CCSVI and Low Blood Oxygen

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby hope410 » Sat Mar 27, 2010 1:41 am

I've worn one of those pulse-ox things on my finger before and my oxygenation levels were normal, I think 100%.

Studies into the effects of hyperbaric oxygen therapy and MS have never shown any benefit to us either in terms of disease progression.

So....???
User avatar
hope410
Family Elder
 
Posts: 125
Joined: Mon Mar 08, 2010 4:00 pm

Advertisement

Postby Vonna » Mon Mar 29, 2010 10:35 pm

Hello Cheer,
Thank you for the links, I did check them out, and they were very helpful!
Yes, it is all so interesting. Anyone who could call this amazing breakthrough discovery a hoax or hope mongering is obviously not taking an objective look. It all makes so much sense!

Hoodyup,
Thanks for your posts, they were very helpful.

Brightspot,
Okay, I will recount a couple of recent events concerning my personal experience with oxygen.

My first clue that something was going on with my oxygen level almost three years ago. After a hospital stay for an MS exacerbation, I was back home. I found myself taking periodic deep breaths of air. It was a strange sensation I had never experienced before. I would simply pull in very deep breaths every few minutes. This concerned me to the point that I was not able to sleep the entire night. This continued a few days, and I guessed that it must be a reaction to one of the new medications I had just been prescribed. I actually stopped all my medications in an attempt to test and see if the strange breathing pattern would also stop. Unfortunately, it didn't, but eventually the deep breaths became fewer and fewer as I recovered from the attack.

Six months later, during another attack, I noticed the strange breathing return. It was also accompanied with shortness of breath, rapid heart rate, chest pressure, and even a little chest pain.

And then, three months ago, another attack. Yes, the breathing returned! All the previous symptoms were more pronounced. And yet, another strange new symptom. I noticed I was yawning in a strange sort of way! How do I explain it? Well, it was like a fake yawn. A yawn where I just open my mouth involuntarily, but it was not refreshing. It is actually very annoying, as my body seems to know I need more oxygen, but is not succeeding very well in satisfying the need.

A few weeks ago, during this ongoing exacerbation, we had a very cold and snowy day. I had spent the day in bed because of extreme fatigue. Sometime in the evening, I noticed something VERY odd. I began to breathe in such a way that was completely refreshing! It actually felt foreign to me as I pulled the breaths in, I could feel refreshment all the way down my chest! It felt ABSOLUTELY WONDERFUL! I can't explain this feeling, but it overwhelmed me so much, I actually cried tears of joy!

My husband came home from work and gasped at how cold it was in the room! He practically never wears a coat. Here I was, with not a single chill bump, and his teeth were chattering! Tears rolled down my cheeks as I tried to explain to him that I didn't remember breathing could be so refreshing. I literally laid there, just enjoying taking in breaths. My husband slept bundled in a coat that night because I begged him not to turn the heater on! My body temperature was doing very weird things, but it allowed me to experience the best breathing I had known since I could remember. I later learned that cold air is more dense, therefore has more oxygen.

And now for today. I had a treadmill stress test because of the rapid heartbeat, shortness of breath, chest pressure, etc... Within four minutes of walking, my heart rate was at 184, which is above my maximum recommended heart rate. Once off the treadmill, my heart rate did not recover very quickly. It stayed well above 100 bpm. The technician kept asking me if I needed oxygen, and I declined. I was actually very curious to see how I would respond to the oxygen, but did not want to appear as someone who over dramatized my condition. She checked my oxygen level by putting the little reader on my finger. My oxygen was at 99%, yet I was breathing very hard, and my face was flushed. I also had tingling in both legs and my lips were starting to tingle. Then as I lay there trying to rest, my heart rate shot back up instead of going down. At that point, she insisted I have oxygen, even though my oxygen level was reading 99%! Ahhhhhhhh, again, the refreshment the oxygen brought was overwhelming! Try as I might, I could not hold back a few stray tears. It was like a rare treat to feel such relief from simply breathing!

As we waited for my heart rate to return to something that was acceptable, I talked to the nurse about CCSVI. She seemed interested, and I brought up a question I had. I have heard that a person can have a different blood pressure in their head than in their arm. If this is true, would it not stand to reason, that the oxygen level (which is carried by the blood) could also be different? Is is possible that we need to be checking the oxygen level in our brains, not our finger?

