Jugular Veins are Important

Recently published in the Journal of Mutiple Sclerosis, a review paper co-authored by Dr. Paolo Zamboni and Dr. Massimo Pedriali on the "Pathology of the Internal Jugular Vein in Multiple Sclerosis".   The complete paper is available on line for free---and I'd recommend it to all.  It is a very thorough review.

http://www.omicsgroup.org/journals/the-pathology-of-the-internal-jugular-vein-wall-in-multiple-sclerosis-2376-0389-1000160.php?aid=63610

As this review outlines, there are observable and documented differences between the jugular veins of healthy controls, when compared to people with Multiple Sclerosis.  These pathological differences involve the endothelial cells which comprise the veins' lining.  Endothelial cell aptosis (death) and derangement, as seen in MS, changes the ability of the jugular veins to drain.  Valvular and intraluminal abnormalities in the jugular veins of people with MS have hemodynamic implications.  There is a shift in collagen in the jugular veins of people with MS which affects venous compliance.

Veins have received little attention and research, when compared to the study and understanding of arteries.  Certainly, in terms of brain health, the carotid arteries are scanned and studied, and neurology and stroke researchers know that blockages, clots, and impairment in flow can be disastrous to the brain.  There are treatment modalities developed to deal with carotid artery issues---from medications to open surgery, to interventional proceedures.  No one questions the importance of healthy blood flow to the brain.

But the venous system and the removal of fluids from the brain is even more important than previously imagined.

During the past two years, international researchers have described a newly discovered lymphatic drainage system, which has actual draining vessels, and relies on the brain's draining veins.  These vessels take lymph fluid, carrying metabolites, proteins and toxins, out of the brain.  This process is aided by sleep.  This science is brand new.   It has reversed what we once believed was the brain's "immune privilege."
http://ccsviinms.blogspot.com/2015/06/rewrite-textbooks.html

This "stunning discovery" of a lymphatic drainage system relies on the jugular veins.

"Instead of asking, 'How do we study the immune response of the brain?' 'Why do multiple sclerosis patients have the immune attacks?' now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels," said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA's Center for Brain Immunology and Glia (BIG). 
http://ccsviinms.blogspot.com/2015/06/a-stunning-discovery.html

The brain is like every other organ in our body---it needs drainage.  Jugular veins are responsible for the exit of blood, cerebrospinal fluid (CSF) and lymph.  Any delays can cause changes to the brain's immune functioning, oxygenation, glucose metabolism and health.  Delays cause neuronal death and inflammation.  Or, what we see in multiple sclerosis.

Dr. Jonathan Kipnis, the discoverer of these lymphatic vessels, will be the keynote speaker at the International Society for Neurovascular Disease.  He will be presenting his research and proposals for studies in MS, alongside Dr. Zamboni and the other members of the ISNVD.

Here's the program.   “How the Extracranial Venous System Influences Neurological Diseases.”

http://isnvd.org/sites/default/files/ISNVD-2016%20meeting%20outline%20program%20guide%209-21-2015.pdf


This is not going away.
jugular veins are important,

Joan



Notice the difference between the top panel---healthy endothelial cells lining the jugular veins in normal controls, compared to the endothelial cells of a person with MS (bottom)

Figure 5: Scanning electronic microscopy. Top panel: regular disposition of the endothelial cells in IJVs of healthy controls, respectively at 800x (right) and 1500x (left). Bottom panel: irregular arrangement of the endothelial cells in the IJV of a MS patient, respectively at 800x (left) and 1500x (right). The cells appear lifted with craters.

2015 ISNVD Conference Abstracts---research breakdown

The International Society for Neurovascular Disease (ISNVD) will be convening for the 5th Annual Conference in Naples, Italy at the end of March.  Abstracts for the presentations have been made available online here:
http://isnvd.org/d/sites/default/files/Invited%20Speaker%20abstracts%20-%20all.pdf

There are many more new presenters and international researchers attending this conference.  The ISNVD continues to grow in its membership and influence.

