rhomberg test and stated that his balance was bad when he walked in the dark.

He received a Doppler ultrasound in Barrie, and this was interpreted as having B-mode abnormalities and reflux on the left side.

I agreed to perform catheterization, venography and intravascular ultrasound.

the IVUS did not show the usual thickening of the valvular tissue seen in PwMS, although there were slight focal areas of echogenicity. I will not show any images.

RIGHT INTERNAL JUGULAR VENOGRAPHY
Image

The venography of his right internal jugular vein was significant for several points.
1. The J2 segment was markedly dilated.
2. The J1 segment was markedly narrowed at the area of the inferior jugular bulb
3. There was tremendous reflux into the largest occiciptal emissary (OEV) vein draining into the external jugular vein.(EJV)

Treatment was performed with a 16mm then 20 mm high pressure balloon with moderate improvement.
Image

The really unusual findings were seen on the left jugular venography.

LEFT IJV venogram
Image

The image on the left shows the inability to catheterize the left internal jugular vein beyond this stump of a vessel. This is the appearance of a completely closed valve. perhaps there is a bit of reflux through the valve just above the stump. After about 30 minutes of trying, i performed a rendevous procedure.

For those unfamiliar with this procedure, the goal is to connect the vein above the obstruction with the vein below it. In the second from left image you can see a sheath extending down the jugular but not quite reaching the catheter that had been placed from the femoral approach. In the third image you can see the wife extending down from the neck beyond the obstruction into the chest. A snare was used to grab the femoral catheter and pull it up through the obstructed valve. After this it was possible to perform the angioplasty you see.

This second image of the left jugular system shows more problems, however.

Image

The fourth and fifth images from left in the top row shows that there is clearly obstruction of the left IJV with stasis above the valve and only a trickle getting down into the chest.

On the lower row, we can see that there is narrowing of the junction of the sigmoid sinus and the internal jugular vein (image on right lower panel shows it better) There is also reflux from the left transverse sinus into the right transverse sinus which ultimately drained into the right internal jugular vein.

In essence this vein is severely obstructed in two locations at the skull base and at the inferior jugular bulb.

There can be no treatment of the lesion at the skull base. angioplasty is not feasible there.

if one looks at the upper left panel of this image one sees something else, a stenosis of the brachiocephalic vein just before it enters the superior vena cava.

This final images shows that better
Image

The two images in the right panel clearly show the obstructive nature of the stenosis. The waist in the balloon was eliminated with about 12 atmospheres of pressure. Such stenosis are usually caused by compression against the left brachiocephalic artery that is tortuous at this age. Is this significant? I think so. Will this angioplasty persist? I doubt it because of the compressive nature of the lesion. However the patient and I agreed to no stents on this visit.

So, he does not have MS proven, his neurologists have excluded this diagnosis. He has chronic fatigue and very severe venous outflow obstructions. I look forward to the followup in this patient because it is of importance to see whether angioplasty can improve his chronic fatigue
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Re: DrSclafani answers some questions

Post by mo_en »

Since IVUS revealed no thickening of the valves, what was the nature of these problems? Local hypoplasia on the right, valve fusion on the left? I guess this case provides evidence that CCSVI deteriorates with time. Which of these vein lesions do you think are congenital? Which could happen during lifetime?
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Re: DrSclafani answers some questions

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mo_en wrote:Since IVUS revealed no thickening of the valves, what was the nature of these problems? Local hypoplasia on the right, valve fusion on the left? I guess this case provides evidence that CCSVI deteriorates with time. Which of these vein lesions do you think are congenital? Which could happen during lifetime?
I think that this is a different disease. Not much was seen on this IVUS because the valve was less echogenic, probably less thickened than in MS. This looks like valve thickening, probably not congenital, possibly related to thrombus formation from the low flow states.
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Re: DrSclafani answers some questions

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Two things

**1. Dr S, has Auckland Radiology (NZ) been in touch about Doppler Ultrasound testing for CCSVI. They are quoting they have made contact and a guided/trained by you?

