Intracranial Pressure or Intracranial Venous Output Resistance. Part 2: Theory of Pathological Variations.

An intracranial space occupying lesion (SOL) has only weight and volume, and does not generate a pressure directly because of its presence or growth. It evolves in the incompressible tissue environment by displacing, parallel with its growth, an equal volume of one or more intracranial contents ‘extracranially’, directly or indirectly, into the dural venous sinuses. The three displaceable intracranial contents are brain tissue fluid, CSF, and blood in the bridging veins and have different rates and resistances to extracranial output. Brain tissue fluid has the slowest rate but the lowest resistance to output. An SOL must grow by displacing the lowest resistance content if its rate of growth is less or equal to the rate of output of brain tissue fluid. Only a very slow growing lesion such as an osteoma or a meningioma evolves by displacing brain tissue fluid. Intracranial venous flow resistance (VFR) and intracranial venous output resistance (VOR), or dynamic ICP (DICP), remain unaffected. Faster growing SOL displaces CSF parallel with its growth. Again VFR and VOR do not rise. An acutely expanding SOL such as a parenchymal haematoma, subarachnoid haemorrhage or acute hydrocephalus can evolve only by displacing venous blood, which has the fastest output rate but the highest output resistance. Consequent narrowing of cortical veins elevates VFR and VOR (DICP). VOR elevates also if SOL obstructs dural venous sinuses. An SOL causes brain herniation by depleting one or more of displaceable intracranial contents across the midline or a foramen but elevates VOR only if there is cortical venous blood depletion with elevation of VFR. Intracranial haemorrhage displaces an equal volume of intracranial venous blood reducing intracranial arterial input, The ruptured vessel or aneurysm stops bleeding not because of a rise in ICP, which in keeping with Pascal’s Law is uniform in all intracranial contents, but because of a reduction or cessation of input of blood to the arterial bed. All neurological signs are the result of regional or global ischaemia and have nothing to do with intracranial pressure.