Venous Hemodynamics in Neurologic Disorders
Clive Beggs, Ph.D. (Centre for Infection Control and Biophysics, University of Bradford, Bradford, UK)
Abstract There is increasing evidence that the cerebral veins and sinuses play an important role in regulating fluids in the intracranial space [1, 2]. There is evidence that venous anomalies may contribute to the pathophysiology of several neurological conditions, including multiple sclerosis (MS) [3, 4], leukoaraiosis [5, 6], normal-pressure hydrocephalus (NPH) , and Alzheimer’s disease (AD) . Here we briefly review the literature regarding venous hemodynamics in neurologic disorders and use 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.
Altered CSF dynamics are a feature of both MS [9, 10] and NPH [11. 13]. Similarly altered dynamics have been shown to be associated with constricted cerebral venous outflow in healthy individuals , suggesting that their origin is primarily biomechanical. The hydraulic resistance of the cerebral venous drainage system is on average 63.5% greater in MS patients diagnosed with CCSVI compared with CCSVI-negative healthy controls . This suggests that CCSVI is associated with mild venous hypertension (<5 mmHg) in the dural sinuses; something that would tend to inhibit the bulk flow of CSF, as has been observed in MS patients [9, 10]. Venous hypertension of this magnitude may also reduce intracranial compliance. Approximately 70% of intracranial blood volume is located within the venous compartment, much of it in thin-walled veins that readily collapse under small changes in transmural pressure. Venous hypertension due to CCSVI would tend to reduce the compliance of these vessels, diminishing the ability of the subarachnoid space (SAS) to accommodate returning CSF during diastole. If this occurs, then it is likely that additional positive CSF flow (towards the lateral ventricles) will occur in the aqueduct of Sylvius (AoS), as has been observed in both patients with MS [9, 10] and healthy subjects with CCSVI . It has been suggested that the change in intracranial compliance seen in patients with NPH may be associated with venous hypertension . In patients with NPH, cortical- vein compliance is significantly reduced ; however, following shunt surgery, compliance greatly increases, suggesting that the compliance changes associated with these veins are functional and not structural [7, 14]. It is therefore plausible that hypertension in the sagittal sinus might increase the pressure in the cortical veins, with the result that the functional compliance of these vessels is reduced . As such, this would explain the increase in aqueductal CSF pulsatility observed in patients with NPH [11, 13].
It has been postulated that venous hypertension arising from CCSVI might be responsible for the reduced cerebral blood flow (CBF) observed in MS patients. However, given that the cerebral perfusion pressure is normally in the region of 70 to 85 mmHg, it is unlikely that venous hypertension of less than 5 mmHg, such as that associated with CCSVI, could account for the large reduction in WM CBF reported in patients with MS [14,15]. It is more likely that the reduction in CBF reported in MS patients is due to morphological changes in the cerebral vascular bed. This may be due to loss of cerebral veins  or alternatively, narrowing of the venous lumen, similar to that observed with periventricular venous collagenosis in patients with leukoaraiosis .
I listen carefully to anything that Clive Beggs says.
From his last paragraph, what does that mean for the concerns about venous hypertension in CCSVI? It's too small to make an impact?