All I know is, I tried the oxygen, and it works. For me, it's like a thirsty traveler in the desert finally getting water.
User avatar
Vonna
Family Elder
 
Posts: 170
Joined: Mon Jan 04, 2010 4:00 pm

Postby bluesky63 » Mon Mar 29, 2010 10:46 pm

Vonna, this is very interesting to me. I was thinking along similar lines and wondering how you measure the difference in oxygen saturation in the brain vs. the rest of the body. I have had the same experience -- the finger clamp gives a beautiful saturation reading, and yet oxygen makes you feel fantastic!

Great observations and details. Thank you. :-)
User avatar
bluesky63
Family Elder
 
Posts: 441
Joined: Mon Apr 18, 2005 3:00 pm

Postby bigfoot14 » Tue Mar 30, 2010 7:58 am

hope410 wrote:I've worn one of those pulse-ox things on my finger before and my oxygenation levels were normal, I think 100%.


The pulse -ox machine measures the oxygen level at your finger tips....
not much help in measuring oxygen perfusion in the brain if the blood flow is slowed by ccsvi
User avatar
bigfoot14
Family Elder
 
Posts: 110
Joined: Mon Nov 30, 2009 4:00 pm
Location: State of confusion (Illinois)

Postby Billmeik » Tue Mar 30, 2010 8:47 am

its pretty important to distinguish between global effects and local. Hypoxia is a measure of o2 in the whole body. MS patients as far as I know don't have low oxygen levels over the whole body. Locally, beause of ccsvi there is probably some deoxygenated blood that isn't escaping the cns correctly and is causing some damage...

I do believe the opening of Jeff's jugular veins allowed for oxygenated blood to flow, and that is why his fatigue and malaise are gone


I dont get this. Oxygenated blood comes from the heart and flows up to the brain where most of the oxygen gets used up.(or is that it, not all?) By opening the jugular deoxygenated blood can flow better. I have ms and in the last few months my mental errors are like 50% but fwiw I need that clarified.

I mean the fatigue thing seems to be from neural turbulance. I was jogging 5 miles a day last spring now I can do a few blocks. This is because after a while it becomes exhausting just to go in a line. There are so many incorrect neural signals to correct in each stride that I get really tired really fast. So a brain that can clear itself isnt going to send as many bad signals, but its nothing global. That metre on the finger isnt going to change because of a ccsvi operation is it?
User avatar
Billmeik
Family Elder
 
Posts: 694
Joined: Fri Nov 27, 2009 4:00 pm

Postby cheerleader » Tue Mar 30, 2010 2:22 pm

It's all about slowed cerebral perfusion and mean transit time. The longer it takes deoxygenated blood to get out, the longer it takes oxygenated blood to get in. Yes, it is localized hypoxia....it's only the brain. A faster mean transit time, thanks to correct venous return, allows for oxygenation.

Dr. Dake believes the relief in Jeff's fatigue is because he no longer has venous congestion. Fatigue in MS is related to slowed perfusion in gray matter.

Here's some research on this:


Deep Gray Matter Perfusion in Multiple Sclerosis
Dynamic Susceptibility Contrast Perfusion Magnetic Resonance Imaging at 3 T

Matilde Inglese, MD, PhD; Sun-Jung Park, MS; Glyn Johnson, PhD; James S. Babb, PhD; Laura Miles, PhD; Hina Jaggi, MS; Joseph Herbert, MD; Robert I. Grossman, MD
Arch Neurol. 2007;64(2):196-202.

Objectives To assess the presence of perfusion abnormalities in the deep gray matter of patients with relapsing-remitting and primary progressive multiple sclerosis (MS) in comparison with healthy controls and to investigate the impact of perfusion impairment on clinical disability and fatigue.



Patients Twenty-two patients with MS and 11 age- and sex-matched healthy volunteers.

Intervention Absolute cerebral blood flow, cerebral blood volume, and mean transit time were measured in the thalamus, putamen, and caudate nuclei.

Main Outcome Measures Decrease of cerebral blood flow in the deep gray matter of patients with MS and correlation between perfusion impairment and the severity of fatigue.

Results The cerebral blood flow value averaged over the thalamus, putamen, and caudate nuclei was significantly lower in patients with primary progressive MS (P<.001) and in patients with relapsing-remitting MS (P = .01) compared with controls, and there was a trend for patients with primary progressive MS to have lower average cerebral blood flow than patients with relapsing-remitting MS (P = .06). With respect to cerebral blood volume, there was a significant difference between patients with primary progressive MS and controls (P<.001) and between the 2 groups of patients (P = .03) but not between patients with relapsing-remitting MS and controls (P>.30). The fatigue score was significantly correlated with cerebral blood flow (r = 0.4; P<.001) and cerebral blood volume (r = 0.5; P = .004).

