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The most important finding of this study is that cerebrospinal fluid “leaks” from the ventricles
of the brain into surrounding brain parenchyma, possibly secondary to trauma induced
blockages of CSF flow and resulting increases in ICP, may be playing an important
etiologic role in the genesis of Multiple Sclerosis. The existence of such possible CSF
“leaks” contributing to MS plaque formation could not be known until MS plaques themselves
became readily visible on medical images. The advent of MRI made this a reality
(1). Such CSF “leaks” could not have been seen prior to MRI, and a role for CSF “leakage”
in the genesis of MS could not have been known prior to the advent of MRI and prior
to the availability of phase coded MR imaging. These combined technologies have now
made CSF flows directly visible and quantifiable.

The first suggestion of this possibility arose from the T2 weighted sagittal brain image
of a patient with MS (Figure 1a, patient #1) displaying an explicit CSF connection between
ventricular CSF and one of the patient’s MS lesions (Figure 1a, arrow #1). Another
lesion in the same image exhibits a similar direct connection to ventricular CSF but in a
less striking manner (Figure 1a, arrow #2). In addition, the peri-ventricular distribution
of MS lesions naturally gives rise to the question that if MS lesions are not correlated in
any way to CSF hydrodynamics, why are they not randomly distributed throughout the
white matter of the brain, instead of being clustered around the ventricles of the brain.
Further consistent with the possibility that MS plaques originate as CSF “leaks” secondary
to trauma, is the existence of Dawson’s fingers (Figure I) where the “long axis of
the (MS) plaque” is “parallel with the white matter fibers in the corona radiata”, i.e., not
within the white matter fibers themselves but parallel to them. “Dawson’s fingers” might
well be the “leak” pathways of cerebrospinal fluid originating in the ventricle and joining
the body of the MS plaque within the brain parenchyma. Parallel to the white matter
fibers would be the path of least resistance for “leaking” CSF to diffuse within the brain
parenchyma, i.e., alongside the white matter fibers.

Protein is the principal ingredient, other than water, of the cerebrospinal fluid. CSF contains
approximately 15 to 40 mg/dL of protein (12). CSF gel electrophoresis has established that there are “more than 300 polypeptides in CSF” (13). In addition, “nine antigenic
species have been demonstrated in CSF that are absent in serum” (14). The question
naturally arises whether the “leakage” of these CSF antigenic proteins, like the
antigenic tau proteins they are known to contain (15), could be the source of the antigens
generating the autoimmune reactions known to be the origin of MS lesions.
If trauma induced “leakage” of CSF proteins into the surrounding brain parenchyma,
and particularly “leakage” of antigenic proteins, is contributing to the formation of MS
plaques, then the vascular expansion stenting of the Azygous and Internal Jugular Veins
recommended by Zamboni et al. (16) could be monitored after installation by UPRIGHT
® phase coded MRI measurements of CSF flow. Upright phase coded imaging of
CSF flow would assure that installed expansion stents are achieving the corrections of
CSF flow dynamics and intracranial pressure (ICP) that are needed to terminate plaque
generating CSF “leaks”.

It is possible that those patients who currently do not respond to the Zamboni vein expansion
stents or those who relapse are relapsing or not responding because the necessary
restoration of normal CSF hydrodynamics and normal ICP has not been fully accomplished
by the initial venous stenting procedure or is not being maintained.
Schoser et al. have reported that an increase in ICP is associated with an increase in
blood velocity in the straight sinus (17). One possible explanation, therefore, for the success
of the Zamboni et al. expansion stent procedure (16) could be that the Zamboni expansion
stent is diminishing blood flow velocity in the straight sinus and BVR (Basil Vein of Rosenthal), thereby reducing ICP and diminishing plaque generating CSF “leaks”.

Myelogenesis is a normal physiologic process that repairs damaged myelin over time
(19). If the myelin injuring process, i.e., “leaked” antigenic CSF proteins, could be terminated,
there is the possibility that with the continuing injury from CSF “leakage” terminated,
the demyelinated axons of MS lesions could be remyelinated by normal
physiologic myelogensis and the MS lesions repaired.

Schoser et al. have reported that an increase in ICP is associated with an increase in
blood velocity in the straight sinus (17).

There is evidence that absorption of CSF by the arachnoid villi occurs by a valve-like process, permitting the one-way flow of CSF from the subarachnoid spaces into the venous sinuses. CSF absorption does not occur until CSF pressure exceeds the pressure within the sinuses. Once this threshold is reached, the rate of absorption is proportional to the difference between CSF and sinus pressures. A normal human can absorb CSF at a rate up to six times the normal rate of CSF formation with only a moderate increase in intracranial pressure.

If obstructions occur at the foramina between the ventricles, the ventricle upstream from the obstruction will enlarge, producing obstructive hydrocephalus. Occasionally, disease processes affect CSF removal. For example, obliteration of the subarachnoid space by inflammation or thrombosis of the sinuses will prevent clearance of fluid. When this occurs, CSF pressure increases and hydrocephalus develops without obstruction of the ventricular foramina. This is called communicating hydrocephalus.

unless there is some einstein hideing in woods that has this all figured out then --ok!

The distribution of CSF is on the outside of the brain, would not explain gray matter degredation, iron deposition in the thalmus, enlarged veins, and lesions we see like Dawson's Fingers in MS, which all occur deep inside brain tissue. CSF surrounds the outside tissue...