Welcome! This blog contains research, information on lifestyle, nutrition, dietary supplements and health for those with MS, as well as continuing information on the understanding of CCSVI and cerebral hypoperfusion. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the immune paradigm of MS, and continues the 15 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Tuesday, November 27, 2012

What's blood got to do with it?




Nov. 27, 2012  10:17 AM

NIH researchers find that fibrinogen appears to be "the trigger" which begins neurodegeneration in MS.

Researchers are honing in on fibrinogen as a mediator in vascular disease, and they are also finding a link in MS.

Fibrinogen is always present in the blood.  The normal range is 200 - 400 milligrams per deciliter (mg/dL).
Fibrinogen is a protein which is made in our livers.  It's the signaling protein for fibrin, which allows our blood to clot.  When people develop venous ulcers on their legs, due to chronic venous insufficiency, it's fibrinogen that leaks from the veins and creates a build up of fibrin, depleting the tissue of oxygen and allowing those hallmark ulcers to form.  This is called a "fibrin cuff."  It's fibrinogen which initiates the coagulation cascade and causes our blood to thicken, as a response to low oxygen levels.

Dr. Zamboni was the first to suggest that MS lesions looked a lot like venous ulcers because of the fibrin cuffs found in both sites of injury.  

And researchers have noted that fibin deposition comes FIRST, before demyelination.


Here is some recent research on this connection:

Compromised vasculature in the nervous tissue is a pathogenic manifestation apparent in traumatic injuries, such as spinal cord, optic nerve, and sciatic nerve injury, as well as in central nervous system (CNS) diseases with autoimmune characteristics, such as multiple sclerosis (MS) (7). 

Blood-brain barrier (BBB) disruption precedes clinical symptoms in MS patients (8), and fibrin is deposited in the lesions (9, 10), apparently before cerebral tissue injury and demyelination (11). Fibrin deposition also coincides with areas of demyelination (12), as well as with areas of axonal damage.

Sunday, November 25, 2012

Normal Pressure Hydrocephalus---the once "controversial" discovery of Dr. Salomon Hakim


November 25, 2012 at 1:59pm

Those of us interested in moving CCSVI diagnosis and treatment forward can always learn from history.

In the 1960s, a neurosurgeon in Bogota, Columbia made the controversial claim that he could reverse neurodegeneration by surgically diverting an excess of cerebrospinal fluid (CSF) by placing a shunt in his patients.

Professor Salomon Hakim first published his thesis in 1964 and then published 6 case reports of "normal pressure hydrocephalus" in The New England Journal of Medicine and the Journal of the Neurological Sciences in 1965. Hakim rose to the forefront of academic medicine as he described a newfound ability to reverse symptoms of “neurodegeneration” that had long been considered irreversible.

It is important to understand that today, 60 years after Hakim's discovery, treating normal pressure hydrocephalus is an accepted practice, even though diagnosing NPH is an inexact science.  There were never any double blinded clinical trials for this surgery.  Hakim claimed he could reverse gait impairment, cognitive problems and urinary incontinence by diverting CSF flow.  And the proof was in his patients' recovery.  No one cries "placebo effect!" after a patient recovers mobility, cognition or bladder control once treated for NPH.

Here is a first hand account of the changes in brain function and recovery, written by a woman treated for NPH.  Her story was published in the New York Times.

I first learned about NPH from Dr. Elliot Frohman in Bologna, Italy--at the first CCSVI conference in September 2009.  It was Dr. Frohman, an MS specialist and neurologist, who commented that CCSVI treatment reminded him of the success he had seen after treating his patients for NPH. Here is what Dr. Frohman said about venoplasty for CCSVI.  I wrote it down in my notes, because his comment literally stunned me.

 I have seen this happen in “normal pressure hydrocephalus- (NPH) Where there is a loss of gait, cognitive and bladder issues and the lesions disappear because the expanded ventricle swallows the lesion. I have shunted the brains of NPH patients, and they showed remarkable improvements. Again, the enlargement of the third ventricle precedes the changes.


So, what's NPH?  And what might it have to do with CCSVI?

The brain and spinal cord are surrounded by a clear fluid called cerebrospinal fluid (CSF). This fluid is produced and stored in cavities in the brain called ventricles. It circulates around the brain, moving from ventricle to ventricle. The purposes of the fluid are to cushion and protect the brain and spinal cord, to supply them with nutrients, and to remove some of their waste products. Any excess fluid drains away from the brain and is absorbed by other tissues.

Hydrocephalus (literally water on the brain) is a condition in which there is too much CSF in the ventricles. This occurs when the natural system for draining and absorbing extra CSF does not work right. The ventricles enlarge to accommodate the extra fluid and then press on different parts of the brain, causing a number of different symptoms. Hydrocephalus has many different causes. Some people are born with the condition, while others develop it during their lives.

Normal pressure hydrocephalus (NPH) is a type of hydrocephalus that occurs in adults, usually older adults. NPH is different than other types of hydrocephalus in that it develops slowly over time. The drainage of CSF is blocked gradually, and the excess fluid builds up slowly. The slow enlargement of the ventricles means that the fluid pressure in the brain may not be as high as in other types of hydrocephalus. However, the enlarged ventricles still press on the brain and can cause symptoms. (The term "normal pressure" is somewhat misleading.)

