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Abstract:

The aetiology proposed for the development of chronic cerebrospinal venous insufficiency (CCSVI) associated with multiple sclerosis (MS) has been the presence of congenital truncular venous malformations. However, this hypothesis is not consistent with the epidemiology or geographical incidence of MS and is not consistent with many of the ultrasonographic or radiographical findings of the venous disturbances found in MS patients. However, the probability of a venous aetiology of MS remains strong based on evidence accumulated from the time the disorder was first described.

The method used in this review was to search PubMed for all past medical publications related to vascular, venous, haematological, epidemiological, biochemical, and genetic investigations and treatments of MS.

Epidemiological and geographical findings of prevalence of MS indicate the involvement of an infective agent. This review of the venous pathology associated with MS describes a hypothesis that the pathogenesis of the venous disease could be initiated by a respiratory infective agent such as Chlamydophila pneumonia, which causes a specific chronic persistent venulitis affecting the cerebrospinal venous system. Secondary spread of the agent would initially be via the lymphatic system to specifically involve the azygos, internal jugular and vertebral veins. The hypothesis proposes mechanisms by which an infective venous vasculitis could result in the specific neural damage, metabolic, immunological and vascular effects observed in MS. The hypothesis described is consistent with many of the known facts of MS pathogenesis and therefore provides a framework for further research into a venous aetiology for the disease.

If MS does result from a chronic infective venulitis rather than a syndrome involving congenital truncular venous malformations, then additional therapies to the currently used angioplasties will be required to optimize results.

Regarding the nature of the venous lesions, I have observed venous diseases closely with ultrasound for the past 24 years and have frequently noted that infalmmation (phlebitis) of the veins will results in localised thrombosis along the wall of the vein, this thrombosis resolves by fibrosis and recanalisation of the vein leaving intraluminal membranes, septa, webs, and fixed and distorted valves. You do not require congenital venous malformations to produce these lesions. I have been looking at these abnormalities in MS patients for the past 2 years, and I personally don't believe that they resemble congenital truncular malformations in any way. This is a very nasty venous vasculitis that we are dealing with, hence the serious consequences.

Third, according to the venulitis theory, the stenoses are an end result of the progressive persistent venulitis caused by the chronic infection rather than the primary cause of the neurological damage. . . . Reversal of the decreased cerebral perfusion may be the mechanism for virtually immediate improvement in symptoms such as fatigue, brain fog and cognition reported by patients following successful angioplasty of stenoses. However, the stenoses and occlusions are not the cause of the MS, they are, along with myelin damage, a result of the infective venulitis.

cheerleader wrote: I'm not completely convinced that it's all about Cpn. I still believe it's more global, and related to endothelial dysfunction. I know a few people who were on the Stratton/Wheldon antibiotic protocol who continued to progress, and one person who was on it and still had stenotic veins. Cpn may be part of the puzzle for some however. I know that Anecdote (Dr. Wheldon's wife who writes in the antibiotic forum here) has recovered from her MS with the antibiotic protocol for Cpn, and she is doing quite well. Obviously, Cpn was involved in her disease process.

cheer

se1956 wrote:Infection ALONE must be wrong.

Because the probability that MS parents transfer the disease to their children is close to 10%.

http://www.neurology.org/content/69/12/1208.abstract

So there must be a congenital part (a metabolism dysfunction?).

But may be it's an/the important trigger.

R.

cheerleader wrote:We're discussing this with Dr. Thibault on Facebook. He says that the venous malformations he's seeing in CCSVI don't look like truncular venous malformations.

NZer1 wrote:I hope that IVUS is going to be used!

se1956 wrote:Infection ALONE must be wrong.
Because the probability that MS parents transfer the disease to their children is close to 10%.

cheerleader wrote:We're discussing this with Dr. Thibault on Facebook. He says that the venous malformations he's seeing in CCSVI don't look like truncular venous malformations.

cheerleader wrote: Robot--The reason I believe MS must be more "global" and not about a single infection is because of the other, scientifically proven environmental and infective associations with MS:
EBV type 1 and 2, smoking,low vitamin D, processed foods, lack of exercise, shift work, obesity, northern European populations, etc.
cheer

...it could be hypothesized that venous stasis in the superior saggital sinus due to extracranial outflow impairment could affect the drainage of bridging veins that pass through the subarachnoid space (near the meninges and EBV-infected B-cell follicles) and contribute to EBV activation. The venous stasis hypothesis in the SSS may contribute to understanding why so many different viruses and bacteria [3,111] have been linked to increased MS susceptibility risk over the last 50 years.