This Is MS Multiple Sclerosis Knowledge & Support Community

elliberato wrote:I tell you what I think...I think there is a nasty bacteria of some kind that is an endothilial fanatic and like the pac-man game devours veins and leaves us with disability...

i wish that were true. imagine ccsvi treated by antibiotic. who wouldnt want that approach!

If you look at the pathology i showed previously, you will see that there just isnt any iniflammation in that vein. no i remain a believer in a congenital theory and that this is congential hypoplasia of the right internal jugular vein and annular stenosis of the left jugular vein

Cece wrote:There was in fact a right jugular vein, that cathether is going through something. (?) And level with the chin as seen in the image, there is a blockage. (?) The dye is very opaque, as Algis noted, indicating very limited flow. (?) The patient is very fortunate to be in the hands of someone who can treat him. (!)

that vein on the right is really small, nothing like a normal sized vein. it gets so small that no flow goes through it.

The thing that I am interested in also is the lack of MS DX. Could this example be what we are looking for in the way that MS may not be used to exclude treatment when these symptoms that the gentleman presented with are so similar to MS symptoms. Does this make sense?
Can a person be defined differently by symptom type and receive treatment for vascular problems rather than the treatment be linked to having MS?
MS dx is the stumbling block?

elliberato wrote:I tell you what I think...I think there is a nasty bacteria of some kind that is an endothilial fanatic and like the pac-man game devours veins and leaves us with disability...

If that was true, because it would be infecting 100's of thousands of "MS" sufferer's world-wide, then it should be rather routine lab practice to find, sample, isolate, and culture the bacteria in question.

Bacteria are relatively easy to kill (especially when compared to a virus).
Lyme disease, for example, has testing available to determine its presence.

Sorry, doesn't pass the sniff test for me.

Donnchadh

Donnchadh wrote:

elliberato wrote:I tell you what I think...I think there is a nasty bacteria of some kind that is an endothilial fanatic and like the pac-man game devours veins and leaves us with disability...

If that was true, because it would be infecting 100's of thousands of "MS" sufferer's world-wide, then it should be rather routine lab practice to find, sample, isolate, and culture the bacteria in question.

Bacteria are relatively easy to kill (especially when compared to a virus).
Lyme disease, for example, has testing available to determine its presence.

Donnchadh

many of the chronic bacteria we harbor are intraphagocytic – meaning they have developed the ability to live inside the nuclei of our cells. Such pathogens thrive in the cytoplasm, or the liquid surrounding the cellular organelles that allow for DNA replication and repair.

link

Studies of autoimmune disease have focused on the characteristics of the identifiable antibodies. But as our knowledge of the genes associated with the disease states expands, we understand that humans must
be viewed as superorganisms in which a plethora of bacterial genomes – a metagenome - work in tandem with our own. The NIH has estimated that 90% of the cells in Homo sapiens are microbial and not human in origin. Some of these microbes create metabolites that interfere with the expression of genes associated with autoimmune disease. Thus, we must re-examine how human gene transcription is affected by the plethora of microbial metabolites. We can no longer assume that antibodies generated in autoimmune disease are created solely as autoantibodies to human DNA. Evidence is now emerging that the human microbiota accumulates during a lifetime, and a variety of persistence mechanisms are coming to light. In one model, obstruction of VDR nuclear receptor-transcription prevents the innate immune system from making key antimicrobials, allowing the microbes to persist. Genes from these microbes must necessarily impact disease progression. Recent efforts to decrease this VDR-perverting microbiota in patients with autoimmune disease have resulted in reversal of autoimmune processes. As the NIH Human Microbiome Project continues to better characterize the human metagenome, new insights into autoimmune pathogenesis are beginning to emerge.

link

Accuracy of the Tests. These tests are very expensive, and none are completely accurate in either identifying Lyme or ruling it out. They should never be used to make a primary diagnosis of Lyme disease in patients who do not have obvious symptoms of the disease.

Both false positive and false negative results are common with these tests.

False positive results occur when the test suggests the presence of the disease, but the person does not actually have an active infection. This may occur in different ways:

* The antibodies to the infectious organism triggering the antibodies are not the Lyme spirochetes. Other organisms that can trigger such antibodies include syphilis and relapsing fever. Dental infections may trigger a false positive response.
* The patient may have been infected with Lyme disease previously and harbor antibodies to the disease.

