blocked veins aren't good for us (stroke research)

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

blocked veins aren't good for us (stroke research)

Postby Cece » Sun Dec 12, 2010 12:58 am

Hypoplasia or Occlusion of the Ipsilateral Cranial Venous
Drainage Is Associated With Early Fatal Edema of Middle
Cerebral Artery Infarction

Conclusions—In this small case series, we demonstrated that only the patients with hypoplasia or occlusion of the
ipsilateral cranial venous drainage developed early fatal edema after large middle cerebral artery infarction. Our results suggest a role of cranial venous outflow abnormalities in the development of brain edema after arterial ischemic stroke.

The intracranial venous compartment occupies approximately
70% of blood volume inside the inflexible cranial
cavity. Following volume-targeted rationale, ICP can be
regulated effectively by the fluctuation of venous blood
volume. Venous hemodynamics passively influence the ICP
through a possible key regulator, outflow obstruction. This
outflow obstruction contributes to intracranial venous congestion
more in patients with high ICP than in patients with
normal ICP. In case of normal ICP, venous collaterals may be
sufficient to prevent cerebral venous congestion and edema.
However, in the setting of large MCA infarction with widespread
ischemic injury, pre-existing abnormalities of cranial
venous drainage may pose significant resistance to venous
outflow, accelerating the development of cerebral edema

This is very specific to our chances of stroke survival, but pwCCSVI would not do well in the aftermath of a stroke.

The specific patients had hypoplasia of the IJV and hypoplasia or atresia of the transverse sinus, or a ligated jugular vein.
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Postby TMrox » Sun Dec 12, 2010 9:02 am

I agree!

Here is more info of vascular involvement and demyelination of the spinal cord:

Transverse Myelitis: A neurological disorder caused by inflammation across both sides of one level, or segment, of the spinal cord. The term myelitis refers to inflammation of the spinal cord; transverse simply describes the position of the inflammation, that is, across the width of the spinal cord. Attacks of inflammation can damage or destroy myelin, the fatty insulating substance that covers nerve cell fibers (thus it is also called a demyelinating disorder).


Researchers are uncertain of the exact causes of transverse myelitis. The inflammation that causes such extensive damage to nerve fibers of the spinal cord may result from viral infections, abnormal immune reactions, or insufficient blood flow through the blood vessels located in the spinal cord...

Some cases of transverse myelitis result from spinal arteriovenous malformations (abnormalities that alter normal patterns of blood flow) or vascular diseases such as atherosclerosis that cause ischemia, a reduction in normal levels of oxygen in spinal cord tissues. Ischemia can result from bleeding (hemorrhage) within the spinal cord, blood vessel blockage or narrowing, or other less common factors.

Blood vessels bring oxygen and nutrients to spinal cord tissues and remove metabolic waste products. When these vessels become narrowed or blocked, they cannot deliver sufficient amounts of oxygen-laden blood to spinal cord tissues. When a specific region of the spinal cord becomes starved of oxygen, or ischemic, nerve cells and fibers may begin to deteriorate relatively quickly. This damage may cause widespread inflammation, sometimes leading to transverse myelitis. Most people who develop the condition as a result of vascular disease are past the age of 50, have cardiac disease, or have recently undergone a chest or abdominal operation.

The Encyclopedia of Autoimmune disease By Dana K. Cassell and Dr Noel Rose Director of Johns Hopkins Center for Autoimmune Diseases, 2003, pp. 237-240
Diagnosed with Transverse Myelitis in December 2008. Inflammatory demyelination of the spinal cord (c3-c5). No MS, but still CCSVI.
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