Dr. Dake at CIRSE

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: Dr. Dake at CIRSE

Postby drsclafani » Fri Sep 16, 2011 9:59 am

while on a working vacation and wine tasting tour to the , I attended CIRSE and was there with a little support for my good friend and colleague, Michael Dake.

Frankly, what i witnessed was a travesty, an insult, a 3 to one attack that at time got personal.

My other good friend, Dr Reekers, simply dismissed CCSVI and nonsense, garbage not worthy of investigation or trial. He argued for evidence based medicine, but did not show any evidence at all. Apparently, his opinion of CCSVI is such that no evidence AGAINST the theary is necessary. It is hard to debate that attitude. Dr Doepp again argued against CCSVI based upon ultrasound and MRv. He showed images of all the areas of the juguilar veins where stenoses are uncommon and showed that these "stenoses" were also seen in healthy controls.

NOBODY discussed thge proponderance of abnormalities seen on every venogram.

i was so frustrated and so sorry for Mike who was just trying to be rational. And so embarrassed that my work hasnot yet been published.
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Re: Dr. Dake at CIRSE

Postby ErikaSlovakia » Fri Sep 16, 2011 11:02 am

drsclafani wrote:while on a working vacation and wine tasting tour to the , I attended CIRSE and was there with a little support for my good friend and colleague, Michael Dake.

Frankly, what i witnessed was a travesty, an insult, a 3 to one attack that at time got personal.

My other good friend, Dr Reekers, simply dismissed CCSVI and nonsense, garbage not worthy of investigation or trial. He argued for evidence based medicine, but did not show any evidence at all. Apparently, his opinion of CCSVI is such that no evidence AGAINST the theary is necessary. It is hard to debate that attitude. Dr Doepp again argued against CCSVI based upon ultrasound and MRv. He showed images of all the areas of the juguilar veins where stenoses are uncommon and showed that these "stenoses" were also seen in healthy controls.

NOBODY discussed thge proponderance of abnormalities seen on every venogram.

i was so frustrated and so sorry for Mike who was just trying to be rational. And so embarrassed that my work hasnot yet been published.

This is so sad :sad: I am sorry :cry:
Erika
Aug. 7, 09 Doppler Ultras. in Poland, left Jugul. valve problem, RRMS since 1996, now SPMS,
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
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Re: Dr. Dake at CIRSE

Postby dania » Fri Sep 16, 2011 11:16 am

It is so hard to convince those doctors to think that the world is not flat. I am always stunned at the attitude that their knowledge is always correct and there is no possibility, not a shred, of them being wrong. Shame on them. Reminds me of the doctor that tried to convince his colleagues that ulcers are caused by a bacteria. We all know how that ended.
Dr S, you said Dr Reekers argued for evidence. I would of liked him to show 100% proof on the existing theory (and it is ONLY a theory, never been proven) that MS is an autoimmune disease. Why cling to a theory for so long that has never been proven?
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Re: Dr. Dake at CIRSE

Postby HappyPoet » Fri Sep 16, 2011 2:00 pm

So sorry, DrS.
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Re: Dr. Dake at CIRSE

Postby Cece » Fri Sep 16, 2011 2:33 pm

Dr. Sclafani is back! You were missed.

cheerleader wrote:Underappreciated in the midst of these clashing positions is one other example of a similar venous lesion with potential relevance to MS – sheathing of retinal veins. This cuffing or sheathing of veins can be appreciated on fundoscopic examination of the eyes and may be associated with retinal vein thrombosis, optic neuritis and vision loss. In the majority of cases when it is diagnosed during an evaluation of disturbed vision, it occurs in patients with MS. Studied extensively at the Mayo Clinic, it is not however singularly associated with cases of established MS. Its frequency among MS patients is estimated to range from 11% to 42%. After fluoroscein dye administration, it is possible to observe leakage of dye around the retinal veins and histologically, the veins display a thickened wall similar to appearances observed in other chronically obstructed venous territories.

When contemplating the possible association between venous obstruction, blood-brain barrier leakage, myelin destruction and immune mechanisms responsible for the initiation of MS, it is interesting to note that the retinal nerve fibres are not myelinated in 99% of the population.