Conclusion The decrease of tissue perfusion in the deep gray matter of patients with MS is associated with the severity of fatigue.


http://archneur.ama-assn.org/cgi/conten ... t/64/2/196

Here's the abstract for Dr. Z's new paper to be presented in Toronto next month at the ANA meeting-

Hypoperfusion of Brain Parenchyma Is Strongly Associated with the Severity of Chronic Cerebrospinal Venous Insufficiency in Patients with Multiple Sclerosis. AAN Annual Meeting 2010. Toronto, 14 Apr 2010 [aan10a].
Abstract.OBJECTIVE: To investigate the relationship between chronic cerebrospinal venous insufficiency (CCSVI) and cerebral perfusion in patients with multiple sclerosis (MS). BACKGROUND: CCSVI is a vascular condition described in MS patients, characterized by stenoses of the main extracranial veins with hampered cerebral venous outflow. We hypothesized that the impaired venous outflow contributes to hypoperfusion of brain parenchyma. DESIGN/METHODS: Sixteen consecutive relapsing-remitting MS patients (mean age 36.1yrs, mean disease duration 7.5yrs and median EDSS 2.5) and 8 age- and sex-matched normal controls (NC), were scanned on a GE 3T scanner using dynamic susceptibility contrast enhanced perfusion-weighted imaging (PWI). Cerebral blood flow (CBF), blood volume (CBV) and mean transit time (MTT) were measured in the gray matter (GM), white matter (WM), normal appearing (NA) GM, NAWM, thalamus, caudate, putamen, globus pallidus, hippocampus, amygdala, nucleus accumbens, red nucleus and substantia nigra. Diagnosis of CCSVI was established based on the venous hemodynamic (VH) Doppler criteria (Zamboni, JNNP, 2009) and the severity was based on fulfilled VH criteria (score 0-5) and VH insufficiency severity score (VHISS) (score 0-16). RESULTS: All 16 MS patients fulfilled the diagnosis of CCSVI (median VH=4, median VHISS=9) and none of the NC. There was a significant association between VH criteria and VHISS, and CBF, CBV and MTT in all examined regions of the brain parenchyma in MS patients. The most robust correlations were observed for lower CBF and higher VHISS in the GM, WM, NAGM and NAWM (r= -0.70 to -0.72, p<0.002), and in the thalamus, caudate, putamen, hippocampus, nucleus accumbens (r= -0.6 to -0.72, p<0.008). The correlation coefficients for CBV and MTT were in a range between r= -0.5 to -0.65. No relationship was observed for NC. CONCLUSIONS/RELEVANCE: This study demonstrates that severity of CCSVI is directly associated with hypoperfusion of the brain parenchyma in MS. Supported by: Hillarescere Foundation and Buffalo Neuroimaging Analysis Center.


Jeff had his first big flare and diagnosis after a week at high altitude in '07....his blood numbers were really weird, looked like the coagulation cascade- but his neuro said it was nothing. I started researching the vascular connection and we found ourselves at CCSVI-
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
User avatar
cheerleader
Family Elder
 
Posts: 5042
Joined: Mon Sep 10, 2007 3:00 pm
Location: southern California

Postby mangio » Tue Mar 30, 2010 3:08 pm

The fatigue is largely from interleukin-6 and other heat cytokines.
Paracetamol will do the trick. One of the most famous anti-pyretics
ever discovered. My guess is the brain is trying to salvage itself
and is creating heat to use as a protective mechanism. Vein blood
is not entirely devoid of oxygen but very low in it. Carbon molecules
are also very important in relation to oxygen.
User avatar
mangio
Family Elder
 
Posts: 288
Joined: Thu Dec 31, 2009 4:00 pm

Postby Billmeik » Tue Mar 30, 2010 3:50 pm

The longer it takes deoxygenated blood to get out, the longer it takes oxygenated blood to get in



didnt know that.
User avatar
Billmeik
Family Elder
 
Posts: 694
Joined: Fri Nov 27, 2009 4:00 pm

Blueberries may improve memory, coordination & balance

Postby WeWillBeatMS » Tue Mar 30, 2010 4:32 pm

I remember reading an article in Prevention magazine about how blueberries, among their many other health benefits, help increase oxygen in the brain. I regularly have a big bag of frozen organic blueberries in my refridgerator which I often put in a morning smoothie with a banana, rice milk or almond milk and frozen acai berry pulp that I get from local Brazilian stores here in South Florida. My toddler daughter loves blueberries too so we will have them fresh every so often too.

http://www.trueblueberry.com/blueberry/memory.asp

WeWillBeatMS
User avatar
WeWillBeatMS
Family Elder
 
Posts: 169
Joined: Wed Feb 03, 2010 4:00 pm

Postby mangio » Tue Mar 30, 2010 4:51 pm

elderberries are also thought to be very good but don't know why
User avatar
mangio
Family Elder
 
Posts: 288
Joined: Thu Dec 31, 2009 4:00 pm

Postby Cece » Tue Mar 30, 2010 5:42 pm

Billmeik wrote:
The longer it takes deoxygenated blood to get out, the longer it takes oxygenated blood to get in



didnt know that.