While neuroimmunologists stubbornly insist that there is no connection between diseases of neurodegeneration and circulation, this illustrious group of international researchers is showing that we are only at the beginning of understanding the impact of blood flow on brain health.

Here is my layperson's breakdown of the research abstracts and presentations.


2D and 3D analysis of vessels in the retina and the brain
Prof. Bart ter Haar Romeny, Ph.D.1,2
1Eindhoven University of Technology, Eindhoven, the Netherlands 2Northeastern University, Shenyang, China
This research is using the imaging of blood vessels in the eye's retina to get a picture of how blood is circulating throught the central nervous system. The blood vessels in the retina give an early picture of how brain diseases and breakdown of the blood brain barrier might be developing. Scanning the eye is easier and more cost-effective, as well.

Venous dysfunction and neurodegenerative diseases
Chih-Ping Chung MD PhD
Taipei Veterans General Hospital, National Yang Ming University, Taipei, Taiwan
Dr. Chung and his group have been studying the venous vasculature in relationship to brain disorders for over a decade. He has spoken at a few of the ISNVD conferences now. His new research focuses on how venous abnormalities are linked to white matter changes and how venous drainage impairment leads to dysfunction in Alzheimer's Disease.

Blood storage within the intracranial space and its impact on cerebrospinal fluid dynamics

Clive B Beggs 1, Simon J Shepherd 1, Pietro Cecconi 2 and Maria Marcella Lagana 2Medical Biophysics Laboratory, University of Bradford, Bradford, BD7 1DP, UK  Fondazione Don Carlo Gnocchi ONLUS, IRCCS S. Maria Nascente. Milan, Italy 
This study measured blood flow throughout the cardiac cycle by using MRI to visualize the flow in the necks of 14 healthy adults.  This study found that it is cerebrospinal fluid (CSF) which controls the volume changes inside the brain.  CSF interacts with the cortical veins to facilitate how much blood is stored.  This is an important finding, because any disturbance in venous outflow of blood and CSF will change the blood storage inside the skull, potentially leading to reduced cerebral circulation.

Advances in Treatment Strategies of Extracranial Venous Disease
Hector Ferral, MD
Senior Clinical Educator NorthShore University Health System
Dr. Ferral has been treating people with CCSVI for a few years now. He has also been an attendee and presenter at the ISNVD before. His new presentation will be looking at the technical advances being made in vein measurement and treatment of CCSVI.

Imaging of Brain Microvascular Disorders: lessons from the CADASIL model.

Hugues Chabriat, MD PhD;Department of Neurology, GH Lariboisiere, APHP, INSERM UMRS1161, University Paris 7 Denis Diderot, Paris France.
This research uses imaging to look at how the small vessel disease related to stroke and dementia develops and progresses.

Endothelin- 1 as a potential target for chronic brain hypoperfusion
Jacques De Keyser, MD, PhD, Free University of Brussels (VUB), Department of Neurology, Brussels, Belgium
This study is near and dear to my heart, as it is looking at how ET-1, a marker of endothelial dysfunction, is related to slowed blood flow in the brain, called hypoperfusion. People with MS have much higher levels of ET 1 in their blood than normals, and much slower cerebral blood flow. We also see this marker elevated in a number of neurodegenerative diseases, like Alzheimer's. In this study, the researchers used bosentan, a blood pressure medication, to treat ET 1 levels. This treatment increased cerebral blood flow in pwMS, and lowered ET-1 levels. (But bosentan has side effects, and is not easy on the liver. Much better, in my opinion, to lower ET-1 levels by addressing endothelial dysfunction, through diet, exercise, and lifestyle.)

TBI and hemodynamic changes in the brain
James R. Stone, MD, PhD
This presentation is looking at how traumatic brain injury induces ischemia, or a low-oxygen state, in the brain. TBI also changes cerebral blood flow and can cause a break in the blood brain barrier, igniting the immune system. New research is showing how explosive devices can cause TBI, even without direct physical contact.

