ICP is determined by the volume of the various intracranial components. Normal ICP is approximately 10 mm Hg. Because the cranium has a fixed volume, an increased volume of any intracranial component must be compensated for by a decrease in the volume of another component. Otherwise, the pressure in the cranium will increase.
There are three major intracranial components.
Brain tissue represents 80% to 85% of the intracranial volume and is composed of a cellular component that includes the neurons and glia, and an extracellular component consisting of the interstitial fluid.
The CSF volume accounts for 7% to 10% of the intracranial volume.
The cerebral blood volume accounts for 5% to 8% of the intracranial volume and includes the blood in the vascular space.
There is an elastance or compliance to the components in the cranium such that a small increase in the volume of one component does not cause an increase in pressure. Once this compliance is exhausted, small increases in volume lead to large increases in ICP (Figure 1).
Increases in cranial volume can be caused by:
Increases in CSF volume due to blockage of the circulation or absorption of CSF.
Increased cerebral blood volume due to vasodilatation (intravascular) or hematoma (extravascular).
Increased brain tissue volume due to a tumor or edema.
Brain edema: Brain edema is classified as cytotoxic or vasogenic and can increase ICP.
Cytotoxic edema is due to swelling of the neuronal and/or glial cellular component and is frequently the result of cerebral ischemia or trauma.
Vasogenic edema is caused by a breakdown of the BBB. The resultant extra-vascularization of protein increases interstitial water due to an increase in osmotic equivalents in the extravascular space.

Figure 1. Idealized Intracranial pressure-volume curve.

 

ICP pathophysiology. An increase in ICP can have severe pathophysiologic consequences.
CPP can be calculated by subtracting ICP from mean arterial pressure (MAP) (i.e., CPP = MAP - ICP).
As ICP increases, CPP decreases. This leads to cerebral ischemia. Normally cerebral ischemia leads to the Cushing reflex, which increases MAP. However, this can compensate only up to a certain point beyond which CPP will fall further, leading to severe ischemia, coma, and death if ICP is uncontrolled.
Increased ICP can also cause herniation of the brain, which can lead to rapid neurologic deterioration and death.