Dr. Fox at ISNVD

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.
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Dr. Fox at ISNVD

Post by Cece » Mon Feb 20, 2012 11:02 am

I have been waiting to hear more about what Dr. Fox has found in his post-mortem studies. He's finally up.
Dr. Robert Fox: Composition of lesions is water. The most important factor is like real estate: location location location
Next up: Dr. Robert Fox "Postmortem assessment of jugular and azygos vein pathology"
Dr. Fox: injected IJV and azygos veins with silicon and removed for analysis. Upper IJVs not extracted.
Dr. Fix: anatomical variation in tri-, bi-, and uni-cuspid IJV valves
Dr. Fox: Valves looked to be normal in function. Hyperplasia sometimes seen (vein narrowings) and abnormal flaps
Dr. Fox: Intraluminal membranes extending 2/3 the way across the vein sometimes found in IJVs
Dr. Fox: intraluminal septum & sheaths found
Dr. Fox: Higher incidence of intravenous abnormalities in MS patients, but no differences in functional abnormalities
What does that mean? Not as much as I'd expected. Higher incidence of intravenous abnormalities, but no differences in functional abnormalities? Valves looked to be normal in function.... Sheaths and septums and membranes were found. The fixing of the veins with silicone may have made it difficult to see if the valves were unnaturally stiff and fixed. How was it assessed that there were no differences in functional abnormalities?
Dr. Fox: Number & location of MS lesions determines disability only in early stages of MS, not in progressive forms

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Re: Dr. Fox at ISNVD

Post by Cece » Mon Feb 20, 2012 2:14 pm

Postmortem assessment of jugular and azygos vein pathology (Robert Fox, USA)

The venous changes of chronic cerebrospinal venous insufficiency (CCSVI) are typically assessed by ultrasound
or MRV, but no gross anatomical description of venous outflow in MS has been reported to date. We harvested
bilateral internal jugular (IJV), subclavian, brachiocephalic, and azygous (AZY) veins from 7 deceased MS
patients and 6 non-MS controls. Veins were injected with silicone, dissected en bloc, incised longitudinally to
expose the luminal surface, and fixed. All valves and structural abnormalities were characterized and
photographed using a stereomicroscope. Vein wall stenosis was defined as a >= 50% reduction in crosssectional
area, defined from vein wall circumference and compared to a normal appearing region in the same
vein. A variety of vein abnormalities were identified. The incidence of vein wall stenoses was similar in MS and
controls. Valvular and other intraluminal abnormalities with potential hemodynamic consequences were
identified in 5 of 7 MS patients (7 abnormalities) and in 1 of 6 controls (1 abnormality). These abnormalities
included circumferential membranous structures (1 MS and 1 control), longitudinally-oriented membranous
structures (3 MS), single valve flap replacing IJV valve (2 MS), and enlarged and malpositioned valve leaflets (1
MS). In addition, many minor anatomic variations without expected hemodynamic consequences were
observed similarly in both MS and controls. These included valves with >2 leaflets, the presence of valves in the
AZY, additional (duplicate) normal-appearing IJV valves, and small membranous septa. In conclusion, post
mortem examination of the IJV and AZY veins of MS patients and non-MS controls demonstrated a variety of
structural abnormalities and anatomic variations. Although vein wall stenosis occurred at similar frequency in
MS and non-MS controls, the frequency of intraluminal abnormalities with possible hemodynamic
consequences was higher in MS patients compared to healthy controls.
Histologic analysis is underway. These
results provide a pathologic explanation for the intraluminal abnormalities observed in ultrasound studies and
emphasize the importance of detailed intraluminal assessment.
ok, that's back to how I understood it before, where the intraluminal abnormalities did have possible effect on blood flow hemodynamics. Good.

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Re: Dr. Fox at ISNVD

Post by cheerleader » Mon Feb 20, 2012 6:46 pm

How can Dr. Fox claim to know what the intraluminal hemodynamic implications are if THE PATIENT IS DEAD???
The truth is, there was NO way to assess functionality in these fixed veins, since there was no longer blood flow.

He can only ask vascular specialists, like Dr. B.B. Lee, who have studied these same truncular venous malformations in living people. And these malformations change hemodynamics.
A few of us have been suggesting that his team consult with the Georgetown team, since they understand VMs. And it is a new area for Dr. Fox.

I had been concerned to learn Dr. Fox had been assigned to head up Dr. Claudu Diaconu's Case Western Research Project. Let's hope the research remains unbiased.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09

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