In recent years there has been much controversy about the possible role that venous anomalies might play in the aetiology of MS. This debate has been precipitated by the work of Zamboni et al. [4], who in 2009 published an ultrasonic study linking a vascular syndrome, chronic cerebrospinal venous insufficiency (CCSVI), with MS. This vascular condition, characterised by stenotic lesions in the extracranial veins, is thought to restrict venous outflow from the brain, resulting in collateral rerouting of the blood flow back to the heart [125]. Although originally linked only with MS, CCSVI has subsequently been associated with Parkinson’s [7], Meniere’s [8, 9] and Alzheimer’s disease [10, 11]. CCSVI has proved to be a highly contentious issue with many doubting its validity, with proponents for [4-6, 126129] and against [130-134] CCSVI publishing contradictory studies defending their respective positions. Although this has led to much confusion, the debate generated by the CCSVI controversy has renewed interest in the role of veins in neurologic disease and has resulted in a considerable amount of new research being undertaken on the cerebral venous and CSF systems, which arguably might not otherwise have occurred [135]. While much of this research has been inconclusive, it has however highlighted the potential for constricted cerebral venous outflow to increase the hydraulic resistance of the venous drainage pathways back to the heart [5, 136], and also to alter the biomechanics of the intracranial space [2, 3]. In particular, it has highlighted the important role that the cortical bridging veins play in regulating both intracranial compliance [73, 74, 119, 137] and intracranial pressure [1]. As such, the CCSVI controversy has helped to raise the profile of the cerebral veins and their importance in regulating the dynamics of the intracranial space.

While clear biomechanical links have been established between cerebral venous drainage and the intracranial fluidic system, it is much more difficult to infer any direct connection between impaired venous drainage and neurodegenerative disease. This is partly because conditions such as MS and Binswanger’s disease are multifactorial in nature but also because the physiology of the intracranial fluidic system is poorly understood. Indeed, such is the complexity and interconnectivity of this system that small anomalies in one part of the intracranial space can lead to multiple changes elsewhere. This makes it very difficult to attribute pathological changes to any single antagonist. Approximately 70% of intracranial blood volume is located within the venous compartment, much of it in thin-walled veins that readily expand or collapse with small changes in transmural pressure. Any constriction of the extracranial venous drainage pathways will therefore tend to cause venous blood to accumulate in these vessels [2, 11, 83, 87] changing their compliance. However, the pathological implications of this are unclear, and further work will be required to fully characterise any pathophysiological mechanisms. Having said this, the venocentric nature of the lesions found in MS and leukoaraiosis points to a vascular connection. While this connection is poorly understood, recent advances in understanding outlined in this review suggest that disturbances of the cerebral venous drainage system can influence the dynamics of the whole intracranial fluidic system and, by implication, the characteristics of the CBF and the motion of the CSF. Although these biomechanical changes have generally been ignored in the past, their importance is increasingly becoming recognised, as they have the potential to shed new light on some of the pathophysiological mechanisms associated with neurologic disease.

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