1) The CSF-circulation is propelled by a pulsating flow, which causes an effective mixing. This flow is produced by the alternating pressure gradient, which is a consequence of the systolic expansion of the intracranial arteries causing expulsion of CSF into the compliant and contractable spinal subarachnoid space. 2) No bulk flow is necessary to explain the transport of tracers in the subarachnoid space. 3) The main absorption of the CSF is not through the Pacchionian granulations, but a major part of the CSF transportation to the blood-stream is likely to occur via the paravascular and extracellular spaces of the central nervous system. 4) The intracranial dynamics may be regarded as the result of an interplay between the demands for space by the four components of the intracranial content, i.e. the arterial blood, brain volume, venous blood and the CSF. This interaction is shown to have a time offset within the cerebral hemispheres in a fronto-occipital direction during the cardiac cycle (the fronto-occipital "volume wave"). 5) The outflow from the cranial cavity to the cervical subarachnoid space (SAS) is dependent in size and timing on the intracranial arterial expansion during systole. Similarly, the outflow from the aqueduct mirrors the brain expansion. The brain expansion is typically very small as evident from the minute aqueductal flow observed in healthy individuals. This expansion occurs simultaneously with an inflow of CSF and will be directed inwards towards the ventricular system. The brain expansion is of decisive importance for the formation of the normal transcerebral pressure gradient. 6) The instantaneous increase of flow in the superior sagittal sinus at the beginning of the systole reflects a direct pressure transmission via the SAS from the expanding arteries to the cerebral veins. It is contended that this early increase in venous pressure together with the volume wave is most likely an important prerequisite for sustaining normal intracranial pressure (ICP) and normal cerebral blood flow. This counter pressure should be reduced in hydrocephalus due to the decreased arterial expansion and could explain the reduced blood flow as well as an increased transmantle pressure gradient causing the ventricular dilatation. An increased pressure in the venous system is likely to be the cause of increases in ICP, including the increased pressure observed in benign intracranial hypertension (BIH).