Ultrasound contrast imaging of brain hemodynamic and perfusion Marcello Mancini, M.D.
Institute of Biostructure and Bioimage – CNR
Naples, Italy

This presentation will be looking at how new MRI and ultrasound technologies are allowing researchers to view cerebral circulation in MS.  People with MS show signs of hypoxia (low oxygen) injury and thrombosis (small clots) in the small veins of the brain. New technologies are allowing us to see that cerebral transit time is slowed in MS. 

Imaging of the Microvasculature
E. Mark Haacke, PhD 
Dr. Haacke, a presenter at all of the ISNVD conferences, returns this year to discuss how his invention of susceptibility weighted imaging (SWI) and MRA can be used to study the neurovascular system, and clarify the relationship between the venous sytem and CSF.


Update in computational fluid modelling of the brain
Mauro Ursino
This presentation is using mathmatical and computer models to simulate the complex mechanisms affecting cerbral circulation. Using these models shows how postural changes and stenosis in extra cranial arteries and veins can change upstream intercranial circulation.

Clinical Applications of Venous Treatment
Dr. Michael Dake, Stanford University

Dr. Dake, last year's ISNVD president and a founding member, will be presenting on the contributions of 2014 studies which have enhanced understanding of how endovascular and open surgical treatment of venous abnormalities has affected patients with MS, Alzheimer's disease, Parkinson's, POTS and other pathologies.

The Heart Brain Connection
MJ Daemen
Dr. Daemen is the keynote guest speaker. He is a neurocardiologist, a member of a new field of experts who are bringing together an understanding of how the heart and brain affect each other. As a member of the Dutch Heart Foundation, his group is looking at how cardiovascular disease is influencing cognitive function and cerebral circulation.

A NOVEL SONOGRAPHIC METHOD FOR REPRODUCIBLE JUGULAR VEIN PULSE WAVE ASSESSMENT
Paolo Zamboni, Francesco Sisini, Erica Menegatti, Giacomo Gadda, Mirko Tessari, Mauro Gambaccini
Vascular Diseases Center, University of Ferrara, Ferrara, Italy 

Dr. Zamboni's group is using ultrasound in the B mode (brightness mode) to measure the pulse wave in the jugular vein.  The way that the wave form looks is currently used to monitor for heart disease, however Dr. Zamboni's group is using this technique to find CCSVI.

Is there a role for mast cells dependent synthesis of Endothelin-1 in neurodegenerative diseases?
Pedro D’Orléans-Juste-1, Louisane Desbiens, Denis Gris-2
Departments of Pharmacoly-1 and of Pediatrics-2, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, PQ, Canada

We know that levels of ET-1 (a marker of endothelial dysfunction) and mast cells (tissue cells of the immune system) occur in higher levels in people with MS.  This study uses the mouse model of EAE as well as a human isoform to study how mast cells found in the vicinity of spinal lesions are involved in the synthesis of ET-1.

Venous abnormalities in Meniere's Disease

P.M.Bavera; P. Cecconi; D. Alpini; F. Di Berardino 

This presentation will be using slides to show the correlation and differences between Meniere's Disease and MS, in regards to CCSVI imaging.  There are specific characteristics to the venous abnormalities seen in Meniere's.

Advances in Idiopathic Intracranial Hypertension Pathogensis: a Focus on Sinus Venous Stenosis
Roberto De Simone, Angelo Ranieri
Headache Centre  Dpt. of Neurosciences, Reproductive Sciences and Odontostomatology University of Naples “Federico II”

This research is focusing on how stenosis of the venous sinus is related to idiopathic intracranial hypertension (IIH)  There is a feedback loop which appears to occur in this situation.  The venous sinus collapses, cerebrospinal fluid pressure builds, which creates more compression.  Endovascular stenting of the venous sinus is a currently approved treatment to end this cycle of stenosis and hypertension.

