Congestive Venous Myelopathy

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

Congestive Venous Myelopathy

Postby cheerleader » Wed Jun 17, 2009 2:16 pm

We've mentioned this disease model as an example of how damaged veins can cause demyelination...without activating the immune system. Veins that become blocked create collateral drainage. This leads to reflux and leakage, which causes demyelination.

I'll be posting studies that prove this model. Look for the tie ins to CCSVI-


Study Number 1
http://www.springerlink.com/content/n086758m65115886/

Y. Narita1, Y. Watanabe1, T. Hoshino2, M. Okada2, Y. Yamamoto2 and S. Kuzuhara3

(1) Department of Neurology, Matsusaka Chuo Hospital, Mie, Japan
(2) Department of Neurosurgery, Matsusaka Chuo Hospital, Mie, Japan
(3) Department of Neurology, Mie University Hospital, Mie, Japan
Received: 12 June 1991

Summary A 45-year-old woman developed a myelopathy 9 years after a spontaneous left caroticocavernous fistula (CCF) was treated by a trapping procedure, with clipping distal to the fistula and ligation of the common carotid artery. Spinal MRI and vertebral angiography revealed recurrence of the CCF and gigantic tortuous veins draining through the brain stem down to the midcervical spinal cord. The abnormal veins and myelopathy disappeared after surgical closure of the CCF.


Here is a woman who had a CCF fistula- an abnormal connection between the internal and external cartoid arteries- treated with ligation of the cartoid artery. This procedure creates a new drainage pattern-
Venous drainage may be anterior via the SOV or posterior via the (IPS) and superior petrosal sinus (SPS). Contralateral venous drainage may also occur via the circular sinus. The latter situation can create contralateral symptoms.


After nine years, an MRI shows the the contralateral veins draining her brain have grown gigantic and tortous...and these veins have created demyelination. After the CCF is closed up...the abnormal veins and myelopathy DISAPPEAR.

cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cheerleader » Wed Jun 17, 2009 2:39 pm

Study # 2
http://jnnp.bmj.com/cgi/content/abstract/79/12/1408

Improvement of paraplegia caused by spinal dural arteriovenous fistula by surgical obliteration more than 6 years after symptom onset
O Kaut, H Urbach and T Klockgether

University of Bonn, Bonn, Germany

Correspondence to:
Dr O Kaut, University of Bonn, Sigmund-Freud-Strasse 25, Bonn 53105, Germany; oliver.kaut@ukb.uni-bonn.de
Spinal dural arteriovenous fistulae (SDAVF) are acquired spinal vascular malformations, in which a small connection between a radicular artery and radicular vein causes venous hypertension, congestive myelopathy and infarction of the spinal cord. Here the case of a 47-year-old man is presented who had pain in his back irradiating to his right leg, numbness of his right leg as well as weakness of both legs. Urination was disturbed with detection of residual urine. Six weeks later he developed a progressive paraparesis of the legs. A T2 weighted MRI of the lower back showed intramedullary hyperintensity. A myelitis was assumed and treatment with acyclovir and dexamethasone was started. Nevertheless, he developed total paralysis of his legs. Six years later, re-evaluation of the initial MRI and a new MRI showed abnormal blood vessels on the dorsal side of the spinal cord, which had been overlooked at the first MRI examination. Spinal angiography demonstrated an arteriovenous fistula. Fistula obliteration was performed. Six months later he was able to stand with canes for 2 min and showed improvement in sensibility. The remarkable aspect of this case of SDAVF is the relevant improvement of complete paraplegia by surgical obliteration 78 months after onset of symptoms. The delay of more than 6 years between onset of first symptoms and final diagnosis underlines the difficulties in making a correct diagnosis of SDAVF. However, even after delayed diagnosis, surgical obliteration should be done, as improvement of neurological function can still be achieved.


Here is a man that becomes paralyzed, is misdiagnosed as myelitis, until his SDAVF - (a problem where the artery meets the vein, which creates venous hypertension and demyelination) is detected. Even after SIX YEARS, surgery and repair of the connection between veins and arteries allows for recovery.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mrhodes40 » Wed Jun 17, 2009 4:20 pm

Cool papers Cheer!!
what a great thread to have begun...

Both of these studies are looking at venous issues in which the veins are stressed by excessive blood flow and both result in myelopathy---
myelopathy= disease or degeneration of the spinal cord with resultant neurological deficits. MSers have myelopathy.

