If congenital, why adult onset?

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

If congenital, why adult onset?

Postby fogdweller » Sat Jan 30, 2010 12:32 pm

This is a very smart, informed and and well educated group of people. Using our creativity, and assuming CCSVI is correct and the venous malformations are congenital, any speculations as to why childhood onset is rare and some cases of MS don't even show up 'til late adulthood?
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Postby Billmeik » Sat Jan 30, 2010 1:43 pm

I think it takes years to build up iron deposits and truly tox the cns with stale blood. if ccsvi is true then management decisions you grow into as a kid work most of you life, but fail as you get older and weaker?
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Postby cathyb » Sat Jan 30, 2010 2:01 pm

Hi

I am no doctor, certainly not a neuroscientist. I was wondering about this very thing myself, and was looking into it online when I saw your post. I'm quite sure that other people in this forum have addressed this issue (and please post threads if you can help), but I just thought I'd let you know that I found quite a few references to myelination 'pruning' occuring in adolescence up until early adulthood, so that could be a red herring ;) Here is a snippet from one of the articles I found, which was actually a legal one:

First, let's consider how the brain matures during adolescence. While significant growth occurs early on—the brain reaches 90 percent of its adult size by the age of 6—a second wave takes place in the years before puberty. During this time, gray matter—areas of the brain responsible for processing information and storing memories—increases in size, particularly in the frontal lobe of the brain, as a result of an increase in the number of synaptic connections between nerve cells. Around puberty, however, a winnowing process begins in which connections that are not used or reinforced begin to wither (hence the "use-it-or-lose-it" hypothesis). This pruning, which begins around age 11 in girls and 12 in boys, continues into the early or mid-20s, particularly in the prefrontal cortex, an area associated with "higher" functions such as planning, reasoning, judgment, and impulse control. As Dr. Jay Giedd of the National Institute of Mental Health has said, the real cognitive advances come with paring down or reducing the number of synaptic connections. During adolescence, the amount of myelin, a fatty, insulating material that coats the axons of nerve cells—similar to the way insulation coats a wire—also increases, improving the nerve cells' ability to conduct electrical signals and to function efficiently; this too continues into adulthood and occurs later in "higher" regions of the brain, such as the prefrontal cortex.

The most detailed evidence for these maturation processes comes from magnetic resonance imaging studies, which underscore the changing arrangement of gray matter and extent of myelination in adolescents and adults. Such research makes the case, for instance, that marked differences do exist between the brain of a 13-year-old and that of a 25-year-old.


Maybe we will find that the damage as a result of CCSVI is mitigated somehow until early adulthood. Time will tell; this is just a response!

Another thought I had was in relation to the development of the internal jugular veins...we know the malformations are congenital, but what happens to them before age 25 (growth, etc)? I could not find anything on this topic, I plan to keep looking.

http://www.slate.com/id/2108284/
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Postby cheerleader » Sat Jan 30, 2010 2:02 pm

Dr. B.B. Lee, vascular surgeon and professor from Georgetown University, who is now studying CCSVI in MS, spoke about this about the Bologna conference. I wrote it up in my notes.
http://www.thisisms.com/ftopict-8105.html

Dr. Frohman asks Dr. Lee-
Why the latency for onset of MS compared to other VM disease?

Dr. Lee states that some cases of Budd Chiari are diagnosed at age 30, not all are pediatric. It depends on the level of vena cava obstruction. It is too late to repair by the time they do a liver biopsy. The venous system is not like the atrial system- extra pressure makes it very vulnerable. Acute venous hypertension is easy to find and obvious, but this is not the issue...it is the slower progress such as CCSVI...what we do not know is what we do not know.


He likens this venous disease to Budd Chiari, a venous disease of the liver which can be pediatric, or show up later (like MS) It is a chronic problem which slowly destroys the liver- and often results in the need for a liver transplant. CCSVI destroys the brain and spine.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby fogdweller » Sat Jan 30, 2010 4:48 pm

Wow, very good ideas and good info!

I also hypothesize that it is something in the nature of active myelinltion pre-young adulthood that compensates for any loss of myeln; the damage thereafter is relatively slow as the veinous back-pressure slowly results in reflux which gradually results in compromise of the BBB which in turn gradually results in accumulation of excess iron in the tissue. Thus symptoms would naturally start sometime after adolescence and take some time before they would manifest themselves.