Did everyone catch this, from Dr. Dake's talk? This fits with some of what's been discussed by Dr. Diana. The lack of myelination on the retinal nerve fibres would mean that an autoimmune disease that attacks myelin should leave those retinal nerve fibres alone. And if people with MS display retinal vein pathology that looks like venous obstruction pathology, then that weighs strongly on the side of CCSVI.
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Re: Dr. Dake at CIRSE

Postby Cece » Fri Sep 16, 2011 2:57 pm

i was so frustrated and so sorry for Mike who was just trying to be rational. And so embarrassed that my work hasnot yet been published.

This is so sad :sad: I am sorry :cry:
Erika

That does sound frustrating. I am sorry too.

The abnormalities are there on every venogram. The fact that CCSVI can be physically observed is in our favor.

Had Stanford neurologists or King's County Hospital IRB seen things differently, there might have been less obstruction for both you and Dr. Dake in your early pursuit of CCSVI research. Still, we'll get there. We are gaining traction, or so I've heard. :)
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Re: Dr. Dake at CIRSE

Postby MrSuccess » Fri Sep 16, 2011 2:57 pm

that also got my attention .... interestingly enough .... ALS does not affect eyesight ....

is that correct Dr.Diana ?



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Re: Dr. Dake at CIRSE

Postby cheerleader » Fri Sep 16, 2011 4:01 pm

Cece wrote:Dr. Sclafani is back! You were missed.

cheerleader wrote:Underappreciated in the midst of these clashing positions is one other example of a similar venous lesion with potential relevance to MS – sheathing of retinal veins. This cuffing or sheathing of veins can be appreciated on fundoscopic examination of the eyes and may be associated with retinal vein thrombosis, optic neuritis and vision loss. In the majority of cases when it is diagnosed during an evaluation of disturbed vision, it occurs in patients with MS. Studied extensively at the Mayo Clinic, it is not however singularly associated with cases of established MS. Its frequency among MS patients is estimated to range from 11% to 42%. After fluoroscein dye administration, it is possible to observe leakage of dye around the retinal veins and histologically, the veins display a thickened wall similar to appearances observed in other chronically obstructed venous territories.

When contemplating the possible association between venous obstruction, blood-brain barrier leakage, myelin destruction and immune mechanisms responsible for the initiation of MS, it is interesting to note that the retinal nerve fibres are not myelinated in 99% of the population.

Did everyone catch this, from Dr. Dake's talk? This fits with some of what's been discussed by Dr. Diana. The lack of myelination on the retinal nerve fibres would mean that an autoimmune disease that attacks myelin should leave those retinal nerve fibres alone. And if people with MS display retinal vein pathology that looks like venous obstruction pathology, then that weighs strongly on the side of CCSVI.


Bingo, Cece....that's a very important point Dr. Dake makes that you clarify. If MS is indeed an autoimmune attack on myelin, it should leave the retinal veins alone, since they are not myelinated. But it doesn't. The blood/retinal barrier is broken on the venous side. Leukocytes infiltrate the area, to clean up after the venous leakage. In the retinal veins, it's easier to see how the venous blood breaks thru. And the lesions on the retinal veins look like MS lesions.

Optical neuritis is another common condition for MS patients. Evaluating periphlebitis retinae involves detecting sheathing and hemorrhage in veins in the retina. Lightman et al. demonstrated that 3.5 years after initial onset of acute idiopathic optic neuritis, eight out of 14 patients who had vascular abnormalities in a first episode of optic neuritis went on to develop MS, while only five out of 32 patients without vascular abnormalities went on to develop MS.[35] The overall incidence of patients with optic neuritis going on to be diagnosed as clinically definite was 13 out of 46 subjects, or 28%. The authors go on to draw the following conclusion: "We therefore suggest that the sheathing of retinal vessels that we observed opthalmoscopically is the visible clinical sign of the perivascular lymphocytic infiltration and accompanying oedema which characterizes the lesions of MS."

http://www.medscape.com/viewarticle/734517_4

I'm so thankful Dr. Dake continues to speak out and press for studies. And I'm glad Dr. S was there to offer support. The intrasigence displayed at this conference was simply terrible.
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dx dual jugular vein stenosis (CCSVI) 4/09
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Re: Dr. Dake at CIRSE

Postby Cece » Thu Nov 17, 2011 5:22 pm

from Hot Topics Session: CCSVI is real, and IRs should treat it with venoplasty
(excerpts)

Dr. Dake
Proposition: Treating MS patients with venoplasty

The present consensual view of interventionalists and hopeful patients is resigned to the conclusion that treatment of CCSVI is not a cure for MS. Debates rage over what roles, if any, CCSVI may play in conjunction with the genesis, progression and symptoms associated with MS, but even the most evangelical CCSVI advocates understand that relief of extracranial venous obstruction will not magically remyelinate compromised axons or reverse existing plaques.

