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PostPosted: Mon Apr 02, 2012 4:39 pm 
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i don't know if article has been posted but should be read.

Quote:
Hypoperfusion of the cerebral white matter in multiple sclerosis: possible mechanisms and pathophysiological significance

This work was supported by MS Anders (Amsterdam, The Netherlands).

Jacques De Keyser1,2, Christel Steen2, Jop P Mostert2 and Marcus W Koch2

1Department of Neurology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium
2Department of Neurology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
Correspondence: Professor Dr J De Keyser, Department of Neurology, Universitair Ziekenhuis Brussel, Laarbeeklaan 101, Brussels 1090, Belgium. E-mail: jacquesdekeyser@gmail.com

Received 2 May 2008; Revised 13 June 2008; Accepted 16 June 2008; Published online 2 July 2008.


Quote:
Accumulating evidence indicates that there is a decreased perfusion throughout the NAWM in patients with MS. It occurs in both relapsing–remitting and primary progressive MS, strongly suggesting that it represents an integral part of the disease process. Ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions). There appears to be a relationship between reduced white matter perfusion and cognitive dysfunction in patients with MS. We provide a hypothetical framework for the reduced perfusion, implicating a key role of astrocyte dysfunction, possibly related to a deficiency in β2-adrenergic receptors resulting in an impaired siphoning and release of K+ in the perivascular spaces. The underlying pathophysiological mechanisms need to be further elucidated as it could ultimately allow us to understand and treat this complex disease better.


http://www.nature.com/jcbfm/journal/v28 ... 0872a.html



Bob


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PostPosted: Mon Apr 02, 2012 7:45 pm 
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Quote:
A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss.
Ok, we know one thing the reduced perfusion is not due to (it is not secondary to axonal loss). The article suggests a complicated theory relating to astrocytes as a possibility.

The idea around here has been that the reduced perfusion is due to the blockages in the neck veins. But there is an easy way to test this idea. Perfusion needs to be measured before and after the endovascular treatment of the stenoses of the neck veins. If improving the outflow through the neck veins also improves the cerebral perfusion, then the reduced perfusion was a result of those blockages.

I do not know if there is as easy of a way to test the astrocyte theory.

Great article, orion. I will read it more closely tomorrow. My astrocytes get a little tired at this time of night.


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PostPosted: Mon Apr 02, 2012 8:03 pm 
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this is a good one, orion.
I wrote a note in Facebook on this paper back in 2009, delving into a bit, and breaking it into bite size chunks. :)
https://www.facebook.com/notes/ccsvi-in ... 9656952210

Quote:
The researchers spend a great deal of time in the paper hypothesizing over causes for this slowed perfusion, and finally admit that there needs to be further study. They write about research into astrocyte (glial cells in the central nervous system) dysfunction, but admit they don't really know what's going on. They haven't found the specific cause for this slowed perfusion and lack of oxygen in the MS brain, and further research needs to be done. The thing they can show is that MS brains have slowed blood flow, damage due to lack of oxygen that is centered around the veins in the brain, and this happens before lesions form.


cheer

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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS


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PostPosted: Thu Apr 05, 2012 2:27 pm 
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I think there is reduced perfusion if the cerebral bloodflow (sum of all flows going in, which equals the sum of all outflows) is low. It's just a question of which part gets the reduced flow, if it isn't evenly perfused. I believe the p in PWI is perfusion, so yes, it can be measured, with MRI. Measuring the astrocytes, no clue.

Further to the thread on metabolism, I think, though flow is the same on both sides of a stenosis (in the jugular), there must be a difference in pressure. I think the pressure should be higher on the upstream side (brain-wards). Also, if the jugulars are a main route (because of the relative diameters of other veins, and the fourth power relationship between diameter and resistance), then any stenosis or obstruction will reduce the overall flow, and thus perfusion. The jugulars appear in parallel with the other veins and collaterals of the neck. The favoured route is the largest vein. That is why after stenosis is removed, the collaterals appear to vanish. The difference in diameters has such a pronounced effect that they now carry only a miniscule amount of the overall low..

So a) which jugular is affected matters, because they are not the same diameter; and b) together they comprise the favoured route, having direct series connection with large brain vessels. Overall, throughout the brain, flow, pressure, and resistance of blood are affected by a jugular stenosis.

Pressure and resistance to flow are increased, and flow (again, thus perfusion) is reduced, over the whole brain.

You can measure it, but it is a fact.

The notion that you will stay alive after ligation of the two largest vessels draining the brain may be technically true, but QOL is definitely in jeopardy.

The way they work in upright humans is mainly when we are lying down. They are a main reason we don't like to sleep standing up.

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PostPosted: Thu Apr 05, 2012 4:25 pm 
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If we assume that low perfusion is the cause of MS then the $64,000 question is what causes the low perfusion rate and more importantly

HOW CAN WE FIX IT?

This article discusses factors that control the cerebral blood flow.
https://en.wikipedia.org/wiki/Cerebral_blood_flow


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PostPosted: Thu Apr 05, 2012 5:01 pm 
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Here is an article on autoregulation of blood flow.
http://www.cvphysiology.com/Blood%20Flow/BF004.htm
Certain organs including the brain, have a means of compensating for a fall in blood pressure by dilating the small arteries and arterioles to allow more blood flow.

So as I see it there are five categories of things that could cause low blood
low:

Low blood pressure.
Blockage or stenosis in the veins
Blockage or stenosis in the arteries
Malfunction of the autoregulation system in the brain.
High viscosity of the blood.

We could probably rule out low blood pressure. I don't have low blood pressure and I think many other MSers also have normal pressure.


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PostPosted: Thu Apr 05, 2012 5:58 pm 
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I asked Dr.Arata about MS patients having high blood pressure and he stated that most of his MS patients have low blood pressure. My bp is low and has been low normal for years.


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PostPosted: Thu Apr 05, 2012 6:18 pm 
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munchkin wrote:
I asked Dr.Arata about MS patients having high blood pressure and he stated that most of his MS patients have low blood pressure. My bp is low and has been low normal for years.


Sounds like we need a poll.


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