Jugular Venous reflux in Leukoaraiosis

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Jugular Venous reflux in Leukoaraiosis

Postby cheerleader » Mon Oct 11, 2010 6:30 pm

New paper out by Dr. Chung (of jugular/transient global amnesia research) It is a hypothetical position paper describing the potential link between Leukaoraiosis and jugular vein reflux. Here is a good definition of LA from Dr. Yasser Metwally (from my computer--can't locate link):

Leukoaraiosis is an ischaemic demyelination of the immediate periventricular white matter associated with astrogliosis, enlarged extracellular spaces and white matter microcavitations. It is secondary to chronic global reduction of brain perfusion. Leukoaraiosis, which appears as an area of hyperintense signal in the white matter on MR images, is an age-related neurodegenerative condition that, when severe, correlates with dementia. It is characterized histologically by demyelination, loss of glial cells, and spongiosis.


What Dr. Chung has suggested with jugular venous reflux in LA sounds a lot like what Dr. Haacke and Hubbard are discussing in CCSVI with hypoperfusion....
Here's is Dr. Chung's abstract:

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.


link

--and not to overstate the obvious, but it doesn't take an autoimmune disease to create white matter lesions, demyelination and cerebral atrophy. These can be caused by venous outflow abnormalities.
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Last edited by cheerleader on Wed Oct 13, 2010 7:05 am, edited 1 time in total.
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Postby Ruthless67 » Mon Oct 11, 2010 9:16 pm

Thank you for this new paper cheerleader.

The research keeps comming in from so many different sources now and an overwhelming amount all seem to point to problems with venous outflow from the brain.

It's really getting exciting.

More pieces for the puzzle.
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Postby sbr487 » Tue Oct 12, 2010 2:43 am

I was reading some notes on depression recently and noticed that a certain type of depression is classified as vascular depression due to its origin ...
A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it
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Postby cheerleader » Tue Oct 12, 2010 8:32 am

There is new research on depression, MS and the atrophy of the hippocampus region from UCLA--
link

this hippocampal atrophy is also seen in diffuse cerebral hypoxia from CO2 poisoning or sleep apnea-
link

Haacke and Hubbard are studying how slowed perfusion and less oxygenation affect the brain's structure and relate to brain atrophy, fatigue and depression...so there will be more research on this connection to CCSVI/MS.

Dr. Chung has been researching the internal jugular veins and neurological disease for the last 10 years. He's in touch with Dr. Haacke now, so there should be more collaborative research going on. Yes, it is exciting.
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Re: Jugular Venous reflux in Leukoaraiosis

Postby scorpion » Tue Oct 12, 2010 11:40 am

cheerleader wrote:New paper out by Dr. Chung (of jugular/transient global amnesia research)

Leukoaraiosis is an ischaemic demyelination of the immediate periventricular white matter associated with astrogliosis, enlarged extracellular spaces and white matter microcavitations. It is secondary to chronic global reduction of brain perfusion. Leukoaraiosis, which appears as an area of hyperintense signal in the white matter on MR images, is an age-related neurodegenerative condition that, when severe, correlates with dementia. It is characterized histologically by demyelination, loss of glial cells, and spongiosis.


What Dr. Chung has found with jugular venous reflux in LA sounds a lot like what Dr. Haacke and Hubbard are discussing in CCSVI with hypoperfusion....

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.


link

--and not to overstate the obvious, but it doesn't take an autoimmune disease to create white matter lesions, demyelination and cerebral atrophy. These can be caused by venous outflow abnormalities.
cheer


Cheer do you really understand what this article is saying????
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Postby cheerleader » Tue Oct 12, 2010 2:54 pm

Yes, I do understand this medical hypothesis paper by Dr. Chung, Scorpion. But let me break it down into simpler terms. I'm sorry if it was too complex.

Leukoaraiosis (LA) is a basic, generic term which describes white matter changes. (MS is actually a sub-category of Leukoaraosis.) Most times, when there is no specific diagnosis, like MS or vasculitis, these white matter lesions are just referred to as LA. They are often seen in the elderly, and show up as bright spots on MRI. My late father had these and was just beginning to show signs of dementia when he died after falling and hitting his head earlier this year. I had some good and heart-breaking discussions with his neurologist. When I saw Dr. Chung's new research on LA and jugular reflux, I wanted to write about this for the forum.

Now, what Dr. Chung is postulating is that jugular reflux may be what is causing these white matter lesions in the elderly. Dr. Chung has written many papers on the jugular veins and their importance in cerebral health. His reasoning for connecting LA and the jugular veins is this:

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.


Since the jugular veins are the "downstream venous outflow" avenue....Dr. Chung connects jugular venous reflux to the slowed perfusion (simply slow blood flow thru the brain) and ischemic changes (simply lack of oxygen) changes seen in LA. What I am saying is...this looks a lot like what Dr. Zamboni has found with venous reflux in CCSVI. And it's a lot like what Dr. Hubbard is seeing with oxygenation levels pre and post angioplasty. And it's what Dr. Haacke is testing with perfusion.

I hope that makes sense. I realize not many people on this forum are as interested in the continuing research--most of the people I discussed research papers with have moved on, but I hope that some on here are still interested. If not, that's fine. This paper will be on the Alliance website at www.ccsvi.org
best,
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Last edited by cheerleader on Tue Oct 12, 2010 3:23 pm, edited 1 time in total.
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Postby hopeful2 » Tue Oct 12, 2010 3:22 pm

Hi Cheer,

Thanks for translating. I didn't understand the posts until you put it in layperson's terminology. (I have particular trouble with the term "ischemia.")

