Saturday, 25 May 2013

Less blood flow for Lesions?

Epub: Juurlink BH. The Evidence for Hypoperfusion as a Factor in Multiple Sclerosis Lesion Development. Mult Scler Int. 2013;2013:598093.


The evidence that hypoxia is a precipitating factor in causing early MS lesions includes increased protein levels of hypoxia-inducible factor-1α; presence of the D-110 hypoxia-inducible protein; increased expression of hypoxia-inducible genes in lesions as well as in adjacent normal-appearing white matter (NAWM); loss of myelin-associated glycoprotein in myelin of early MS lesions; a 50% reduction of blood flow through NAWM with areas of lowest blood flow having the greatest probability of lesion development. Why MS-like lesions develop following hypoxemic insults in some individuals but not in others is likely dependent upon the presence of immune predisposing factors that are governed genetically. Hypoperfusion may be due to decreased arterial supply, restricted venous return, or a combination of these. There are clinical trials ongoing or planned to treat chronic cerebrospinal venous insufficiency (CCSVI) through angioplasty. I suggest that it is important that clinical trials addressing vascular issues in MS should examine how the vascular intervention affects white matter perfusion and determine whether the extent of perfusion recovery and maintenance of this recovery is related to functional recovery and maintenance of functional recovery. Consideration should also be given to the possibility of arterial problems playing a role in hypoperfusion in some MS patients.

This is a hypothesis paper and one persons view; is it yours?

8 comments:

  1. As the authors state and I paraphrase: "the schema of hypoxia in stroke mechanism does not lead to MS-like lesion formation...." If hypoxia was causative the pathology between stroke and MS be more congruent. I would say that hypoxic damage is more consequence than causative. Hyperbaric O2 and CCSVI have failed to ameliorate the disease.

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    1. Rather you have failed to understand what kind of damage is favoured by CCSVI. It's ok, all neurologists and most patients have the same (lack of) opinion.

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    2. True, CCSVI proposes insufficient venous drainage leading to backflow, iron deposition and subsequent immune pathogenesis. Evidence for venous occlusion causing MS lesions is lacking.

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    3. Hypoxia in stroke leads to breakdown of the BBB. What triggers the inflammation and the breakdown of the BBB in MS??? What's going on with astrocytes and microglia and integrity of BBB?

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    4. No, Steve S, that's not how it works. The damage is purely mechanical, caused by the force of the backflowing blood on the walls of the periventricular veins and the perivenous soft tissue. Iron deposition is one of many processes that follow, including BBB disruption and immune cell invasion.

      That's why MS lesion have nothing to do with stroke damage.

      CCSVI is a static venous condition that becomes hazardous under combinations of everyday movements. The paradigm shift that one has to assimilate is quite demanding. I could send you a recent article that clears all up, if interested.

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    5. Thanks , I would like to see the link to the paper mentioned.

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    6. http://www.jle.com/e-docs/00/04/83/56/resume.phtml

      The full article is not free. I can send it to you if you provide an email address.

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  2. 1- increased protein levels of hypoxia-inducible factor-1α;
    2 - presence of the D-110 hypoxia-inducible protein;
    3 - increased expression of hypoxia-inducible genes in lesions as well as in adjacent normal-appearing white matter (NAWM);
    4 - loss of myelin-associated glycoprotein in myelin of early MS lesions;
    5 - a 50% reduction of blood flow through NAWM with areas of lowest blood flow having the greatest probability of lesion development

    Are these established as true, or would any of these be in debate among neurologists?

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