In Endothelial function, the glymphatic system and New Drug Development
Endothelial dysfunction in neurodegenerative disease
J. Winny Yun, Emily Stevenson, Seiichi Omura, Fumitaka Sato, Ikuo Tsunoda, Alireza Minagar, Felix Becker, Trevor Castor, Adam Xiao, J. Steven Alexander, LSUHSC-Shreveport Molecular and Cellular Physiology, Microbiology, Virology, Neurology, Shreveport, Louisiana, USA.
Dr. Steven Alexander from LSU returns to the ISNVD to again discuss the endothelium in neurovascular disease. There is a vascular association of specific biomarkers found in MS. This new research is looking for a means to regulate these neurolymphatic markers, to help those with neurovascular diseases.

Fluid Dynamic Influences on Cerebrovascular Endothelial Activation Responses
Dr. Alexander and the LSU team look at how blood flow over endothelial cells affect their health. Laminar shear stress (regular blood flow) over endothelial cells is essential to their function. Disrupted flow causes endothelial cells dysfunction and death. Shear stress alterations could lead to a break down of the endothelial layer in the brain, and create a disturbance in the blood brain barrier and inflammation.

Cardiovascular risk factors and neurodegenerative disorders
Dr. Robert Zivadinov
Buffalo Neuroimaging Analysis Center, Department of Neurology, University at Buffalo, State

This research finds an association with cardiovascular risk factors (smoking, obesity, inactivity, high blood pressure) and MS.  MS patients who had one or more CV risk factors had higher lesions loads and more brain atrophy.

Avanti!

Joan

New blinded study finds CCSVI associated with MS, and NOT found in normals

While CCSVI studies lead by neurologists claim they can't seem to find CCSVI, or conversely, they find it in everyone---

Here are the details of a recent blinded study lead by vascular specialists utilizing correct diagnostic protocols.  It was undertaken at Sapienza Hospital in Rome and lead by Dr. Luciana Tromba.   It's all about specificity and sensitivity of the study, which is reflected in their method and p values.  I'll explain below the abstract.
http://phl.sagepub.com/content/30/1/52.short


We enrolled 112 patients with multiple sclerosis and 67 healthy subjects from 20 to 67 years of age. All the patients underwent Duplex and color-Doppler sonography of the neck vessels, transcranial colour duplex sonography, M-mode study of the valve system and of venous abnormalities. Subjects were positive for chronic cerebrospinal venous insufficiency when at least two of five hemodynamic criteria of the Zamboni protocol were fulfilled

No healthy subjects were positive for chronic cerebrospinal venous insufficiency, while in the sample of patients affected by multiple sclerosis the diagnosis was made in 59.8% of cases (p < 0.0001). 

I want to point out that very, very small p value number, that number which is smaller than .0001 means these scientists are very sure about their results.  In statistics, the p value is the number which reflects the testing of a hypothesis. The smaller the p value, the larger the significance of results.

What this means is that the study found a significant difference between normals and people with MS, and this is backed up scientifically.  It is not random, or chance.  This was a highly specific, highly detailed study.


The first criterion was the most frequent in patients affected by multiple sclerosis and chronic cerebrospinal venous insufficiency (respectively 54.4% and 76.1%, p < 0.001). The second, third and fourth criteria were never present in healthy subjects but were detected in patients with multiple sclerosis. The positivity of the second criterion was associated with diagnosis of chronic cerebrospinal venous insufficiency in 100% of cases. The third criterion had a prevalence of 52.2% in the subgroup of chronic cerebrospinal venous insufficiency patients. It was positive in 36 multiple sclerosis patients and was associated with chronic cerebrospinal venous insufficiency diagnosis in all cases except one.

This highly detailed study looked at all the CCSVI diagnostic criteria in those with MS and normals and saw very dramatic results.  This leads them to the conclusion---

Chronic cerebrospinal venous insufficiency is a haemodynamic condition strongly associated with multiple sclerosis and is not found in normal controls. The addition of M-mode ultrasound to the diagnostic protocol allows improved observation of venous valve abnormalities.

Again, this study was blinded, followed the correct Zamboni protocol, looked at blood flow (or hemodynamics) using M mode ultrasound.  M mode stands for "motion", and this ultrasound shows problems with delayed blood flow caused by issues inside the veins, like webs or problems with valves.

