New understanding of the role of cerebrospinal fluid: offsetting of arterial and brain pulsation and self-dissipation of cerebrospinal fluid pulsatile flow energy.

Many theories have been postulated to date regarding the mechanisms involved in the absorption of the intracranial arterial blood flow energy in the intracranial space, but it is as yet nor clearly defined. The blood flow energy that is transmitted from the heart formulates the cerebrospinal fluid (CSF) pulsatile flow, and is known to constitute the major energy of the CSF flow, while the bulk flow carries only small energy. The intracranial space that is enclosed in a solid cranium and is an isolate system as in the Monroe-Kellie doctrine, and the authors propose to re-analyze the Monroe-Kellie doctrine concept in terms of energy transfer and dissipation of the Windkessel effect. We propose that the large blood flow energy that initiates in the heart is transferred in order of precedence to the arteries, arterioles, brain parenchyma, and finally to CSF within the cranium, in which the energy is confined and unable to be transferred, so that the final transfer of energy to the CSF pulsatile flow is self-dissipated in terms of direction and chronology in CSF pulsatile flow. In order for the CSF pulsatile flow that is transferred from arterial blood flow energy to be dissipated in the intracranial space, this cannot be explained with bulk flow energy in any perspective, since the pulsatile flow kinetic energy is greater than the bulk flow kinetic energy by at least a 100-fold. The pulsatile flow energy within the closed intracranial space cannot be transferred and is confined, as postulated by the Monroe-Kellie doctrine, and therefore the authors propound that the pulsatile flow dissipates by itself. The dissipation of the CSF pulsatile flow kinetic energy will be in all directions in a diffuse and random manner, and is offset by the CSF flow energy vector due to the CSF mixing process. Such energy dissipation will lead to maintenance of low CSF flow energy, which will result in maintaining low intracranial pressure (ICP), and sufficient brain perfusion. It is our opinion that our hypothesis will be able to explain the decreasing offsetting effect of arterial pulsation in chronic obstructive hydrocephalus, and the mechanisms for the ventricular dilatation in communicating hydrocephalus without changes in the mean ICP, and therefore highly justifying our hypothesis.