This Is MS Multiple Sclerosis Knowledge & Support Community

selkie wrote:Whenever I don't understand a too technical paper, I skip right to the conclusion like Daisy did.

The other thing you can do is wait until Dr. Sclafani gets back, post the link in his thread, and ask *specific* questions you may have.

Overall, I would say from reading the conclusion that this study - done by neurologists - certainly confirms Dr. Zamboni's theory that the vascular system plays a role in the development of MS.

It makes me so angry I could spit, that my neurologist said of Dr. Z's theories (w/out even reading his paper that was published in at least two medical journals) and of CCSVI, "that nothing much will come of it" - simply parroting another neuro he knows who made that comment.

This kind of blindness in the medical field is why we're all having to become vascular "experts" (ha) ourselves and spend our own money to be treated for a very real medical condition, a vascular deformity that our insurance companies should be paying for.

But calling attention to papers like this, will hopefully get more of the medical community to wake tf up.

Selkie, I totally agree with you on this one. Ever since wife's dx of MS 6 weeks ago all I've been doing is researching and reading articles pertaining to MS.

Wife is currently on Rebif and sees the nuero at the end of this month to
check her liver count. At this point in time is when I'm going to ask more
question and show him all the research papers pertaining to the relationship vascular disorders can play a key role in MS. This is when I'm going to request the dx for MS that is required for the Hubbard Foundation to test wife for CCSVI. I'm not going to get her treated at this
time but just dx. I don't see that this is too much to ask for. Hopefully all goes well!

not sure if this is important ........but .... the Editor -in-Chief of the Neurology Journal - Neurological Research - is Professor Manuel Dujovny
of [/b]WAYNE STATE UNIVERSITY in Detroit Michigan.

Is this not the place - Wayne State University - that some neurologist came out swinging AGAINST .... CCSVI and Dr. Zamboni ?

Correct me if I'm wrong .

If I'm RIGHT ..... then something stinks in WSU ..... when a underling makes outragous statements that contradict the opinion of the professor .......... that may have been his mentor.

This needs to be sorted out asap.

And this makes me ..........

To have this information ..... for so long ........2005 ........ and just sit on it ........is just outragous .......





Mr. Success - still learning how to start and stop BOLD

MrSuccess wrote:not sure if this is important ........but .... the Editor -in-Chief of the Neurology Journal - Neurological Research - is Professor Manuel Dujovny
of [/b]WAYNE STATE UNIVERSITY in Detroit Michigan.

Is this not the place - Wayne State University - that some neurologist came out swinging AGAINST .... CCSVI and Dr. Zamboni ?

Correct me if I'm wrong .

If I'm RIGHT ..... then something stinks in WSU ..... when a underling makes outragous statements that contradict the opinion of the professor .......... that may have been his mentor.

This needs to be sorted out asap.

And this makes me ..........

To have this information ..... for so long ........2005 ........ and just sit on it ........is just outragous .......





Mr. Success - still learning how to start and stop BOLD

Dr. Haake of Haake protocol in dx CCSVI. is from Wayne State. They recently (aug. 10?) held a conferenc on CCSVI. I doubt they were the ones that came out swinging. We must be careful about who/what we accuse. If you have reference?

I understand this paper perfectly well.
Unfortunately has nothing to do with CCSVI.
This is the classical "MS is an immune disease" paper.
They talk about the vasculature because that is where the Blood Brain Barrier(BBB) resides. They are hoping that a drug can be found to strenghten the BBB and they noted that this is part of interferon effect.
So nothing new and nothing supporting the vascular theory in MS.

Hi Fog - thanks for correcting me. I thought Dr. Haacke was tied to Wayne State U - in some way. I was too lazy to research the connection .

This is much WORSE than I thought.

I disagree with Nunzio ..... and value Daisy3's post ...

IT CANNOT BE STATED MORE CLEARLY

WSU has researched and produced an opinion that MS may be affected by vascular disorders

They - WSU- concluded the association in 2006



And still we have the Neurology community in CCSVI denial. Or at least a good portion of them.

I thought Dr. Zamboni was a genius ..... now I know he is.




