a paper from 2004 saying ms is primary vascular pathogenesis

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a paper from 2004 saying ms is primary vascular pathogenesis

Postby Cece » Wed Jun 02, 2010 9:56 pm

Microvascular Abnormality in Relapsing-Remitting Multiple Sclerosis: Perfusion MR Imaging Findings in Normal-appearing White Matter1
Meng Law, MD, Amit M. Saindane, MD, Yulin Ge, MD, James S. Babb, PhD, Glyn Johnson, PhD, Lois J. Mannon, RT, Joseph Herbert, MD and Robert I. Grossman, MD
- Author Affiliations

1From the Departments of Radiology (M.L., A.M.S., Y.G., J.S.B., G.J., L.J.M., R.I.G.) and Neurology (J.H.), New York University Medical Center, MRI Department, Schwartz Building, Basement HCC, 530 First Ave, New York, NY 10016. Received June 24, 2003; revision requested September 3; revision received October 16; accepted November 12. Supported by National Institutes of Health grants RO1CA093992, NS29029, NCRR M01 RR00096 GCRC, and R37 NS 29029–11. Address correspondence to M.L. (e-mail: lawm01@med.nyu.edu).

We interpret our findings of diminished perfusion in NAWM as evidence that MS has a primary vascular pathogenesis, and there is histopathologic evidence to support this hypothesis: Adams et al (9) described frequent edematous onion-skin changes and lymphocytic infiltration of vein walls in NAWM without adjacent parenchymal inflammation; this suggests that MS represents a form of subacute or chronic vasculitis that could precede lesion development. Allen and McKeown (46) have also observed perivascular inflammation in areas of macroscopic NAWM.

and this:
Nonetheless, the vascular or ischemic basis for demyelination is intriguing. Provocation of symptoms in response to a hot bath, exercise, and food and alcohol intake are features of MS (56); similarly, experimental neural ischemia produces both conduction block and focal demyelination (57). All of these provocative stimuli share a common denominator—namely, vasodilatation of the extraneural vascular bed. Hence, despite autoregulation in regions of impaired perfusion, shunting of vascular reserve away from critically perfused regions in the central nervous system may trigger an acute deterioration. Although it has long been noted that there are vascular occlusive changes in MS (19), attention has been drawn to evidence in recent histopathologic studies of MS of hypoxia-like tissue injury (58)."

So do MSers have their symptoms provoked after a hot bath, exercise, food or alcohol intake because these are all things that vasodilate the extraneural vascular bed (?) and shunt vascular reserve away from the already underserved brain? I don't think so, I've understood vasodilation to be good for us, but I dunno?

I did a search for this article here and it does look like it was discussed in cheerleader's original long sticky, but I was not able to find where.

My other reason for posting this is that: these guys at New York University Medical Center should have been all over CCSVI, has anyone contacted them?
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Postby mangio » Wed Jun 02, 2010 10:18 pm

I have read other papers as well by Yulin Ge. I think some of these
researchers presented papers in Toronto at the American Neurology conference? Lets hope they are big on CCSVI.
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Postby cheerleader » Wed Jun 02, 2010 10:35 pm

Hi Cece--Yes, people on here have been "all over" New York University--some of the MS patients from there found this paper and other research the neurologists there did with Dr. Mark Haacke in 7 Tesla MRI studies, and tried to talk about doing CCSVI testing, but the doctors were not interested in CCSVI studies. At all. THere's a thread on here somewhere where people were talking about demanding NYU get involved....but it's been buried and I'm too tired to find it.

This paper you've linked is all about hypoperfusion, and how that can create ischemia in the brain. Here it is....Marie found it in March '09 (you can search by posts, in order to find specific ones on longer threads....)


The vasodilitation mentioned is inside the brain-not good, since it takes vascular reserves away from an already slowly perfused brain....CCSVI patients want vasodilation outside the brain ...in the extracranial veins. It was this paper that confirmed to me what we saw when Jeff came home from a week at high altitude with his first MS flare...low oxygen further damaging an already injured brain, due to venous congestion and slowed perfusion.

here's a good thread on hypoperfusion.

Dr. Hubbard is now testing fMRI BOLD (oxygenation levels) in CCSVI before and after angioplasty and finding a large change in oxygenation rates once veins are opened. more to come---

Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
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Postby Badger » Wed Jun 02, 2010 11:48 pm

I have had problems going for hot baths since I was young. I would get a sensation running through my body and then my head would feel weak almost like I was going to faint.

I just called it "a funny feeling" but it is making sense now. :wink:
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Re: a paper from 2004 saying ms is primary vascular pathogen

Postby sbr487 » Thu Jun 03, 2010 7:20 am

Cece wrote:I don't think so, I've understood vasodilation to be good for us, but I dunno?

I think the author is saying exactly what you think. According to him, vascodilation results in drawing of additional blood flow in extra neural network resulting in more starvation ...
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