Sclafani mentioned it too in his thread a week or two ago...reduced outflow means reduced inflow...
"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition
Cece
Family Elder
 
Posts: 9022
Joined: Mon Jan 04, 2010 4:00 pm

Postby gibbledygook » Fri Apr 02, 2010 2:39 am

Just got this through from the Journal of Cerebral Blood Flow and Metabolism. It shows how hypoxia breaks down the blood brain barrier.

Blood–brain barrier (BBB) disruption, resulting from loss of tight junctions (TJ) and activation of matrix metalloproteinases (MMPs), is associated with edema formation in ischemic stroke. Cerebral edema develops in a phasic manner and consists of both vasogenic and cytotoxic components. Although it is contingent on several independent mechanisms, involving hypoxic and inflammatory responses, the single effect of prolonged hypoxia on BBB integrity in vivo was not addressed so far. Exposing mice to normobaric hypoxia (8% oxygen for 48 h) led to a significant increase in vascular permeability associated with diminished expression of the TJ protein occludin. Immunofluorescence studies revealed that hypoxia resulted in disrupted continuity of occludin and zonula occludens-1 (Zo-1) staining with significant gap formation. Hypoxia increased gelatinolytic activity specifically in vascular structures and gel zymography identified MMP-9 as enzymatic source. Treatment with an MMP inhibitor reduced vascular leakage and attenuated disorganization of TJ. Inhibition of vascular endothelial growth factor (VEGF) attenuated vascular leakage and MMP-9 activation induced by hypoxia. In conclusion, our data suggest that hypoxia-induced edema formation is mediated by MMP-9-dependent TJ rearrangement by a mechanism involving VEGF. Therefore, inhibition of MMP-9 might provide the basis for therapeutic strategies to treat brain edema.

[color=blue]
It's also on Pubmed but the url is just generic to the site for some reason.

I believe minocycline inhibits MMP9 as does salvia miltiorrhiza:



Zhong Xi Yi Jie He Xue Bao. 2009 Feb;7(2):145-50.

Salvianolic acid B in vitro inhibited matrix metalloproteinases-1, -2, and -9 activities.
Liang YH, Li P, Huang QF, Zhao JX, Liu X, Dai MK.

Department of Pathology, School of Preclinical Medicine, Beijing University of Chinese Medicine, Beijing 100029, China.

OBJECTIVE: Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases, which as a group can degrade essentially all extracellular matrix components. The proteolytic property of the MMPs is important during wound healing to remove debris and facilitate cell migration. Targeting towards the decreased MMPs activities is a new treatment strategy for healing chronic wounds. Salvia miltiorrhiza is a popular Chinese herb that could promote chronic ulcers healing for topical use. Salvianolic acid B (Sal B) is the most abundant bioactive component in Salvia miltiorrhiza. The research was designed to explore the inhibitory effects of Sal B on MMP-1, MMP-2 and MMP-9 activities. METHODS: Pure human interstitial collagenase (MMP-1) or gelatinase A (MMP-2) was activated by p-aminophenylmercuric acetate (APMA), and was incubated with Sal B for 1 h. The activities were observed by quenched fluorescent substrate. Gelatinase B (MMP-9) is rich in polymorphonuclear neutrophils (PMN), so the rat PMN was used as a source of MMP-9 for MMPs activity assays. In vitro MMP-9 from rats' PMN lysate was incubated with Sal B for 1 h, and its activity was tested by gelatin zymography. RESULTS: Sal B dose-dependently inhibited the human MMP-1 and MMP-2 activities in the range of 0.002 4 to 0.3 g/L, with 50% inhibiting concentration (IC(50)) of (0.090<0.015) g/L and (0.080<0.005) g/L respectively. In the range of 0.003 to 0.3 g/L, Sal B could inhibit the MMP-9 activity (P<0.01). CONCLUSION: The broad-spectrum inhibitory effects of Sal B on MMPs may reveal one of the mechanisms for the effects of Salvia miltiorrhiza on chronic wounds.

PMID: 19216858 [PubMed - in process]
[color=blue]

J Am Coll Cardiol. 2010 Mar 23;55(12):1240-9.

