Ashton's letter

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

Ashton's letter

Postby Gordon » Wed Aug 25, 2010 2:44 pm

An Open Letter to the Honourable Gene Zwozdesky, Alberta Minister
of Health Regarding the August 6, 2010, Alberta Health Services
Report on MS and CCSVI
Dear Minister Zwozdesky,
Introduction
I recently read the “Alberta Health Services Information Sheet
On Multiple Sclerosis (MS) and Chronic Cerebrospinal Venous Insufficiency
(CCSVI)” which was prepared by members of your department and made
available to the public on August 6, 2010. I found this report to contain numerous
factual errors, misleading statements and half truths. It also included blatant, fear
mongering and an incredibly biased view of the relationship between the
pathology of chronic cerebral spinal insufficiency (CCSVI) and multiple sclerosis
(MS). Given that the authors of this “Information Sheet” are public civil servants
who report to you, and who are ultimately responsible to the citizens of Alberta, I
felt compelled to write to you to both point out the major deficiencies of this report
and to ask for a retraction of it.
You also need to investigate whether or not any of the authors/contributors have
a conflict of interest regarding a non-drug therapy for MS. As discussed later, the
existence of such conflicts of interest is the only reasonable explanation for the
erroneous and biased nature of the report. Given that the public relies on AHS
information sheets as sources of factual and unbiased data and analyses, I am
sure you agree that those who write AHS information sheets must be free of such
conflicts of interest. I also assume that the existence of conflicts of interest will
not be tolerated by your department.
I am writing to you in various capacities including: 1) An Alberta taxpayer, 2) A
research scientist who is very familiar with the MS data base and the only
Albertan scientist who has published on CCSVI and MS in a recognized medical
journal (Embry, 2010), 3) The president and research director of Canada’s
second largest MS charity, Direct-MS (www.direct-ms.org), and 4) A father of a
person with MS. The combination of these roles gives me a unique perspective
as well as the expertise and the incentive to comment on the AHS report. I would
have expected an AHS report to contain factual information and unbiased
analyses on CCSVI and MS but I found just the opposite.
I will now provide comments on numerous statements in the report that conflict
with either the established science or with the data we currently have at hand
regarding CCSVI and MS. I will also highlight statements which have no basis in
fact and are merely unfounded and unjustifiable speculations. I hope you agree
that Albertans should expect AHS information sheets, on important health issues
which affect our citizens, to be fact-based and objective.
Publicly funded AHS staff members, who are responsible for the production of
such reports, must be counted on to be “honest brokers” of scientific information
so as not to jeopardize the health of the citizens of Alberta or your department’s
credibility. Given that the authors of the MS and CCSVI information sheet
ultimately report to you, and that you are ultimately responsible for the
information being given to Albertans, I hope you will take my evaluation of the
AHS information sheet seriously and then act to rectify a most unfortunate and
potentially harmful situation.
Section 1 “Are CCSVI and MS related?”
The first unwarranted statement in this section is “CCSVI and MS may be
related” (emphasis on the word may from the report). Currently, and at the time
the report was written, there is no reasonable doubt that MS and CCSVI are
associated - that is, there are abundant data that demonstrate that a significantly
higher % of persons with MS have CCSVI as compared with the general
population.
The University of Buffalo work demonstrated an almost 3X higher prevalence of
CCSVI is persons with MS in a large study of 500 people (University of Buffalo,
2010). Notably, the person doing the determination of whether or not CCSVI was
present was properly trained and had months of experience. Most importantly,
the results were checked and corroborated with selective venography, the
accepted gold standard for the determination of CCSVI, and thus can be
considered to be very reliable.
The AHS report also refers to the recently published Doepp et al (2010) study
which found no CCSVI in persons with MS. Notably this study was done in a few
months, included only a small number of subjects, and the technician doing the
CCSVI detection was not properly trained in venous ultrasound work (much
different from arterial ultrasound work). Furthermore, this study did not include
any selective venography to demonstrate the reliability of the ultrasound
interpretations. Given the above, this study is widely discounted as highly
suspect science within the CCSVI research community.
It was very surprising that the AHS report did not refer to other published studies
of CCSVI/MS association which include Al-Omari and Rousan (2010) which
found 84% of persons with MS had CCSVI (sample size 25) and no healthy
controls had CCSVI (sample size 25) and Simka et al (2010) which found CCSVI
in 90% of persons with MS (70 sample size). Notably, both these results were
supported by selective venography which leaves no doubt as to the accuracy of
