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Monday, June 3, 2013 1:20 AM | Tony Miles Volg link

Conclusions to the paper presented:

Although much research work has been undertaken into
the contribution of venous abnormalities to various
neurological conditions, there has generally been a lack
of any hydrodynamic analysis to interpret the data
collected. Without such analysis, it is possible to misinterpret results and come to potentially erroneous conclusions [174]. In the analytical review presented here,
we have sought to redress this issue, and have been able
to show that CCSVI-like anomalies in the extracranial
venous system are unlikely to account for the reduction
in CBF reported in patients with MS. Rather, our analysis suggests that other pathophysiological mechanisms
must be a work, which are increasing the hydraulic resistance of the cerebral vascular bed in patients with
MS. Similarly, changes in the cerebral microvasculature
seem to be responsible for reduced CBF in leukoaraiosis.
CBF in the WM is markedly reduced in both MS and
leukoaraiosis, and in both conditions, lesions exhibit
signs of ischemia, although to a lesser extent in the case
of MS. Under conditions of hypoperfusion, the laws
governing mass transfer indicate that the cerebral veins
are more likely to be affected by hypoxic stress compared with the arterioles and capillaries, and this might,
in part, explain why the plaques in MS tend to be
perivenular in nature. With respect to this, the hydrodynamic properties of the periventricular veins appear to
make these vessels particularly vulnerable to plaque
Venous hypertension in the dural sinuses seems to be
associated with marked changes in intracranial compliance. There is sound theoretical reason to believe that
this will alter the dynamics of the intracranial CSF system, which in turn may affect the finely tuned intracranial windkessel mechanism. With respect to this, MS
and NPH appear to share some similar characteristics.
In particular, both conditions seem to be characterized
by increased CSF pulsatility in the AoS.
Despite conflicting studies, there is increasing evidence
that CCSVI is a real physiological phenomenon, and that
it is in some way associated with MS. The evidence from
Beggs BMC Medicine 2013, 11:142 Page 12 of 17 studies in patients with MS, and the hydrodynamic analysis presented here, suggests that CCSVI
causes venous hypertension in the dural sinuses. However, the role that CCSVI might play in the pathophysiology of MS remains unclear, and more work is
urgently needed to understand the clinical relevance
of this condition.
ADC: Apparent diffusion coefficient; AoS: Aqueduct of Sylvius; AV: Arachnoid