Also the pre-adult developing vascular system might provide adequate drainage. I don't know enough about the development of the vascular system to give a meaningful opinion on that.

This could be one great advantage of CCSVI. Up til MRI's, MS was pretty much a differential diagnosis, and even thereafter only if the MRI's showed a big patch of damaged tissue. We didn't know what caused MS so we couldn't diagnose it before a lot of damage had been done. If we do now, then we can check and correct the cause before people have to go through the rest of their lives with the permanent nerve damage!
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Postby sbr487 » Sun Jan 31, 2010 12:38 am

congenital reason is still a hypothesis.
It could be a genetic defect and might take years to manifest (mutate) into actual MS (similar to what happens people who have cancer/diabetes risk).
Too early to conclude anything I guess
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Postby ozarkcanoer » Sun Jan 31, 2010 8:47 am

I was diagnosed with MS at age 60, with somewhere on the order of 40 lesions. Now how could I get to age 60 with this lesion load and had no (obvious) symptoms until then ? I don't know. But I do know that MS is hard to diagnose. I conjecture that if MS is congenital then it takes years for damage to be done. Similar to Parkinsons. Congenital problems with blood flow may not show up as symptoms in children because they are still developing and maybe collateral veins or maybe more elastic veins in the young postpones reflux and the older we get and the nature of the venous malformations and other health issues play a role in if/when we get diagnosed. My neuro has told me that many many people are not diagnosed with MS until the autopsy !!!

Just my speculations...

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Re: If congenital, why adult onset?

Postby frodo » Mon Feb 01, 2010 3:25 am

fogdweller wrote:This is a very smart, informed and and well educated group of people. Using our creativity, and assuming CCSVI is correct and the venous malformations are congenital, any speculations as to why childhood onset is rare and some cases of MS don't even show up 'til late adulthood?


Other important factor is that people grow up after puberty. It is expected that the veins of a tall person have harder load that the veins of a children.

This explains the low frequent onset before puberty. About the late adulthood onset, that can only be explained by the time of iron accumulation.
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Postby eve » Mon Feb 01, 2010 3:53 am

For myself I am convinced that I had my first relapse at age 11. I had my left arm go numb, didn't hurt one bit, just wouldn't work - for over three weeks. Had all sorts of tests done, xrays, I had large number of white bloodcells but my arm was not inflammated at all, complete mystery.

Since that time my arm would feel 'funny' on and off but I could use it fine. Also my left foot had turned inwards a bit around the same time and made me trip.

My parents were going through a very, very nasty divorce and had been for 4 years at the time, I was under tremendous stress ... in that same summer I developed an ulcer.

My puberty was pretty normal healthwise till I had another stressfull period at age 20 - and I went to my GP with complaints of extreme fatigue, dizzyness and stiff legs, which was not recognised (I had her look it up once I had my diagnosis at age 34).


So my two cents ... I think I was born with it and I think the stress I had to deal with just made it show up early, I guess otherwise I would not have any complaints till up in my twenties or maybe even later... I don't know.

I'm a bit hesitant to post this as you all approach it scientific and well I have no proof what so ever to offer you but my personal conviction. But just my two cents, for what it's worth.
dx 2002,RRMS,  suspected begin of MS 1978 (age 10)
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Postby sbr487 » Mon Feb 01, 2010 4:02 am

similar experience here ...

I had sudden weakness in my legs at 12 years or so.
I used to fall when I lift my legs to climb (say a vehicle)
This went on for a month and resolved by itself.
Dr's attributed this to exam stress and what not.

I never had any major issues until 25 years (kind of relapse for 13 years)
and then problems simply started accumulating ...

So kind of confirms that it could be congenital ...

Hurray Zamboni ...
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Postby harryp » Mon Feb 01, 2010 4:14 am

Hi, Is there enough information on the speed of growth of colaterol veins to be a guide to the time of onset of CCSVI? You may have guessed I'm not a medic just a very interested researcher.
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Postby mrsilkykat » Mon Feb 01, 2010 8:51 pm

What about the geographic distribution of MS? What about gender? How do these MS issues fit into congenital CCSVI. Not that they have ever been explained by the autoimmune theory either, as far as I know.

