- 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, 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
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?
Friday, January 4, 2013
CCSVI doppler diagnostics presented at vascular conference
January 4, 2013 at 2:09pm
The 34th Congress of the SIAPAV (Italian Society for Angiology and Vascular Medicine) http://www.siapav.it had an extensive review session of CCSVI diagnostics.
There were three lectures presented by specialists in doppler ultrasound for CCSVI. All of these specialists agree that CCSVI exists, it creates a delay of cerebral blood flow, hypoperfusion, and cerebral lesions, and there are very specific tests to measure this process.
The specialists also stated that operators who are finding between 0-50% of CCSVI in people with MS are NOT utilizing correct doppler technique. They stated that the SAME problem happened 35 years ago, when technicians began analysing the carotid arteries. There is a very specific protocol that must be followed, or the results are inaccurate. A lack of knowledge of the venous return system from the brain is part of this problem.
The fact that neurologists continue to ignore this clarion call from vascular specialists, and proceed with badly designed studies, is disturbing. There have been millions of dollars of wasted money and years of wasted time, pursuing studies that are of no value.
Below is the very specific review from this conference.
It is translated by google translate from Italian, and because if this, is not perfect. But BNAC offers training for American doppler technicians, based on this protocol. BNAC is the only center with a published US study that has worked with the experts in this doppler protocol. None of the NMSS funded researcher utilized the complete and correct protocol.
Refresher Course of the 34th Congress SIAPAV dedicated to CCSVI has provided an extensive updating on the diagnosis of chronic cerebrospinal venous insufficiency. The report that follows is intended as a reference for those interested in the clinical picture characterized by hemodynamic abnormalities and / or abnormalities of the refluxing veins from the Central Nervous System.
Three lectures were devoted to the physiology and pathophysiology of cerebral venous return (M. Mancini, Naples), which is essential for understanding the clinical phenomena, paintings echo-color-Doppler normal and pathological (G. Cacciaguerra, Catania), prerequisite for obtaining a correct diagnosis, limiting as much as possible the false negative and false positive and, finally, to the diagnostic protocol with the main criteria and / or accessories must be based on which the diagnosis (G. Arpaia, Vimercate).
Mancini has outlined the salient features of venous hemodynamics in the brain, illustrating the intracranial circulation time measured with echo contrast (landmarks carotid artery, jugular vein and thyroid) that are significantly delayed in CCSVI. From the point of view the speaker presented the map of cerebral perfusion and the prevalence of MS plaques in the hypoperfused areas in the form of clinical progressive MS, while the prevalence in areas hypoperfused would be greater in relapsing-remitting clinical form. This could explain the greater effectiveness of the correction hemodynamics in relapsing-remitting MS, compared to progressive MS.