these data. Given there are not a large number of references on CCSVI and MS,
the omission of these key references, which are readily found on Pubmed, shows
a definite lack of scholarship by your staff regarding the question of CCSVI and
MS association.
Furthermore, given the importance of the question of the association of CCSVI
and MS, your staff should have contacted the various centres around the world
which are presently testing and treating persons for CCSVI. Importantly, these
centres are doing selective venography as part of the testing. If they had done
such a common sense and fundamentally necessary investigation, they would
have found that all centres are reporting 80 – 95% of the MS patients they are
seeing have CCSVI and that number now exceeds 2000 subjects. Furthermore,
Dr Sandy MacDonald, a vascular surgeon in Barrie Ontario, testified before a
Parliamentary Subcommittee on Neurological Diseases in June (available for
viewing on the Internet) that 95% of almost 300 MS patients that his clinic tested
had CCSVI. The omission of these most important data is most troubling.
In summary, the current information leaves no reasonable doubt that CCSVI is
strongly associated with MS. Thus the claim made by the authors of the AHS
report that this is not yet established is not true and is very misleading.
It is accepted that the established association of CCSVI with MS does not mean
that CCSVI is necessarily a causal factor for MS. The second paragraph of this
section looks at the important question which naturally stems from an established
CCSVI/MS association - Does CCSVI contribute to the MS disease process, that
is, does it have a causal role in MS?
The question of cause for an established association of a condition such as
CCSVI with a disease needs to be addressed by examining various criteria that
were first clearly enunciated by Hill (1965) in a classic paper entitled “The
Environment and Disease: Association or Causation”. In this paper, Hill
demonstrated that for a causal relationship to be reasonably well established, the
important criteria that need to be satisfied are a consistent association, the
occurrence of the condition before the disease onset, and biological plausibility
for the condition to contribute to the disease process.
The two examples provided by the authors in the second paragraph of the AHS
report to support their contention that association does not prove cause include
differences in genetics (male versus female) and the concept that some tested
therapies don’t work. Both these examples have absolutely nothing to do with
determining if an association is causal or not. It is imperative that your staff take
the time to read the Hill (1965) paper which sets the standards for evaluating
cause versus association. It was disconcerting to read this paragraph because
of the lack of reasoning regarding association versus cause.
The third paragraph in this section also shows a major lack of understanding of
CCSVI and a complete unfamiliarity with the CCSVI literature. The statement
“the association between MS and CCSVI may actually be explained by MS
causing CCSVI (original emphasis on “MS causing CCSVI”) is not tenable
because it has been established that the venous malformations, which are
responsible for CCSVI, are congenital in origin (i.e. formed during pregnancy)
(Lee et al, 2009; Lee et al, 2010).
If the authors had done adequate research into the types of venous
malformations constituting CCSVI, they would not have made such a
scientifically unsupportable statement. A few examples of the venous
malformations associated with CCSVI include completely inverted or missing
jugular valves, bony spines impinging on a vein, a completely absent jugular
vein, and grossly malformed veins. A number of others such as septa and webs
within the veins are described in the literature and are readily viewed on online
videos produced by vascular surgeons.
It is untenable to postulate that “inflammatory proteins” could be responsible for
such venous malformations and abnormalities. It is clear the authors of the AHS
report lack basic knowledge about the vascular malformations which cause
CCSVI. Their speculation that the malformations are the result of “inflammatory
proteins” has no basis or merit and is very misleading as to the relationship of
CCSVI and MS.
Section 2 “How could MS actually cause CCSVI?”
The information in this entire section is completely irrelevant and inappropriate
given that the established data show beyond a reasonable doubt that the venous
malformations which constitute CCSVI are congenital in origin and could not
have been caused by “inflammatory proteins” by any stretch of the imagination. It
is very clear the authors of the AHS report have no idea as to the nature of the
venous malformations in CCSVI and it is important for them to do proper
research on this subject. The data which answer the question of the origin of the
venous malformations are readily available. The irrelevant and erroneous
speculations which constitute this entire section of the AHS report, reflect badly
on the credibility of your department.
Section 3 “What is the relationship between CCSVI, MS, and iron
accumulation in the brain?”
I am not sure why the authors included this section in the report but I can only
assume they did so because they are trying to discredit the concept that CCSVI
is a causal factor of MS. As they note, iron is associated with MS lesions and this
