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

Sunday, October 30, 2011

Venous intraluminal abnormalities in MS

October 30, 2011 at 12:02pm

A medical student from Case Western University has been providing some interesting research in the US for CCSVI.

Claudiu Diaconu first presented his research proposal to study CCSVI in November 2010 at the Lepow Day at Case Western.  This is a yearly event, where medical students present their research projects.  Diaconu's was called:  An Assessment of Chronic Cerebrospinal Venous Insufficiency -Tissue Analysis of the Cerebrospinal Veins.  His study was funded with a grant from the NMSS.

In his proposal, Diaconu set out how he would harvest the autopsied veins and inject them with a silicone gel in the lab, so that the interior of the vein could be studied.  This was one part of his study, which also included doppler ultrasound and MRV assessment of CCSVI.

At ECTRIMS, Claudiu Diaconu's research created a bit of a stir.  A year after his proposal he came forward with evidence of the truncular venous malformations associated with CCSVI.  The intraluminal defects that Dr. Zamboni has been describing for years.
The same Cleveland Clinic group also has begun examining cerebrospinal veins from cadavers of MS patients and controls.
Some results from the first 13 cadavers were presented during a platform session at ECTRIMS by Case Western University medical student Claudiu Diaconu. He confirmed that venous structures in the brain and brainstem appear to be far more complicated and variable than previously thought.
In fact, the postmortem study revealed the presence of a novel venous valve that had not been described in anatomy textbooks.
Perhaps the most important finding was that most of the stenoses identified in the study were not associated with vessel wall thickness or circumference.

As a result, Diaconu said, cerebrospinal vein scans in live patients "should focus on identifying intraluminal abnormalities, not just vessel wall narrowing or thickening.


And the results of his study, so far, are found in this abstract-
Anatomical and histological analysis of venous structures associated with chronic cerebrospinal venous insufficiency

Marked valvular and other intraluminal abnormalities with potential hemodynamic consequences were identified in 5 of 7 MS patients (7 abnormalities) and in 1 of 6 controls (1 abnormality). These abnormalities included circumferential membranous structures (1 MS and 1 control), longitudinally-oriented membranous structures (3 MS), single valve flap replacing IJV valve (2 MS), and enlarged and malpositioned valve leaflets (1 MS). In addition, minor anatomic variations without expected hemodynamic consequences were observed similarly in both MS and controls. These included valves with >2 leaflets, the presence of valves in the AZY, additional (duplicate) normal-appearing IJV valves, and small membranous septa. 

Conclusion: Post mortem examination of the IJV and AZY veins of MS patients and non-MS controls demonstrated a variety of structural abnormalities and anatomic variations. Vein wall stenosis occurred at similar frequency in MS and non-MS controls. However, the frequency of intraluminal abnormalities with possible hemodynamic consequences was higher in MS patients compared to healthy controls, although the current sample size is limited.

It is this type of inquisitive and open collaboration of medical practices which will elucidate the connection of CCSVI and MS, and help us move forward, as doctors understand the best means to deal with these intraluminal defects.  

These are mechanical defects, which means there is no money for pharmaceutical companies, and less money for research.  But there are answers to be found, and help and healing for those with MS.   


At the Cleveland Clinic, technician Larry Raber and physician Mei Lu practice the ultrasound technique to measure CCSVI in patients with MS on medical student Claudiu Diaconu. Cleveland Clinic Center for Medical Art

Wednesday, October 19, 2011

Shift Work, Cortisol and Environmental Factors in MS

October 19, 2011 at 8:11am

In the news yesterday, a new study showing how shift work (night time work outside of normal daytime hours) doubles a teen's risk of developing Multiple Sclerosis.  

This is considered an "environmental factor" as opposed to a genetic factor.  This new paper comes from the Karolinska Institute in Sweden and was published in the Annals of Neurology.  The researchers did not propose a specific theory as to how shift work might increase the risk of MS, but they did comment on how circadian rhythm disruption might affect melatonin and the immune system.

Here is the complete paper:

Oddly enough, just last week, another published study showed how shift work raises the risk of metabolic disease, higher body mass index (BMI) and cardiac problems in young adults vias cortisol release. This study was undertaken by Dutch researchers and published in the Journal of Clinical Endocrinology-- only a week prior to the Swedish study.  

Here's the abstract for that paper on shift work:

Shift work, or work outside standard daytime hours, has been associated with an increased incidence of metabolic syndrome, and cortisol plays a major role in the development of the disease.