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http://onlinelibrary.wiley.com/doi/10.1 ... 2/abstract

This provides some support for the use of MR imaging to study hemodynamics of the azygous. It also says that in patients with portal hypertension, when the portal hypertension is treated through an angioplasty procedure called TIPS, the blood flow in the azygous decreases by 46%!

For those of us with CCSVI, anytime flow is added to the cerebrospinal drainage in a person with compromised cerebrospinal drainage is not a good thing.

Portal hypertension would be caused by liver disease.

Determining the cause of portal hypertension involves the following: History of jaundice, History of blood transfusions, intravenous drug use (hepatitis B and C), Pruritus, Family history of hereditary liver disease (hemochromatosis, Wilson disease), History of alcohol abuse

http://emedicine.medscape.com/article/182098-clinical

Here are some doppler images of enlargened azygous veins due to portal hypertension. It states that the doppler is done from the esophagus. We have frequently said that the azygous cannot be directly dopplered but perhaps it can? Would the doppler have to be literally within the esophagus?
http://www.eusatlas.ro/page-119~Portal+ ... +flow.html

Cece wrote:http://onlinelibrary.wiley.com/doi/10.1 ... 2/abstract

This provides some support for the use of MR imaging to study hemodynamics of the azygous. It also says that in patients with portal hypertension, when the portal hypertension is treated through an angioplasty procedure called TIPS, the blood flow in the azygous decreases by 46%!

For those of us with CCSVI, anytime flow is added to the cerebrospinal drainage in a person with compromised cerebrospinal drainage is not a good thing.

Portal hypertension would be caused by liver disease.

Determining the cause of portal hypertension involves the following: History of jaundice, History of blood transfusions, intravenous drug use (hepatitis B and C), Pruritus, Family history of hereditary liver disease (hemochromatosis, Wilson disease), History of alcohol abuse

http://emedicine.medscape.com/article/182098-clinical

Here are some doppler images of enlargened azygous veins due to portal hypertension. It states that the doppler is done from the esophagus. We have frequently said that the azygous cannot be directly dopplered but perhaps it can? Would the doppler have to be literally within the esophagus?
http://www.eusatlas.ro/page-119~Portal+ ... +flow.html

this is endoscopic ultrasound where an endoscope is placed within the gastrointestinal tract and then ultrasound is done through that entry.

I have spoken about this topic with a world class vascular radiologist whose major practice is liver disease. He has stated that he has never noticed symptoms of ccsvi in one of his patients. But he hadnt really looked for it either. So he will now look for the association.

drsclafani wrote:this is endoscopic ultrasound where an endoscope is placed within the gastrointestinal tract and then ultrasound is done through that entry.

I have spoken about this topic with a world class vascular radiologist whose major practice is liver disease. He has stated that he has never noticed symptoms of ccsvi in one of his patients. But he hadnt really looked for it either. So he will now look for the association.

Very interesting!!
I saw this as similar to the effect of nutcracker on collateral flow to the azygous.

The main symptoms and complications of portal hypertension include:
Gastrointestinal bleeding; black, tarry stools or blood in the stools; or vomiting of blood due to the spontaneous rupture and hemorrhage from varices.
Ascites, an accumulation of fluid in the abdomen.
Encephalopathy, confusion and forgetfulness caused by poor liver function and the diversion of blood flow away from your liver.
Reduced levels of platelets or decreased white blood cell count.

http://my.clevelandclinic.org/disorders ... nsion.aspx

It would be difficult to distinguish the symptoms of CCSVI from the symptoms of encephalopathy.
http://en.wikipedia.org/wiki/Hepatic_encephalopathy
Some of this sounds familiar, including the abnormal Babinski's sign seen in hepatic encephalopathy and in MS. In encephalopathy there are the toxins, especially ammonia, that the liver is not cleansing that are doing brain damage. But if CCSVI is present in the increased flow in the azygous due to being used as a collateral for the portal vein, there might be slowed drainage and impaired clearance of toxins from the brain, which could only make the situation worse. And some of the confusion and cognitive impairment might be CCSVI related instead of encephalopathy related.

West Haven Criteria

The severity of hepatic encephalopathy is graded with the West Haven Criteria; this is based on the level of impairment of autonomy, changes in consciousness, intellectual function, behavior, and the dependence on therapy.[1][7][8]
Grade 1 - Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction
Grade 2 - Lethargy or apathy; minimal disorientation for time or place; subtle personality change; inappropriate behaviour
Grade 3 - Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation
Grade 4 - Coma (unresponsive to verbal or noxious stimuli)

http://en.wikipedia.org/wiki/Transjugul ... emic_shunt

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPSS). This is used in the treatment of refractory ascites, bleeding from oesophageal varices and hepatorenal syndrome.[5][6] TIPSS-related encephalopathy occurs in about 30% of cases, with the risk being higher in those with previous episodes of encephalopathy, higher age, female sex and liver disease due to causes other than alcohol.

Why would encephalopathy occur AFTER the portal vein is treated with a shunt? 30% of the time?
I would expect it to be relieved by TIPSS, not caused.
The jugular is punctured as part of the TIPSS procedure but I don't know how common jugular clotting or intimal hyperplasia is after a jugular puncture.