Just wondering if anyone has ideas, speculation on the subject.
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Postby Cece » Mon Feb 01, 2010 10:58 pm

mrsilkykat wrote:What about the geographic distribution of MS? What about gender? How do these MS issues fit into congenital CCSVI.


For gender I believe women are more susceptible to chronic venous insufficiency (varicose veins?) when compared to men.

Epstein-Barr virus impacts the endothelium negatively and is implicated in CCSVI and MS. Does epstein barr follow a geographic distribution? Also a fattier inland diet, lack of fish and lack of sunshine (vitamin D) may contribute to it.
"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition
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Postby eve » Tue Feb 02, 2010 1:54 am

If you google on veins most articles concern varicose veins - but I thought this was interesting..


Who Is Affected by Varicose Veins?

Although the underlying cause of varicose veins is unknown, a number of risk factors have been identified.

Heredity. Varicose veins tend to run in families. If your parents, grandparents, aunts, uncles, or other family members have had varicose veins, it’s likely that you’ll develop them. A defect in the vein walls or valves is the greatest contributing factor in 70 percent of cases.

Age. Varicose veins are a progressive condition that worsens in frequency and severity with age. As we age, elastic fibers in our bodily tissues break down, leading to wrinkles in the skin and weakening of the blood vessels.

Gender. Primarily due to the production of progesterone (one of the major female hormones), women are more likely than men to get varicose veins—by a ratio of approximately four to one.

Hormonal changes. Changes in hormone levels brought on by puberty, contraceptives, pregnancy, menopause, and hormone replacement therapy are risk factors for varicose veins.

http://www.advancedveinctr.com/veinhealth_varicose.htm



Are varicose veins more common in African Americans or Caucasians?

Varicose vein related problems are self reported in approximately 10% of African Americans and 24% of all Caucasians in the United States - based on a national survey in 1961.

http://www.veinsveinsveins.com/faq_freq ... tions.html



Interesting look into the venous sytem

http://www.3dscience.com/Resources/3d_Human_Anatomy.php
dx 2002,RRMS,  suspected begin of MS 1978 (age 10)
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Postby Donnchadh » Tue Feb 02, 2010 12:17 pm

While I don't doubt that some percentage of MS cases are indeed due to congenital origins, perhaps others are due to accidental damage?

I believe that this is true of my own personal situation. I suffered a very bad fall back in 1990, sliding down the edge of a building (about 30 feet). I was holding onto a ladder, and the impact was so severe that my forehead bent the aluminum rung.

Prior to this accident, I was in great overall health and had absolutely NO neurological problems of any kind. I never had any infectious diseases (other had a rare case of the common cold); and my neurological conditions never changed as a result of being sick.

I broke a toe, damaged my left shoulder, and then that's when the problems started. By 11:00am every day, I would become so tired I couldn't keep my eyes open; I wasn't physically tired but rather "head" tired. I would sleep for about 2 hours and then be OK again. I would sleep overnight with no problems.

A dull pain in my neck, just below my skull, was constant. A pain located in the back of my skull lasted for weeks (my ex told me that a nickel-sized area became bald-the hair has since grown back along with the cessation of this pain).

There was some minor tingling in my hands; classic "pins and needles" symptom's.

After surgeries for my shoulder and foot, my neurological symptom's gradually diminished (over the course of about two years).

I had one MRI taken back in 1992 of my neck (which was kind of cutting edge back then) which shows some lesions on the spinal cord. However, the images are small (about 2 inches square) and very grainy so the lesions were overlooked. No one picked up on this damage.

Fast forward to today.

My symptom's have progressively worsened. The minor tingling in both hands develop into a severe case of bilateral carpal tunnel syndrome, and I have had release surgery on both hands. The surgeon said he never saw a worst case; describing the entrapped nerves as being "hourglassed" by the inflammation against the wrist ligaments.

My walking is effected; feels like I am partially "tightened-up" with the classic foot drag.

My looking over MRI's taken in the last couple of years, it would seem that around the neck injury site, there is some vein damage (appears smooth and round both below and above it).

My plan to is approach my neurologist to see if he will OK a CCSVI MRV tests to determine if there is in fact vein damage at the neck injury site.

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