It makes me crazy when I hear a neurologist who has been presented this idea has declared this "can't" be the cause of MS. A look at the literature and en effort to study this shows it most certainly can cause demyelination and inflammation and in legs we know we get lesions. So based on what scientific principle is it rejected out of hand? And given that we seem to have these stenoses it seems to me perhaps it is up to them to show that such an anomaly CAN'T harm the MS brain before they tell us to ignore it.

I really appreciated the note that it took some years for the lady with the altered blood flow to develop neuro problems after her repair. It may show how it can be that people can have a jugular removed and they seem "fine" at least if you check them the next week. Question is does the body cope with that over years? MY guess is no and in around a decade you see these issues.

HERE"S another onealong the same "veins" :lol:
Spinal dural arteriovenous fistula: the pathology of venous hypertensive myelopathy
RW Hurst, LC Kenyon, E Lavi, EC Raps and P Marcotte
Department of Radiology, University of Pennsylvania Medical Center, Philadelphia, USA.

Spinal dural arteriovenous fistulas (SDAVFs) are the most common type of spinal vascular malformation. The arteriovenous shunts, located entirely outside the spinal cord, cause a clinical picture of chronic progressive myelopathy believed to arise from the effects of increased venous pressure and impaired venous drainage on the spinal cord. Despite their well-described clinical and angiographic features, no reports have documented the spinal cord pathology in a case of angiographically or pathologically proven SDAVF. We report such a patient in whom a spinal cord biopsy supported increased venous pressure as a mechanism of neurologic dysfunction.



So increased pressure caused this neurologic problem for this patient.

The question is can this kindof injury cause demyelination?



Paper here

Evidence of Acute Demyelination Around a Developmental Venous Anomaly: Magnetic Resonance Imaging Findings
JUNG, GREGOR MD; SCHRÖDER, RITA MD; LANFERMANN, HEINER MD; JACOBS, ANDREAS MD; SZELIES, BRIGITTE MD; SCHRÖDER, ROLAND MD

Abstract
The authors report on the occurrence of a focal demyelination showing a mass effect around a developmental venous anomaly in the cerebellum. Because the latter presented as a single lesion, the differentiation from intraparenchymal neoplasms or infarction was difficult. Follow-up magnetic resonance imaging and histology from a biopsy specimen give useful information to find the appropriate diagnosis.


Another one
Found here
Cerebral venous thrombosis in the rhesus monkey
W. D. Sheffield, R. A. Squire and J. D. Strandberg


Cerebral venous thrombosis was identified in four rhesus monkeys. Two initially showed neurologic signs and three had diarrhea or dysentery. All four had severe intestinal disease, including three cases of ulcerative colitis complicated by extracerebral thromboembolic disease. Central nervous system lesions, confined to the centrum semiovale, were multiple thrombi of internal cerebral veins, perivenular demyelination, and gemistocytic astrocytosis. The lesions resembled those found in people with cerebral venous thrombosis, and support the hypothesis that perivenular demyelination may occur as a sequela to venous occlusion. The lesions were identical to those found in "leukoencephalosis and perivascular myelosis," an entity of unknown cause previously described in monkeys.


The monkeys had actual clots and sudden complete occlusion but the fact remains; demyelination as a result of venous changes.

And then here is something to add
CLICK HERE

Evidence for subacute fat embolism as the cause of multiple sclerosis.James PB.
The neurological features of decompression sickness, which is thought to be due to gas embolism, are similar to those of multiple sclerosis (MS). This similarity suggested the re-examination of a concept, first proposed in 1882, that the demyelination in MS is due to venous thrombosis. Unfortunately, although the plaques of MS are often perivenular, thromboses are not always present. Nevertheless, vascular theories can explain the topography of the lesions in MS. Embolism is generally associated with arterial rather than venous damage, and with neuronal infarction rather than loss of myelin. However, the intra-arterial injection of a range of substances can cause venous damage and perivenous demyelination in the brain, although it does not exactly reproduce the plaques seen in man. There is also evidence in man that fat may lodge in the microcirculation of the nervous system and cause distal perivenous oedema with the loss of myelin from axons. Since acute fat embolism may produce lesions not only in the white matter of the brain, but also in the cord, the retina, the meninges, and the skin, and since all these have been described in MS, subacute fat embolism may be the cause of MS.



That guy was close he is almost there if only he'd known about the venous stenoses and backups............... The kinds of injuries that happen to tissue secondary to the CVI (in legs) are similar to thromobsis so if he'd have known...........

So many years ago............
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
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Postby Loobie » Thu Jun 18, 2009 5:00 am

Have you guys ever seen the movie "Minority Report"?. If you have you remember how computer screens were just virtual and you could just absolutely fly through research because you just manipulated everything trough touch. You guys remind me of that! How you guys just mow through this stuff is amazing!

