- MS patients with gadolinium-enhancing lesions (inflammatory lesions) had 54% faster thinning
- MS patients with new T2 lesions had 36% faster thinning that those with MS who did not have these features of MRI activity
- Participants whose level of disability got worse during the study had 37% more thinning, compared to patients whose level of disability did not change
- Participants who had the disease less than five years showed 43 percent faster thinning than those who had the disease more than five years
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
Saturday, January 5, 2013
Retinal thinning and MS. Why?
January 5, 2013 at 3:02pm
The OCT (optical coherence tomography) test for retinal thinning in MS is in the news again. You may have seen the press releases on "the eyes have it" and MS. OCT has been around for many years. It is a test which uses light instead of sound waves to visualize an area of the body. Because the eyeball can let light in, OCT scans are a great way to monitor what's going on inside and behind the eyeball. The retina is made up of light sensitive neurons that form layers at the back of the eye.
The retina is a very important part of monitoring the MS process. But something which is NEVER mentioned in this discussion is that, unlike the optic nerve, the retina does not have myelin. Myelination is rarely extended into the retina.
If MS is an inflammatory disease which targets myelin, why is the retina being affected during an MS relapse?
Something else that is never mentioned in these MS OCT stories is that retinal thinning is seen in other diseases of neurodegeneration, including Parkinson's and Alzheimer's Disease. Retinal thinning is not unique to MS. The Michael J. Fox Foundation is looking at retinal thinning in Parkinson's, and there have been other "eyes may be a window" stories on OCT and Parkinson's
Here's the new study from Johns Hopkins MS Center:
Peter Calabresi, MD. and team recruited 164 participants from Johns Hopkins MS Center. They all underwent eye scans every six months to check for thinning of a part of their retinas. Repeat scans were carried out for an average of 21 months. Fifty-nine of the volunteers had no MS disease activity.
Here are some of the findings.
The editorial authors also noted that the study results provide indirect evidence that active inflammation — even if subclinical or occurring in a different functional system — is connected with greater rates of retinal neurodegeneration.
The more inflammation and swelling the researchers found in the retinas of the MS patients, the more inflammation showed up in their brain MRIs.
So, optical coherence tomography appears to be a good test to monitor MS relapses, maybe better/easier/less expensive than MRI.
But some questions need to be asked-----
The retina does not have myelin. Why is the retina thinning during an MS relapse? What is happening? Why is there retinal atrophy during an MS relapse?
Dr. Dake has written about this conundrum. Why should the retina, which does not have myelin, be thinning during active MS relapses?
Because it is drained by the retinal vein, and if there is venous insufficiency in the area of the brain and eye, the retina will be affected. Venous insufficiency can cause retinal atrophy.
The culprit may well be retinal vein sheathing and/or venous insufficiency caused by CCSVI.
Here's Dr. Dake on the subject:
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.
Here is a paper from 1945 which noted retinal vein sheathing and thinning of the retina in MS patients:
Finally, here is a paper from 2012 where neurologists noticed that some of their MS patients had macular oedema (swelling) that was unexplained. Macular oedema is linked to venous congestion and an increase in venous pressure.
Macular oedema typically results from blood–retinal barrier disruption. Multiple sclerosis is not otherwise thought to be associated with macular oedema except in the context of comorbid clinical uveitis. Despite a lack of myelin, the retina is a site of inflammation and microglial activation in multiple sclerosis and demonstrates significant neuronal and axonal loss. We unexpectedly observed microcystic macular oedema using spectral domain optical coherence tomography in patients with multiple sclerosis who did not have another reason for macular oedema.
It's all well and good to find new ways to monitor MS progress, like the OCT scan.
But shouldn't researchers also be asking WHY? Why do we see retinal atrophy in active MS relapses? Why is there macular oedema? Why do other diseases of neurodegeneration also have retinal thinning, without inflammation? What is this process teaching us?
Perhaps the Dr. Calabresi would like to chat with Dr. Dake? Perhaps the Johns Hopkins MS Clinic might like to work with vascular researchers? Maybe they'd like to speak to other specialists in Parkinson's and Alzheimer's?
I keep hoping.