Mr. Success

Nunzio wrote:I understand this paper perfectly well.
Unfortunately has nothing to do with CCSVI.
This is the classical "MS is an immune disease" paper.
They talk about the vasculature because that is where the Blood Brain Barrier(BBB) resides. They are hoping that a drug can be found to strenghten the BBB and they noted that this is part of interferon effect.
So nothing new and nothing supporting the vascular theory in MS.

The proposed mechanisms about how CCSVI causes the lesions is because the BBB is weakened and T-cells and iron can cross it and produce the damage. We know now that this happens because the hypoperfusion, but this paper is previous to Zamboni research.

This paper was very innovative. To strength the BBB with chemicals was the only option at that time.

To be very frank I have not understood why the opposition from Neuro community. After all, Dr. Z seems to be only taking the argument to a logical conclusion.

All along it has been postulated that immune attack is of unknown origin.
Dr. Z says, its due to what is happening in the brain.

I would like to believe that BBB change, immune attack etc. are all co-ordinated rather than being incidental.

In the auto-immune approach, its difficult to believe that immune response went bad and at the same time the BBB changes also happened.

Just to add another point about Wayne State University in Michigan, Dr. Haake who is one of the leading researchers on MRIs/MRVs for CCSVI has a dual appointment at Wayne State in Michigan and McMaster University in Hamilton. Ontario. This is leading edge, cross-border collaboration.

Based on everything I know, Wayne State is very supportive of Dr. Hakke's research, as is McMaster University.

hi there

i also did some research and foud some interesting vascular papers before Zamboni:

Immunohistochemical study of vascular injury in acute multiple sclerosis.

AIMS--To examine the vascular changes occurring in three archival cases of acute multiple sclerosis, and to provide immunohistochemical evidence of early endothelial cell activation and vascular occlusion in this condition.

CONCLUSION--It is proposed that vascular endothelial cell activation may be an early and pivotal event in the evolution of multiple sclerosis, and that demyelination may have an ischaemic basis in this condition. The vascular endothelium may contain an early element in the evolution of multiple sclerosis.

source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC501826/

Subcortical vascular cognitive impairment: Similarities and differences with multiple sclerosis

Abstract
Subcortical vascular cognitive impairment is caused by lacunes and widespread ischemic white matter damage which closely resembles white matter abnormalities seen in multiple sclerosis. Recent evidence suggests that the progression rate of ischemic white matter lesions on MRI is very similar to that observed in multiple sclerosis.

source: http://www.jns-journal.com/article/S002 ... X/abstract

Vascular Endothelial Growth Factor Is Expressed in Multiple Sclerosis Plaques and Can Induce Inflammatory Lesions in Experimental Allergic Encephalomyelitis Rats

....
These results suggest that overexpression of VEGF may exacerbate the inflammatory response in autoimmune diseases of the CNS by inducing focal BBB breakdown and migration of inflammatory cells into the lesions .

source: http://journals.lww.com/jneuropath/Abst ... _in.9.aspx

ABSTRACT

PURPOSE: To prospectively determine hemodynamic changes in the normal-appearing white matter (NAWM) of patients with relapsing-remitting multiple sclerosis (RR-MS) by using dynamic susceptibility contrast material–enhanced perfusion magnetic resonance (MR) imaging.

CONCLUSION: The NAWM of patients with RR-MS shows decreased perfusion compared with that of controls.

source: http://radiology.rsna.org/content/231/3/645.full

regards
alex

Hi Alex--
Those are great papers--we discuss them in the very long original CCSVI thread which began all of this last year. Yes, there are many, many research papers regarding endothelial dysfunction, hypoperfusion, the vascular system and the MS brain. What Dr. Zamboni did was discover a reason why all of this was happening.

Please note that the same researchers at Louisiana State University who published the original paper cited on this thread from 2006--MS as a vascular disease-- have recently published a brand new follow-up and worked with Dr. Zivadinov of SUNY Buffalo:

These papers are linked at www.ccsvi.org-
under Advanced Topics---published papers:

Pathophysiology. 2010 Jul 19. [Epub ahead of print]
Multiple sclerosis and cerebral endothelial dysfunction: Mechanisms.
Alexander JS, Zivadinov R, Maghzi AH, Ganta VC, Harris MK, Minagar A.