False negative results miss the actual presence of the disease. These results are also common. (If the results are negative but Lyme disease is highly suspected, the doctor will probably prescribe antibiotics anyway.) False negative results occur for a number of reasons:

* The test is taken too early in the course of Lyme disease. In such cases, the antibodies that fight the spirochete might not have reached a level that is high enough to be detected. (Only about 20 - 30% of patients can be identified using immune system tests in the first 2 - 4 weeks. By the fourth week, up to 80% of patients will have detectable antibodies.)
* The patient has taken certain medications, such as steroids or certain anti-cancer drugs, which reduce the immune system's ability to produce antibodies, including those in response to Lyme disease.
* There are too many infection-fighting antibodies attached to the bacteria. In this case, there are not enough loose antibodies in the blood sample to trigger a response.
* The laboratory itself has set its sensitivity point too high. Some laboratories establish a standard of very high antibody levels before the test results will trigger a finding of Lyme disease. (They do this to avoid too many false-positive responses.) In so doing, however, their tests may miss the disease in patients with lower antibody levels. A related diagnostic problem concerns the possibility of missing persistent Lyme disease after antibiotic treatments, when antibody levels would be low.

All of this means that a negative blood test does not rule out a diagnosis of Lyme disease, particularly if symptoms strongly suggest its presence. Conversely, a positive blood test does not prove that Lyme disease is causing the symptoms. A second blood test, taken several weeks later, may help.

link

Lyme is known as "The Great Imitator", as it appears as all kinds of "auto-immune" disease. The microbes can hide inside our own cells - including macrophages. They can and do affect gene transcription. It cannot be said that there is no connection - yet.

*emboldening and italicizing is mine

havent i taught you well algis?

Will try harder next time

Dr. Sclafani
On this forum we talk mostly about the jugular veins and the azygous. But further up there are a multitude of small veins that drain various parts of the brain. If a stenosis existed in one of those smaller veins inside the skull could it be detected by doppler ultrasound? Also, if a stenosis was found inside the brain would it be possible to balloon it or would there be too great a risk of injuring the brain?

zamboni says you need two or more major veins servicing the brain/spine to be obstructed to develop MS. Does your 61 year old have MS? Has he been given an MRI for MS (there's a special MRI protocol for this scan...just like an MRV for CCSVI requires a special protocol). I remember after I was first diagnosed with MS I discussed some of my symptoms with the radiologist. I had a massive prssure at one point in my head. He said "may be a tumour". I thought he would pick it up during the brain MRI...but he said no - they use special instrumental settings to probe for each suspected condition.

Anyway - I later went back to him with the Haacke CCSVI protocol and was diagnosed with CCSVI (confirmed with Doppler Ultrasound).

NZer1 wrote:The thing that I am interested in also is the lack of MS DX. Could this example be what we are looking for in the way that MS may not be used to exclude treatment when these symptoms that the gentleman presented with are so similar to MS symptoms. Does this make sense?
Can a person be defined differently by symptom type and receive treatment for vascular problems rather than the treatment be linked to having MS?
MS dx is the stumbling block?

Bingo!

It is my understanding that no one can explain the fatigue associated with MS. Since I do not think that MS causes stenoses of the veins, the diagnosis of ms is not relevant to our discussion. This patient does have two comorbidities: MS and thyroid disease.

David1949 wrote:Dr. Sclafani
On this forum we talk mostly about the jugular veins and the azygous. But further up there are a multitude of small veins that drain various parts of the brain. If a stenosis existed in one of those smaller veins inside the skull could it be detected by doppler ultrasound? Also, if a stenosis was found inside the brain would it be possible to balloon it or would there be too great a risk of injuring the brain?

generally those smaller veins do not impact in the way the larger ones necessarily do. they just get bypassed. but if the main vessels are obstructed, the impact is greater. There is no question that other veins not draining the brain and spine and smaller veins draining the brain and spine are affected by the same mechanism as we see in the larger veins. I will show one some day.

Stenoses of the dural sinuses and intracranial veins likely occur as well. However the current wisdom is that these venous structures have wide variation. I think we have to do a lot more study in order to unravel that mystery

drsclafani wrote:

NZer1 wrote:The thing that I am interested in also is the lack of MS DX. Could this example be what we are looking for in the way that MS may not be used to exclude treatment when these symptoms that the gentleman presented with are so similar to MS symptoms. Does this make sense?
Can a person be defined differently by symptom type and receive treatment for vascular problems rather than the treatment be linked to having MS?
MS dx is the stumbling block?

Bingo!

It is my understanding that no one can explain the fatigue associated with MS. Since I do not think that MS causes stenoses of the veins, the diagnosis of ms is not relevant to our discussion. This patient does have two comorbidities: MS and thyroid disease.

Hi Dr, the only reasoning/theory that I have heard regarding fatigue that may hold water is that it is due to cross firing and misfiring of the motor nerves which gives the worn out feeling.
So the fatigue from vascular problems is the clue?