With that said, Dr. Chung's research and findings seem very helpful for CCSVI. If some of the issues are understood and treated for elderly patients then younger patients presenting with similar symptoms and a diagnosis of MS may receive better treatment.

Plus (if I understood correctly) the findings may validate what Zamboni, Hubbard and Haacke are saying plays a part in CCSVI. :)

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Postby Cece » Tue Oct 12, 2010 4:53 pm

Cheer, this is good research with good implications and this is more discussion than it had previously gotten.

One of my first introductions to MS was of course the MRI, after which I received the diagnosis. On that MRI, it mentioned that the finding of a white matter lesion was abnormal for a patient of my age and it was one of the first of what I did not know would be a long string of unanswered MS-related questions: why would a white-matter lesion be a nonfinding if it were in a 60-year-old? A WML is nothing to scoff off, it would hurt a 60-year-old just as much as a 30-year-old, only then it is swept under the rug as senile dementia, needing a cane, and all of that?

I don't think we can leap ahead and draw too many conclusions the way I'd want to, but it feels like this has potential for more than just MSers.
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Postby patientx » Tue Oct 12, 2010 6:34 pm

Cece wrote:Cheer, this is good research with good implications and this is more discussion than it had previously gotten.


The thing is, this paper is not research. It is a hypothesis (note, it was published in a journal called Medical Hypothesis). It is presented as a possible explanation for leukoaraiosis, which describes white matter hyperintensities of unknown etiology.

Reading the entire paper, the author refers to venous hypertension and edema, neither of which are seen in MS (nor CCSVI, for that matter). He also writes repeatedly about reflux seen during a Valsalva maneuver, which was previously blasted as not following the Zamboni protocol.
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Postby cheerleader » Tue Oct 12, 2010 6:42 pm

Cece wrote: why would a white-matter lesion be a nonfinding if it were in a 60-year-old? A WML is nothing to scoff off, it would hurt a 60-year-old just as much as a 30-year-old, only then it is swept under the rug as senile dementia, needing a cane, and all of that?

I don't think we can leap ahead and draw too many conclusions the way I'd want to, but it feels like this has potential for more than just MSers.


Cece--great point, and thanks for making it. A white matter lesion in a 60 yr. old is usually explained by venous insufficiency, or a mini-stroke, or some other vascular situation. It is never linked to an autoimmune disorder. My Dad's lesions were just considered part of the aging process...never defined, perhaps Parkinson's perhaps dementia.

Dr. Chung noticed this, too. And here is his other new paper on how aging affects the jugular venous return. You guessed it....it gets worse with age-

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)

link

When we consider that MS is a continuing, progressive disease that worsens as patients age---and that CCSVI was worse in those with progressed or longer-term diagnosis, we can see how this might fit in with Dr. Chung's research on aging and jugular venous return.
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Postby cheerleader » Tue Oct 12, 2010 6:46 pm

patientx wrote:
The thing is, this paper is not research. It is a hypothesis (note, it was published in a journal called Medical Hypothesis). It is presented as a possible explanation for leukoaraiosis, which describes white matter hyperintensities of unknown etiology.


I know, I said exactly that in my response to scorp. Please read the 2nd Chung paper on aging and the venous return, patient. It is research. I should have included that in the beginning. It makes more sense in understanding Chung's hypothesis. He is noting jugular venous reflux associated with aging.
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Postby CureOrBust » Wed Oct 13, 2010 12:55 am

Cheer, in your first post, you included two quotes, which to me implied that they were both extracted from the same paper by Dr Chung. When I did a search on the internet for the first quote, I came across the quote, but it was not by Dr Chung, and they didn't reference his paper either. :?

I do not have access to the full article, but would like to know if both the original quotes extracted directly from Dr Chung's paper? or did you combine the quotes to clarify the link between Leukoaraiosis and MS?
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Postby cheerleader » Wed Oct 13, 2010 7:02 am

CureOrBust wrote:Cheer, in your first post, you included two quotes, which to me implied that they were both extracted from the same paper by Dr Chung. When I did a search on the internet for the first quote, I came across the quote, but it was not by Dr Chung, and they didn't reference his paper either. :?

I do not have access to the full article, but would like to know if both the original quotes extracted directly from Dr Chung's paper? or did you combine the quotes to clarify the link between Leukoaraiosis and MS?


Cure--you're right...the first quote is from the writings of neurologist Dr. Yasser Metwally explaining LA (I had it on my computer from when my Dad was diagnosed...and grabbed it without providing the link)--and for the life of me I can't find the link now...Dr. Chung's abstract follows---I will edit the first post to clarify. I wrote too quickly... Apologies.
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Postby CureOrBust » Thu Oct 14, 2010 3:30 am

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Postby 1eye » Fri Oct 15, 2010 12:52 pm

cheerleader wrote:
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)


When we consider that MS is a continuing, progressive disease that worsens as patients age---and that CCSVI was worse in those with progressed or longer-term diagnosis, we can see how this might fit in with Dr. Chung's research on aging and jugular venous return.


Two things jump out at me. One, if "IJV haemodynamic parameters across a large population... could be used as a normal reference for clinical and research purposes", isn't this set of data very useful in describing the normal population, and can't it be used at least as a guide as to what can be expected from experimental controls?

The other is the reference to only left IJV reflux. What is it that distinguishes the left IJV, and does this mean the right IJV doen't get reflux?
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