Cerebral vein changes in relapsing-remitting multiple sclero

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

Cerebral vein changes in relapsing-remitting multiple sclero

Postby Robnl » Thu Sep 20, 2012 2:49 am

http://www.springerlink.com/content/x74m208nl60j78p0/
Abstract

Objective
To investigate characteristics of the internal cerebral veins (ICVs) and their main tributaries and the deep medullary veins (DMVs) in patients with relapsing-remitting MS (RRMS) with enhanced T2*-weighted angiography imaging (ESWAN).

Methods
Fifty-three RRMS patients and 53 normal controls underwent conventional MRI and ESWAN. ESWAN venograms were created by performing minimum intensity projections of the phase images, and the resulting venograms were used to observe characteristic vascular changes, including scores of the ICVs and their main tributaries and manifestations of the DMVs. Two experienced radiologists analysed all data.

Results
Patients showed decreased mean scores of the ICVs and their main tributaries compared with controls. The mean score in acute patients was higher than in stable patients. Furthermore, the DMVs diminished and shortened in 48 patients with longer disease duration, whereas the DMVs increased and elongated in 5 patients with shorter disease duration. The penetrating veins were well defined in 30 active lesions, whereas the veins were ill defined in 69 non-active lesions. Interestingly, well-defined penetrating veins were shown in 15 non-active lesions in the stable patients.

Conclusions
Enhanced T2*-weighted MR angiography can detect cerebral vein characteristics in relapsing-remitting MS patients, which may provide important information on the pathogenesis of MS.
Key Points
• Enhanced T 2 * -weighted magnetic resonance angiography (ESWAN) provides new insights into multiple sclerosis
• ESWAN venograms clearly demonstrate the internal cerebral and deep medullary veins
• The internal cerebral veins exhibit abnormalities in patients with relapsing-remitting MS
• Deep medullary veins exhibit different manifestations in patients with different disease duration
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Re: Cerebral vein changes in relapsing-remitting multiple sc

Postby Cece » Tue Dec 11, 2012 6:31 pm

The cerebral vasculature is different in pwMS than in controls. The longer the disease duration, the shorter the deep medullary veins were.

full paper is here http://download.springer.com/static/pdf ... 6&ext=.pdf
CCSVI is mentioned in the paper:
Several vascular dysfunction mechanisms may exist. Firstly, there may be reduced blood oxygen utilization from chronically damaged
brain tissue that leads to decreased levels of oxygen extraction [18]. Secondly, MS patients are at higher risk of ischaemic stroke, which might involve endothelial dysfunction secondary to inflammatory disease activity [29]. Alterations in endothelial function have been reported in MS [30–32]. Wakefield et al. demonstrated fibrin deposition and vessel thrombosis in the absence of cellular infiltration in three acute cases of MS, suggesting that the thrombosis of small veins and capillaries could represent an ischaemic basis for disease [33]. Thirdly, MS patients have global cerebral hypoperfusion, which might predispose them to ischaemic stroke development. Using dynamic susceptibility contrast-enhanced MRI, Law and colleagues found that cerebral blood flow (CBF) was markedly decreased and that the mean transit time was prolonged throughout the NAWM in 17 RRMS patients compared with 17 control subjects [14]. Finally, several studies have suggested that the pathogenesis of MS might be the consequence of CCSVI, which has proved controversial [34–36]. It could be hypothesised that decreased venous outflow from the brain parenchyma to the periphery might lead to increased intracranial pressure and subsequent venous stasis, especially in the small vein vasculature. However, the exact pathogenesis of this process remains unknown
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Re: Cerebral vein changes in relapsing-remitting multiple sc

Postby 1eye » Mon Dec 17, 2012 1:30 pm

This paper and the supporting references show that "MS" is a venous disorder during which the veins undergo significant changes and degradation, proceeding along the vasculature. My personal contention is that it has been shown, by Zivadinov et al., that CCSVI patients (not "MS" patients) have problems with their venous vasculature, and now this study finds, by different imaging techniques, the same result in "MS" patients.

Yes, there is auto-immunity. Yes, the brain, and spine (and probably other organs, including the heart) are oxygen-starved. Yes, the nerves are directly in the line of fire. Oh, boy, fun.

When will the "MS" thought-junta stop propagating the lie that CCSVI and "MS" are different things? Who cares if the chicken or the egg came first, if both are fresh and you are hungry? Turn on the stove!
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'MS' is over - if you want it
Patients sans/without patience
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Re: Cerebral vein changes in relapsing-remitting multiple sc

Postby 1eye » Tue Dec 18, 2012 7:18 pm

I understand that biases are possible, and that statistics may be questioned, but can similar study results be combined to strengthen the statement that CCSVI is the same disease as "MS", that treating one thing treats the other, that the CCSVI procedure is safer and more effective than say, Tysabri?

Further, can some of the massive expenditures of public funds on drug treatments for the private profits of corporations be diverted towards research into making the procedure safer and more effective?
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'MS' is over - if you want it
Patients sans/without patience
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Re: Cerebral vein changes in relapsing-remitting multiple sc

Postby 1eye » Fri Dec 21, 2012 4:38 pm

As none of my questions have been answered, I thought I might bump this back up.

I add the following, to be answered by anyone who thinks they know:

1. What are the known differences in the following aspects of CCSVI and "MS"?

a) expected length of disease course
b) known cause
c) symptoms
d) treatment strategies known to have efficacy
e) cost of living with the disease for i) the patient
ii) the caregiver/ family member (if any)
iii) the insurer (if any)
iv) the health care system/government

2. How many a) patients b) caregivers/family c) doctors have the existence/treatment of CCSVI caused direct harm to? treatment of"MS"?

3. direct benefit? from CCSVI treatment? from "MS" treatment?

4. Has anybody/how many have been able to go back to work following any treatment for CCSVI vs "MS"?

5. have had to quit work following any treatment for CCSVI vs "MS"?

6. same as 5., only substitute death as the result.

7. same as 4. only substitute living longer than expected.
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'MS' is over - if you want it
Patients sans/without patience
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