Friday, 11 March 2016

Variability in jugular vein size varies

Buch K, Groller R, Nadgir RN, Fujita A, Qureshi MM, Sakai O.
Variability in the Cross-Sectional Area and Narrowing of the Internal Jugular Vein in Patients Without Multiple Sclerosis.
AJR Am J Roentgenol. 2016:1-5. [Epub ahead of print]

OBJECTIVE:Chronic cerebrospinal vascular insufficiency is a proposed condition of intraluminal stenosis of the internal jugular vein (IJV) that impedes venous flow from the brain. Calculations of IJV stenosis are vague and described in veins with at least a 50% reduction in IJV calibre at a specific level. The purpose of this study was to assess normal changes in anatomic calibre of the course of the IJV in a generalized population.
MATERIALS AND METHODS: Images from 500 consecutive contrast-enhanced neck CT studies performed in January-July 2011 were reviewed. Cross-sectional areas of the IJV were calculated at the jugular foramen, C1-C7 levels, and jugular angles bilaterally. Patients were excluded if they had severely motion-limited studies; limited clinical data; a history of multiple sclerosis, neck mass, or neck dissection; or known IJV occlusion. Normalized IJV cross-sectional areas at each level were compared with an averaged normalized cross-sectional area from all patients at each level.
RESULTS: Greater than 50% narrowing compared with a normalized average was found in 133 of 363 patients (36.6%) and was seen at all IJV levels. In 36.1% of patients this narrowing occurred at the C1 level. Most of the areas of narrowing greater than 50% occurred above the C4 level.
CONCLUSION: The IJV has marked variability in its course in the neck. Areas of narrowing greater than 50% occur most commonly in the upper cervical and skull base regions. Given the normal anatomic variations in IJV calibre, caution should be used when making the diagnosis of and treating IJV stenosis.

Well the subtext is clear , if you are thinking of CCSVI, have more of a think


  1. Zomboni was right all alomg! :-)

    1. Uh no, this study specifically states people without MS. I've done quite a bit of reading on CCSVI. There is a good deal of interesting things to note. Is it the cause of MS? Clearly not. May it be a trigger in some people? Possibly and in a more indirect way, that being essentially TIA's resulting in an immune attack as small amounts of blood get misconstrued as an antigen by a malfunctioning immune system. Similar was found late last year in mice models where a single drop of blood set off an immune response.

      Some people who have surgery in respect to CCSVI do state they have some levels of symptoms relief and others not. This does not display anything causal of MS again but perhaps does display that proper oxygenation of brain cells results in stronger signaling which makes a certain amount of sense.

      At the sametime on the other side of the coin may make no sense. People who undergo arterial stents and blockages in the neck seldom seem report what one would think would be a variety of symptoms based on lack of oxygenation.

      The reality is our bodily systems appear rather loosely bound conceptually but are rather tightly bound in function. This results in a highly complex biological machine per se. When disease and disorders enter into the picture these complexities and being both better understood by science but at the sametime are displaying far far more complexity than might be commonly understood.

      MS in its own right is extremely complex and like other diseases more than likely has multiple entry points into the disease. CCSVI may be a indirect trigger in some fashion. But we cannot expect every healthy individual who has CCSVI to undergo surgery to avoid the prospect of MS or TIA's.

      Further it is not a procedure to be taken lightly.

      A proper long term clinical study of people who endure MS would be interesting. However, to engage in such a study the patients would really need not be taking a disease modifying therapy to see if those with CCVSI .vs. those who have underwent surgical correction see a significant change in relapse.

      Such a study would IMHO be completely irresponsible placing both cohorts at risk of relapse. Additionally there is no foundation in that relapse is not attempted to be induced. One persons relapse has no bearing on if another person would have relapse.

      I do not know if CCSVI could be simulated in mice. That might be interesting?

    2. No it is not interesting?

      Likewise there is no evidence that CSSVI is a trigger this is supposition

    3. Thank you for this, I was unaware of the study.

    4. So for study quoted above to carry weight as a true replication it would be fine to tie your IJVs off for 3 months and one would see no noticeable difference ? ;-)

      Regards as always

  2. The fact that they are talking about jugular veins does not mean they know what they are talking about. They are completely ignorant of the implied theory. What they do is just spread the misconception that has been carefully built around it.

  3. Neither of the two comments above make any sense to me - are the posters trying to say that CCSVI is supported by this report or not?

    The way I read it (which could be wrong) is that the study was done on normal people without MS or a range of other conditions which could potentially influence or skew the results. Of these normal people, 36.6% of them had narrowing of more than 50% - i.e. the study does not support the theory that CCSVI is involved directly with MS.

    1. The calibre of the internal jugular veins is irrelevant. What is of key importance, according to CCSVI, is the competence of the internal jugular vein VALVES. In MS patients these valves are immobile, or overgrown, or fused together. The authors make to comment on this, possibly because they aren't aware of it, as most people as well. Instead, they present a finding of no importance at all.


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