Severe Criticism & MOCKERY of CCSVI BY A Doctor SPAMMING

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

Postby ikulo » Sat Mar 12, 2011 4:25 pm

colros wrote:Changes in refraction over time are universal, have nothing to due with the retina and nothing to do with MS. That "colors brightened immediately" is highly subjective. What was the evidence that you brain blood flow was so reduced as to cause cerebral hypoxia? If blood flow was that reduced you would have lost consciousness long before color perception changed.

With all due respect to Dr Sclafani, the ONLY way venous occlusion can potentially cause brain damage is by an increase in intracranial pressure which could secondarily reduce blood flow. No study has ever shown a primary reduction in cerebral flow causing MS. Cerebral flow will be reduced secondarily in long-standing MS secondary to loss of active brain tissue. Indeed, we do not know what breaks the BBB and leads to infiltration of inflammatory cells, but it has nothing to do with blood flow or pressure.

We all care very much about MS. Unfortunately, "CCSVI" and its surgical treatment, as superficially attractive as it is, is not the answer.


Dr. Rose, just wanted to bring this study to your attention.

Correlation of Diffusion Tensor and Dynamic Perfusion MR Imaging Metrics in Normal-Appearing Corpus Callosum: Support for Primary Hypoperfusion in Multiple Sclerosis
A.M. Saindanea, M. Lawa, Y. Gea, G. Johnsona, J.S. Babba and R.I. Grossman

From the Department of Radiology, New York University Medical Center, New York, NY

. . . .

Fundamentally, there are 2 possible causes for NAWM hypoperfusion, which can be categorized as primary or secondary. In the first scenario, a primary vascular pathologic lesion results in decreased perfusion in the NAWM with consequent ischemic parenchymal injury. In the second scenario, axonal damage in MS lesions leads to WD of axons traversing distant areas of white matter, resulting in decreased axonal attenuation, regional hypometabolism, and secondary hypoperfusion of the NAWM. The distinction between these mechanisms has potentially important implications, because ischemia may be an early and potentially reversible finding, whereas hypometabolism from axonal degeneration would represent advanced and irreversible disease.

. . . .

We interpret these findings as support for primary hypoperfusion (ischemia) in MS.

. . . .

This study does not refute the presence or importance of WD in MS; however, it suggests that hypoperfusion is due to alternative (primary vascular) pathologic conditions.

. . . .

Considerable histopathologic evidence supports a primary vascular pathologic lesion in MS. Studies have described perivascular inflammatory changes such as lymphocytic infiltration and edematous onion-skin changes of vein walls in NAWM lacking adjacent parenchymal inflammation, suggesting that MS could represent a form of subacute or chronic vasculitis.31,42 Vascular occlusion in MS was described on histopathologic examination by Putnam43,44 in the 1930s and later by Wakefield et al,45 who demonstrated fibrin deposition and thrombosis of vessels in the absence of cellular infiltration, suggesting that thrombosis of small veins and capillaries could represent an ischemic basis for disease. More recent studies have demonstrated the presence of extensive oligodendrocyte apoptosis46 and preferential loss of myelin-associated glycoprotein,47 which is suggestive of hypoxic-ischemic-type tissue injury.

. . . .

The results of this study correlating DTI and perfusion changes are more consistent with what would be expected in primary ischemia than in secondary hypoperfusion from WD. Further investigation, including larger and longitudinal studies are warranted to additionally support the concept of ischemic injury in MS. A better understanding of the role of ischemia could aid in predicting clinical course, monitoring response to therapy, and designing novel targets for therapeutic intervention for MS.



http://www.ajnr.org/cgi/content/full/28/4/767
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Postby colros » Sat Mar 12, 2011 4:52 pm

I should have qualified my statement by saying that no blinded study has shown a primary reduction in cerebral blood flow in MS.

The paper to which you refer uses a very complex analysis with proprietary software without blinding, very similar to what Zamboni did. So their conclusion is not justified. Confirmation with well-blinded studies using conventional techniques is required.

