Terry wrote:My question is... what could twist a vein? Did you see that thing?
Zamboni does not define these blockages, or posit what these "venous obstructions" are, but they are in the blood vessels, and they are hampering the correct flow of blood in people with MS.
mrhodes40 wrote:But another thing I thought of--I did read both papers-- was whether or not it is possible the tortuous veins and insufficiency is SECONDARY to the sclerotic area in the brain.
If MS were autoimmune we would be able to control it much better than we can with current therapies.
They keep telling us "more complicated than we thought...." Yes, it's very complicated when you are trying to force something that doesn't fit ....
the azygous vein in the MS group was affected in 86% of cases.Most cases involved membranous obstruction of the junction with the superior vena cava, twisting, or, less frequently, septum and atresia as can be seen in the x-rays in Figure 2a; in 12 cases the azygous system presented stenoses at several points up to even atresia of the lumbar plexuses
As for the jugular veins, they were found to be stenosed unilaterally or bilaterally in 59/65 patients (91%). The stenoses were frequently annulus and septum, followed by atresia; no twisting was observed.
Although investigations on the role of iron in MS are
still few, some evidence supports a pivotal role for iron in
MS inflammation. The effect of manipulation of iron level
was investigated in EAE, a form of induced autoimmune
encephalomyelitis in mice used as an experimental model of
MS.31 The incidence of EAE was 60–70% in mice with a
normal iron level and in iron-overloaded mice, but 0% in
iron-deficient mice. The findings suggest that iron
deficiency provides protection from the development of
EAE31 and also challenge traditional views on what
constitutes a normal level of stored iron.14 The authors31
noted that, ‘The failure of iron-deficient mice to develop
EAE is impressive. Many of the pharmaceutical approaches
to inhibiting EAE are less effective than iron deficiency.’
Another group32 investigated the serum concentration
of soluble transferrin receptor (sTFR) in a group of MS
patients. The levels were found to be significantly higher in
patients with active MS, either in progressive or relapsingremitting
clinical form, than in controls. Serum ferritin
levels were also significantly elevated in patients affected by
the active and progressive form.32 Both findings support the
hypothesis above described, which proposes local iron
overload as the initial signal of the inflammatory chain in MS.
Although the primum movens of MS is still elusive, these
studies suggest that iron-dependent mechanisms of inflammation
seen in CVD could be relevant to MS. Future work
on MMPs and on iron/macrophage interactions appears
especially promising. However, because of its relevant
epidemiology and its easily visualized lesions, CVD is an
ideal model for investigating iron mediated mechanisms of
tissue injury of venous and inflammatory origin, as well as
the use of deliberate induction of iron deficiency as a
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