a publication on normal cerebral outflow

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a publication on normal cerebral outflow

Postby Cece » Mon Dec 27, 2010 7:43 pm

Here is a publication that is looking at what is normal cerebral outflow in 18 participants. This one sounds to me like he has CCSVI:
Venous flows in EV were peculiar in three participants. V11 and V14 had a unilateral IJV responsible for the totality of cerebral venous drainage. On the contrary, V18 had an increased and dominant EV drainage (flow was null in the right IJV and significantly reduced in the left).

http://www.nature.com/jcbfm/journal/v29 ... 0929a.html

EV drainage means epidural drainage which means the vertebral veins. Null flow in one IJV and significantly reduced in the other - I can't imagine that wouldn't get a CCSVI diagnosis!
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Postby Rokkit » Mon Dec 27, 2010 8:06 pm

There's a Journal of Cerebral Bloodflow and Metabolism? Who knew!? Cool find, Cece.
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Postby Cece » Mon Dec 27, 2010 8:39 pm

Thanks, Rokkit. It has all its archives up to 2009 available in full, which is nice. And there's stuff like this:
Hypothermia reduces neuronal damage after cerebral ischemia and traumatic brain injury, while hyperthermia exacerbates damage from these insults. Previously we have shown that temperature-dependent modulation of excitotoxic neuronal death is mediated in part by temperature-dependent changes in the synaptic release/translocation of Zn2+. In this study, we hypothesize that brain temperature also affects hypoglycemia-induced neuronal death by modulation of vesicular Zn2+ release from presynaptic terminals. To test our hypothesis, we used a rat model of insulin-induced hypoglycemia. Here we found that hypoglycemia-induced neuronal injury was significantly affected by brain temperature, that is, hypothermia inhibited while hyperthermia aggravated neuronal death. To investigate the mechanism of temperature-dependent neuronal death after hypoglycemia, we measured zinc release/translocation, reactive oxygen species (ROS) production, and microglia activation. Here we found that hypoglycemia-induced Zn2+ release/translocation, ROS production, and microglia activation were inhibited by hypothermia but aggravated by hyperthermia. Even when the insult was accompanied by hyperthermic conditions, zinc chelation inhibited ROS production and microglia activation. Zinc chelation during hyperthermia reduced neuronal death, superoxide production, and microglia activation, which was comparable to the protective effects of hypothermia. We conclude that neuronal death after hypoglycemia is temperature-dependent and is mediated by increased Zn2+ release, superoxide production, and microglia activation.

http://www.nature.com/jcbfm/journal/v30 ... 9229a.html

which may be relevant but I need to work on my science background (or lack thereof) to make sense of it. It ties in to my previous thinking about the role of glucose (as needed by the brain and limited by CCSVI) and the effect of heat on glucose in the bloodstream (it fluctuates more wildly; diabetics have to account for this in the summer) and now to add insult to injury, if overheated the brain will endure worse damage from this lack of glucose. And taking zinc is protective?
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Postby David1949 » Mon Dec 27, 2010 9:29 pm

Excellent detective work Cece. Reading up on all the terms will take some work but I think you will do that. You may not have a medical background but as Thomas Edison once said; "Genius is 1% inspiration and 99% prespiration."

Thank you for all your hard work!
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Postby Leonard » Tue Dec 28, 2010 2:15 am

Cece wrote:Thanks, Rokkit. It has all its archives up to 2009 available in full, which is nice. And there's stuff like this:
Hypothermia reduces neuronal damage after cerebral ischemia and traumatic brain injury, while hyperthermia exacerbates damage from these insults. Previously we have shown that temperature-dependent modulation of excitotoxic neuronal death is mediated in part by temperature-dependent changes in the synaptic release/translocation of Zn2+. In this study, we hypothesize that brain temperature also affects hypoglycemia-induced neuronal death by modulation of vesicular Zn2+ release from presynaptic terminals. To test our hypothesis, we used a rat model of insulin-induced hypoglycemia. Here we found that hypoglycemia-induced neuronal injury was significantly affected by brain temperature, that is, hypothermia inhibited while hyperthermia aggravated neuronal death. To investigate the mechanism of temperature-dependent neuronal death after hypoglycemia, we measured zinc release/translocation, reactive oxygen species (ROS) production, and microglia activation. Here we found that hypoglycemia-induced Zn2+ release/translocation, ROS production, and microglia activation were inhibited by hypothermia but aggravated by hyperthermia. Even when the insult was accompanied by hyperthermic conditions, zinc chelation inhibited ROS production and microglia activation. Zinc chelation during hyperthermia reduced neuronal death, superoxide production, and microglia activation, which was comparable to the protective effects of hypothermia. We conclude that neuronal death after hypoglycemia is temperature-dependent and is mediated by increased Zn2+ release, superoxide production, and microglia activation.

http://www.nature.com/jcbfm/journal/v30 ... 9229a.html

which may be relevant but I need to work on my science background (or lack thereof) to make sense of it. It ties in to my previous thinking about the role of glucose (as needed by the brain and limited by CCSVI) and the effect of heat on glucose in the bloodstream (it fluctuates more wildly; diabetics have to account for this in the summer) and now to add insult to injury, if overheated the brain will endure worse damage from this lack of glucose. And taking zinc is protective?