The main problem with the hypoperfusion hypothesis is that reduction in cerebral blood flow will affect the high oxygen consumption neurones of the grey matter long before it affects the low oxygen consumption glial cells of the white matter, the cells involved in producing myelin disease of which causes MS.
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Postby ikulo » Sat Mar 12, 2011 5:08 pm

So you completely dismiss the findings of the paper because it wasn't blinded?

I'm not familiar with the consumption differences between grey and white matter, but am interested in learning more. Could you provide a paper or source to learn more?
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Gray Matter Atrophy in CIS

Postby Shayk » Sat Mar 12, 2011 5:25 pm

Hi
The main problem with the hypoperfusion hypothesis is that reduction in cerebral blood flow will affect the high oxygen consumption neurones of the grey matter long before it affects the low oxygen consumption glial cells of the white matter, the cells involved in producing myelin disease of which causes MS.

It seems that grey matter atrophy is present quite early in the disease process. Brain atrophy in clinically isolated syndrome
CONCLUSIONS: This is the first study dealing with brain atrophy in a CIS sample from Latin America in which brain atrophy, mainly grey matter atrophy, was shown in early stages of the disease compared with healthy individuals.

So it seems that grey matter atrophy can occur prior to a diagnosis of MS.

Sharon
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oxygen consumption of grey vs white matter

Postby colros » Sat Mar 12, 2011 5:55 pm

Ratio of the volume of grey matter to white matter in the cerebral hemipheres (20 yrs. old) = 1.3 (Miller, A.K., Alston, R.L. and Corsellis, J.A., Variation with age in the volumes of grey and white matter in the cerebral hemispheres of man: measurements with an image analyser, Neuropathol Appl Neurobiol., 6:119-132, 1980)
Ratio of the volume of grey matter to white matter in the cerebral hemipheres (50 yrs. old) = 1.1 (Miller et al., 1980)
Ratio of the volume of grey matter to white matter in the cerebral hemipheres (100 yrs. old) = 1.5 (Miller et al., 1980)
% of cerebral oxygen consumption by white matter = 6%
% of cerebral oxygen consumption by gray matter = 94%


http://faculty.washington.edu/chudler/facts.html
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Postby frodo » Sat Mar 12, 2011 5:55 pm

colros wrote: I am against any surgical procedure or drug that has not been proven in good controlled trials to be of any long-term benefit


Dear doctor,

I suppose you are aware that CRABs drugs have been shown to reduce gadolinium enhanced lesions, but nobody has ever established a relationship between the existence of these lesions and MS progression.

Do you consider acceptable to use this kind of drugs?
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Re: oxygen consumption of grey vs white matter

Postby ikulo » Sun Mar 13, 2011 2:48 pm

colros wrote:Ratio of the volume of grey matter to white matter in the cerebral hemipheres (20 yrs. old) = 1.3 (Miller, A.K., Alston, R.L. and Corsellis, J.A., Variation with age in the volumes of grey and white matter in the cerebral hemispheres of man: measurements with an image analyser, Neuropathol Appl Neurobiol., 6:119-132, 1980)
Ratio of the volume of grey matter to white matter in the cerebral hemipheres (50 yrs. old) = 1.1 (Miller et al., 1980)
Ratio of the volume of grey matter to white matter in the cerebral hemipheres (100 yrs. old) = 1.5 (Miller et al., 1980)
% of cerebral oxygen consumption by white matter = 6%
% of cerebral oxygen consumption by gray matter = 94%


http://faculty.washington.edu/chudler/facts.html


I was hoping for a study demonstrating that reduced CBF in the brain affects the gray matter more than the white matter. You would undoubtedly admit that just knowing the percentage of oxygen consumption does nothing to prove the effect of hypoperfusion. That would require many assumptions and leaps of logic.
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Postby MSBOB » Sun Mar 13, 2011 3:39 pm

J Neuroimmunol. 2011 Jan;230(1-2):173-7. Epub 2010 Sep 9.
Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis.
Casiraghi C, Dorovini-Zis K, Horwitz MS.

