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

Friday, August 27, 2010

Blood Flow and white matter lesions

August 27, 2010 at 10:58pm

The idea that MS is related to hypoperfusion, or slowed blood flow, is not new.
Here's is Dr. Juurlink's proposal from 12 years ago--

Hypoperfusion in the MS brain explained:

"Hypo"; meaning under or sub-par and "perfusion"- meaning the delivery of blood to the capillary bed.

In MS brains, there is a below normal delivery of blood into brain tissue.  Neurologists have never given a good explanation as to why this happens.  Here's a great paper that looks at this phenomena.

(terms to know -NAWM  is normal appearing white matter, or healthy myelin.  
Ischemia means a lack of oxygen or hypoxia.)

"Accumulating evidence indicates that there is a decreased perfusion throughout the NAWM (normal appearing white matter) in patients with MS. It occurs in both relapsing–remitting and primary progressive MS, strongly suggesting that it represents an integral part of the disease process. Ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions). There appears to be a relationship between reduced white matter perfusion and cognitive dysfunction in patients with MS.

Ge et al (2005) interpreted the hypoperfusion in NAWM as a vasculopathy in the context of the perivascular inflammations that occur in focal MS lesions. However, although inflammatory infiltrates in MS are typically located around small- or medium-sized veins (Adams, 1989) and in the perivascular spaces surrounding arterioles (Gay, 2006; Gay et al, 1997), microvessel thrombosis is only exceptionally being observed within these lesions (Aboul-Enein and Lassmann, 2005; Wakefield et al, 1994)."

So, this paper comes pretty close to saying that this slowed perfusion and white matter lesions could be created by slowed blood flow and a lack of oxygen in the brain.  This is exactly what Dr. Juurlink was proposing.

Here's a study that shows that white matter lesions in rats were formed when cerebral hypoperfusion was created in their brains.

"Cerebrovascular white matter lesions represent an age-related neurodegenerative condition that appears as a hyperintense signal on magnetic resonance images. These lesions are frequently observed in aging, hypertension and cerebrovascular disease, and are responsible for cognitive decline and gait disorders in the elderly population. In humans, cerebrovascular white matter lesions are accompanied by apoptosis of oligodendroglia, and have been thought to be caused by chronic cerebral ischemia. In the present study, we tested whether chronic cerebral hypoperfusion induces white matter lesions and apoptosis of oligodendroglia in the rat. Doppler flow meter analysis revealed an immediate reduction of cerebral blood flow ranging from 30% to 40% of that before operation; this remained at 52–64% between 7 and 30 days after operation. Transferrin-immunoreactive oligodendroglia decreased in number and the myelin became degenerated in the medial corpus callosum at 7 days and thereafter."

There is NO NEED for any auto- immune system activation to create white matter lesions or myelin destruction.  NONE.  Dr. Juurlink knew this.  Many doctors who study stroke know this.   All that is needed is slowed blood flow.  

Did you know that most elderly people have white matter lesions in their brains?  We don't see them, because they are not routinely given MRIs.  But it's a known fact that the aging brain has slower perfusion, slower circulation and decreased blood flow, resulting in less oxygenation.  Why has the correlation of circulation in MS and other neurodegenerative diseases been ignored?  This chaps my hide.

Here's a paper where they created white matter lesions in rats' brains by clamping their carotid arteries closed.  Remember, the arteries bring the blood in, the veins take it out.  Slowed perfusion can be created by slowed delivery of blood, or slowed removal.  It works both ways.

Notice in this study, the first areas of white matter lesions were on the optic nerve after only THREE DAYS of ligation.  This mimics the order of problems we see in pwMS. RRMS patients typically present with vision problems first and show white matter lesions.

"Cerebral white matter (WM) lesions are observed frequently in human ischemic cerebrovascular disease and have been thought to contribute to cognitive impairment. This type of lesion can be experimentally induced in rat brains under chronic cerebral hypoperfusion by the permanent occlusion of both common carotid arteries. However, it remains uncertain whether chronic ischemia can damage both the gray and white matter, and whether it can induce demyelination with or without axonal damage. Therefore, we examined axonal damage using immunohistochemistry for the amyloid β/A4 precursor protein (APP), chromogranin A (CgA) and demyelination using immunohistochemistry for the encephalitogenic peptide (EP) in this model. Severe WM lesions such as vacuolation and the loss of nerve fibers appeared in the optic nerve and optic tract after 3 days of ligation, and less intense changes were observed in the corpus callosum, internal capsule, and fiber bundles of the caudoputamen after 7 days with Klüver–Barrera and Bielschowsky staining. These WM lesions persisted even after 30 days. The APP, CgA, and EP-immunopositive fibers increased in number from 1 to 30 days after the ligation in the following WM regions: the optic nerve, optic tract, corpus callosum, internal capsule, and fiber bundles of the caudoputamen. "

When neurologists say that Dr. Zamboni's research is not based on fact....give them a lecture on hypoperfusion and white matter lesions.  This is science, this is fact, this is real.



  1. You propose a bold conjecture by stating equivalence between arterial and venous system insofar each one's effect on the cerebral perfusion: "Slowed perfusion can be created by slowed delivery of blood, or slowed removal. It works both ways." It does work both ways, but how do we know, if analogous flow alterations produce comparable effects? In fact, many people, who have severely altered venous hemodynamics don't experience by far the same problems as people whose arterial hemodynamics is altered.

    1. You comment is not completely true--publications prove that many people with altered venous hemodynamics do experience problems. As venous specialist Dr. Byong B. Lee likes to say, "We do not know what we do not know." This is largely because the venous system has been ignored in preference for the arterial. But we have known about venous stroke, venous congestion and venous dural sinus stenosis causing intracranial hypertension. The newly discovered lymphatic vessels of the CNS run through the brain's dural venous sinus and into the jugular veins. Quite obviously, venous flow matters. The mission of the International Society for Neurovascular Disease is to fully understand this relationship , and I would recommend you to their site for information and presentations on these issues. http://www.isnvd.org

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