Cece, great finding! I may add a further observation, perhaps it is related.

I have been liberated twice now. Things are restenosing again so a further intervention has been planned. The doctors and me will get it under control, in particular as doctors learn how to best keep the veins open.

My experience is that after liberation, I sweat normal again, in the neck and on my head. At night, in my pillow. But now, as things restenose again, the skin is as dry as it can be. In the intermediate period, if I sweat well during the night, the next day is quite OK.

I think this strengthens your thinking above and may be related to the blood stream through the head and in fact the blood supply to the hypocampus?.
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Postby pairOdime » Tue Dec 28, 2010 6:52 am

What a great journal for CCSVI related research...from their home page.

Welcome to Journal of Cerebral Blood Flow & Metabolism
The Journal of Cerebral Blood Flow & Metabolism stands at the interface between basic and clinical neurovascular research, and features timely and relevant research highlighting experimental, theoretical, and clinical aspects of brain circulation, metabolism and imaging.
It's a paradigm shift
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Postby Leonard » Thu Dec 30, 2010 8:53 am

Thanks Cece for your link http://www.nature.com/jcbfm/journal/v30 ... 9229a.html
This led me to make the following analysis of the situation.

When Zamboni first published his findings in December 2008, this must have gone like a storm through the MS medical and research communities. Obviously, they could not deny the results. Where they rejected the proposition in public, they must have started a vigorous searching for the clue in their own world. Perhaps to help us in the long run, in the short term most certainly for their own benefit. And a new patent race was born. In the meanwhile, to fend off the competition, they made public statements like this is a hoax.

Now, what does it do if you open the veins and reduce the resistance? Of course, the flow increases. And oxygen rich blood can pass through the head. But there is more. A number of clues can be found in research papers that had already been published over recent years and that are related to a low glucose level and everything that is surrounding it. And guess what: Mark Freedman's name is there, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2850589/ and he even registered a patent in 2009.

When I mentioned the low glucose hypotheis to my neurologist the week before last, there was no response and as I said here earlier the meeting was a total failure. But somehow I could feel that my neuro knew more about this and the developments around ccsvi and low glucose levels.

To cut a long story short: the patent race is on… what's new, this sector is no different from any other sector… and our interests to get honest and fair information about what's happening around ccsvi is secondary to the short term interests for filing patents and the profit motive.

I hope that the delays in ccsvi treatment are not caused or due in some way to this patent race.
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Postby Cece » Thu Dec 30, 2010 10:08 am

Leonard, that is interesting, I will look into that more, thanks.

For anyone else coming in on this conversation, the low-glucose hypothesis (which which sounds so official when you give it that name and call it a hypothesis! See what we have wrought) :) is looking at just the glucose side of the three things that blood flow to the brain does. Blood flow delivers oxygen, delivers the glucose to the very hungry brain as well as other nutrients, and takes away waste products. The other two are important, but the glucose is important too, and it was months before I looked at that instead of focusing only on the oxygen. It's an explanation too for the post-liberation increase in dreams and REM sleep, since REM has high glucose demands, Joan has posted about this.

I once saw a MS physical therapist, she was convinced that yeast causes MS because of research showing that pwMS get chronic yeast infections. Now like so many other things, I tie that bit of info into CCSVI and say that we are consuming more sugar than the average person, to get it elevated in our blood streams, to try and meet the unmet needs of the brain. And the result of greater sugar consumption are a greater prevalence of yeast infections.

Leonard, sorry that your neurologist rejected the idea, I can only imagine it getting a blank stare there because first you have to buy into CCSVI and then take it further to look at the glucose side of things. It's only a hypothesis, but I find it convincing.
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Postby pairOdime » Thu Dec 30, 2010 10:34 am

Stroke. 2010 Jun;41(6):1278-84. Epub 2010 May 6.
A mouse model characterizing features of vascular dementia with hippocampal atrophy.
Nishio K, Ihara M, Yamasaki N, Kalaria RN, Maki T, Fujita Y, Ito H, Oishi N, Fukuyama H, Miyakawa T, Takahashi R, Tomimoto H.

Department of Neurology, Faculty of Medicine, Kyoto University, Sakyo-Ku, Kyoto 606-8507 Japan. ihara@kuhp.kyoto-u.ac.jp.
Abstract
BACKGROUND AND PURPOSE: We have previously described effects of chronic cerebral hypoperfusion in mice with bilateral common carotid artery stenosis (BCAS) using microcoils for 30 days. These mice specifically exhibit working memory deficits attributable to frontal-subcortical circuit damage without apparent gray matter changes, indicating similarities with subcortical ischemic vascular dementia. However, as subcortical ischemic vascular dementia progresses over time, the longer-term effects that characterize the mouse model are not known.

