I will ignore the discussion with the naysayer Lyon. He seeks to mislead anyone who wants factual info on CCSVI syndrome.
Early in this thread Ikulo and Cheerleader disagreed with my statement. Its worth considering the papers mentioned in full:
The hypoperfusion may occur early or late in MS progression, no one knows.
..there have been a few studies noting hypoperfusion in MS as compared to severity of MS. Dr. Grossman has done incredibly fastinating radiological studies regarding this matter. Here is a quote from one of his papers:
Compared to RR-MS, PP-MS patients showed significantly lower CBF in the periventricular NAWM (p=0.002) and lower CBV in the periventricular and frontal NAWM (p values: 0.0029 and 0.022). EDSS was significantly correlated with the periventricular CBF (r=-0.48, p=0.0016) and with the periventricular and frontal CBV (r=-0.42, p=0.015; r=-0.35, p=0.038, respectively)
MarkW - The whole paper is complex....... Towards the end of the discussion it states:
Further studies are warranted to better explore the relationship between clinical and perfusion measures and to establish the role of the molecular mechanisms causing MS-related neurodegeneration. In particular, longitudinal studies in patients in the earliest stages of the disease will have to establish whether hemodynamic impairment is a mediator or a marker of degenerative tissue.
That's a great paper, Ikulo...
here's an entire thread on hypoperfusion. This was the reason I started on the vascular path in the first place. Dr. Haacke has some research coming out on perfusion as well. This is a trememndous piece of the MS puzzle.
Hypoperfusion comes first. We do know this....
MarkW - The abstract says:
Hypoperfusion of the normal-appearing white matter in multiple sclerosis (MS) may be related to ischemia or secondary to hypometabolism from wallerian degeneration (WD). This study evaluated whether correlating perfusion and diffusion tensor imaging (DTI) metrics in normal-appearing corpus callosum could provide support for an ischemic mechanism for hypoperfusion.
Thus, the purpose of this study was to evaluate the relationship between perfusion and DTI changes in the normal-appearing corpus callosa of patients with relapsing-remitting MS (RRMS), with the hypothesis that correlations between perfusion and DTI measures would be more consistent with what would be expected in primary ischemia.
The discussion says:
Numerous histopathologic and biochemical studies have demonstrated that in addition to the characteristic discrete white matter lesions found in patients with MS, there is diffuse abnormality involving grossly NAWM. Findings in the NAWM include decreased myelin-specific protein,1 diffuse astrogliosis,31 and infiltration by macrophages and T lymphocytes.3,4 Although MS has prototypically been characterized as a demyelinating disease, axonal damage, including axonal transection and decreased fiber attenuation, has been demonstrated in both lesions as well as within the NAWM.2,32
Hypoperfusion is an interesting part of the MS jigsaw. It is too early to say it comes first in MS. I agree with the first paper 'longitudinal studies in patients in the earliest stages of the disease will have to establish whether hemodynamic impairment is a mediator or a marker of degenerative tissue'.
The neuros saw the immune system issues and concluded that MS was immune in origin. Let us not fall into the same trap with haemodynmic issues. MS is complex and multifactorial. Any theory on its etiology must explain the whole jigsaw not just part of it.