Intracranial pressure (ICP) is pressure inside the bony calvarium and therefore reflects the pressure of the brain parenchyma and cerebrospinal fluid (CSF). The Monro-Kellie doctrine operates under the assumption that the cranium is incompressible and the volume inside the cranium is fixed.1Because the intracranial compartment is in contiguity with the spinal canal, which contains epidural fat and openings via neural foramina between segmental vertebra, the assumption of a rigid system is not completely accurate, but provides a useful framework for understanding ICP. The principal intracranial components (blood, CSF, and brain tissue) are in a state of volume equilibrium, and any increase in volume of one of these intracranial components must be compensated for by a decrease in volume of another; otherwise, ICP will increase.2 The principal buffers for increased ICP are CSF and (to a lesser degree) intravascular blood, which respond to increases in volume of the other intracranial constituents. For example, the development of an intracranial meningioma will attempt to be compensated for by a decrease in CSF volume to maintain ICP. Rapid and large volume shifts are difficult for the system to compensate for and will generally result in elevation of ICP.
There are a variety of causes of elevated ICP, which can be primarily related to intracranial masses and edema, obstruction of CSF flow and reabsorption, and obstruction of venous outflow. Space-occupying masses include subdural and epidural hematomas, primary brain tumors, metastatic disease, and cerebral abscess. Spaceoccupying brain edema may have a variety of etiologies such as trauma, infarction, encephalitis, postictal swelling, and disordered autoregulation in the setting of posterior reversible leukoencephalopathy syndrome. CSF accumulation may be from intraventricular obstructive processes and extraventricular barriers to normal CSF reabsorption, such as meningitis and subarachnoid hemorrhage. Elevation of ICP from obstruction of venous outflow may be due to obliteration of venous sinus by mass lesions, venous sinus thrombosis, or elevated venous pressure from dural arteriovenous fistulas. It is important to recognize that these various etiologies are not mutually exclusive and that multiple causes can simultaneously contribute to elevation of ICP.