Abstract The human craniovertebral cavity, although practically completely surrounded by bone, is subject to relatively wide variations in pressure. The activity of the cerebrospinal fluid is dependent upon: (1) a stable production-absorption mechanism; (2) the phenomena occurring in the intracraniospinal veins which very sensitively reflect pressure changes to that fluid. The almost constantly shifting variations in pressure which occur in the cerebrospinal veins and which are secondary to pressure changes in the extracranio-vertebral veins, indicate the elastic nature of the craniovertebral cavity in contrast to the older conception of the closed box character of the cavity. Under most physiologic and many pathologic conditions, variations in cerebrospinal fluid pressure are readily explained by changes in venous pressure. It is only under unusual pathologic conditions that variations in osmotic pressure affect the level of the fluid pressure. Although the cerebral arteries have an intrinsic nerve supply, changes in caliber of the intracranial arteries probably rarely, if ever, disturb the normal cerebrospinal fluid pressure, except during severe abnormal states, such as during oxygen-carbon dioxide disequilibrium. It is true that these vessels react sensitively to changes in metabolites circulating in the body, metabolites, however, which remain remarkably constant under physiologic conditions. Even under very unusual conditions, it is difficult to effect changes in caliber of the cerebral arteries, and great and sudden increases in arterial pressure are necessary before the diameter of the cerebral arteries alters. Again, removal of fluid from the cistern does little, if anything, to the caliber of these vessels. On the other hand, during such procedures, marked changes occur in the size and pressure of the cerebral veins. If it is a dictum that the cerebrospinal fluid pressure is closely related to the venous pressure, it is also true that the cerebral blood flow is closely related to the arterial blood pressure and the width of the cerebral vascular bed. These two factors tend to keep the oxygenation of the brain at a steady state or within normal limits, so that, for example, a great fall in arterial pressure is compensated by a widening of the vascular bed. Thus, the blood flow may be slower, but the oxygen uptake by the brain is relatively greater. It is remarkable that unconsciousness or convulsions do not supervene until the cerebral arterial pressure falls to a level of approximately 20 mm. of mercury, at which point the oxygen saturation of the internal jugular blood is in the neighborhood of 20 volumes per cent. The difficulty in affecting the cerebral blood flow is again observed in states of increased intracranial pressure, which must be extremely high before collapse occurs. One of the most remarkable of the vascular adjustment mechanisms is the ability of the cerebral circulation to continue in the face of almost complete and prolonged venous obstruction. Under such conditions, the emissary pathways increase in their activity so that the cerebral venous pressure becomes partially adjusted, and the production-absorption mechanism becomes reestablished with a fall of cerebrospinal fluid pressure to its original level. These examples suffice to demonstrate the remarkable resiliency of the cerebral circulation during widely adverse circumstances.