Cece wrote:

West Haven Criteria

The severity of hepatic encephalopathy is graded with the West Haven Criteria; this is based on the level of impairment of autonomy, changes in consciousness, intellectual function, behavior, and the dependence on therapy.[1][7][8]
Grade 1 - Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction
Grade 2 - Lethargy or apathy; minimal disorientation for time or place; subtle personality change; inappropriate behaviour
Grade 3 - Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation
Grade 4 - Coma (unresponsive to verbal or noxious stimuli)

http://en.wikipedia.org/wiki/Transjugul ... emic_shunt

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPSS). This is used in the treatment of refractory ascites, bleeding from oesophageal varices and hepatorenal syndrome.[5][6] TIPSS-related encephalopathy occurs in about 30% of cases, with the risk being higher in those with previous episodes of encephalopathy, higher age, female sex and liver disease due to causes other than alcohol.

Why would encephalopathy occur AFTER the portal vein is treated with a shunt? 30% of the time?
I would expect it to be relieved by TIPSS, not caused.
The jugular is punctured as part of the TIPSS procedure but I don't know how common jugular clotting or intimal hyperplasia is after a jugular puncture.

This is very commonly seen and relates to worsening of hepatic function and worsening toxins. Removing the toxins allows patients to have cflearer mental functions without any change in the hemodynamics of portal hypertension.

This is not like nutcracker in that patients are rarely asymptomatic with liver failure and cirrhosis

So the main significance would be that, in liver disease, we have vascular specialists who look at the azygous vein, and we can find out if the sorts of stenoses seen in the azygous in the MS patient population are ever seen in the azygous in patients with liver failure but with presumably healthy azygous veins.

They even check for compressibility of the azygous vein, in the endoscopic ultrasound images that I linked, with the compressibility being reduced when flow is increased. Who knew the azygous vein could even be reached to be imaged in this way! But it does not sound like a viable follow-up imaging alternative for CCSVI patients with azygous disease.

I might still say that if basic research can show that the removal of toxins in the brain is hindered by CCSVI conditions and the blood brain barrier weakened, then patients with liver failure who are at risk of toxins damaging the brain would benefit from a simple doppler test to check for CCSVI and a simple venoplasty to treat it, if found. Especially since it's known that there is excessive flow being routed into the azygous.

We don't yet know who all might benefit from the discovery of CCSVI. Possibilities expand before contraction...

Cece wrote:So the main significance would be that, in liver disease, we have vascular specialists who look at the azygous vein, and we can find out if the sorts of stenoses seen in the azygous in the MS patient population are ever seen in the azygous in patients with liver failure but with presumably healthy azygous veins.

They even check for compressibility of the azygous vein, in the endoscopic ultrasound images that I linked, with the compressibility being reduced when flow is increased. Who knew the azygous vein could even be reached to be imaged in this way! But it does not sound like a viable follow-up imaging alternative for CCSVI patients with azygous disease.

I might still say that if basic research can show that the removal of toxins in the brain is hindered by CCSVI conditions and the blood brain barrier weakened, then patients with liver failure who are at risk of toxins damaging the brain would benefit from a simple doppler test to check for CCSVI and a simple venoplasty to treat it, if found. Especially since it's known that there is excessive flow being routed into the azygous.

We don't yet know who all might benefit from the discovery of CCSVI. Possibilities expand before contraction...

i can agree to that possibility

SORRY FOR MY IGNORANCE BUT I´D LIKE TO ASK IF IT COULD BE POSSIBLE ANY CONNECTION BETWEEN FATTY LIVER DISEASES: ALCOHOLIC LIVER DISEASE (ALD), NONALCOHOLIC FATTY LIVER DISEASE (NAFLD), IRON OVERLOAD AND FATIGUE.

One connection is for those who have hemochromatosis, which contributes to excessive iron potentially being stored both in the brain and the liver.

But the liver disease that's relevant to the azygous vein is liver disease caused by thrombosis of the portal vein or hypertension of the portal vein. These cause the redirection of flow to the azygous.

Any kind of liver disease would result in toxins not clearing well from the bloodstream, which could lead to fatigue and encephalopathy?

Sorry for my ignorance as well! I am better versed on the subject of jugulars than on livers...

edited to add: Dr. Hector Ferral is co-coordinator of a workshop on portal hypertension at the upcoming SIR conference.
http://www.sirmeeting.org/index.cfm?do= ... Ev&ev=2616

That's really interesting.

Any kind of liver disease would result in toxins not clearing well from the bloodstream, which could lead to fatigue and encephalopathy?

That's how I felt when I got sick and got my brain lesion, like I was being poisoned. I also have no spleen (because of a car accident 35 yrs ago), so I guess my blood doesn't get cleaned so well. Anytime I bled when I was really sick, I felt much better, (menstrual, large blood tests, blood donation) the fatigue would disappear within 3 hours, like magic really, a bit like some people get almost instant results from CCSVI treatment. It's been nearly two years since I discovered my iron levels were well above normal, and that I was a C282Y carrier, and I've had 8 pints of blood taken since then. I feel really good, and have had no more brain events since reducing the iron/hemoglobin levels. My ferritin now sits at 62 and my hemoglobin is around 150. I do start to go backwards if I don't give one point every three months, feel tired and toxic again.

I'm quite sure I have some other error of iron metabolism, that matched with my C282Y gene is causing problems, or maybe porphyria going by my family problems for myself and probably my sister with MS also. The classic Hereditary Hemochromatosis can only be a small part of the story. Different genes regulate iron absorption, transport, storage and export from cells. Virus's can cause your body to store iron away, to hide it from the virus, so iron metabolism and the immune system are one system

The other hemochromatosis gene is the H63D (more common than C282Y), and it looks like this one may be more importantly linked to brain iron. I'm sure there will be more on this soon.