Iron in the Brain or the Immune System

September 17, 2009 at 9:36am

Many disease modifying treatments use the reduction of immune activated lesions as shown on MRI as proof a treatment is "working" in MS. This has baffled me, since we know that the number of lesions does not correlate to level of disease progression. Someone like my husband can have 20 brain lesions and function quite well. Someone else can have one or two lesions and be wheelchair-bound. Also, at a certain point, lesion progression stops when MS turns progressive. There must be another mechanism of injury, along with the immune system, at work in the MS brain.

In Bologna, Dr. Mark Haacke addressed another means of measuring brain tissue injury in MS. Susceptibility Weighted MRI. What SWI MRI shows us, is that iron deposited in the brain is a bio marker for MS progression.

What is different in SWI-MRI, according to Dr. Haacke, is that brain damage shown due to iron deposition actually CORRESPONDS to disability in MS.

The more iron deposed in the brain, the more disability, the more progressive MS is. This is different than the usual measuring of hyperintense lesions on MRI, which have no specific correlation to disease severity.

Here's the rub:
Pharma companies use the lesions shown on MRI as "proof" that their particular drug is working. Look! We've reduced hyperintensities on MRI! Our amaze-a-bub is slowing MS! Stock prices go up, investors are happy, and MS patients continue to decline.

If we look at the TRUE cause of disability- the only measurement in the brain that correlates to disability is iron deposition and brain atrophy.

This is why my husband had 20 lesions at his diagnosis and could mountain bike, and someone with one lesion is in a wheelchair. It's not just about the white matter lesions.

If we understand that the macrophages and immune system are activated as janitors to clean up the cellular death in the brain, we understand that the lesions we see on standard MRI may be secondary--just as they are a stroke patient, or someone with an ischemic brain ijury.

Thank goodness for Dr. Haacke, and other scientists who are speaking out.  It is not simply about the lesions on MRI. We will be told it is, because we can be sold drugs that halt these lesions---but that has not stopped MS progression.  There is no drug to stop reflux, iron deposition and hypoxic injury in the brain, and this is why it has not been explored since TJ Putnam in the 1940s, and will be fought.

Notes from CCSVI conference, 

Bologna, Italy --September 8, 2009

September 9, 2009 at 7:37pm

Notes from the CCSVI presentation
September 8, 2009


Dr. Ellliot Frohman, University of Texas Southwestern Medical Center Neurology, Dallas, Texas and Robert Zivadinov, Jacobs Neurological Institute, Buffalo, NY are chairs for the morning session:

Dr. Frohman makes the introduction. CCSVI is removed from how we think about MS or any other immune mediated diseases. Could other diseases we currently classify as autoimmune be related to venous disease? Autoimmune diseases share in common molecular adhesion molecules. Perhaps Crohn’s could be venous? Validating CCSVI in MS may affect the classification of other autoimmune disorders. This venous model has been overlooked.

Micrographs, histopath proficles, periventricular cuffs, red cells we see in post capillary venules. This is not new. In 1863 -before Charcot.- G.E. Rindfleisch writes of venous congestion in MS.

Could the immune system go anywhere blood goes? Is this why there is an inappropriate immune response? He notes the large crowd in the room (it’s packed) and says he hopes people will speak out. (they will!)

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Dr. Paolo Zamboni- Universita degli Studi di Ferrara, Italy director of vascular studies

The drama of CCSVI and MS is that of severe stenosis of the extracranial pathways. Everyone in this room can return home and establish a cooperation between vascular and neurology departments. A simple demonstration - he shows a video demonstration of doppler protocol to aid diagnosis. There is a blocked outflow of blood.

In the normal control groups, there is a monodirectional flow of blood. In MS the periventricular vein has a bidirectional flow. Substitute circles avoid intracranial hypertension. Mean transit time is increased.

Dr. Zamboni proposes a “Menu” for the day-

1. Entree- what is the origin of venous stenosis?
2. Pasta- May we assess consequences of CCSVI in the brain. Perhaps microbleeding is the source of lesions.  Just like CVI in other parts of the body- there is microcirculation
Cerebral spinal fluid ultrafiltration and reabsorption depends on transmural pressure.
TMP = IVP-EVP
In venography, there is much higher pressure in MS patients then controls.
Histology- research cited:
-red blood cell extravastion during relapse
-fibrin cuffs in venous hypertension
-iron laden macrophages
are ALL found in MS patients.

3. Main Course- Is CCSVI treatable?
measuring pressure before and after Liberation procedure is significantly changed.

4. Dessert- What are the effects of CCSVI treatment?

and for Today’s Special---Chronic fatigue as a symptom of CCSVI
(you have to love the Italians and their food analogies.)