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

Friday, September 16, 2011

Dr. Dake on "retinal vein sheathing": MS-like lesions, but no myelin

September 16, 2011 at 7:57pm

Dr. Dake made a very important point for the CIRSE conference with his in depth essay on the importance of CCSVI research. 

Retinal Vein Sheathing in MS--  The veins of the retina in pwMS become enlarged and thickened and there is damage to the retinal nerves.  Without myelin.  99% of the time, there is no myelin on retinal nerves, but there is MS damage.  

Here's Dr. Dake---

Underappreciated in the midst of these clashing positions is one other example of a similar venous lesion with potential relevance to MS – sheathing of retinal veins. This cuffing or sheathing of veins can be appreciated on fundoscopic examination of the eyes and may be associated with retinal vein thrombosis, optic neuritis and vision loss. 

In the majority of cases when it is diagnosed during an evaluation of disturbed vision, it occurs in patients with MS. Studied extensively at the Mayo Clinic, it is not however singularly associated with cases of established MS. Its frequency among MS patients is estimated to range from 11% to 42%. After fluoroscein dye administration, it is possible to observe leakage of dye around the retinal veins and histologically, the veins display a thickened wall similar to appearances observed in other chronically obstructed venous territories.

When contemplating the possible association between venous obstruction, blood-brain barrier leakage, myelin destruction and immune mechanisms responsible for the initiation of MS, it is interesting to note that the retinal nerve fibres are not myelinated in 99% of the population.


Lesions due to MS, occuring on nerves that do not have myelin.  Leaking veins--in people who develop MS.  "Cuffs" that contain immune cells around these leaking veins.
The optic nerve, which exits the back of the eyeball, DOES have myelin.  The retinal nerve sheath, inside the eyeball, does not.

These vascular abnormalities of the eyes in pwMS have been noted by opthamologists for decades.
Here's a paper from 1986

The occurrence of perivenular abnormalities in a region free of myclin and oligodendrocytes provides evidence that the vascular changes in MS can occur independently of contiguous demyelination, and may be the primary event in the formation of a new lesion.

Optical neuritis is another common condition for MS patients. Evaluating periphlebitis retinae involves detecting sheathing and hemorrhage in veins in the retina. Lightman et al. demonstrated that 3.5 years after initial onset of acute idiopathic optic neuritis, eight out of 14 patients who had vascular abnormalities in a first episode of optic neuritis went on to develop MS, while only five out of 32 patients without vascular abnormalities went on to develop MS.[35] The overall incidence of patients with optic neuritis going on to be diagnosed as clinically definite was 13 out of 46 subjects, or 28%. The authors go on to draw the following conclusion: "We therefore suggest that the sheathing of retinal vessels that we observed opthalmoscopically is the visible clinical sign of the perivascular lymphocytic infiltration and accompanying oedema which characterizes the lesions of MS."

Dr. Dake's point is---If MS is indeed an autoimmune attack on myelin, then why are these eye nerves, which do NOT have myelin, affected in MS?  Why do these retinal veins show venous congestion, leaking and immune activation?  MS specialists do not have an answer.  And they have not looked any further.  

Here is the pre-eminent neurologist of the UK, commenting on the above study---many years later, in 2010.

Although the perivenous localization of cellular cuffing and plaque formation in multiple sclerosis is well known, and vascular abnormalities of the retinal vessels detected by ophthalmoscopy have also been reported, no one is yet clear on the frequency and significance of these findings.
Alastair Compston 

"No one is yet clear".  Shouldn't MS specialists, like you, Dr. Compston,  try to understand why there is retinal vein sheathing in MS?  Dr. Dake has only been in the MS world for three years, and he is curious.  He believes there is a correlation with venous congestion due to CCSVI.  He understands blood flow.  He sees the connection.  Actually, anyone who can read sees the connection.

The truth is, doctors have noted this connection of the retinal veins and MS since 1944.

Rucker CW: Sheathing of the Retinal Veins in Multiple Sclerosis. Proc Staff Mtg Mayo Clinic 1944,
Here is the full paper from Dr. Rucker-

My outrage continues.  I do NOT understand how MS specialists can continue to put up roadblocks to further investigation of CCSVI. 


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