ICP: tumor: corrected mechanism

The process by which intracranial tumors produce cerebral compression was initially described over one hundred years ago. (Source 1)

In the normal adult, intracranial contents (i.e. cellular mass, blood, and CSF) have a combined volume of 1200-1500 cm^3. (Source 2). The presence of a tumor (or other mass lesion, e.g. hematoma) increases intracranial volume. When the cranium is closed, an increase in intracranial volume would necessarily result in an increase in intracranial pressure (ICP) due to the rigid enclosure of the skull. This change in pressure given a change in volume is commonly referred to as elastance (the inverse of compliance).

However, initially an increase in cellular mass can be compensated for by a reduction in volume of the other intracranial components i.e., CSF and blood. This compensation allows for a degree of increase in tumor volume without any change in ICP, therefore prolonging the onset of clinical symptoms. When this compensatory mechanism is exhausted, ICP increases (Monro-Kellie doctrine). This increase in ICP may cause a decrease in cerebral perfusion pressure, defined as MAP – ICP (or CVP if it is higher than ICP), or may cause herniation of brain tissue from one compartment to another (e.g. across meningeal barriers, down the spinal canal, or, in the case of skull fracture, outside the skull). Both of these processes can lead to ischemia, mechanical injury, and cerebral dysfunction.

Neurologic injury triggers a complex host of processes that result in cerebral cytotoxic and vasogenic edema, which worsens ICP by further increasing intravascular volume (Ref. 1, 2). This vicious cycle leads to worsening clinical symptoms: drowsiness and headache progressing to hypertension and bradycardia, followed ultimately by loss of consciousness, fixed and dilated pupils, hypotension, and death (Source 3).