How can we achieve the new status required for treatment?

hwebb wrote:zamboni says you need two or more major veins servicing the brain/spine to be obstructed to develop MS. Does your 61 year old have MS? Has he been given an MRI for MS (there's a special MRI protocol for this scan...just like an MRV for CCSVI requires a special protocol). I remember after I was first diagnosed with MS I discussed some of my symptoms with the radiologist. I had a massive prssure at one point in my head. He said "may be a tumour". I thought he would pick it up during the brain MRI...but he said no - they use special instrumental settings to probe for each suspected condition.

Anyway - I later went back to him with the Haacke CCSVI protocol and was diagnosed with CCSVI (confirmed with Doppler Ultrasound).

i do not understand the focus on ms. the patient has venous disease, that is pure and simple. No one can deny that the right jugular vein is hypoplastic. There is no history of any proven pathological process that might cause this appearance. He never had a catheter in his neck, no trauma, no obvious infectious processes.

So since there is no evidence that MS causes stenotic veins, what do we do about this hypoplastic vein?

Let's review the essential features of the right jugular venogram. For the moment accept that the left ijv is stenotic at the confluens



The right jugular vein (horizontal black arrow) is very small. you can see the difference in dimensions compared to the left side. The normal jugular vein measured more than 8 millimeters and can distend greatly beyond that. This measures about 3 m illimeters.

The contrast media comes to an abrupt end (curved orange arrow). meaning that the diameter is no more than the diameter of the catheter which is 1.66 millimeters in diameter.

We cannot tell how long that occlusion is but it must end somewhere along its lower half. Occlusion is not the same as thrombosis which is an occlusion caused by or resulting in clot filling the vein.

Looking up, one sees that the contrast media is refluxing up in to the head predominantly through the sigmoid sinus (vertical arrow) but also through veins at the skull base such as the squiggly one near the middle. The white curved arrow points to intracranial veins that are refluxing, trying to find a way out of the skull and into the left internal jugular vein.

Given symptoms, something should be done to improve intracranial outflow.

NZer1 wrote:

drsclafani wrote:

NZer1 wrote:The thing that I am interested in also is the lack of MS DX. Could this example be what we are looking for in the way that MS may not be used to exclude treatment when these symptoms that the gentleman presented with are so similar to MS symptoms. Does this make sense?
Can a person be defined differently by symptom type and receive treatment for vascular problems rather than the treatment be linked to having MS?
MS dx is the stumbling block?

Bingo!

It is my understanding that no one can explain the fatigue associated with MS. Since I do not think that MS causes stenoses of the veins, the diagnosis of ms is not relevant to our discussion. This patient does have two comorbidities: MS and thyroid disease.

Hi Dr, the only reasoning/theory that I have heard regarding fatigue that may hold water is that it is due to cross firing and misfiring of the motor nerves which gives the worn out feeling.
So the fatigue from vascular problems is the clue?

How can we achieve the new status required for treatment?

but there are patients without motor dysfunction who have fatigue. i cannot refute your hypothesis. I dont want to focus on it at all. i want to treat an obvious venous disease.

drsclafani wrote:

NZer1 wrote:

drsclafani wrote:
Bingo!

It is my understanding that no one can explain the fatigue associated with MS. Since I do not think that MS causes stenoses of the veins, the diagnosis of ms is not relevant to our discussion. This patient does have two comorbidities: MS and thyroid disease.

Hi Dr, the only reasoning/theory that I have heard regarding fatigue that may hold water is that it is due to cross firing and misfiring of the motor nerves which gives the worn out feeling.
So the fatigue from vascular problems is the clue?

How can we achieve the new status required for treatment?

but there are patients without motor dysfunction who have fatigue. i cannot refute your hypothesis. I dont want to focus on it at all. i want to treat an obvious venous disease.

This would appear to mean that a published research paper with conclusion needs to magically appear and be accepted, stating that venous disease causes fatigue and can be relieved by Angio treatment?

NZer1 wrote:

drsclafani wrote:

NZer1 wrote:
Hi Dr, the only reasoning/theory that I have heard regarding fatigue that may hold water is that it is due to cross firing and misfiring of the motor nerves which gives the worn out feeling.
So the fatigue from vascular problems is the clue?

How can we achieve the new status required for treatment?

but there are patients without motor dysfunction who have fatigue. i cannot refute your hypothesis. I dont want to focus on it at all. i want to treat an obvious venous disease.

This would appear to mean that a published research paper with conclusion needs to magically appear and be accepted, stating that venous disease causes fatigue and can be relieved by Angio treatment?

there are papers that describe fatigue caused by venous outflow obstruction from superior vena caval syndrome, stenosis of jugular veins from dialysis catheter, and from ligation of jugular veins

fatigue has not been explained very well by any mechanism.

further the national ms society in us suggests as an off label use modafininl (provigil) as a treatment of fatigue. in the absence of conclusive data showing efficacy or even a mechanism of action