Welcome! This blog contains research & information on lifestyle, nutrition 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 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

Tuesday, October 19, 2010


Two new papers from Dr. Chung

October 19, 2010 at 8:11am

For those who have been following this page for a bit, you may remember my references to Dr. Chung in Taiwan who has been studying the jugular veins in relationship to transient global amnesia (TGA) and other neurological disorders.  

Dr. Chung found that in those with internal jugular vein valve problems, or valves that didn't close properly,  there was reflux of blood in their jugulars when they used a "valsalva maneuver"--that means pushing air up against a closed airway, or straining.  The valves opened and this sent blood back up into the brain, and created temporary ischemic (low oxygen) events.  Dr. Chung postulated this is what causes temporary amnesia.   Some activities that create valsalva manuever are coughing, straining, opening up plugged up ears, lifting, and stressful responses. 

Dr. Chung has two new papers out on aging and the jugular veins.  I thought these were important to discuss after the ECTRIMS conference-- in which a researcher from the American University in Beirut stated that CCSVI could not be important in MS, because he only found CCSVI in older or more progressed MS patients.  He and his team found CCSVI in 92% of what he called "late MS" patients---those who had MS 10 years or more.  To anyone who knows MS, 10 years is not "late MS." 

I know many people who have had MS 30 years and more, but let's get on with what Dr. Chung discovered.  Dr. Chung is now measuring venous return in the jugular veins of the "healthy"  elderly.





Cerebral venous outflow insufficiency via the internal jugular vein (IJV) is associated with several neurological disorders. However, a normal reference set of IJV hemodynamic parameters derived from a large, healthy population over a wide range of age has, until now, been lacking. Color-coded duplex sonography was performed on the IJVs of 349 subjects (55.60 ± 17.49,16 to 89 y; 167 M/182 F). With increasing age, increased lumen area and decreased time-averaged mean velocity of bilateral IJV and a decreased proportion of total flow volume, drainage in the left IJV were found. The frequency of left jugular venous reflux (JVR) also increased with aging. We report IJV hemodynamic parameters across a large population, which could be used as a normal reference for clinical and research purposes. Furthermore, we found a decreased proportion of venous drainage, increased JVR prevalence, dilated lumen and slowed flow velocity in the left IJV, all of which suggest increased left IJV outflow impedance with aging. (E-mail: hhhu@vghtpe.gov.tw)

Now, this is very, very different than CCSVI.  In this situation, the jugular vein is dilated, which is stretched out or enlarged.  Not like CCSVI where the jugulars are pinched or tiny.  But what interests me is that in the elderly, there is less flow in the left jugular, more reflux and slowed venous drainage.  This appears to occur naturally with aging.  Do you see where I'm going with this?  Add aging to someone with malformed jugular veins and CCSVI, and you have a recipe for further disability in those who are older and have had MS for more years.

Dr. Chung takes his research into slowed jugular vein flow in the elderly one step further, and postulates that perhaps THIS is why we see white matter lesions in the brains of the elderly.  I, sadly, know all about this.  Since my Dad had these white matter lesions before he died earlier this year.  My Dad had been slowing down, acting more confused and having cognitive problems.  His neurologist explained that he had "leukoaraiosis" or LA.  This simply means my Dad had white matter lesions. 

So, Dr. Chung writes the following about LA-----

Leukoaraiosis (LA) is a major cause of vascular dementia and disability in the elderly. Age and hypertension are the most two important risk factors. Despite its clinical significance, the etiology is so far unclear. Chronic cerebral hypoperfusion associated with vasogenic edema, microbleeding or/and endothelial dysfunction found in LA favors venous ischemia, in stead of arterial ischemia, as its pathogenesis. The involved regions in LA, periventricular and subcortical regions, are the drainage territory of deep cerebral venous system and the watershed region between the superficial and deep cerebral venous system respectively. Adding the facts that periventricular venule collagenosis, and retinal and intraparenchymal venules dilatation are related to the severity of LA, cerebral venous hypertension caused by downstream venous outflow impairment might play a major role in the pathogenesis of LA. Internal jugular vein is the main venous outflow pathway for cerebral venous drainage. The frequency of jugular venous reflux (JVR) is increased with aging. Hypertension, which has a decreased venous distensibility, might further exacerbate the sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency caused by JVR. Clinically, JVR caused by a dural AV fistula does lead to cerebral hypoperfusion, white matter abnormalities, vasogenic edema and cognitive impairment in several published reports. JVR is suggested to play a key role in the pathogenesis of LA through a sustained or long-term repetitive retrograde-transmitted cerebral venous pressure and venous outflow insufficiency, which might lead to chronic cerebral venous hypertensions, abnormal cerebral venules structural changes, decreased cerebral blood flow, endothelial dysfunction, and vasogenic edema in cerebral white matters.


Do you see that?  Decreased cerebral blood flow, due to hypoperfusion....JUST like what we have been discussing in CCSVI.  Retrograde cerebral pressure, in other words, reverse blood flow back into the brain.  All creating a low oxygen environment and leading to white matter lesions in the elderly.  Makes sense, doesn't it?

I hope Dr. Chung joins up with the International Society of Neurovascular Diseases.  They can use his specialized research into the jugular veins...and I've suggested that they invite him to join in the conversation.  There is so much to be learned!!
Joan 

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