Monro-Kellie Doctrine

Original Author: Rose Ingleton
Last Updated: May 6, 2019
Revisions: 2

The Monro-Kellie Doctrine was first described by Dr Alexander Monro and Dr George Kellie. It describes the relationship between the contents of the cranium and intracranial pressure.


The cranium (or neurocranium) describes the part of the skull encasing the brain, made up of 8 bones (frontal, ethmoid, sphenoid, occipital, paired parietals, and paired temporal). As the cranium is made from solid bone*, its structure is fixed and therefore the volume contained within cannot be changed.

Alongside the brain tissue, the other major components found within the cranium are blood (mostly venous blood from within dural sinuses) and the cerebrospinal fluid (CSF). The volume of each of these components is restricted by the fixed space within the cranium.

*This concept only applies to adults, as the presence of fontanelles and open suture lines in infants that have not yet fused means there is potential for a change in size and intracranial volume

In an average adult, the intracranial volume is approximately 1700ml and is distributed as shown in Figure 1.

In normal cranial physiology, these three components exist in equilibrium with each other to satisfy this fixed volume. As such, if the volume of one component increases, the volume of another must decrease.

Figure 1 – The intracranial components and their respective volumes

Intracranial Pressure

The intracranial pressure (ICP) is the pressure within the cranium of the skull. Due to the fixed nature of the cranium, an increase in volume of any one of the intracranial components will also cause an increase in pressure.

Therefore, in the absence of pathology, an equilibrium between these three components must be maintained to preserve a normal intracranial pressure. If the volume of one of the components within the cranium increases, the volume of a different component must decrease to maintain this equilibrium and sustain a normal ICP.

The normal value for intracranial pressure is 5–15mmHg. A value above 20mmHg usually signifies the point at which intervention may be required to avoid significant or life-threatening consequences.

Intracranial Pathology

If a pathological condition affects any one of the three components or a new component is introduced in to the fixed volume of the cranium, then this equilibrium may be disrupted.

For example, if a patient develops a brain tumour, a new component (with its own volume and own contribution to intracranial pressure) is introduced in to the cranial cavity. Initially, as the tumour is growing, its volume may be small enough that the skull volume can accommodate it and compensatory mechanisms can be employed to maintain a normal intracranial pressure.

The main compensatory mechanisms are increased drainage of blood or cerebrospinal fluid from the cranial cavity, in turn allowing for space to be created for this new lesion. This means that the intra-cranial pressure remains normal (Figure 2).

Figure 2 – Intracranial compensation in the presence of pathology to maintain a normal intracranial pressure

However, if the tumour continues to grow, it will reach a certain size where these compensatory mechanisms will become exhausted, whereby no further drainage of blood or CSF will be possible.

At this point, the equilibrium becomes disrupted and the patient enters a decompensated state where intracranial pressure will begin to rise (Figure 3).

Figure 3 – Intracranial decompensation in the presence of pathology causing a rise in intracranial pressure


Figure 4 – Types of Herniation

If the tumour continues to grow without intervention, the intracranial pressure will rise to such a degree that the final cranial component, the brain parenchyma, will shift in position and become displaced, this is termed herniation.

There are several types of herniation depending on which part of the brain is being displaced, the most serious of which are uncal and tonsillar herniation (Figure 4):

  • Uncal herniation refers to displacement of the medial part of the temporal lobe (uncus) below the tentorium cerebelli
  • Tonsillar herniation occurs when the cerebellar tonsils are forced downwards through the foramen magnum, causing compression on the brainstem (fatal if left untreated)

Volume-Pressure Curve

In the absence of pathology, normal homeostatic mechanisms maintain a normal intracranial pressure in response to small fluctuations in intracranial volume. Indeed, in the presence of pathology with a small volume, our compensatory mechanisms also ensure that the intracranial pressure remains maintained.

As the intracranial pathology increases in size, the patient will enter decompensated state, whereby small increases in intracranial volume result in a large increase in intracranial pressure* (Figure 6). If the intracranial pathology increases further in size, without intervention, the intracranial pressures rises even more rapidly, that can lead to brain herniation.

This is termed the volume-pressure relationship.

*Although this does mean that a neurosurgeon only has to remove a small volume (blood/CSF/brain tissue) in order to significantly reduce the intracranial pressure.

Figure 5 – The intracranial volume-pressure curve (1) No pathology (2) Small volume pathology in a compensated state with normal ICP (3) Large volume pathology in a decompensated state with elevated ICP (4) Very large volume pathology with a significantly elevated ICP and brain herniation

Key Points

  • The Monro-Kellie Doctrine describes the relationship between the contents of the cranium and intracranial pressure
  • In non-pathological states, three components exist in equilibrium to maintain normal intracranial pressure, the brain tissue, the blood, and the cerebrospinal fluid
  • Small volume changes can be accommodated by compensatory mechanisms to maintain the intracranial pressure
  • Larger volume changes can lead to the compensatory mechanisms being exhausted, leading to significant increases to intracranial pressures and potential herniation

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