Obviously, no one denies that interventionalists are ill-equipped to exclusively shepherd clinical treatment trials aimed at providing meaningful results informed by prior experiences that refined safety and efficacy metrics to objectively investigate new drug therapies. On the other hand, what has been learned from the initial observational phase of CCSVI treatment is informative and should not be wholesale discounted.

Currently, the long-term results of endovascular treatment of patients with CCSVI are unknown. Although it is estimated that 15,000 patients have been treated worldwide, many have not received adequate follow-up surveillance. This is often due to the lack of local or regional opportunities for undergoing the initial procedure. In many cases, this results in patients tra - velling long distances to undergo therapy, but subsequently leaves them without any continuity in medical care for follow-up at home.

As CCSVI is just one of many potential considerations that may fit as single pieces in a large puzzle that ultimately influences the development of MS in a particular individual, it is not terribly troublesome at our level of disease understanding to allow that not all MS subjects possess the identical predisposing conditions.

The specific contributing elements may be different among MS patients and an individual’s disease severity, tempo of progression, symptoms and response to therapies may be highly dependent on his/her collection of characteristic factors
.
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Re: Dr. Dake at CIRSE

Postby Cece » Thu Nov 17, 2011 5:26 pm

http://ccsvinews.blogspot.com/search?up ... results=50
Dr. Reekers
Opposition: There is no evidence for CCSVI or its treatment in MS patients

In actual fact, these statements ought not to be discussed by those who care for good clinical practice, evidence-based medicine and doing the best for our patients.

However, the whole discussion of CCSVI has been taken out of the scientific discourse and has moved instead to what is called “emotionbased medicine”. Although there is growing evidence for the non-existence of CCSVI, this does not seem to make any difference to the discussion. There are even rumors that there is a lobby by neurologists and the pharmacy industry to kill the theory of CCSVI. Those who are promoting the CCSVI treatment see proof and compelling data when there is nothing there: it all shows disorganized thinking.

There also seems to be a strange fascination in medicine for the anatomy at both ends of the Gaussian curve. To call a normal variant an abnormality is both clever, from a selling point of view, and deceptive. This is unfortunately not unique in medicine. For decades “patients” have been treated with septoplasty for nasal septum deviation or children by tonsillectomy for large tonsils to prevent all sorts of common cold diseases. It is not that long ago that many psychological diseases were connected to being left-handed. Heilpraktiker connected poor posture to learning and concentration problems. And there are many more examples where normal anatomic variations triggered wrong-thinking to support a delusion. But as the singer-songwriter Randy Newman sings, “short people are just the same as you and I.”

All scientific opinions create complex discussion, and the blend of passion and science that CCSVI and MS bring forth require tempered deliberation that should focus on data and facts. This necessitates a balance between scepticism and openness to new ideas. Although I am absolutely sure that there is no scientific proof for the existence of CCSVI and the pathologic relation in the development of MS, it is hard to believe that some of the people I have always known as honest scientists, with important contributions to the field of IR, have now adopted the habit of spreading false information, for whatever reason.

Inflammation of the central nervous system (CNS) (neuroinflammation) is now recognised to be a feature of all neurological disorders. In multiple sclerosis, there is prominent infiltration of various leukocyte subsets into the CNS with resultant elevation of many inflammatory mediators within the CNS. An extensive dataset describes neuroinflammation to have detrimental consequences, but results emerging largely over the past decade have indicated that aspects of the inflammatory response are beneficial for CNS outcomes. Nevertheless, these inflammations might be the cause of what is now called CCSVI. If this is true, patients with longstanding MS would be particularly affected. If you then add this to the natural distribution of venous variations, it might lead to the observation of something like CCSVI, which would than better be named Chronic Post- Inflammation Venous Abnormality (CPIVA). If this is true, and I am just speculating, it is not the venous abnormalities which cause MS, but vice versa: the inflammation with MS is causing the venous abnormalities. Off course, this is as much as a hypothesis as the existence of CCSVI and should first be investigated in a blinded study with a control group. We have to look at early MS and late MS, and patients with other inflammatory diseases of the CNS and control groups. CPIVA could easily explain what we are discussing today.

