Why "CCSVI" is Surreal

[cheerleader]

BTW, unlike "liberation", there are good randomized controlled trial showing that the current DMD drugs do slow the progression of plaques. Otherwise they could not be sold.

But progression of plaques (lesions) does not equal progression of MS disability...or someone like my husband, with 20 lesions, would not be able to mountain bike, while our friend, with one lesion, cannot walk.

DMDs do not address the true disability, which is brain atrophy and loss of gray matter. That continues, even on DMDs.--
http://archneur.ama-assn.org/cgi/reprint/63/8/1175.pdf

Clinically relevant GM atrophy occurs in the cerebellum of MS patients and is more prominent than WM atrophy. As such, it may provide complementary data to other regional atrophy and intrinsic tissue measures.

http://msj.sagepub.com/content/15/7/811.abstract
http://onlinelibrary.wiley.com/doi/10.1 ... 7/abstract

The Review of DMDs by the British Medical Journal showed that even when DMDs stop relapses, MS disability continues. It's not about white matter lesions.....this is why the DMD program was called a failure in the UK. Because the drugs don't work.

To make things even more difficult, the calculations assessing whether disease modifying treatments might be affordable in the NHS were predicated on the putative effects of preventing the accumulation of disability in multiple sclerosis, not on relapse rates. To many this seemed hazardous—firstly, because only a proportion of patients (who are unidentifiable) become progressively disabled; and secondly, because the relation between relapses and disability is more complex and more indirect than many imagined.5 Reducing the frequency of relapses does not necessarily reduce the progression of disability. Indeed, studies with powerful monoclonal antibodies show that progression can continue unabated even when relapses are abolished completely.6

http://www.bmj.com/content/340/bmj.c2882.full


So...even with all of those wonderful trials of the drugs...we are not any further along in understanding the true cause of disability in MS....but it looks to be gray matter atophy, not white matter lesions. Interestingly enough, my husband's brain atrophy was reversed by increased blood flow after his angioplasty.
Which is why I find the autoimmune theory of MS to be surreal.
cheer

[Cece]

The initial scientific proof of endovascular treatment for CCSVI is in Dr. Zamboni's 2009 paper. Peer reviewed and published.

Here is an abstract of Dr. Mandato's safety study on CCSVI treatment as presented at the SIR conference:
www.jvir.org/article/S1051-0443(11)00005-4/fulltext

[CaptBoo]

What she said!

[cheerleader]

I'd like to continue to explain what Dr. Zamboni has discovered. But what if MS disability is about gray matter atrophy and the deep cerebral veins, as new research is indicating. The DMDs do not stop progression, even if relapses are completely stopped (see Bristish Medical Journal link in earlier post)

Now that we've seen how disability in MS is not connected to relapses and white matter lesions (see my earlier post w/all the research on gray matter atrophy) we can understand the connection to extracranial venous stenosis, reflux and gray matter injury.

Here is a diagram of the deep cerebral venous system...please click for the picture.

link

Reflux flow mapping in the cerebral venous system found in CCSVI-MS. Map of venous reflux flow in MS and in healthy controls. In the diagram, areas investigated by means of high resolutions vascular ultrasounds. Legends: Yellow arrows normal flow direction, red arrows reflux flow; SSS (superior saggital sinus), CS (confluence sinus), TS (transverse sinus), SS (straight sinus), DCVs (deep cerebral veins including Galen vein (GV), internal cerebral veins (ICVs), Rosenthal vein (RV)), IPS (inferior petrosus sinus), IJVs (internal jugular veins). A Area: reflux rate in the extracranial main pathways, IJVs and azygous vein; B Area: reflux rate in the TS; C Area: reflux rate in the DCVs; D Area: reflux rate in the veins connecting the subcortical gray matter with the DCVs..

This is how extracranial venous blockage and reflux damages the MS brain. Once again, not about white matter lesions....Dr. Zamboni is a brilliant and caring doctor, and his discovery has saved my husband's brain. I am forever indebted to his brilliance and compassion. And I will continue to clarify his discovery...
cheer

[Cece]

Cheer, great work pulling the research together and explaining it.