And the researchers found CCSVI in pwMS, and not in normals.

Dr. Zamboni has always stated that CCSVI is about blood flow, not just how veins look, or measuring stenosis.   As he has said numerous times, "CCSVI is about flow, not architecture."

When scientists work with him, utilize his protocol, they find CCSVI in MS.  That's what scientific replication is about.  It is not about agendas, conflicts of interest, or p values that show no specificity.  It is not about ignoring his protocol, casting aspertions, or creating new measurements for stenosis never before seen in vascular journals, like the Traboulsee study at UBC, which I believe was scientific misconduct.
http://ccsviinms.blogspot.com/2014/12/scientific-misconduct.html

This exploration of CCSVI is far from over, despite the "death knell" editorials by neurologists.   Thanks to the vascular researchers willing to do the hard work.

Joan

What has Changed?

In the five years since Dr. Zamboni's first publication on the connection of MS to extracranial hemodynamics, there have been many changes in mainstream MS treatment and new discoveries made by researchers around the world.

The relationship of the vascular system in MS is being explored, and dealt with in a sideways manner by neurologists.  I do not expect we will ever hear that CCSVI is valid science from neurologists--they will attempt to rename it, requantify slowed venous return and hypoperfusion, and make it their own.  They will call Dr. Zamboni's discovery of CCSVI junk science- while they are working on patenting drugs to address blood flow in pwMS.  This is because neurologists work with pharma and write prescriptions.  They do not deal with the mechanistics of the brain's circulation or with the venous malformations Dr. Zamboni has discovered.  They are not phlebologists or vascular surgeons. For MS specialists, this discovery of hemodynamic alterations goes beyond their practical expertise.

However, one neurologist recently published a paper on the vascular connection to MS, and said this:

"...vascular contributions in MS do appear to support the notion of the vasculature being an initiating target in MS etiology and not simply a bystander presentation of other disease processes. Perhaps the strongest support for this is the number of MS therapies that have been developed, which target leukocyte binding to activated endothelial cells, a central component of the blood-brain barrier (BBB)."
http://www.biomedcentral.com/1741-7015/11/219

Here are drugs being developed by neurologists to address blood flow:
http://ccsviinms.blogspot.com/2013/08/medications-for-ms-addressing-blood.html

What have we learned since Dr. Zamboni first began publishing his research on CCSVI?  

1. People with MS (pwMS) have slower cerebral hemodynamics than normal people.  Their blood flow exits the brain at a slower rate. There are hemodynamic differences between normal people and those with MS. Hypoperfusion is real, it opens the blood brain barrier and it damages the brain.  Whether it is a cause or effect of MS will be debated for decades, however vascular researchers have shown better perfusion and cerebral blood flow (CBF) and cerebral spinal fluid (CSF) flow after venoplasty for CCSVI.

http://www.hindawi.com/journals/msi/2013/598093

http://www.ncbi.nlm.nih.gov/pubmed/23523158

2. People with MS do better with exposure to UV rays, which may explain the long-established link of MS rates and northern latitudes. UV ray exposure relieves symptoms in many.  This may be due to increased vitamin D levels, but it might also be due to the way in which UV rays release nitric oxide, change the endothelium and increase blood flow. 

http://ccsviinms.blogspot.com/2013/06/photorelaxation-uv-rays-and-ccsvi-june.html

3. People with MS are being advised to consider their nutrition and to eat more fruits, vegetables and whole foods and less saturated fats and processed foods.   When Dr. Swank suggested this 60 years ago, it was called "junk science" and people with MS were told it wouldn't do them an ounce of good.  It is now given as helpful advice by the NMSS and the AAN.   

