IJV stenoses found post-mortem in 2 MS patients

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

IJV stenoses found post-mortem in 2 MS patients

Postby Cece » Sat Apr 30, 2011 4:31 pm

http://jnnp.bmj.com/content/82/4/355/reply

We performed complete post-mortem examination of two patients with MS, died for different causes. One patient, a 74 year-old-woman, was hospitalized for acute respiratory illness and died because of bacterial pneumonia; the other one, a 35 year-old-woman, died for otogenic bacterial meningitis complicated with internal jugular thrombosis as demonstrated on MR venography.

Postmortem examination demonstrated in both patients a marked stenosis of left internal jugular vein at the apex of the angle formed by the two heads of the sternocleidomastoid muscle where the IJV overlie the carotid artery with ectasia and congestion of the intracranial veins. Venous flow slowing, caused by the stenosis, had predisposed to IJV thrombosis, histologically demonstrated in the second case. Severe inflammatory disease may be a risk factor for deep venous thrombosis but also chronic cerebrospinal venous insufficiency.

We demonstrate, for the first time as far as we are aware, the presence of anatomical alteration in the veins of the neck with impaired venous drainage from the central nervous system in two patients with multiple sclerosis who died from other causes.

We do not know the exact implications in MS pathology and certainly there is no doubt that this area warrants a great deal more study. Clinical trials for evaluating new therapeutic agents and other clinical experimental protocols may be required.
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Re: IJV stenoses found post-mortem in 2 MS patients

Postby Brainteaser » Sat Apr 30, 2011 6:32 pm

Cece wrote:http://jnnp.bmj.com/content/82/4/355/reply

We performed complete post-mortem examination of two patients with MS, died for different causes. One patient, a 74 year-old-woman, was hospitalized for acute respiratory illness and died because of bacterial pneumonia; the other one, a 35 year-old-woman, died for otogenic bacterial meningitis complicated with internal jugular thrombosis as demonstrated on MR venography.

Postmortem examination demonstrated in both patients a marked stenosis of left internal jugular vein at the apex of the angle formed by the two heads of the sternocleidomastoid muscle where the IJV overlie the carotid artery with ectasia and congestion of the intracranial veins. Venous flow slowing, caused by the stenosis, had predisposed to IJV thrombosis, histologically demonstrated in the second case. Severe inflammatory disease may be a risk factor for deep venous thrombosis but also chronic cerebrospinal venous insufficiency.

We demonstrate, for the first time as far as we are aware, the presence of anatomical alteration in the veins of the neck with impaired venous drainage from the central nervous system in two patients with multiple sclerosis who died from other causes.

We do not know the exact implications in MS pathology and certainly there is no doubt that this area warrants a great deal more study. Clinical trials for evaluating new therapeutic agents and other clinical experimental protocols may be required.


Anyone think the bacterial connection significant to CCSVI/MS? - Johnson, Anecdote?
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Postby Cece » Sat Apr 30, 2011 7:14 pm

Postmortem examination demonstrated in both patients a marked stenosis of left internal jugular vein at the apex of the angle formed by the two heads of the sternocleidomastoid muscle where the IJV overlie the carotid artery with ectasia and congestion of the intracranial veins

Ectasia means dilation...I think this may be significant. It's linking our stenoses in our jugulars with this dilation and congestion of the intracranial veins, isn't it?

I like that it's 2 out of 2 (100%) even if that's a very very small study. These malformations are anatomical, it is to our advantage; they are there and can be seen.
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Postby orion98665 » Sat Apr 30, 2011 8:05 pm

Cece wrote:
Postmortem examination demonstrated in both patients a marked stenosis of left internal jugular vein at the apex of the angle formed by the two heads of the sternocleidomastoid muscle where the IJV overlie the carotid artery with ectasia and congestion of the intracranial veins

Ectasia means dilation...I think this may be significant. It's linking our stenoses in our jugulars with this dilation and congestion of the intracranial veins, isn't it?

I like that it's 2 out of 2 (100%) even if that's a very very small study. These malformations are anatomical, it is to our advantage; they are there and can be seen.



Great find Cece, especially coming from the journal of Neurology, Neuro-
surgery and Psychiatry.

Bob
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Re: IJV stenoses found post-mortem in 2 MS patients

Postby frodo » Sun May 01, 2011 2:49 am

In some thread somebody said that, as we cannot perform an invasive venography to healthy patients, we will never know how often vein irregularities appear in the healthy population.

Well, I didn't thought of autopsy at that time. Now we know how to test the veins problems prevalence. Thanks Cece.
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Postby Cece » Sun May 01, 2011 7:35 am

credit goes to Joan, she posted this first on the CCSVI in MS facebook site.

I remember mention of cadaver studies before but had forgotten about them. I agree, this is a very informative way to go.

As for the inability to do invasive venograms in healthy volunteers, according to eric593, UBC is doing exactly this!! I was surprised by that.