has been known for a long time. One possible explanation is that it is contributed
by oligodendrocytes which die through some MS disease process. It is equally
possible that the iron deposits are related to CCSVI as described in detail by
Singh and Zamboni (2009). A key point these authors make is that iron deposits
are associated with venous problems in other parts of the body (e.g. legs, torso)
and thus it would be consistent to have iron deposits associated with extracranial
venous problems.
In this regard, I refer you and the authors to the Zavadinov et al (2010) paper
which concludes on the basis on some robust and impressive MRI-based data,
that “CCSVI may be an important mechanism related to iron deposition in the
brain parenchyma of MS patients”.
In summary, the available data and theoretical considerations support the
concept that CCSVI might be responsible for some, or even all, the iron
associated with MS lesions. Thus the occurrence of iron adds support to the
proposition that CCSVI is a causal factor in MS. The authors’ statement that
“studies of iron in the brain do not help sort out the relationship between MS and
CCSVI” is both erroneous and misleading. We can definitely say that the current
data tell us that the study of iron may well sort out the relationship between MS
and CCSVI but that we need more studies in this field. The authors’ failure to
reference and discuss the findings of Singh and Zamboni (2009) and Zivadinov
et al (2010) regarding iron and CCSVI again reveals a distinct lack of scholarship
and understanding of the CCSVI literature.
Section 4 “Why do most neurologists doubt that MS could be caused by
blocked or sluggish veins?”
This is the strangest part of the AHS report and the authors provide little scientific
support for rather bold statements which are stated as “beliefs”. Beliefs belong
more to religion that they do to science and what is required are cogent, properly
referenced statements and arguments rather than unsupported “beliefs”.
For example we have the statement “They [neurologists] also know that MS or an
MS-like condition has never been shown to be a result of blocked or sluggish
veins”. Exactly how neurologists know this is of course unknown (extrasensory
psychic powers?), and such pompous bluster has no place in an objective
analysis of an important health issue.
Currently, the possibility exists that CCSVI (blocked veins) may well be a causal
factor in MS and we know this by applying the criteria of Hill (1965) for
determining cause from association. It is well established that:
1) CCSVI is strongly and widely associated with MS and this has been
demonstrated by using selective venography in centres around the world (USA,
Canada, Italy. Poland, Bulgaria, India, Jordan to name a few).
2) CCSVI is congenital in origin and thus precedes the start of the MS disease
process.
3) There are a number of plausible biological mechanisms which relate CCSVI to
the MS disease process, including decreased perfusion, upregulation of
adhesion molecules and deposition of iron.
4) Animal experiments carried out by Putman (1935) showed that blockages in
the extra-cranial veins of dogs produced CNS lesions which closely resembled
those of MS.
The sum of all these criteria, which essentially satisfy Hill’s criteria for causation,
leave little doubt that CCSVI is very likely a causal factor in MS. Any other
interpretation would require incredible special pleading and astronomical odds for
chance co-occurrences.
Thus, although the authors believe that neurologists believe that CCSVI cannot
cause CCSVI, they do not provide any solid reasoning to support such beliefs. I
would further note that arguments presented in this section such as “There are
many people with true venous insufficiency but they never get MS” are simplistic
and irrelevant. No one is saying CCSVI is the only causal factor of MS and it is
openly acknowledged that most people with CCSVI (20-25% of the population)
do not get MS.
There is no doubt that MS involves a number of causal factors including genetic
susceptibility, vitamin D deficiency and Epstein-Barr infection (Ebers, 2008). The
key point is that, when CCSVI is present in a person with MS (perhaps as often
as 75-80 % of the time), it contributes to the disease process as determined by
the data discussed above. This is also nicely shown by the University of Buffalo
data that revealed that those persons with MS and CCSVI have more severe
disease than those with MS and no CCSVI (University of Buffalo, 2010). This is
exactly what would be expected if CCSVI is one of the causal factors of MS in
many cases.
In the next two paragraphs in this section, the authors argue that blockages are
not present in the veins of persons with MS. Notably, they ignore all the
published imaging and venous flow data from Ultrasound and MRV studies that
demonstrate beyond any doubt that such blockages are present. They also
ignore all the venous catheter interventions which actually found the blockages in
thousands of people.
As part of their circuitous arguments they state “Dr Zamboni reported that venous
pressure did not differ above and below the regions of narrowing”. Such a
statement is completely false and in the 2009 article that first discussed CCSVI in
MS, Zamboni et al state “the pressure gradient measured in CDMS across the
stenosies was significantly different” (Zamboni et al, 2009, p.395). Such blatant
