The cerebrospinal fluid (CSF) not only provides mechanical protection to the central nervous system, but also acts as a transport medium for nutrients, neuroendocrine substances and for the removal of toxic metabolites, preserving the chemical environment of the brain (Davson et al. 1987). As outlined in the second part of this work (Holman et al. 2010), it is hypothesized that the disruption of CSF flow may be linked to neurodegenerative diseases such as Alzheimer's through disturbed regulation of intracranial pressure, through accumulation of toxic metabolites or through a combination of both (Segal 2000; Stopa et al. 2001; Kivisakk et al. 2003; Silverberg et al. 2003; Abbott 2005; Johanson et al. 2005).
You can read about cerebrospinal fluid here:http://rsif.royalsocietypublishing.org/ ... .0033.full
and then watch the accompanying '3D visualization of CSF flow velocity vectors in a human subarachnoid space during one cardiac cycle' here:www.youtube.com/watch?v=mGy55iRHTlg&feature=related
The latter was pretty but not intuitively understandable to me...
We show in the work at hand that there are large spatial variations in the velocity distribution in the cranial SAS that will influence the transport behaviour of toxic metabolites and neuroendocrine and other substances released into the CSF. Assuming there are physiological reasons for these variations, we hypothesize that not all regions of the brain will be affected with the same severity by disrupted CSF flow.
Lots of equations follow, reminiscent of Dr. Tucker's or Dr. Beggs' work....
But skipping ahead:
Large variations in the CSF velocity field indicate substantial spatial differences in transport characteristics. For flow in the third cerebral ventricle, there are indications that the ventricle shape is optimized with regards to substance transport between the pituitary gland and the hypothalamus (Kurtcuoglu et al. 2007b). It is conceivable that, similarly, the flow variations in the SAS reflect an optimization with regards to efficient transport of toxic metabolites and other substances used for communication through the CSF space. This would suggest that different areas of the brain would be affected dissimilarly by a disruption of CSF flow. As an example, a brain region requiring very efficient flushing of toxic metabolites may experience accumulation of waste products that could lead to or accelerate neurodegenerative processes, whereas, in other areas, the disruption may have little to no effect.
Presuming that our IJV obstructions could cause disruption to the cerebrospinal flow, this might affect different areas of the brain differently. Substance transport might be disrupted. Removal of toxic metabolites might be disrupted. In some areas the toxins might accumulate, while in others they might not, with neurodegenerative processes as a result.
So the big question is: what effect, if any, do IJV obstructions have on cerebrospinal flow?