This Is MS Multiple Sclerosis Community: Knowledge & Support

Conclusions
The finding of significant differences between normal controls and MS patients in BOLD response patterns associated with a cognitive task in both task-positive and task-negative cortical networks sheds light on neuronal mechanisms of cognitive impairment in MS patients. Most remarkably, the inhibition of the default network appears to be impaired in posterior parietal and anterior medial prefrontal cortex and this impairment is reversed and in fact normalized by venoplasty. Since BOLD response is a function of cerebral blood flow and volume, and also oxygen metabolism rate, the reduced BOLD responses in both task positive and task-negative networks may reflect not only altered neuronal function but also change in cortical venous blood volume in MS. Thus the recovery of the suppression in the default network by angioplastic treatment may reflect recovered neuronal and/ or vascular function. Moreover the increase in the venous undershoot component of the BOLD response in MS as compared to controls and its reduction after venoplasty provides evidence of impaired clearance and CNS venous insufficiency and holds out the promise that this method may provide an objective diagnostic test.

ABSTRACT: BACKGROUND: Several studies have reported hypoperfusion of the brain parenchyma in multiple sclerosis (MS) patients. We hypothesized a possible relationship between abnormal perfusion in MS and hampered venous outflow at the extracranial level, a condition possibly associated with MS and known as chronic cerebrospinal venous insufficiency (CCSVI). METHODS: We investigated the relationship between CCSVI and cerebral perfusion in 16 CCSVI MS patients and 8 age- and sex-matched healthy controls. Subjects were scanned in a 3-T scanner using dynamic susceptibility, contrast-enhanced, perfusion-weighted imaging. Cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) were measured in the gray matter (GM), white matter (WM) and the subcortical GM (SGM). The severity of CCSVI was assessed according to the venous hemodynamic insufficiency severity score (VHISS) on the basis of the number of venous segments exhibiting flow abnormalities. RESULTS: There was a significant association between increased VHISS and decreased CBF in the majority of examined regions of the brain parenchyma in MS patients. The most robust correlations were observed for GM and WM (r = -0.70 to -0.71, P < 0.002 and P corrected = 0.022), and for the putamen, thalamus, pulvinar nucleus of thalamus, globus pallidus and hippocampus (r = -0.59 to -0.71, P < 0.01 and P corrected < 0.05). No results for correlation between VHISS and CBV or MTT survived multiple comparison correction.
CONCLUSIONS: This pilot study is the first to report a significant relationship between the severity of CCSVI and hypoperfusion in the brain parenchyma. These preliminary findings should be confirmed in a larger cohort of MS patients to ensure that they generalize to the MS population as a whole. Reduced perfusion could contribute to the known mechanisms of virtual hypoxia in degenerated axons.

It amazes me that we have ground breaking science being reported on this site--- (in some cases because posters from this site brought research to universities, and encouraged dialogue regarding CCSVI in MS) which is neglected in favor of squabbling and incessant name calling.