2. A follow up on to my search for answers for lots of things that are linking the MS experience of us all.
[url]http://www.CPn%20Help.org/pdfs/ChronicDisease.pdf[/url]

"Viable C. pneumoniae circulating
in peripheral blood mononuclear cells (PBMCs)
may reach various human
tissues after an inflammatory trigger
event occurs in the tissue and then
cause chronic infection in the tissue.
This might create or worsen a chronic
disease process. The purpose of this
article is to review the association of
C. pneumoniae with chronic human
diseases."
This article I have seen before and discounted it's content. Now I have a dx of CPn persistent infection I started to look around at data on the subject of CPn and Lyme and have found many links to a 'big picture' of what our symptoms are doing.
When the CPn dies off it creates two endotoxins which the immune system responses to and works to remove. This has a by product of Iron being deposited, interesting! The actual endotoxins cause symptoms that are very much the same as PwMS experience and a host of other diseases depending on where in the body the process occurs.
In my day 5 experience of being on the David Wheldon protocol with antibiotics I am finding that my symptoms are on the increase, and most of all any muscular injuries from the past are where I am feeling the most effect, I am also more Fatigued and weak.
My history of spine injuries are all noticeable in the increase of discomfort/pain and especially weakness. Places such as both shoulders where I have torn rotator cuffs are sore and weak. Leg muscle strains from the past sporting injuries are sore and weak. Injuries to my hands/fingers muscles and joints are sore and weak. I had an eye socket injury to my left eye as a teenager, the same problematic 'MS' eye is discharging on the first couple of days on the ABx.

Co-incidence?

Regards,
Nigel

I read the article several times before it sank in, thoughts Team?
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Re: DrSclafani answers some questions

Post by allynz »

Auckland Radiology did a scan on my husband a couple of weeks ago following instructions from Dr S. he provided in a letter when my husband was treated by Dr S. in July. Dr S. now has that report and last Thursday we posted him the CD of the scan. On Sunday my husband is heading back to NY for another round of treatment by Dr S. based on the results of that scan and the progress reports my husband has emailed to Dr S.

The ultrasound tech called in the radiologist because she couldn't locate the jugular vein. I wasn't there but my husband was happy with the level of service he got, knowing they are not experienced in identifying ccsvi. Not being able to find my husband's jugular vein was not unexpected - we had the same issue in NY, his veins are not in great shape.

This was not the only CCSVI related scan they have done - they told us another woman had been to them asking for it. I have also suggested a friend go see them as she is keen to visit Dr S but suffers from Chronic Fatigue not MS so the situation is not so straight forward as she has no assurance that ccsvi is actually her problem although I know she will find the post above interesting.

My friend works there - they are skeptics, in fact of all the people that we have told about ccsvi she is the most skeptical but that is just her nature anyway. She told me that at a recent conference of some kind ccsvi was a hot topic of conversation and at that conference there was quite a bit of debate between the believers and non-believers. I try not to get into the details too much with her though as I don't want it affecting our friendship.

FYI for any kiwis there is a story on SUNDAY this Sunday about a guy from Cromwell going to see Dr S. We were going to be part of the story too but the timing wasn't right and our experience/outcome wouldn't have been suited to advancing the ccsvi cause and we wouldn't want to contribute to any negative views of ccsvi as a result of not having a miraculous result.
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Re: DrSclafani answers some questions

Post by drsclafani »

NZer1 wrote:Two things

**1. Dr S, has Auckland Radiology (NZ) been in touch about Doppler Ultrasound testing for CCSVI. They are quoting they have made contact and a guided/trained by you
They hve not been in contct or trained by me. Only with my patient. I asked them to do a simple ultrasound to assure patency and did not guide them in a CCSVI study. I cannot comment on their ability to detect CCSVI.
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Re: DrSclafani answers some questions

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allynz wrote:On Sunday my husband is heading back to NY for another round of treatment by Dr S. based on the results of that scan and the progress reports my husband has emailed to Dr S.
I hope this is successful. Best wishes, allynz.
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Re: DrSclafani answers some questions

Post by Cece »

drsclafani wrote:I think that this is a different disease. Not much was seen on this IVUS because the valve was less echogenic, probably less thickened than in MS. This looks like valve thickening, probably not congenital, possibly related to thrombus formation from the low flow states.
I wonder if this ties in to the abnormal collagen seen in MS veins ( http://www.sciencedirect.com/science/ar ... 0712000592 ). If chronic fatigue patients do not have abnormal collagen, it might lead to less echogenic valves and greater ability of the vein to dilate. There is a large degree of dilatation in that right jugular.

It's interesting to think that IVUS could be used to distinguish between IJV valves from MS or Lyme's or chronic fatigue: the usual smooth thickened appearance of MS valves; the wavy splotched appearance of Lyme's valves; and near-normal appearance of chronic fatigue valves. Even if all showed similar-looking stenosis on flouroscopy. Definitely need greater sample size/more patients to know if these observations are correct.

For this patient, two areas were treated and hopefully resolved (lower right and left jugular stenoses) and two areas not treated (upper left jugular stenosis) or treated but not expected to last (brachiocephalic stenosis). So the question is if partial treatment is enough for symptom resolution.
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