Old paper from Hans Lassman

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Old paper from Hans Lassman

Post by frodo » Thu Dec 11, 2014 9:29 am

I have just found a paper from Hans Lassman from 2007. This author is quite important because he colaborates in the forefront of research, with Lucchinetti, Vanda Lennon and the people from the Mayo Clinic.

Though he has never used the term CCSVI this is what he writes in his paper:

Taken together, all these studies agree that the most initial
tissue changes in focal white matter lesions occur on a
background of mild perivenous inflammation. However,
initial damage of myelin sheaths is associated with activated
microglia in the absence of local tissue infiltration by T-cells

I would say that this is very compatible with the CCSVI theory.

I have never seen this paper mentioned around here. My apologies if it is repeated. The second section is worth reading.

http://cbr.meduniwien.ac.at/fileadmin/d ... rt_103.pdf

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Re: Old paper from Hans Lassman

Post by cheerleader » Sun Dec 14, 2014 1:19 pm

Hi Frodo-

I haven't seen that specific review by Lassmann--thanks for posting. In it, he summarizes his earlier reseearch on hypoxic like injury in MS.

We discussed Lassmann's research on TIMS, especially during the early days on CCSVI exploration. Dr. Bernard Juurlink has used his papers to further explain his understanding of CCSVI/MS and hypoperfusion and ischemic injury. And Marie Rhodes refers to his papers in her CCSVI book. It's very important, and yes it is completely compatible to the vascular theory of MS. There is demyelination in the MS brain without infiltration of T cells. Here's more on Lassmann, Ge, Adams, and Dr. Juurlink's observations of MS as a disease of hypoperfusion. From my blog, written in 2010.
http://ccsviinms.blogspot.com/2010/08/b ... sions.html

The idea that MS is related to hypoperfusion, or slowed blood flow, is not new.
Here's is Dr. Juurlink's proposal from 12 years ago--

http://www.nature.com/jcbfm/journal/v28 ... 0872a.html

"Accumulating evidence indicates that there is a decreased perfusion throughout the NAWM (normal appearing white matter) in patients with MS. It occurs in both relapsing–remitting and primary progressive MS, strongly suggesting that it represents an integral part of the disease process. Ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions). There appears to be a relationship between reduced white matter perfusion and cognitive dysfunction in patients with MS.

Ge et al (2005) interpreted the hypoperfusion in NAWM as a vasculopathy in the context of the perivascular inflammations that occur in focal MS lesions. However, although inflammatory infiltrates in MS are typically located around small- or medium-sized veins (Adams, 1989) and in the perivascular spaces surrounding arterioles (Gay, 2006; Gay et al, 1997), microvessel thrombosis is only exceptionally being observed within these lesions (Aboul-Enein and Lassmann, 2005; Wakefield et al, 1994)."

So, this paper comes pretty close to saying that this slowed perfusion and white matter lesions could be created by slowed blood flow and a lack of oxygen in the brain. This is exactly what Dr. Juurlink was proposing.

Here's a study that shows that white matter lesions in rats were formed when cerebral hypoperfusion was created in their brains.

"Cerebrovascular white matter lesions represent an age-related neurodegenerative condition that appears as a hyperintense signal on magnetic resonance images. These lesions are frequently observed in aging, hypertension and cerebrovascular disease, and are responsible for cognitive decline and gait disorders in the elderly population. In humans, cerebrovascular white matter lesions are accompanied by apoptosis of oligodendroglia, and have been thought to be caused by chronic cerebral ischemia. In the present study, we tested whether chronic cerebral hypoperfusion induces white matter lesions and apoptosis of oligodendroglia in the rat. Doppler flow meter analysis revealed an immediate reduction of cerebral blood flow ranging from 30% to 40% of that before operation; this remained at 52–64% between 7 and 30 days after operation. Transferrin-immunoreactive oligodendroglia decreased in number and the myelin became degenerated in the medial corpus callosum at 7 days and thereafter."

Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09

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