Department of Microbiology and Immunology, The University of British Columbia, Vancouver, British Columbia, Canada.
Abstract
Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis.

Copyright © 2010 Elsevier B.V. All rights reserved.

Does anyone care about this?

This is in response to the breach of the BBB question, that was kind of hinted that only CCSVI could be responsible for.

Correction: I don't think that EBV is a retrovirus, but it has some associations.
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Postby colros » Sun Mar 13, 2011 3:52 pm

No need for studies. We have lots of clinical examples. Ischemic (lack of blood flow) stokes demonstrate the principle quite well. When a large cerebral artery is blocked by thrombosis, the part of the cerebral cortex it supplies dies; white matter that needs much less blood flow is generally not affected particularly in transient ischemic attacks. For images see these publications for example.

http://stroke.ahajournals.org/cgi/reprint/31/3/680
http://stroke.ahajournals.org/cgi/reprint/34/4/932
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Postby MSBOB » Sun Mar 13, 2011 6:17 pm

colros wrote:No need for studies. We have lots of clinical examples. Ischemic (lack of blood flow) stokes demonstrate the principle quite well. When a large cerebral artery is blocked by thrombosis, the part of the cerebral cortex it supplies dies; white matter that needs much less blood flow is generally not affected particularly in transient ischemic attacks. For images see these publications for example.

http://stroke.ahajournals.org/cgi/reprint/31/3/680
http://stroke.ahajournals.org/cgi/reprint/34/4/932


Very interesting. "chronic cerebral ischemia" I read some studies that white matter was affected in in chronic cerebral ischemia, but usually as a course of natural aging and atrophy. The mechanisms look similar to MS, but not exactly. I suppose anyone back 40 years ago treating MS with warfarin didn't have much success for the same reasons you are trying to explain here.


Thanks for the info.

Peace
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Postby colros » Sun Mar 13, 2011 7:21 pm

"Chronic cerebral ischemia" really means small lacunar (white matter) infarcts due to occlusion of the small penetrating arteries by emboli or stenosis due to hypertension.

http://en.wikipedia.org/wiki/Lacunar_stroke
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Postby MSBOB » Sun Mar 13, 2011 7:50 pm

colros wrote:"Chronic cerebral ischemia" really means small lacunar (white matter) infarcts due to occlusion of the small penetrating arteries by emboli or stenosis due to hypertension.

http://en.wikipedia.org/wiki/Lacunar_stroke


Wow! Thanks for the info again. From the Wiki link: "They may be more frequent in men and in African Americans, Mexican Americans, and Hong Kong Chinese."

That strikes me kind of funny, because it is like the exact opposite of the risky demographics for MS.

My opinion on the CCSVI thing has grown. It is really too bad that it is such a divisive issue. A little study done in Italy that inspired a bunch of people to go out on their own and get surgeries on their major jugulars. I don't feel very good about it at all. I don't want to argue with anyone either. Not anymore.

Thank you, colros. Be kind and patient.
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Postby frodo » Mon Mar 14, 2011 4:46 am

Hi MSBOB

my question is open for you too. As Mr Colros refuses to answer, maybe you can help me with my doubts.

I repeat the question. Being CRABs drugs only able to reduce gadolinium enhanced lesions, with no established relationship to MS progression, do you consider acceptable to use this kind of drugs?
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Postby Lyon » Mon Mar 14, 2011 6:18 am

..
Last edited by Lyon on Fri Jun 24, 2011 7:41 pm, edited 1 time in total.
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Postby frodo » Mon Mar 14, 2011 7:59 am

Lyon wrote:I'd be the last person to defend the CRABs or the pharmas but I don't see any of them claiming that their product's (supposed) benefit to the patient is based only on it's ability to control lesions?


Thanks for your answer Lyon, but still none of them claims to have influence in the long term. It could happen that they help in the short term making things worse later. Therefore the question is still open. Is it ethical to diagnosize these things with unknown long-term effects?
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