Plus it's a really good movie if you like Sci-Fi thrillers.
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Postby cheerleader » Thu Jun 18, 2009 7:27 am

mrhodes40 wrote:That guy was close he is almost there if only he'd known about the venous stenoses and backups............... The kinds of injuries that happen to tissue secondary to the CVI (in legs) are similar to thromobsis so if he'd have known...........

So many years ago............


More excellent papers! This doctor is cool, Marie...Dr. Phillip James of University of Dundee, Scotland. He said MS looked like divers' disease to him, and puts his patients in hyperbaric oxygen chambers. He was hung up on the fat embolism angle- but you're right, the mechanism for injury is there. I actually e-mailed him the Zamboni, and let him know the vascular research was still continuing. Never heard back, but I'd like to think it encouraged him.
Loved Minority Report, Lew - would enjoy a computer screen like that...but as you can see, Marie and I are thrilled to have so many medical journals on line for FREE! This is only in the last ten years they've been published online, so it's good timing-
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby akaheather » Thu Jun 18, 2009 10:19 am

It makes me crazy when I hear a neurologist who has been presented this idea has declared this "can't" be the cause of MS.


Be prepared to be crazy! I saw my neuro today (in Austin) and he pretty much shut me down. The good news is that he really didn't have any good reasons to disprove the CCSVI theory. His response was pretty unoriginal, just the same old rhetoric about how this unproven, which came first the myelopathy or stenosis, yada, yada, yada. I was disappointed, but not surprised.

At one point he did question/retort that if I did indeed have a stenosis why wouldn't it be more apparent in me? (I have RRMS with no noticable disability.) I chose not to argue about how location/degree of stenosis could affect disability over time.

At this point, I am pretty much done with him. In my mind he is a pharmacist at best and, unfortunatly, cannot really help me.

Heather

PS
So based on what scientific principle is it rejected out of hand? And given that we seem to have these stenoses it seems to me perhaps it is up to them to show that such an anomaly CAN'T harm the MS brain before they tell us to ignore it.


My thoughts exactly.
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Postby peekaboo » Thu Jun 18, 2009 10:56 am

Don't give up Heather!

A few of us at a time are proving that we MS'rs have the stenosis regardless its relationship to MS! Of ourse we think otherwise but since MRV's are minimally invasive hopefully you can convince someone to give it a try? (in network preferrably)
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Postby Sharon » Thu Jun 18, 2009 11:06 am

Marie and I are thrilled to have so many medical journals on line for FREE!


And we are just thankful you and Marie understand this stuff and can explain it.
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Postby akaheather » Thu Jun 18, 2009 2:22 pm

Well, if I can't find anyone local I may be looking into California. This early in the game, with as few exacerbations as I've had, I am wondering how difficult it might be to find a stenosis or if it would even qualify for surgery? Any thoughts?
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Postby Arcee » Thu Jun 18, 2009 2:51 pm

I suspect that I will be a good test case for that. So far so good as far as relapses and symptoms go for me, but I do have bunches of lesions. Very curious to hear what they see in the veins, and I will pass along that info.
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Postby daniel » Thu Jun 18, 2009 7:14 pm

cheerleader wrote:...snip...
but as you can see, Marie and I are thrilled to have so many medical journals on line for FREE! This is only in the last ten years they've been published online, so it's good timing-
cheer


Every time I search google for titles of medical papers, I get results wanting me to pay $20-30 for access to the full paper. Which sites do you use to get access to and search through the papers for free?
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Postby NHE » Thu Jun 18, 2009 11:11 pm

daniel wrote:Every time I search google for titles of medical papers, I get results wanting me to pay $20-30 for access to the full paper. Which sites do you use to get access to and search through the papers for free?


From time to time, I take a stack of abstracts that I've printed out from PubMed and go to the library of the local university in my town. I take a USB flash drive with me so I can download the PDFs. I print them out when I get home as it's usually cheaper than paying for the printouts at the library. If the journal article is too old and there isn't a PDF for it, then you can usually just photocopy it if the library has the actual journal on the shelf. In addition, PubMed usually lists if an article is available for free so for those articles you should be able to get them without any problems.

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Postby cheerleader » Tue Jun 08, 2010 6:52 pm

OK...
At Rhonda's request, I am going to begin reposting the threads that got us to where we are today. Really want the new people to understand where these discussions came from. This is an oldie, but a goodie.
cheer
Husband dx RRMS 3/07
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http://ccsviinms.blogspot.com
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