This Is MS Multiple Sclerosis Community: Knowledge & Support

This may be a very basic question, but my Aunt is a Medical Doctor and she was wondering what Zamboni's theory is for why plaques form in the spinal area, not the brain?

How does CCSVI explain non-cranial (brain) plaques?

Thanks...

The veins that are looked at are the jugulars and the azygous. The jugulars drain the brain, the azygous drains the spine....

But what if both jugulars were found to be stenosed and the azygous is checked and found to be fine? What would explain the spinal lesions? Just a question that I have had myself

The blood will find its way out of the brain through the vertebral veins/plexus (vertebra are in the spine). This is the main pathway while standing or sitting.

Supposedly a jugular obstruction can cause a spinal lesion but I don't fully understand how.

If Dr. Sinan is correct in finding 95% of pwMS have a stenosis or web in the azygous, then I am highly suspicious that anyone found not to have azygous stenosis might actually have one that went unfound.

Very recently this happened to someone here, she received treatment in the jugulars in Poland but nothing found in her azygous, then received treatment in NY where the doctor found a valve issue in her azygous (there's a link to her blog in the AAC thread).

I found this in one of Zamboni's paper

"Although investigations into the role of iron in MS are still few, many high-resolution MR techniques have shown stored iron regions inside the brain and spinal cord...

Blocked extracranial venous blood outflow causes a high rate of cerebral venous reflux in MS patients, as shown in earlier studies (Zamboni et al, 2007, 2009a, 2009b, 2009c). This detected reflux, propagated from the chest and neck veins into the parenchymal veins of the brain, may have an important function in explaining the mechanism of iron overload in MS...


Autoimmune cells mainly destroy oligodendrocytes, the cells responsible for creating and maintaining a fatty layer known as the myelin sheath, which helps the neurons to carry action potentials across axonal pole. In MS, this myelin sheath becomes thin or completely disappears. Most importantly, due to the repeated attacks of autoimmune cells, the remyelination capacity of the insulating sheath is lost, leading to scar-like plaques or lesions situated around the damaged axons (Chari, 2007). However, in such a scenario, iron overload and oxidative stress may be the underlying cause that leads to immunomodulation in chronic MS"

http://www.nature.com/jcbfm/journal/v29/n12/full/jcb

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Diagnosed with Transverse Myelitis in December 2008. Inflammatory demyelination of the spinal cord (c3-c5). No MS, but still CCSVI.

There is also the idea from Dr Schelling and Dr Flanagan that axon damage can occur from stretch and stress tears of the cord and dural sac, which can set off the BBB breach and then lesion formation as the body attempts to heal the breach and lesion area. The immune involvement is thought to happen after the healing process is begun and the immune involvement is there to clean up the byproducts of the process.
The immune involvement after the lesion forms was shown by Australian Researchers working with pathology study of lesions known to be new, against various older ones.
So there may well be several ways that lesions form and the CSF is likely to circulate within the spinal fluid various 'items of interest' yet to be studied and again these 'items' can accumulate in the CNS passages as well.
So as well as the vein walls there is the CSF walls to consider.