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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).

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.

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.

If the internal jugular veins are obstructed and the dural sinuses drain slowly, this may cause congestion of the cerebrospinal fluid as well, which may affect steps 1-7 of the cerebrospinal fluid flow.

When internal jugular vein obstructions are treated, there may be an immediate improvement in cerebospinal fluid flow.

This part was from me, not from the links. Before that it was factual but this part needs proving. Evidence based medicine takes forever.

A painfully slow, but educational, neuroanatomy youtube clip about cerebrospinal flow: http://www.youtube.com/watch?v=PUb8iLgpY8E

I don't remember that one. I'll look for it, thanks.

In my non medical mind, surely the poor flow of CSF, the fluid that is responsible for waste disposal of matter in and around the brain, could be the very thing that is leaving "deposits" of material where they aren't meant to be, triggering an autoimmune response - leading to lesions? Is

Is that so far fetched?

I know this question is not about CSF, directly, but is there an average velocity of venous blood, say in the jugulars, if everything is working? Can't Doppeler measure it? Wouldn't an outlying number indicate something is wrong?

Flow rate of cerebrospinal fluid (CSF) — A concept common to normal blood-CSF barrier function and to dysfunction in neurological diseases

Hansotto Reiber∗
Neurochemisches Labor, Universität Göttingen, Robert-Koch-Straβe 40, D-3400 Göttingen, Germany

Abstract
Many neurological diseases are accompanied by increased protein concentrations in the cerebrospinal fluid (CSF), described as a blood-CSF barrier dysfunction. The earlier interpretation as a “leakage” of the blood-CSF barrier for serum proteins could be revised by introduction of a “population variation coefficient” of the CSF / serum quotients for IgG, IgA and IgM (ΔQ/Q̄) which is evaluated as a function of increasing albumin quotients (QAlb). The data presented here are based on specimens from 4380 neurological patients. These population variation coefficients were found to be constant over two orders of magnitude of normal and pathological CSF protein concentrations (QAlb = 1.6 · 10−3 - 150 · 10−3). This constancy indicates that there was no change in blood-CSF barrier related structures with respect to diffusion controlled protein transfer from blood into CSF and hence no change in molecular size dependent selectivity. The pathological increase of plasma protein concentrations in CSF in neurological diseases could also be explained quantitatively by a decrease of CSF flow rate due to its bifunctional influence on CSF protein concentration: reduced volume exchange, and as newly stated, increased molecular net flux into CSF without change of permeability coefficients. Again, on the basis of a changing CSF flow rate, the hyperbolic functions, which describe empirically the changing quotient ratios between proteins of different size (e.g. QIgG : QAlb) with increasing CSF protein content (QAlb) can likewise be derived from the laws of diffusion as the physiologically relevant description. The hyperbolic discrimination line between brain-derived and blood-derived protein fractions in CSF in the quotient diagrams for CSF diagnosis can be further improved on the basis of the large number of cases investigated. Other physiological and pathological aspects, such as high CSF protein values in the normal newborn, in spinal blockade, in meningeal inflammatory processes, CNS leukemia or polyradiculitis as well as animal species dependent variations can each be interpreted as due to a difference or change in the CSF flow rate.