By endorsing and offering treatment for CCSVI at high costs to the patient, based on very poor and debatable data, we will not be seen as clinicians who protect their patients, but as trigger-happy cowboys. This last issue is the main reason I am so involved in this topic. The CCSVI debate will eventually be resolved, but whether our loss of credibility can be restored, remains to be seen.
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Re: Dr. Dake at CIRSE

Postby MrSuccess » Thu Nov 17, 2011 11:17 pm

How sad it is to read some rant - rather than some well reasoned thoughts - from some highly educated medical professional. I'm speaking of Dr.Reekers.

Can this fellow be any more condescending ? Cowboys ?

Let me say this : An old saying goes .......

" If it weren't for differences of opinion .... there would not be horse races ".


Perhaps Dr.Reekers should consider this. Better yet .... DO A TRIAL ..... and THEN ....
draw his conclusions from the results.


Ride 'em Cowboy !!!!!!!


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Re: Dr. Dake at CIRSE

Postby Robnl » Thu Nov 17, 2011 11:48 pm

I'm from Holland; Dr Barkhoff, Dr. Reekers and 'chief' Dr. Polman...i'm ashamed about their CCSVI attitude...They are really super-doctors but locked-up in what they know....

When i read about these 'discussions' i always think about the following example; I work in IT, if i can't install a piece of software and my colleague can, i just say that it can't be installed (comparing it to the ccsvi no-sayers).
That doesn't work that way, does it?
Doctors treat ccsvi and see improvements....if i was one of these neuro's, i would select some of these treated people and turn them inside-out. I mean; these patients got a MS history and MRI results etc etc, there are several official tests to measure the 'status' f MS and symptoms.....i really do not understand why this doesn't happen....ego-problem?? Fear???

Maybe CCSVI has nothing to do with MS, but then a lot of us don't have MS but CCSVI :mrgreen:
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Re: Dr. Dake at CIRSE

Postby sumsum » Fri Nov 18, 2011 12:30 am

Hi there,

one question in regard to the retinal nerve: in the German Wikipaedia version I read that the retinal nerve is not myelinated with Schwann cells but with oligoden-droctyes. Can we hence really say that the retinal nerve is not myelinated? I am asking, because I would like to put this question to my (skepitcal) neuro in December and want to make sure that my argument is water-proof...

Cheers!

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Re: Dr. Dake at CIRSE

Postby cheerleader » Fri Nov 18, 2011 11:34 am

sumsum wrote:Hi there,
one question in regard to the retinal nerve: in the German Wikipaedia version I read that the retinal nerve is not myelinated with Schwann cells but with oligoden-droctyes. Can we hence really say that the retinal nerve is not myelinated? I am asking, because I would like to put this question to my (skepitcal) neuro in December and want to make sure that my argument is water-proof...

Cheers!

sumsum


Sumsum-
Dr. Dake refers to 99% of the population that does not have myelination of retinal nerve fibers, and he's right. Normal retinal nerves do not have myelin. When the nerves do, it shows up in vision problems in children, and is noted by retinal lesions.

Retinal nerve myelination is considered a birth defect, and found in less than 1% of the gp. It is related to congenital conditions such as Down Syndrome, and would show up in vision tests of psMS, if they had myelinated retinal nerve cells.

http://www.cfp.ca/content/56/4/357.full
Myelinated retinal nerve fibre layer (MRNFL) is a retinal lesion caused by the abnormal myelination of the nerve fibres of the retina. The lesion typically appears as striated gray or white opacification with feathery edges, and often follows the distribution of the nerve fibres.1 The estimated incidence of MRNFL is 0.98%.1 This paper is an update of a previous paper on MRNFL published by Baxter and Sharma in 2001.2 Myelinated retinal nerve fibre layer is a condition that produces opaque lesions on the retina. It can be asymptomatic, as in the case of our patient, or cause varying degrees of visual impairment. Although there is no treatment for the condition itself, any associated negative prognostic conditions such as axial myopia, amblyopia, and retinovascular lesions should be treated promptly. Asymptomatic patients need only be followed on a routine basis.

cheer
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