Same thing with exercise.  Only a few years ago, pwMS were advised not exert themselves, but to rest and conserve their energy.  Now we know that physical exercise and activity delays progression, and reverses gray matter atrophy.  Same thing with smoking cessation, stress reduction, and better sleep.  All of these cardiovascular lifestyle changes can make a difference.

http://www.nationalmssociety.org/living-with-multiple-sclerosis/healthy-living/index.aspx

4. Oxidative stress and inflammation are recognized as driving forces in MS progression.  This has lead to exploratons of new modalities of treatment, like the Nrf2 pathway. 

http://ccsviinms.blogspot.com/2012/09/oxidative-stress-multiple-sclerosis-and.html

5. Gray matter health has been recognized as a more accurate biomarker of MS progression than white matter lesions.  Gray matter atrophy will become the new target for MS therapies.

http://ccsviinms.blogspot.com/2012/01/iron-and-gray-matter-what-do-we-know.html

6. PwMS have much higher levels of the clotting proteins- fibrin and endothelin-1 in their serum than normals. These are markers of endothelial dysfunction.

http://ccsviinms.blogspot.com/2012/11/whats-blood-got-to-do-with-it-nov.html

7. Upright MRI has allowed us to see how cerebrospinal fluid and blood return to the heart is slowed and impeded in pwMS.

http://www.fonar.com/news/100511.htm

8.  The venous endothelium is being studied, and researchers are noting that there are changes happening to the lining of the veins in people with neurodegenerative disease.

http://www.biomedcentral.com/1741-7015/11/219

9.  CCSVI is being explored around the globe.  There are literally hundreds of papers published in vascular and neurological journals.  New papers come to press every day.  The connection of blood flow and diseases of neurodegeneration continues, as doctors admit that lifestyle interventions and prevention are staving off Alzheimer's and dementia, while none of the drugs have helped one bit.

http://www.ccsvi.org/index.php/component/search/index.php?option=com_search&task=search

10.  The ISNVD has been established.  There is now an international society of researchers working on understanding the venous connection to neurovascular disease.  Their fourth conference will be held in San Francisco in February, 2014.  The International Society for Neurovascular Disease is convening, publishing, and moving this research forward.
http://isnvdconference.org

All of these connections between MS and the cardiovascular system are new.  And this has happened in just the past five years.  

For those waiting for venoplasty to be accepted as an MS treatment, we have to step back and view the other changes that have happened in MS care.  

The American Academy of Neurologists has several papers featured on their page which connect slowed blood flow and neurodegenerative disease.  They have a patient outreach branch--The American Brain Foundation-- and they have a yearly Brain Fair to discuss diet and lifestyle changes people with neurodegenerative diseases, including MS, should consider.  So much for Dr. Swank's junk science.

Here's a wonderful video Christopher Alkenbrack found on Dr. Roy Swank's work.  It was made in 1989 as part of a Canadian news investigation into the success of Dr. Swank's diet in pwMS as compared to a vastly more expensive and failed chemotherapy trial.  If you haven't seen it, it's a must watch.  

Because today, 25 years later, the NMSS is making these very same dietary and lifestyle recommendations to pwMS.  Yet when asked about dietary changes for pwMS, the neurologist in this video from 1989 says there is "little to no benefit."

https://www.youtube.com/watch?feature=player_embedded&v=lEnn_AZT-SU 

When reporters, scientists, neurologists, MS specialists and others say, "Oh, the connection of CCSVI to MS, that's junk science."  We've investigated it, and there's nothing there"---remind them about Dr. Roy Swank.  Remind them how long it took his observations of "capillary fragility", slowed blood flow, increased fibrin and hypercoagulation to be accepted as part of MS.    

He was noting endothelial dysfunction decades before scientists knew about nitric oxide and how environmental factors contributed to blood flow.  And he has never once been credited by mainstream neurology.  You won't see his name or read his research in their journals.  But he was right.

Dr. Zamboni's discovery has revolutionized how we look at cerebral blood flow, by studying the under-researched extracranial venous system, and utilizing doppler ultrasound to understand venous malformations which alter cerebral hemodynamics.  Like Dr. Swank, Dr. T.J.Putnam and others, he is decades ahead of his time.  His discovery of CCSVI may very well be the rest of the equation in understanding the slowed venous return and endothelial dysfunction found in pwMS.   To say that it is junk science, and that there is no connection of venous return in MS, is to negate scientific fact.  

