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Small internal jugular veins with restricted outflow are associated with severe multiple sclerosis: a sonographer-blinded, case--control ultrasound study.
Krsmanovi E, Ivkovi M, Lepi T, Stankovi A, Rai Evi R, Din I E.
BMC Neurol. 2013 Jul 17

Abstract
BACKGROUND:
Recent evidence has indicated an association between chronic cerebrospinal venous insufficiency (CCSVI) and multiple sclerosis. Small internal jugular veins (IJVs) (with a cross-sectional area of less than 0.4 cm2) have been previously described as difficult to catheterize, and their presence may potentially affect cerebrospinal venous drainage. In this blinded extracranial color-Doppler study we had two principal aims: first, to assess prevalence of CCSVI among Serbian MS patients compared to healthy controls; and second, to assess prevalence of small IJVs (with a CSA <= 0.4 cm2) among MS patients and controls.
METHODS:
The sixty seven unrelated patients with clinical isolated syndrome (CIS), relapsing-remitting (RR), secondary progressive (SP) and primary progressive (PP) multiple sclerosis and 21 healthy controls were examined by high-resolution color-Doppler.
RESULTS:
The ultrasonographic criteria of CCSVI (according to Zamboni) were positive in 11.9% of the patients and in none of the control subjects. The CCSVI-positive patients had significantly longer disease durations and were significantly more disabled (measured by their Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Severity Score (MSSS) scores), but after adjustment for gender and disease duration, CCSVI was not an independent risk factor for multiple sclerosis severity. The small IJVs were found in 28.4% of the patients and 28.6% of the controls. The patients with small IJVs were associated with decreased venous outflow from the brain and presented with longer disease durations and significantly higher EDSS and MSSS scores compared to patients without small IJVs. A multivariate logistic regression analysis adjusted for gender and disease duration showed that small IJV is an independent factor associated with multiple sclerosis severity (EDSS >=6) (adjusted OR = 8.9, 95% CI: 1.8-45.6, p = 0.007). Among patients with small IJVs the 36.84% were also CCSVI positive.
CONCLUSIONS:
Both, CCSVI and small IJVs seem to influence or follow MS severity, but only small IJVs turned out to be an independent factor in this study. Thus, small IJVs with restricted outflow, which might be aspects of CCSVI different from the criteria originally described by Zamboni, emerge as a cofactor in the multifactorial pathophysiology of multiple sclerosis.

Full text is here: http://www.biomedcentral.com/1471-2377/13/90

I hope this can be replicated. They looked specifically at hypoplastic very small jugular veins, and found an association between those and severity of MS.

Hypoplastic jugular veins might be easier to identify than Dr. Zamboni's 5 doppler criteria. The onus is on CCSVI researchers to find evidence of CCSVI that can be replicated. This could be it.

The prevalence of small IJVs differed significantly according to different clinical courses of MS (p = 0.0002), with the highest prevalence in the CP group (68.4%, all SP). Small IJVs were significantly more common among the patients with severe MS (EDSS ≥ 6) (n = 15 were sIJV positive out of 25 patients with EDSS ≥ 6, p = 0.00001, Figure 1). The mean MSSS was significantly higher among the patients with small IJVs (p = 0.002, Table 3).

Those are high percentages. This could be a strong association?

The presence of small IJVs is associated with the increased probability of a severe clinical course of the disease.

One of the scariest things when diagnosed with MS was not knowing the prognosis. Imagine getting diagnosed, getting an ultrasound, they find the small IJVs, and they can then recommend that you go on Tysabri or a risky but more effective drug right away. Especially since hypoplastic IJVs can't be increased in size, as far as current methods are available, this makes sense to me. (Getting angioplasty asap of any treatable stenoses also makes sense to me.)

Cece wrote:Imagine getting diagnosed, getting an ultrasound, they find the small IJVs, and they can then recommend that you go on Tysabri or a risky but more effective drug right away. Especially since hypoplastic IJVs can't be increased in size, as far as current methods are available, this makes sense to me. (Getting angioplasty asap of any treatable stenoses also makes sense to me.)

I'm not a healthcare professional, but I cannot see this as an ethical option. From my understanding: the disease modifying drugs [DMD] are designed to limit demyelinating events on MRI, which, in turn, is associated with the rate of relapse [unless, of course, there are lesions in so-called silent areas]. Nonetheless, the minimization of accumulated lesion load is supposed to be a backstop against the rate of progression, or the rate at which the brain and spinal cord atrophy. This is, essentially, the whole premise of DMD therapy.

Hypothetically, if I had a patient with neither, positive MR scans and/or physical affectations, I cannot see how prescribing a DMD would be beneficial. I would refer to another specialist whose is trained in therapeutic options aimed at correcting precisely the pathology exhibited in the patient: the small, or, as you call them: hypoplastic vasculature, whether it be via percutaneous transluminal angioplasty [PTA], or something else.

Likewise, the reason why interventional radiologists [IRs] are performing angioplasty for CCSVI is not because of MS, but because of the presence of CCSVI; it just so happens to be that CCSVI and MS are coincidentally associated with one another; i.e., no IR will tell you he/she is treating MS.

Caveat lector: I could be totally wrong in my assessment of evidence-based medicine as I am not a healthcare professional. Yet, from my point of view, it appears unethical.

If there is an actual medical professional on this board [Scalfani? et al.] I would be interested in their approach to this issue.

CuriousRobot wrote:Hypothetically, if I had a patient with neither, positive MR scans and/or physical affectations, I cannot see how prescribing a DMD would be beneficial.

I meant that they'd been diagnosed with MS, which usually involves a positive MRI and clinical presentation, and at that time a DMD is usually prescribed? The idea would be to go with a more aggressive treatment, rather than the 1st generation DMDs, if the patient is at greater risk of severe MS.

understanding: the disease modifying drugs [DMD] are designed to limit demyelinating events on MRI, which, in turn, is associated with the rate of relapse [unless, of course, there are lesions in so-called silent areas]. Nonetheless, the minimization of accumulated lesion load is supposed to be a backstop against the rate of progression, or the rate at which the brain and spinal cord atrophy.

I thought the association between lesion load and disability (the real hallmark of progression) had been discredited. Isn't that why the UK won't pay for them anymore? Isn't it why they won't prescribe them (in Ottawa, Canada, anyway) for anything but certified genuine "relapsing-remitting-type-MS"?. "RRMS' is not supposed to feature "progression", which really should say 'disability past a certain point'.

That point, I believe, is supposed to be an EDSS score of 6. After that, you are said to be, or have, "SPMS". That in my opinion is just discrimination against the disabled, and is very convenient for everyone but the "RR" patients. They have to come up with the bucks, at least until even they, too, "convert". So disability doesn't happen in "RRMS", and remissions don't happen in "SPMS". All of which is bullshit.

I think the "Caring Professionals" think that, with DMDs, at least you can hope for a delayed conversion, but there's no proof of that either. So DMDs end up being very expensive, ineffective, wishful thinking. But I think they, rather, than the CCSVI procedure, are placebos. Their high cost, in a jaded view like mine, is merely a hedge against Nocebo effect.

Maybe people with small, inoperable IJVs should be the ones called "SPMS". Then nobody would have to do a CCSVI procedure, and they could continue the "diagnose and adios" treatment. Nobody will ever notice that the paper also says the same number of healthy controls as people with both "MS" and an EDSS >6 have small IJVs.

The small IJVs were found in 28.4% of the patients and 28.6% of the controls.

Does that mean having "MS" versus none, has nothing to do with whether your IJVs are small, too? ...

EDSS >6:

p = 0.007