Venous hemodynamics in neurological disorders: an analytical review with hydrodynamic analysis

Abstract

Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.Venous hypertension in the dural sinuses can alter intracranial compliance. Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.

Validation of a Hemodynamic Model for the Study of the Cerebral Venous Outflow System Using MR Imaging and Echo-Color Doppler Data

“…1 The interest in understanding the hemodynamics of the brain arises from human brain function being critically dependent on the proper values of cerebral blood inflow and outflow. 2 Unfortunately, experimental access to cerebral circulation dynamics is limited.…”

Increased Tissue Pressure Induces Demyelinated Lesions and Necroses in the Brain

“…In tissue with reduced blood circulation, hypoxemia will be greater at the venous than at the arterial side of the vascular network (Beggs, 2013). This fact may illustrate the regular occurrence of venous vessels in the center of MS plaques.…”

“…Juurlink (2013) writes that hypoxia is a precipitating factor in causing early MS lesions and that hypoperfusion may be due to a decrease in an arterial supply, restricted venous return, or a combination of these. Beggs (2013) suggests that other pathophysiological mechanisms must be at work, which are increasing the hydraulic resistance of the cerebral vascular bed in patients with MS and leukoaraiosis. No consideration was given to a possible increased tissue pressure (e.g., by edema) as a cause for the reduction of blood flow and for hypoxemic lesions.…”

“…Large periventricular demyelinated lesions of both cerebral hemispheres, such as seen in Schilder's disease (a special form of MS), mainly occur in young patients (Allen and Kirk, 1992). The increased pressure in the periventricular white matter, resulting in inadequate blood perfusion, may explain the formation of the spatial periventricular demyelinated lesions in disorders of the white matter like Binswanger's encephalopathy and leukoaraiosis (Baust et al, 1963;Beggs, 2013). Arteriosclerosis, arterial hypertension and every general brain swelling (e.g., edema in cases of uremia or blood pressure crisis) act synergistically with demyelinating processes.…”

“…However, such venous stenosis or other changes causing narrowing of blood vessels can hardly be proven (Valdueza et al, 2013). Nevertheless, the regular demonstration of venules in the center of the MS lesions offer a valuable link for the understanding of the mechanism for the formation of the lesions and point to an ischemic origin (Beggs, 2013).…”