Joan

Bologna---18 months later

March 12, 2011 at 10:18am

To those who are new to the page, or those who may not have read the notes from the first Bologna  CCSVI conference when they were posted in September 2009, I'm linking them here:

http://ccsviinms.blogspot.com/2009/09/notes-from-ccsvi-conference-bologna.html

This coming week many of the same doctors are reconvening in Bologna to discuss ongoing studies of CCSVI.  When I was invited to the first conference in 2009, Dr. Zamboni asked me if I could help out by inviting some press from the US to cover the meeting.  I called all of my press contacts, as well as several medical writers. None were available.  One medical writer yelled at me for calling and bothering her.  She  told me "no one is interested in this."  Her big medical story the week I called was Steven Tyler falling off stage and breaking his arm.  I told her she was wrong, people were interested.  

Things are different in 2011.  People with MS, their caregivers, doctors and activists around the world have focused a light on the proceedings in Bologna.  It turns out that people are interested in CCSVI.  Very interested.  

As the doctors reconvene and discuss all that they have learned in 18 months, as new doctors step up to the podium and bring innovative perception to the research, I'll be at home with my family.  I don't need to fly by myself to cover the meeting and post it online, because there will be many more witnesses.  There will be international press and a host of participants transcribing the presentations.  And that makes me very, very happy.

Thanks to Dr. Zamboni for continuing the research, in the face of some very powerful opposition.  Thanks to all of the doctors who have taken up this cause.  Thanks to all of you for researching, reading and sharing this information.  Thanks to those who have reached for the baton and are running forward, so I can go to a concert, make dinner, go to church, walk the dog and enjoy my weekend with my husband and son in sunny California.  And to all those in Italy, make sure to step outside during breaks, walk the lovely ancient streets and have a gelato!

Here is the link to the International Society of Neurovascular Disease site and information about the conference next week:

www.isnvd.org

Stay tuned.  As reports come in from the meetings, we'll be posting them all over the internet.  And who knows?  Maybe that medical writer will discover that people really do care about Multiple Sclerosis and the vascular connection.

Joan

Dr. Zamboni and Dr. Zivadinov's hypoperfusion study

March 7, 2011 at 1:59pm

This research was presented in April 2010 at the American Academy of Neurology conference as a poster, but we have the full paper available to us online.   Those who have read the notes on this page know that this has been an area of research near to my heart.  Hypoperfusion simply means slowed blood flow through the brain.

Here is a link to the complete paper in pdf form:

http://www.biomedcentral.com/content/pdf/1741-7015-9-22.pdf

To the best of our knowledge, this pilot study is the first to report a significant relationship between the presence and severity of CCSVI and hypoperfusion in the brain parenchyma. These preliminary findings should be confirmed in a larger cohort of MS patients to ensure that they generalize to the MS population as a whole. Reduced perfusion could contribute to the known mechanisms of virtual hypoxia in degenerated axons.

 An altered CBF (cerebral blood flow) pattern may be a consequence not only of local circulatory disturbances due to inflammatory mechanisms in acute or chronic phases, but instead could result from an outflow blockage situated far away from the lesions. CCSVI is a vascular condition described in MS patients that is characterized by stenoses caused by intraluminal defects such as web, septum, malformed valve or, rarely, by segmental hypoplasia/agenesis [1,2]. Stenosing lesions of CCSVI have been classified among the truncular venous malformation in a consensus document [18,19].

Therefore, CCSVI may impact local hemodynamics and overload microcirculation at places distant fromthe location of the mechanical stenosis, as in any condition of venous obstruction of the major trunks.

Such a mechanism may lead to capillary hypertension and leakage, consistently contributing to inflammation

[20]. In this pilot study, we have shown a strong relationship between the severity of CCSVI and hypoperfusion in the WM, GM and SGM.

Please note:

All 16 pwMS had CCSVI, none of the healthy controls had CCSVI.  All pwMS had slowed cerebral blood flow, or hypoperfusion, which affected the white matter and gray matter of their brains.

100% pwMS had hypoperfusion, which was related to the severity of CCSVI.