Department of Cellular and Molecular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Abstract
Multiple sclerosis (MS) is believed to be an immune-mediated neurodegenerative disorder of the human central nervous system which usually affects younger adults with certain genetic backgrounds. The causes and cure for MS remain elusive. Based on the recent advances in our understanding of the pathogenic mechanisms of MS, it appears to represents a heterogeneous group of disorders with dissimilar pathophysiology and neuropathology. Currently, there is no unifying hypothesis to explain the pathogenesis of this complex disease. The three prevailing concepts on the pathogenesis of MS include viral, immunological, and vascular hypotheses. This review presents MS as a neuroinflammatory disease with a significant vascular component and examines the existing evidence for the role of cerebral endothelial cell dysfunction in the pathogenesis of this progressive central nervous system (CNS) inflammatory disorder.

PMID: 20663648 [PubMed - as supplied by publisher]

cheer

frodo wrote:

Nunzio wrote:I understand this paper perfectly well.
Unfortunately has nothing to do with CCSVI.
This is the classical "MS is an immune disease" paper.
They talk about the vasculature because that is where the Blood Brain Barrier(BBB) resides. They are hoping that a drug can be found to strenghten the BBB and they noted that this is part of interferon effect.
So nothing new and nothing supporting the vascular theory in MS.

The proposed mechanisms about how CCSVI causes the lesions is because the BBB is weakened and T-cells and iron can cross it and produce the damage. We know now that this happens because the hypoperfusion, but this paper is previous to Zamboni research.

This paper was very innovative. To strength the BBB with chemicals was the only option at that time.

The reason I do not value this paper much is that , according to the classical MS-autoimmune theory, two events have to happen:
#1 The immune system has to be primed against myelin.
#2 You need a breach of the Blood-Brain Barrier.
Every MD will agree with this, including neurologist.
The BBB is formed primarily by the tight junction between the endothelial cell that line the inside of the blood vessel in the brain.
So, in this sense, MS is a vascular disease, but not because CCSVI.
Try to show that paper to a neurologist and see what happen.
Naturally any advances in understanding MS is welcome, but do not think this will advance our CCSVI cause.
This paper is from 1990 so, nothing new.
http://www.ccsvi.co.uk/resources/Kermod ... t%2090.pdf
BREAKDOWN OF THE BLOOD-BRAIN BARRIER
PRECEDES SYMPTOMS AND OTHER MRI SIGNS
OF NEW LESIONS IN MULTIPLE SCLEROSIS
Such perivascular inflammation has also
been seen in normal-appearing white matter of the brain and in the retinal venules in the absence of subjacent parenchymal inflammation , leading to the conclusion that perivascular inflammation in MS can occur in the
absence of myelin breakdown, and the suggestion that a vascular event is a necessary preliminary to the development of structural damage.
Magnetic resonance imaging (MRI) provides a noninvasive means of studying disease.

I think the paper is relevant because, in the autoimmune theory, there is the unanswered question: why does the BBB break-down? It is accepted that it does break down and that this comes first. So now CCSVI is presented as a possible explanation for that unanswered question.

If a neurologist is pooh-poohing the CCSVI theory, then that question (why does the BBB break down?) can be raised, followed by the idea that this is a place where CCSVI may click right into place with what is already known about MS.

Nunzio wrote:
This paper is from 1990 so, nothing new.
http://www.ccsvi.co.uk/resources/Kermod ... t%2090.pdf
BREAKDOWN OF THE BLOOD-BRAIN BARRIER
PRECEDES SYMPTOMS AND OTHER MRI SIGNS
OF NEW LESIONS IN MULTIPLE SCLEROSIS

Yes. It is true that some people had found the same before, but nobody was reading those papers. You only have to remember the Schelling case.

The vascular involvement in MS has been rediscovered and forgotten several times, just because vascular papers were lost inside a sea full of EAE papers. It is impossible to find a needle in a haystack.

These researches were not so close to the solution as Schelling or Zamboni or others, but nevertheless they did their research in an environment that was biased against vascular involvement. Maybe their contribution was not the most important, but it was worthy anyway. Their article can be a tool for us.