And cerebrospinal fluid is affected by venous return.  Open jugular veins are essential for CSF clearance.  link

The less blood flowing through the brain back to the heart, the more CSF can build up and reabsorption is hindered.  For those who want to learn more about this connection, I highly suggest reading Dr. Michael Flanagan's book and blog, The Downside of Upright Posture.

Venoplasty for CCSVI changes cerebrospinal fluid flow rates.  

The reseachers at BNAC noted that even 12 months after venoplasty, the patients treated for CCSVI had a faster rate of CSF flow going through their brains.  


My husband had a profound relief of fatigue, cognitive fog, heat intolerance, spasms and sleep apnea after being treated for CCSVI in May 2009. These improvements still continue, now 3 and a half years later.  His third ventricle is now normal on MRI, he has no gray matter atrophy.  

Dr. Frohman and his neurological community would have you believe that Jeff's benefits from CCSVI venoplasty are placebo, while the patients they have treated for NPH benefits are real.  Why this cognitive dissonance?  

Only more research, publications like the BNAC paper on cerebrospinal fluid changes after venoplasty, and more pressure from patients and caregivers will provide answers.

Joan




Sunday, November 18, 2012


 Seasonal Affective Disorder (SAD) and MS

November 18, 2012 at 9:54am

The days are shorter.  Sunlight is hard to find.  We bundle up against the cold.  We also put on the extra winter pounds, sleep more and move less.  For those who live in the northern latitudes, the shorter days of winter are a reality.  And this can affect our mood and general health.  As we exercise less, our blood flow slows down. We feel more fatigued, more hopeless. The risk of cardiovascular disease increases.

There is a syndrome doctors know about---called "seasonal affective disorder"  or SAD.  It is very prevelant in northern latitudes.  Most of the association is with mood, or levels of depression.  But it is also linked to cardiovascular disease.

What connection does this have with MS?  
MS is a disease linked to northern latitudes, lack of vitamin D and lack of ultraviolet rays.  And with the link to CCSVI, we are learning more about the vascular risk.

For 68 years latitude has been identified as an important risk factor in the occurrence of multiple sclerosis (MS), but not satisfactory explanation has been offered for this relationship. Epidemiological studies of MS, however, have failed to take into account the degree of change in the amount of ambient light over the course of the year, a variable which is closely related to photoperiod and latitude. Seasonal affective disorder (SAD), another illness for which latitude is a risk factor, appears to be related to the decrease in ambient light during the winter months, and offers some relevant insights into the geographical distribution of risk for developing MS. 

 There is a very strong correlation between UV rays, photorelaxation and cardiovascular disease.
Here's a small sampling on this research.

Dr. Furchgott and the Discovery of Photorelaxation
I've been reading up on the effect of UV rays on the body, and I came back to  the research of Nobel prize winning researcher, Dr. Robert F. Furchgott.  He passed away in 2009, and his university keeps his web page online.  Dr. Furchgott was a professor at SUNY Downstate in Brooklyn, NY---the same place where Dr. Sal Sclafani recently retired and where the first CCSVI conference was held in the US!   Here's Dr. Furchgott's page--

Dr. Furchgott discovered the process of photorelaxation over 40 years ago.  What he noted in the lab was that exposure to UV rays changed the endothelium, encouraging nitric oxide production and vasodilation of arteries.   

Tuesday, November 13, 2012


Nicoletta Mantovani-- A Woman Reborn

November 13, 2012 at 8:47am

Today, there are over 50 publications reporting on this story, which is important news in Italy.  I've translated one more link, from Ferrara, where Dr. Zamboni's trial is beginning.  Please note that the reporter states that Dr. Zamboni is going up against powerful opponents--namely the pharmaceutical industry and neurologists in their employ.   Miss Mantovani and Dr. Zamboni and all of us around the world are requesting clinical trials for his procedure. Independent research, without corporate interest.  Joan



Zamboni Method, Nicoletta Mantovani is reborn from multiple sclerosis

The weekly People Pavarotti's widow says her relief from this illness is thanks to the care created by the Professor from Ferrara. But his clinical trial Brave Dreams, operating for just a short time, is already receiving criticism from some medical journals
by Marco Zavagli | Ferrara | 13 November 2012

A woman reborn. Reborn from the disease, multiple sclerosis. Thanks to the care of Dr. Zamboni.  She has always believed and experimented in care for MS, with which she has struggled for years.

She is the honorary president of CCSVI in MS society, a non-profit organization and she is also sick. A president who has been known to be such. Nicoletta Mantovani, the widow of Luciano Pavarotti has been able to get in line and wait her turn. She did not "run away" abroad, as they must do in Canada, where the angioplasty intervention for obstructed neck veins is now on the agenda. She was patient like everyone else. Without utilizing the benefits that the money and fame could provide.

And today, as she confided in an interview published in People, she is "a woman reborn."