errors in the AHS report demonstrate a further lack of scholarship and call into
question the accuracy of all statements.
The last two statements in this section are especially egregious and unscientific.
Firstly the authors state “Neurologists are not convinced that there are truly
blockages in the veins of people with MS, unless the vein is frankly clotted. This
latter condition is only seen in some MS patients after they have angioplasty.”
This statement has no scientific basis and represents fear mongering.
The neurologists have apparently not looked at the overwhelming database that
that has demonstrated the existence of the blockages. Furthermore they are
ignoring the fact that every day 75 venous angioplasties are done in centres in
many parts of the world (over 2000 procedures done so far) and this daily
number continues to increase as more centres open up. If the venous blockages
did not exist there would not be a large and ever expanding medical service
which treats such blockages in centres as reputable as the prestigious Arizona
Heart Institute in Phoenix, Arizona.
The claim of the authors of the AHS report that the only venous blockages that
do exist are clots caused by angioplasty is not true and is another blatant
example of fear-mongering.
The last statement is this section was bolded – “Thus, without blockage, it is
hard to imagine how venous angioplasty can possibly do anything but risk
injury to a vein.” This baseless, inflammatory, fear-mongering statement, which
has no place in an AHS information sheet, leaves little doubt as to the anti-
CCSVI bias of the authors of the AHS document.
Section 5 “Arterial angioplasty is done all the time. What is the concern
about angioplasty for CCSVI?”
The first three paragraphs describe arteries and problems associated with them.
There are various inaccuracies such as the statement that “a stent will only get
properly secured into an artery by its high pressure blood flow.” It is well known
that stents stay in place due to the fact they are flexible and are chosen so that
they are slightly larger than the artery. Furthermore, the arterial epithelial cells
grow into the stent mesh thus incorporating the stent into the artery wall. Stents
have been used in low pressure veins for a number of years using the same
principles.
The authors of the AHS report rightly note that veins opened by angioplasty can
suffer restenosis and no one is arguing this point. We currently do not have
enough data on the rate of restenosis or on which angioplasty techniques are
best for preventing restenosis. Notably such experience for arterial angioplasty
was developed during the first 5 years of doing the procedure and the same thing
is happening right now as venous angioplasty becomes more and more common
a procedure in centres throughout the world. This is how all medical procedures
are improved upon and the thesis put forward by the authors of the AHS report
that venous angioplasty should not be done because we don’t know the
restenosis rate is illogical and meaningless.
The authors statement that “there are no situations where venous
angioplasty is an accepted and satisfactory treatment.” (original bolding) is
not factual. A quick search of Pubmed reveals the use of venous angioplasty for
various conditions including its use in kidney patients. There is no doubt it is not
perfect (few if any medical procedures are) but is certainly often satisfactory in
that it achieves the desired result. At present no one is claiming venous
angioplasty is routinely done and the reason for this is, that in the past, there has
not been a widespread need for such a procedure.
The final bolded statement in this section – “However, given that we can be
confident that many people will sustain completely occluded veins from the
procedure, we must be very sure that there is enough evidence to suggest
that CCSVI actually contributes to ongoing brain injury in MS before we
undertake such trials.” – is a most curious and somewhat confusing one. First
of all there is no basis whatsoever to “be confident” that many people will sustain
completely occluded veins following venous angioplasty. In fact this problem has
not been reported by any of the clinics doing venous angioplasty and again this is
another example of blatant fear-mongering. The strangest thing about this
statement is that the neurologist have been repeatedly saying that only proper
trial results will tell us if CCSVI is related to the MS disease process and now this
statement says we need evidence that CCSVI is part of the MS disease process
before trials are done. They have constructed a classic Catch-22 out of no data
and no logic.
In summary, venous angioplasty is an accepted procedure but has been used
sparingly in the past for a variety of somewhat rare conditions. Its current use for
opening up blockages in extra-cranial veins in persons with MS is no different
than its previous usages and no vascular doctors have raised any concerns
about this usage. In fact, more and more interventional radiologists in centres
around the world (including numerous sites in the USA) are doing venous
angioplasty on blocked extra-cranial veins. This trend has been steadily growing
over the past year indicating that the procedure is not causing any problems that
would have resulted in reassessment and pull back.
Section 6 “What does it mean when people return from having venous
