Dr. Schelling's wrote
" Spread of Acute Rises in Central Venous Pressure into the Brain?
Any momentary excess central venous pressure tends to revert the flow in any venous drainage which is not guarded by competent valves. If a venous drainage system lacking competent valves is not vented by venous anastomoses (lacking opposing valves) and its pathways are nowhere compressed, regurgitant blood can most easily and rapidly be pushed back in any affluent vein as far as its outermost tributary vessels.
But so long as its circumvallation is intact and nowhere substantially yields to pressure, the craniovertebral space can accommodate regurgitant blood volumes only as long as a commensurate venting, i.e. evacuation of blood from separate venous drainages of cranial cavity and spinal canal, is possible. If back-jets into different cerebral or spinal venous drainage systems compete, length and flow resistance of the respective venous pathways will also influence the pressure load to which walls and neighborhood of the involved veins will be exposed.
Skull radiographs of supposed victims of multiple sclerosis, showing striking widenings of the main venous passageways out of (and into) the cranium first stirred the present author's particular interest in the diverse anatomical pathological specifications of multiple sclerosis (119). A closer scrutiny of the truly unique post-mortem observations of multiple sclerosis led him to the conclusion that the specific cerebral changes evolve under the following circumstances and in the following ways:
The first prerequisite for plaque veins' injurious activities appears to be a disproportionately severe valvular incompetence of that internal jugular vein by which these plaque veins are specifically drained (Plate XIV , figg. A, B). Via this vein regurgitant blood then must be conducted into a relatively minor intracranial catchment area – meaning, in a classic instance of cerebral multiple sclerosis, directly up into the straight sinus affluents. Provided there are no venous anastomoses strong enough to provide for the involved venous pathways' sufficient venting, venous regurgitations of injurious intensities into the straight sinus’ affluent veins must occasionally result (119,120).
The remarkable functional isolation of the straight sinus system of venous drainage has been consistently illustrated not only anatomically (9,120), but also – more dramatically -- in the literature on the disastrous effects of (especially thrombotic) straight sinus occlusions. The evidence presented demonstrates that, if the venous outflow through the straight sinus is blocked, the collateral venous drainage from the brain's central parts tends to decompensate under the mere perfusion load of blood circulation (). It becomes clear that the potentially far more massive overloading of the straight sinus affluents by intense venous back-jets can certainly not be expected always to be dissipated in a harmless fashion.
Apart from their typically being limited to affluents of the straight sinus, the brain plaques of multiple sclerosis expand from only certain small section(s) of a plaque vein's surface. The question arises as to what may limit and localize the particular venous regurgitation effects. A consideration of the acute, both absolute and relative rises in intra-abdominal and intra-thoracic pressure reveals the existence of a number of factors which can limit a spread of venous regurgitation into particular cerebral veins. The primary limiting factor against a strong retrograde venous invasion of a particular part of the brain lies in the rapidity with which the thrust of any correspondingly localized venous regurgitations is counterbalanced by separate competing venous regurgitant and ordinary arterial flows into the craniovertebral space. A regurgitation into particular cerebral veins may also end precipitously, due to an exhaustion of its own volume or, in cases involving a larger intracranial venous domain, because the veins providing for a venting of the craniovertebral space are emptied too quickly. Finally, the ordinary course of trans-diaphragmal pressure gradients makes it probable that venous regurgitations into the brain will often be stopped by competing venous back-jets from intra-abdominal collecting veins into the epidural vein plexus of the lower spinal canal.
The Development of Venous Back-Jets into the Brain
The conditions predisposing to injurious venous back-jets via one internal jugular vein into the brain are rather complex, and research must be initiated to directly determine when and how such potentially disastrous events take place. If the venous drainage of the straight sinus is critically isolated and the other venous tributaries of the large collecting veins of the trunk are guarded by competent valves, potentially disastrous back-jets of central venous blood will begin as soon as the valve of the straight sinus-related internal jugular vein has been burst through, become too distended, or if its valve-leaflets have critically shrunken.
However, this is only one requirement for the occurrence of potentially disastrous venous back-jets into the brain. The presence of opportunities for sufficiently massive venting effluxes out of the craniovertebral space is equally necessary. As soon as the venous back-jet has become established, it will always tend to become more severe -- simply because of its continual "washing out" of its own pathways into, and of the channels of concurrent venting effluxes out of, the craniovertebral space. Thus initially harmless venous regurgitations may, sooner or later, reach injurious intensities.
The physical impacts causing "Dawson's fingers" and "Steiner's splashes" thus appear comprehensively accounted for."