Not sure about the bacterial connection. The IJV thrombosis in the younger woman is another way in which these stenoses are doing harm when they are untreated (causing the turbulent flow that can cause thrombosis).
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Postby jimmylegs » Sun May 01, 2011 8:11 am

ms patients tend to be low in zinc. low zinc status is associated with higher rates of bacterial infection.

Volume 12, Issue 7, Pages 515-518 (July 1996)
Zinc levels and infections in hospitalized patients with AIDS
Abstract
Impaired cellular and humoral immunity and phagocytic function have been attributed to zinc deficiency. This study examined the association between low serum zinc concentration and opportunistic infections in hospitalized patients with the acquired immune deficiency syndrome (AIDS). We examined the records from all 505 inpatient consultations performed by our Nutrition Service from May 1992 through June 1994. The medical records from all 228 patients with AIDS with known serum zinc levels (determined by atomic absorption spectrophotometry) were reviewed. The length of HIV seropositivity, most recent CD4 count, presence of diarrhea, and degree of malnutrition were noted. The principal diagnosis accounting for the admission was grouped according to the type of infection: Pneumocystis carinii pneumonia (PCP), viral, fungal, bacterial, and other. Sixty-seven patients (29%) had abnormally low serum zinc levels (LSZ < 55 μg/dL), 49 patients (21%) had borderline low serum zinc (BSZ ≥ 55 and ≤ 65 μg/dL), and 112 (49%) patients had normal serum zinc levels (NSZ > 65 μg/dL). There was no significant difference among the groups in CD4 count, length of HIV seropositivity, presence of diarrhea, or severity of malnutrition. Patients with zinc deficiency (LSZ) had a significantly higher incidence of bacterial infection than did patients with normal zinc. Patients with borderline zinc levels had an intermediate incidence of bacterial infection. There were no significant differences among the three groups in the incidence of PCP, viral, or fungal infections. Severe zinc deficiency was noted in 29% and borderline levels in an additional 21% of hospitalized AIDS patients. A low zinc level was not associated with the length of HIV seropositivity, CD4 count, or degree of malnutrition. Hypozincemia was associated with an increased incidence of concomitant systemic bacterial infections.

using conversion factor 0.153 these cutoffs for low, and normal zinc levels given above, we get:

low: 55 μg/dL * 0.153 = 8.415 umol/L
"normal": 65 μg/dL * 0.153 = 9.945 umol/L

both those numbers are about half the zinc level you see in (thai) healthy controls. (ie tight averages around 18 umol/L - but keep in mind that thai diet is low- to no- gluten.. without the zinc drain caused by gluten consumption, and the high zinc content of common thai food ingredients like oyster sauce, it's easier for them to achieve a healthy zinc level with diet alone).

posted dec 24 2009
http://www.thisisms.com/ftopicp-82549.html#82549
Galvanising forces in vascular health and disease: is dietary zinc protective?
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Postby jimmylegs » Sun May 01, 2011 8:18 am

FYI

selenium is antiviral:

http://tinyurl.com/3q9x55a
High Risk of HIV-Related Mortality Is Associated With Selenium Deficiency
selenium deficiency is an independent predictor of survival for those with HIV-1 infection


selenium is low in ms patients:

http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
SELENIUM, VITAMIN E AND COPPER IN MULTIPLE SCLEROSIS

the vascular connection:

http://www.ncbi.nlm.nih.gov/pubmed/21053344
J Cell Biochem. 2010 Dec 15;111(6):1556-64.
Selenium suppressed hydrogen peroxide-induced vascular smooth muscle cells calcification through inhibiting oxidative stress and ERK activation.
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Postby bluesky63 » Sun May 01, 2011 8:27 am

I had also asked johnson about boluoke, an earthworm-based enzyme that dissolves biofilm, implicated in chronic infections. (It just seemed like something he would have heard of.) It also affects fibrinolysis.

boluoke

https://www.researchednutritionals.com/ ... ode=CBD202

Not sure of details, but this does fit in with other nutritional information. Jimmy, you are a treasure trove!

This is a fascinating approach. I am so sorry for these people and their families. But we can hope that this contributes to developing knowledge that can save other people.
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Postby Cece » Tue May 03, 2011 11:23 am

In MS the permeability of cerebral capillaries is increased, as demonstrated by studies on post-mortem material and neuroimaging techniques. This phenomenon is called breakdown of the blood-brain barrier (BBB) and it appears to be an integral part of the pathological process. If this barrier is compromised, by a variety of other pathological conditions, in a patient with existing MS, it has been shown that new fresh lesions will occur at this site in the brain. There is no connection that has been proven between blood-brain barrier defects and CCSVI.

www.telegraph.co.uk/health/healthnews/8 ... tions.html

Further research in this area would be very informative! The link between the jugular stenoses and the ectasia and congestion of the intracranial veins can be linked through as-of-yet-undone research to the increased permeability of cerebral capillaries as shown on post-mortem material and neuro-imaging techniques.

I don't think our researchers are researching fast enough. :)
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