angioplasty elsewhere and report that they feel better?”
In this section the authors of the AHS report try to discount the very numerous
anecdotal accounts of substantial improvements that persons with MS have
enjoyed after having their extra-cranial veins opened by angioplasty. Such
accounts have been described in detail in various media including newspaper
articles, TV documentaries and short clips, and video and written personal
accounts on the internet. The one thing that stands out about these very
numerous accounts is that the gained benefits are very substantial and tend to
address balance, fatigue and brain fog issues. Furthermore, never in the history
of MS has any conventional (e.g. drugs) or unconventional treatment ever
resulted in such a huge volume of positive reports of major gains. There is no
doubt that the positive results from venous angioplasty are unprecedented in
their strength and numbers.
The authors of the AHS are suggesting that all the major benefits reported by
hundreds of patients from numerous different countries are all due to placebo
effect. This is completely unsupportable given the types and strengths of
improvements that have been reported and the fact they have remained or, in
many cases, got even better with time. The placebo effect does not allow a
person who could barely get out of bed most days before angioplasty to start
running 10 km marathons a month after venous angioplasty.
The statement that “As of today, no Canadian neurologist has found
significant or sustained improvement upon examination of patients who
had had venous angioplasty performed, despite the fact that most
returning patients report feeling better and sometimes note improvement in
sensation or walking.” (original bolding) has absolutely no basis in fact. First of
all this implies that the authors contacted every neurologist in Canada to
determine if any of their patients had actually improved after venous angioplasty.
We can be sure the authors of the report did not do this. Furthermore, I know of a
number of cases where people have enjoyed major gains and that their
neurologists were impressed and pleased with such gains. Once again the
inclusion of patently false statements in the AHS report is most disturbing and
causes one to have little faith in the veracity of any information in the report.
In the last paragraph of the report the authors offer the advice to “Be careful
about where you get information” and I can only second this. The AHS report,
with its lack of scholarly research, numerous false statements, fear mongering
and illogical discussions, is a good example of questionable information which is
best avoided. Although not mentioned in the AHS report, the best information on
CCSVI and its treatment can be obtained from vascular doctors and
interventional radiologists. Seeking advice on impaired venous drainage from
doctors who do not specialize in vascular issues is probably not a good idea.
Summary
The authors of the AHS report have done an unacceptable job of presenting the
facts about CCSVI and its treatment and have included inaccurate information
and fear mongering statements. This report is below any acceptable standard for
a government information sheet which should include only factual data and an
objective analysis of it. The AHS report is blatantly biased in its anti-CCSVI
stance that one has to wonder about the motivations behind its origin and the
expertise of its authors.
The main failings of the one-sided report include:
1) The overwhelming database which indicates CCSVI and MS are
associated is not acknowledged and key references on this topic were
omitted.
2) The data and reasoning which demonstrate CCSVI is most likely a causal
factor in MS were not properly addressed and an untenable and baseless
speculation of “inflammatory proteins” causing CCSVI was emphasized.
3) The relationship between iron and CCSVI was poorly analysed and the
two key references on this subject were omitted.
4) The overwhelming evidence for the existence of impaired venous drainage
in many persons with MS was completely ignored and was replaced by
unsubstantiated pronouncements and unsupportable “beliefs” that such
blockages simply do not exist.
5) Fear mongering, which has no place in an AHS document, is commonly
used and included the false claims that the only venous blockages that
exist are clots caused by angioplasty and the only results of venous
angioplasty are injuries to the vein.
6) The established and widely accepted use of venous angioplasty for
various conditions is ignored and unsupported insinuations are made that
venous angioplasty is a very unsafe, experimental procedure.
7) All the impressive improvements reported by hundreds of persons with MS
who have had venous angioplasty done are simply written off as placebo
effect despite the impossibility of this in many documented cases. The
authors fail to recognize the unprecedented strength and numbers of the
reported improvements.
8) Outright erroneous statements such as there is no pressure gradient
across the venous stenosis, and no neurologist has seen any
improvement in a person who has had venous angioplasty, are scattered
throughout the report.
Given that we can assume the AHS was written by professionals, the only
reasonable interpretation of why the report lacks scholarly and unbiased
information is that the one or more of the authors had a conflict of interest.