Effect of an antimicrobial agent on atherosclerotic plaques: assessment of metalloproteinase activity by molecular imaging.
Ohshima S, Fujimoto S, Petrov A, Nakagami H, Haider N, Zhou J, Tahara N, Osako MK, Fujimoto A, Zhu J, Murohara T, Edwards DS, Narula N, Wong ND, Chandrashekhar Y, Morishita R, Narula J.

University of California Irvine School of Medicine, Irvine, California, USA.

OBJECTIVES: Technetium-99m-labeled matrix metalloproteinase inhibitor (MPI) was used for the noninvasive assessment of matrix metalloproteinase (MMP) activity in atherosclerotic plaques after minocycline (MC) intervention. BACKGROUND: MMP activity in atherosclerosis contributes to plaque instability. Some antimicrobial agents may attenuate MMP activity. METHODS: Atherosclerotic lesions were produced in 38 rabbits with a high cholesterol diet for 4 months; 5 groups of rabbits, in the fourth month, received fluvastatin (FS) (n = 6), low-dose MC (n = 7), high-dose MC (n = 7), a combination of low-dose MC and FS (n = 6), or no intervention (n = 12); 8 unmanipulated rabbits were used as disease controls. Micro-single-photon emission computed tomography imaging was performed in all animals after intravenous MPI administration, followed by pathologic characterization of the aorta. A cell culture study evaluated the effect of MC on MMP production by activated human monocytes. RESULTS: MPI uptake was visualized best in untreated atherosclerotic animals (percent injected dose per gram MPI uptake, 0.11 +/- 0.04%). MPI uptake was reduced in the FS (0.06 +/- 0.01%; p < 0.0001), high-dose MC (0.05 +/- 0.01%; p < 0.0001), and MC-FS (0.05 +/- 0.005%; p < 0.0001) groups. Low-dose MC did not resolve MPI uptake significantly (0.08 +/- 0.02; p = 0.167). There was no incremental benefit of the combination of MC and FS. MPI uptake showed a significant correlation with plaque MMP-2, and MMP-9 activity. MMP-9 release from tumor necrosis factor-alpha-activated macrophages was abrogated by incubation with MC. CONCLUSIONS: Molecular imaging of MMP activity in atherosclerotic plaque allows for the study of the efficacy of therapeutic interventions. MC administration resulted in substantial reduction in plaque MMP activity and histologically verified plaque stabilization. MC was found to be equally effective as FS. Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

PMID: 20298932 [PubMed - in process]
[color=blue]
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
User avatar
gibbledygook
Family Elder
 
Posts: 1414
Joined: Mon Feb 14, 2005 4:00 pm
Location: London

Postby Vonna » Fri Apr 02, 2010 8:58 am

gibbledygook,
This was very technical information for my simple mind, but I did get the part about hypoxia breaking down the blood brain barrier. Very interesting!
User avatar
Vonna
Family Elder
 
Posts: 170
Joined: Mon Jan 04, 2010 4:00 pm

Postby Cece » Fri Apr 02, 2010 11:00 am

gibbledygook wrote:I believe minocycline inhibits MMP9 as does salvia miltiorrhiza:


Wow, that does tie together.
"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition
Cece
Family Elder
 
Posts: 9022
Joined: Mon Jan 04, 2010 4:00 pm

Re: CCSVI and Low Blood Oxygen

Postby Ruthless67 » Thu Jan 24, 2013 11:56 am

Here is an older piece of research into Minocycline as it relates to RA & scleroderma skin manifestations & atherosclerosis

http://www.roadback.org/index.cfm?fusea ... lay_id=113


In an interview, Dr. Trentham was asked his impression of the results of the study. "(The results) were highly, highly significant. . . we had hoped to see remissions, and we did see them. What surprised us was that we also saw a reversal of symptoms. We had not expected to see that."

"The evidence that minocycline is a safe and effective treatment for Rheumatoid arthritis
led us to believe it might also be helpful in related diseases such as scleroderma. This study shows that premise was correct."

Rheumatoid arthritis and scleroderma are not the only diseases found to respond to antibiotics. It seems that several diseases, ulcers and atherosclerosis among them, show indications of a possible microbial component.

The mechanism of action of antibiotics in RA and scleroderma will most likely not be determined until an organism is either proven or eliminated as a participant in the disease process.


Good article & food for thought.
User avatar
Ruthless67
Family Elder
 
Posts: 422
Joined: Tue Oct 27, 2009 4:00 pm
Location: Montana, USA

PreviousNext

Return to Chronic Cerebrospinal Venous Insufficiency (CCSVI)

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: Robnl


Contact us | Terms of Service