METHODS: Comprehensive behavioral test batteries and histological examinations were performed in mice subjected to BCAS for up to 8 months. Laser speckle flowmetry and F-fluorodeoxyglucose positron emission tomography were performed to assess cerebral blood flow and metabolism at several time points.

RESULTS: At 2 hours after BCAS, cerebral blood flow in the cerebral cortex temporarily decreased to as much as 60% to 70% of the control value but gradually recovered to >80% at 1 to 3 months. At 5 to 6 months after BCAS, reference and working memory were impaired as demonstrated by the Barnes and radial arm maze tests, respectively. Furthermore, F-fluorodeoxyglucose positron emission tomography demonstrated that hippocampal glucose utilization was impaired at 6 months after BCAS. Consistent with these behavioral and metabolic abnormalities, histological analyses demonstrated hippocampal atrophy with pyknotic and apoptotic cells at 8 months after BCAS.

CONCLUSIONS: These results suggest that the longer-term BCAS model replicates advanced stages of subcortical ischemic vascular dementia when hippocampal neuronal loss becomes significant.
Last edited by pairOdime on Thu Dec 30, 2010 2:44 pm, edited 1 time in total.
It's a paradigm shift
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Postby Leonard » Thu Dec 30, 2010 11:37 am

Cece wrote:Leonard, sorry that your neurologist rejected the idea, I can only imagine it getting a blank stare there because first you have to buy into CCSVI and then take it further to look at the glucose side of things. It's only a hypothesis, but I find it convincing.


I think they know deep inside about ccsvi; and they may even buy into the broader ideas behind the glucose hypothesis. But then, if this is all about patents, the golden rule is you don't talk, believe me, I know although from another sector... And when I say you don't talk, I mean really you don't talk. And that is exactly what is happening..
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Postby Leonard » Sun Jan 02, 2011 12:22 am

I think that I found another link to the glucose hypothesis. And this significantly strengthens the idea that MS has to do something with a low glucose condition.

I just googled on Vitamine D and glucose transport, and guess what, the link between the two is definitely there.
<shortened url>

This would help explain the role of Vitamine D in MS; the sun exposure of the mother during her first months of pregnancy, how well she metabolised Vit D; the prevalence of MS in families that move south during the childhood; perhaps even the disease modulating properties of Vit D intake by patients etc.

It seems that a number of things now start to align quite nicely and all point in teh same direction: that the glucose condition is an important factor. And -what's more important for us as patients- that if you fix it, many things may restore to normal!!
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Postby HappyPoet » Sun Jan 02, 2011 6:04 am

Cece, you're on quite a roll!
Thanks for getting this thread started!

Thank you, everyone else, for your contributions!

So, who is going to contact The Journal of Cerebral Blood Flow & Metabolism to tell them all about CCSVI, or has someone already done so?
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Postby Cece » Sun Jan 02, 2011 10:47 am

Leonard wrote:I think that I found another link to the glucose hypothesis. And this significantly strengthens the idea that MS has to do something with a low glucose condition.

Interesting, I will read up on this. A vitamin D/glucose connection?

Rather than saying MS has to do with a low glucose condition, my thoughts are that the level of sugar in the blood would be adequate except for the poor draining of the brain, in which the normal levels of glucose get used up and so the brain benefits if the MSer maintains a higher than normal sugar level in the body.
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Postby Leonard » Sun Jan 02, 2011 12:00 pm

Cece, I fully share your view. Where I say low glucose condition, I mean to say the low glucose level inside the part of the nervous systeem or the brain that is affected by the poor blood flow. And yes, a higher than average sugar level will help MS patients to cranck up the glucose level in the affected areas.
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Re: a publication on normal cerebral outflow

Postby 1eye » Sun Jan 02, 2011 1:32 pm

Cece wrote:Here is a publication that is looking at what is normal cerebral outflow in 18 participants. This one sounds to me like he has CCSVI:
Venous flows in EV were peculiar in three participants. V11 and V14 had a unilateral IJV responsible for the totality of cerebral venous drainage. On the contrary, V18 had an increased and dominant EV drainage (flow was null in the right IJV and significantly reduced in the left).

http://www.nature.com/jcbfm/journal/v29 ... 0929a.html

EV drainage means epidural drainage which means the vertebral veins. Null flow in one IJV and significantly reduced in the other - I can't imagine that wouldn't get a CCSVI diagnosis!


People who have worked with resistors know that the lowest resistance in a parallel network gets hottest. It will wear out quickest. It gets the most flow. This is why we need working IJVs and vertebral veins. There is a lot of blood trying to get through, and normal is a specific cross-sectional area. The pipe is no wider than its narrowest point. A small collateral vein cannot take the place of a large jugular. If it has valves you need collateral valves too, which sounds tricky to me.

Back to your regularly scheduled program. Sounds like hypoglycemia and hypoxia can result from not enough flow.
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