Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. 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 auto-immune paradigm of MS, and continues the 20 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

Monday, March 7, 2011

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:


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.


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