Consequently, it is most important that your department do an investigation of the
authors to determine if any of them has a conflict of interest when it comes to
CCSVI and its treatment.
One obvious conflict would be past or current ties to pharmaceutical companies
that manufacture drugs for MS. Because the treatment of CCSVI has the
potential to replace current drug treatments, it is to be expected anyone with
financial ties to pharmaceutical companies might have the incentive to denigrate
and marginalize CCSVI as a phenomenon in MS and venous angioplasty as a
useful treatment for MS because of potential future financial losses. Needless to
say this is a very important and sensitive issue that needs immediate attention.
I assume that the report will immediately be retracted if such conflicts of interest
are found. Furthermore, failure to investigate such likely conflicts of interest
would itself constitute a serious breech of ethics given the potential influence of
AHS information sheets and the need for them to be factual and unbiased.
Finally I would like to express my thoughts on the AHS report from the four
perspectives that I have.
1) As an Alberta taxpayer I am most disturbed that my tax money was spent
on such an unscientific and biased report. Government revenues should
be spent on fact-based, objective reports on important subjects which
allow the consumer to make informed decisions regarding their health
care.
2) As a research scientist, I am dismayed that AHS would publish such an
unscientific document. I expect good, solid scientific analyses of important
issues, not unsubstantiated opinions and vapid pronouncements.
3) As the president and research director of Canada’s second largest MS
charity, I am disappointed by the lack of honest, unbiased and worthwhile
information in the AHS report. Persons with MS need reliable information
and thoughtful and unbiased analyses of such data to help them make
important decisions regarding their treatment choices and ultimately their
health. All the erroneous conjecture and misinformation in the report is
potentially harmful for persons with MS.
4) As a father of a person with MS, I am very angry that I cannot count on the
government of Alberta to provide reliable information to help our family
deal in the best possible way with a serious disease.
The people of Alberta, and especially all those who are dealing with MS, deserve
far better from the government of Alberta when it comes to providing factual and
objective data and analyses on the important topic of CCSVI and its treatment.
I look forward to hearing from you in the near future regarding the results of the
investigation into probable conflicts of information of the authors and what your
department plans to do to rectify the unacceptable and potentially harmful
situation regarding the current lack of reliable and objective information on
CCSVI and its treatment from AHS.
Sincerely,
Dr Ashton Embry
References
Al-Omari MH, Rousan LA, Internal jugular vein morphology and hemodynamics in patients with multiple
sclerosis, Int Angiol. 2010 Apr;29(2):115-20
Doepp F, Paul F, Valdueza JM, Schmierer K, Schreiber SJ, No cerebrocervical venous congestion in
patients with multiple sclerosis. Ann Neurol. 2010 Aug;68(2):173-83.
Ebers GC, Environmental factors and multiple sclerosis. Lancet Neurol. 2008 Mar;7(3):268-77.
Embry AF, Integrating CCSVI and CNS autoimmunity in a disease model for MS. Int Angiol. 2010
Apr;29(2):93-4.
Hill AB. The environment and disease: association or causation? Proc R Soc Med 1965;58:295–300.
Lee BB, Bergan J, Gloviczki P, Laredo J, Loose DA, Mattassi R, et al. Diagnosis and treatment of venous
malformations Consensus Document of the International uni0n of Phlebology (IUP)-2009. Int Angiol. 2009;
28: 434-51
Lee AB, Laredo J, Neville R, Embryological background of truncular venous malformation in the extracranial
venous pathways as the cause of chronic cerebro spinal venous insufficiency. Int Angiol. 2010 Apr;29(2):95-
108.
Putnam T, Studies in multiple sclerosis iv. "encephalitis" and sclerotic plaques produced by venular
obstruction. Arch Neurol Psychiatry 1935;33(5):929-940
Simka M, Kostecki J, Zaniewski M, Majewski E, Hartel M, Extracranial Doppler sonographic criteria of
chronic cerebrospinal venous insufficiency in the patients with multiple sclerosis. Int Angiol. 2010
Apr;29(2):109-14.
Singh AV, Zamboni P, Anomalous venous blood flow and iron deposition in multiple sclerosis. J Cereb
Blood Flow Metab. 2009 Dec;29(12):1867-78.
University of Buffalo. First Blinded Study of Venous Insufficiency Prevalence in MS Shows Promising
Results. Press release, February, 10, 2010. Available at http://www.buffalo.edu/news/10937
Zamboni P, Galeotti R, Menegatti E, et al. Chronic cerebrospinal venous
insufficiency in patients with multiple sclerosis. J Neurol Neurosurg Psychiatry
2009;80:392-399.
Zivadinov R, Schirda C, Dwyer MG, Haacke ME, Weinstock-Guttman B, Menegatti E, Heininen-Brown M,
Magnano C, Malagoni AM, Wack DS, Hojnacki D, Kennedy C, Carl E, Bergsland N, Hussein S, Poloni G,
Bartolomei I, Salvi F, Zamboni P, Chronic cerebrospinal venous insufficiency and iron deposition on
susceptibility-weighted imaging in patients with multiple sclerosis: a pilot case-control study. Int Angiol. 2010
Apr;29(2):158-75.
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Re: Ashton's letter

