A murine model of CCSVI is associated with mild but significant impairment of gait as assessed by neurobehavioral testing - P. Thanaporn USA
Mice that have their jugular veins ligated to simulate CCSVI do not develop any brain inflammation or demyelination, suggesting yet again that ‘veinous insufficiency’ does not cause multiple sclerosis.
Researchers from Harvard Medical School in the US took 20 mice, ligated both jugular veins and observed them for six months.
Fifteen control mice were given a sham ligation procedure and another eight were induced with experimental autoimmune encephalomyelitis as negative controls.
Despite CT venography confirming the ligation produced hemodynamic changes, MRI demonstrated there were no signs of blood-brain barrier breakdown or neuroinflammation.
In addition, cytometry and histopathology showed ligation didn’t result in any increase in inflammatory cell populations or demyelination.
Moreover, no clinical signs were observed in any of the ligated mice.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/2944
After confirming successful bilateral JV ligation, we investigated whether JVL resulted in altered cerebral hemodynamics. The JVL group demonstrated significantly increased cerebral retention of nuclear perfusion agent, Tc-99m-exametazime, compared to the sham group expressed as the percentage of the injected dose per gram of tissue (%IDGT = 7.09±0.42 (sham) vs. 8.29±0.11 (JVL), p = 0.024, Fig. S1) at 5 months post surgery. These results indicate that bilateral jugular vein ligation altered cerebral hemodynamics in the JVL group. Together with the structural abnormalities seen on CT venograms, these results confirm that we have established a mouse model of chronic cerebral venous insufficiency.
Both posture and activity may therefore potentially play a role in exacerbating the effects of venous congestion resulting from venous stenosis. To address these possible confounding variables, we aimed to maximize the resting state of venous pressure by surgically ligating both JVs in order to create an extreme scenario of increased venous cerebral venous insufficiency. Some studies have reported that 91% of MS patients having either unilateral or bilateral JV stenosis, with 14% exhibiting bilateral stenosis in the jugular veins . In this way, we believe we have accounted for possible differences in cerebral venous hemodynamics between mice and humans by creating a murine model with relatively greater cerebral venous insufficiency than previous positive studies have reported in humans . The mice were followed for up to 6 months after JVL, a considerable part of the lifespan of SJL mice (typically around 400 days) which, particularly given the maximization of venous pressure by bilateral JVL, should be more than sufficient for disease manifestation if there was a relationship between venous congestion and demyelination.
drsclafani wrote:The cerebral venous drainage of the mouse is not like that of the human.
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