The arachnoid villi, most numerous on both sides of the superior sagittal sinus, are also present at the base of the brain and around the spinal cord roots and have been thought to act as functional valves that permit unidirectional bulk flow of CSF into the vascular lumen. However, electron microscope studies show that the arachnoid villi have a continuous membranous covering. This layer is extremely thin, and CSF passes through the villi at a linearly increasing rate as CSF pressures rise above 68 mm H2O. This passive route is not the only manner in which CSF water and other contents are transported. Tripathi and Tripathi, in serial electron micrographs, found that the mesothelial cells of the arachnoid villus continually form giant cytoplasmic vacuoles that are capable of transcellular bulk transport. Certain substances, such as penicillin and organic acids and bases, are also absorbed by cells of the choroid plexus; the bidirectional action of these cells resembles that of the tubule cells of the kidneys. Some substances have also been shown to pass between the ependymal cells of the ventricles and to enter subependymal capillaries and venules.
By infusing and withdrawing CSF under controlled circumstances, the resistance to CSF absorption and its rate of replacement can be calculated. The resistance to the passage of CSF into the venous system has been termed R0 and can be expressed in terms similar to the Ohm law (E = IR): the voltage (E) reflects the difference in pressure between the CSF and the venous system (PCSF – PV), which drives CSF into the dural sinuses, and the equivalent of electrical current, termed If, represents the flow rate of CSF. In the steady state, this flow rate is equal to the rate of CSF production (0.3 mL/min). R0, the resistance to absorption, which under normal circumstances is approximately 2.5, rises when there is a blockage in the CSF circulation. The equation for CSF pressure can therefore be expressed as PCSF – PV = If × R0; when rearranged, PCSF = PV + If × R0. Because the product of If × R0 is only 0.8 mm Hg, it can be appreciated that the main contribution to CSF pressure—as measured by spinal puncture—is the venous pressure, PV. Restated, the intracranial pressure and CSF pressure, which are in equilibrium, are the result predominantly of vascular pressures and not CSF outflow resistance. However, in pathologic conditions such as bacterial meningitis and subarachnoid hemorrhage, R0 may rise to levels that impede CSF circulation, raise pressure.
In the recumbent position, ICP and, consequently, CSF pressure are normally about 8 mm Hg or 110 mm H2O (1 mm Hg equals 13.7 mm H2O), with an upper limit of normal that is higher in children than in adults according to Huh and colleagues. As the head and trunk are progressively elevated, the weight of the column of CSF is added incrementally to the pressure in the lumbar subarachnoid space, and the intracranial CSF pressure drops correspondingly, so that it is close to zero in the standing position. As described above, the CSF pressure is in equilibrium with the capillary and prevenous vascular pressures, which are influenced mainly by circulatory changes that alter arteriolar tone. Elevations in systemic arterial pressure cause little or no increase of pressure at the capillary level because of cerebrovascular autoregulation, and hence, little increase in CSF pressure. Extremely low blood pressure (BP), in the range of a mean of 40 mm Hg, however, cannot be compensated for and correspondingly, lowers the CSF pressure (it follows that CSF pressure is zero, when the heart stops).