Postby frodo » Thu Aug 26, 2010 2:36 am

Gordon wrote:Given that the authors of this “Information Sheet” are public civil servants
who report to you, and who are ultimately responsible to the citizens of Alberta, I
felt compelled to write to you to both point out the major deficiencies of this report
and to ask for a retraction of it.


This is the part I like the most. They really have to retract if they are wise, because If they do not, and CCSVI turns out to be true, they will have a legal problem.

And they cannot say "we didn't know better". The letter is public and contains undisputable statements.
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Postby Billmeik » Thu Aug 26, 2010 7:05 am

I thought the alberta info sheet was good beause it made some scientific point rather than a bunch of childish whining. Their science is easy to pick apart. If ccsvi was caused by scarr tissue flowing down the veins, whey would the cells stop in the jugulars? Why not the heart?
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Postby Billmeik » Thu Aug 26, 2010 7:06 am

I thought the alberta info sheet was good beause it made some scientific point rather than a bunch of childish whining. Their science is easy to pick apart. If ccsvi was caused by scarr tissue flowing down the veins, whey would the cells stop in the jugulars? Why not the heart?
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Postby frodo » Thu Aug 26, 2010 1:25 pm

Billmeik wrote:I thought the alberta info sheet was good beause it made some scientific point rather than a bunch of childish whining. Their science is easy to pick apart. If ccsvi was caused by scarr tissue flowing down the veins, whey would the cells stop in the jugulars? Why not the heart?


One of the most (negatively) remarkable things of the pre-Zamboni research in MS is that they do not even agree what they speak about. For some MS researches, MS means the presence of scars in the CNS. Some other ones mean the underlying condition that produced the scars. For some others MS means just to be positive in the Poser or McDonald criteria, forgetting about the different existing types of distributed scars.

The whole research has been so sick that now is possible to sustain nearly any argument because MS means a lot of things.

Now these people is using the confusion to discredit the CCSVI theory. They say sometimes MS for the underlying condition that causes scars (when they say that MS can cause CCSVI they mean this) but when they feel like it, they change the meaning of MS and they state something about the scars. This is really awfull situation.
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