Intracranial Pressure or Intracranial Venous Output Resistance Part I: Theory of origin and physiological variation

Intracranial Pressure (ICP) has two components, static or gravitational and dynamic or vascular. Dynamic intracranial pressure (DICP) is the unspent fraction (or entirety) of the intracranial arterial blood pressure and equals intracranial venous output resistance (ICVOR), which is the sum of intracranial venous flow resistance (ICVFR) in the bridging veins and the dural venous sinus pressure (DVSP). Intracranial contents possess only volume and weight, and cannot directly create or vary ICP. Contraction of voluntary, cardiac or smooth muscle is the sole mechanism for generating a pressure in the living body. All perpetually dynamic pressures in the living body, such as ICP, derive from cardiac systole, the only muscular contraction that recurs unceasingly during life, and disappear at asystole. Intracranial contents possess physical properties of fluids, are constant in volume in physiological state and are incompressible at biological pressures. Input to an intracranial content equals and parallels output from it, directly or indirectly, to ‘extracranial’ dural venous sinuses. The total volume of these contents has no relationship with ICP and the so-called elastance and compliance are not known physical properties of matter in the fluid state and do not, therefore, merit a role in the origin or variation of ICP. DICP varies because of changes in ICVFR, DVSP or both. ICVFR varies, in accordance with Poisieulle’s equation, with passive changes in the lumens of bridging veins that occur due to opposite and parallel active changes in the lumens of intracranial arteries and arterioles. Changes in DVSP are secondary to changes in CVP or obstruction in dural sinuses. ICVOR or DICP is uniform throughout the intradural compartment and dynamic pressure gradients do not exist in intracranial contents. In the incompressible intracranial environment, blood input, flow and tissue perfusion occur because the arterial bed, from the large arteries to the ends of arterial capillaries, expands and contracts during the cardiac cycle creating equal, parallel and opposite volume changes in the venous bed, and balanced inputs to and outputs from arteries, veins and capillaries.