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PostPosted: Thu Feb 02, 2012 1:38 pm 
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This is from an article written by K.K. Jain, MD on Medlink. It was originally released in 1998, but Dr. Jain updates this article, as new research emerges. The last update was in 2011. And it includes CCSVI. Professor Jain is a nanotechnology and neurological expert, and serves as associate editor of Medlink Corporations online encyclopedia of neurology.


http://www.medlink.com/subscribe_server ... D=MLT000L9


Quote:
Multiple sclerosis. Contrast-enhanced MRI in patients with multiple sclerosis show that increased permeability of the blood-brain barrier commonly occurs with this disease. Lymphocyte recruitment into the brain across endothelial cells of the blood-brain barrier, which is otherwise restricted and well regulated, represents a critical event in pathogenesis of multiple sclerosis (Correale and Villa 2007). The changes in capillary permeability often precede T2-weighted MRI evidence of tissue damage. Increased gelatinase B (a type of matrix metalloproteinase) is associated with an open blood-brain barrier on MRI. Steroids may improve capillary function by reducing activity of gelatinase B.

Various inflammatory factors produced by perivascular cells in multiple sclerosis affect the permeability of the blood-brain barrier. One of these, the intercellular adhesion molecule-1, binds to its leukocyte ligands and allows activated leukocytes entry into the central nervous system. According to 1 hypothesis, pathological reflux of venous flow in the cerebral and spinal veins increases the expression of intercellular adhesion molecule-1 by the cerebrovascular endothelium, which, in turn, could lead to increased permeability of the blood-brain barrier (Simka 2009).



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PostPosted: Thu Feb 02, 2012 2:16 pm 
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I think that reference is to Dr. Simka's paper where ICAM-1 is said to be up-regulated by shear stresses. Sounds like a plausible hypothesis to me. Since it actually lets unwanted leukocytes through the BBB it also looks to me like an autoimmune mechanism, the same one addressed by Tysabri.

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PostPosted: Thu Feb 02, 2012 3:14 pm 
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What about the thing that I read a couple of days ago, that post-mortum research of the lesions of diseased MSers showed the presence of a virus in them? Because of stale blood, the virus cells get more numerous and the white blood cells, trying to fight it of, cross the BBB and in the process of killing the virus, the myelin gets damaged as well. This sounds way too simple, but so did CCSVI...


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PostPosted: Thu Feb 02, 2012 3:28 pm 
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If the cerebral endothelium becomes permeable, all kinds of particles can cross into brain tissue. Viruses (like EBV), bacteria (like Cpn and borrelia burgdorferi), plasmic particles, microhemorrages, iron and the immune system. All of these have been found in MS brains. Dr. Simka's hypothesis, which is included in this new medical article, is that-

Quote:
pathological reflux of venous flow in the cerebral and spinal veins increases the expression of intercellular adhesion molecule-1 y the cerebrovascular endothelium, which, in turn, could lead to increased permeability of the blood-brain barrier (Simka 2009).


Here is Simka's full paper--He suggests studying a "hemodynamic approach" in MS
http://www.direct-ms.org/pdf/CCSVI/Simk ... S%2009.pdf

Quote:
Perhaps, in addition to or instead of pharmacotherapy, surgical correction could be an option in some anatomical variants of pathological venous outflow, such as in the localized occlusion of the azygous vein.
Hopefully, a hemodynamic approach to the multiple sclerosis pathogenesis can open a new chapter of investi- gations and treatment of this debilitating neurologic disease.


The point I was hoping to make in this post is that this theory is being included in a new, updated encyclopedia entry for Medlink on the blood brain barrier. And that was pretty exciting to see.
cheer

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PostPosted: Thu Feb 02, 2012 4:32 pm 
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I was unfamiliar with Medlink, but I agree that it's an exciting development.

Here's something from the linked article:
Quote:
Clinical assessment of the blood-brain barrier. Two main approaches are used for studying the integrity of human blood-brain barrier in vivo: (1) structural imaging employs contrast agents that only penetrate the blood-brain barrier at sites of damage, and (2) functional imaging is used to study the transport of substances across the blood-brain barrier- both intact and damaged. Structural imaging employs contrast agents with CT scanning and is relatively insensitive. MRI with the contrast agent gadolinium is more sensitive. Hyperintense acute reperfusion injury marker (HARM) is gadolinium enhancement of cerebrospinal fluid on fluid-attenuated inversion recovery MRI and may be a useful imaging biomarker to evaluate matrix metalloproteinase-9, which may play a role in blood-brain barrier disruption after ischemic stroke (Barr et al 2010).

Is HARM present in MS patients?
If MRIs with gadolinium enhancement measure blood brain barrier integrity, then the results we heard awhile back about 12 out of 13 MS patients having no enhancement on their MRIs done post-CCSVI treatment mean that we go from leaky blood-brain barriers to intact blood-brain barriers post-treatment. And that is a wonderful thing.


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PostPosted: Thu Feb 02, 2012 4:47 pm 
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Cece wrote:
Is HARM present in MS patients?
If MRIs with gadolinium enhancement measure blood brain barrier integrity, then the results we heard awhile back about 12 out of 13 MS patients having no enhancement on their MRIs done post-CCSVI treatment mean that we go from leaky blood-brain barriers to intact blood-brain barriers post-treatment. And that is a wonderful thing.


I hadn't heard that about the post CCSVI MRIs, Cece...but it makes sense. Great news! Jeff hasn't had any enhancing lesions since his venography 3 years ago. I think Dr. Dake showed that 22 out of 23 patients did not have any enhancing lesions after 2 years....need to dig out that post.

What I've been told is that the gadolinium enhancing lesions on MRI found in MS brains are due to "disruptions" in the BBB, due to active inflammatory lesions. Neurologists claim that it is the immune system doing the disrupting. But if you note in the article in the first post---disruption of the BBB has been found before any immune activity.

Here is more info on HARM (Hyperintense Acute Reperfusion Marker)---a marker in stroke
http://stroke.ahajournals.org/content/e ... 6.abstract

I couldn't find any info on HARM in MS brains. interesting,
cheer

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PostPosted: Thu Feb 02, 2012 5:56 pm 
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827673/
Here's something! In this article it says:
Quote:
Post-Gd-DTPA FLAIR identification of HARM has been confirmed in subsequent studies of stroke and multiple sclerosis, identifying its utility in clinical practice as a marker of BBB disruption.
and cites this article:
http://www.ncbi.nlm.nih.gov/pubmed/18581384
Quote:
In vitro investigation of poor cerebrospinal fluid suppression on fluid-attenuated inversion recovery images in the presence of a gadolinium-based contrast agent.

I'm not sure what to make of this but it seems to be one more way in which MS is similar to ischemia, which is vascular.

I wish I remembered more about the post CCSVI MRIs findings I mentioned, like who the researcher was. Edit: I found it, Cheer posted it originally, and I was off on some of the details! :oops:
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic17572.html#p173450
Quote:
Magnetic resonance imaging (MRI) blindly demonstrates a trend for fewer T2 lesions in the ITG (p = 0.081), corresponding to a 10% decrease in the ITG compared with a 23% increase in the DTG over the first 6 months of the study.
It was a decrease in lesions, but not an end to all enhancement.


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