Monday, June 3, 2013 1:20 AM
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Tony Miles
http://www.biomedcentral.com/content/pdf/1741-7015-11-142.pdf Conclusions to the paper presented: Conclusions 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 formation. 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 http://www.biomedcentral.com/1741-7015/11/142CSF-related 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. Abbreviations ADC: Apparent diffusion coefficient; AoS: Aqueduct of Sylvius; AV: Arachnoid
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