[MegansMom]

specifically the cases of CCSVI found post- mortem and several studies looking at hypoperfusion and the changes in perfusion pre and post venoplasty.

Zamboni deserves a Nobel prize for medicine not being ridiculed by someone that doesn't keep up with the peer reviewed studies/research.
and please refrain from saying derogatory things about patients and patient choices. Ask any physician that deals with MS patients. They are some of the best educated about their disease and it's treatments.

I encourage any new folks to study the research and then make the decision that s best for you.

Buy a copy of Marie Rhodes book on CCSVI
It's called :

"CCSVI as the cause of Multiple Sclerosis : The Science behind the controversial theory."

[colros]

@cheerleader
MS is not a primary disease of neurones of the grey matter. It is a primarily a disease of the myelin producing glial cells of the white matter. Grey matter atrophy is due to retrograde degeneration secondary to axonal injury, NOT due to hypoxia of neurones. There is a direct correlation between plaques and grey matter atrophy. Here is the abstract from the first paper you mention:

"Background: Gray matter (GM) atrophy has been reported
in multiple sclerosis (MS). However, little is known
about its regional distribution.
Objective: To investigate the regional distribution of
GM atrophy in clinically early primary progressive MS
(PPMS).
Design and Patients: Thirty-one patients with PPMS
within 5 years of symptom onset (mean age, 43.2 years;
median Expanded Disability Status Scale score, 4.5) and
15 healthy control subjects (mean age, 43.7 years) were
studied.All subjects underwent a 3-dimensional inversionrecovery
fast spoiled gradient-recalled echo sequence that
was repeated after 1 year in patients only. Magnetic resonance
images underwent an optimized voxel-based morphometric
analysis that segments magnetic resonance data
volumes in a normalized space and quantifies tissue atrophy
on a voxel-by-voxel basis. A lesion mask was created
for each patient and used in normalization and segmentation
steps to minimize bias from lesions. A
multisubject design was used in the cross-sectional study
to compare patients with PPMS and controls. A 1-way
analysis of variance (within-subjects) design was used in
the longitudinal study.
Results: At baseline, patients with PPMS displayed bilateral
thalamic atrophy compared with controls. In addition,
a significant association between lesion load and
decreased GM volume was found for the thalami. Loss
ofGMin the putamen, caudate, thalami, and cortical and
infratentorial areas was observed in patients after 1 year
of follow-up.
Conclusions: Atrophy is most obvious in deep GM in
clinically early PPMS. This may reflect increased sensitivity
of these regions to neurodegeneration. Cortical and
infratentorial atrophy developed as the disease evolved."

You have made a selective quote that does not reflect the overall conclusions.

To repeat, there is no way that blockages in neck veins could selectively cause ischemia of white matter. They could only potentially cause reduction in TOTAL cerebral blood flow which would result in unconsciousness before ever affecting cells of the white matter. There is no such thing a chronic cerebral ischemia. Like light switches, neurones are either on or off. They cannot tolerate chronic hypoxia like other tissues such as skeletal muscle.

[cheerleader]

It is a disease of gray matter. The white matter disease is secondary.

Gray matter demyelination is frequent and extensive in most patients with multiple sclerosis (MS) and has recently received much attention in neuropathologic and imaging studies. Gray matter lesions show distinct pathologic features that make their detection difficult with conventional imaging techniques. Thus, despite their high prevalence, their impact on clinical symptoms has not been defined well so far. This review focuses on recent information from pathologic and imaging studies and summarizes our current knowledge on cortical pathology derived from human and experimental studies.

http://www.mendeley.com/research/gray-m ... sclerosis/

Here's more about demylination of the gray matter of the hippocampus--
http://onlinelibrary.wiley.com/doi/10.1 ... 7/abstract

new MRI technology is allowing doctors to see the deep gray matter. The same gray matter that is drained by the deep cerebral veins. Research moves on.... it is changing.
cheer

[colros]

There is zero evidence that MS is a primarily a disease of grey matter neurones. Zamboni's study was totally UNBLINDED and should never have been published. He selected variations in the normally large spectrum of venous flow patterns and associated them with MS in subjects for whom he knew the diagnosis. Blockages in neck veins could only possibly cause damage to the brain if intracerebral pressure were increased and there is zero evidence that MS patients have such. Zamboni's "reflux" is some phenomenon that he proposes to explain how blockages in neck veins could cause damage to the brain without an increase in intracerebral pressure. This is not science. Your husband's brain would be the same even without "liberation".

