This Is MS Multiple Sclerosis Community: Knowledge & Support

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.

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.

This is so sad I am sorry
Erika

Dr. Sclafani is back! You were missed.


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.

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."

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.

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.

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

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.