[cheerleader]

Zamboni's research was blinded. He did not know who had MS and who did not. He research was peer-reviewed and published. I have spoken to neurologist Dr. Salvi in person about this. Dr. Salvi was very dubious, and is now convinced.
What he found is real. Reflux of the deep cerebral veins is not normal, and is injurious to the brain. It harms the deep gray matter. And new MRI technology is showing the injury to this area in the MS brain.
the facts will not change.
cheer

[colros]

Indeed there are also demyelinating lesions in the grey matter that are harder to detect with MRI and that may explain some of the discrepancy between white matter lesions and disability. But that has nothing to do with the existence or not of "CCSVI". There is no way that blockages in neck veins can cause damage to the brain without an increase in intracerebral pressure which as never been demonstrated in MS patients.

[Shayk]

Hi--I haven't read all of this thread...but this caught my eye.

colros

To repeat, there is no way that blockages in neck veins could selectively cause ischemia of white matter. They could only potentially cause reduction in TOTAL cerebral blood flow which would result in unconsciousness before ever affecting cells of the white matter. There is no such thing a chronic cerebral ischemia.

It seems to me this MS research contradicts your comment.

Subcortical vascular cognitive impairment: similarities and differences with multiple sclerosis.

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.

White matter hemodynamic abnormalities precede sub-cortical gray matter changes in multiple sclerosis

CONCLUSIONS:

CBF (CBF = cerebral blood flow) was decreased in the NAWM of both CIS and RR-MS patients and in the subcortical NAGM of RR-MS

Looks to me like we do have a reduction in cerebral blood flow without becoming unconscious--quite contrary to your statement.

Sharon

[colros]

Zamboni's research was blinded. He did not know who had MS and who did not. He research was peer-reviewed and published...

Not true. Here is a quote from the Methods section of his paper:

"Sixty-five subjects with MS fulfilling the ECD-TCCS screening criteria and 48 controls of the HAV-C group underwent selective catheterism of the azygous and IJV system via the transfemoral route. Venography was performed, being aware of patients’ diagnoses."

To repeat, this study was unblinded and should never have been published.

[cheerleader]

Idiopathic Intercranial Hypertension and MS have been linked, Dr. Rose. I heard Dr. Eliot Frohmann, neurologist, discuss this in Bologna. There is an enlargement of the third ventricle in both diseases.

http://www.mevis-research.de/~klein/pub ... ctrims.pdf

Here's a paper noting the relationship

link

Here's another case:
http://www.ncbi.nlm.nih.gov/pubmed/18539995
cheer

[griff]

My purpose with posting this article was to get opinions from both sides. I appreciate any opinions that try to give us scientific information on CCSVI, regardless of its nature whether it is supportive or not. Lets face it the cause of MS and the role of CCSVI to it is still unknown. Different scientists might have different ideas about it. I think tims give us a good forum to learn about these ideas and we can decide what we accept and what we do not. I would be happy if I could see more posts from doctors who are familiar with CCSVI and they would tell us their opinions about it regardless whether it is favorable or not.

A personal note. I talked to a neuro surgeon who supports CCSVI research and he thinks patients should be given the right to get the operation until its real role in MS is decided even though he thinks that CCSVI is not a major factor to MS. Two of his close friends and fellow doctors just recently died of MS, so he has a strong feeling for MS patients. Now, is he a bad guy just because he thinks based on his experience that CCSVI is not a major factor to MS? He might be wrong, but he might be right, but I do not think that he and others who think like him should be hated for their opinions.