Monro-Kellie hypothesis

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• Brain Edema Formation and Functional Outcome After Surgical Decompression in Murine Closed Head Injury Are Modulated by Acetazolamide Administration

The pressure-volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine or the Monro-Kellie hypothesis ^{1) 2)}

The Monro-Kellie hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is a fixed volume. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.

The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g. epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.

These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100–120 mL.

So what's the big deal? If the abnormality becomes large enough, the pressure within the skull can increase rapidly. Eventually the pressure can become so great that the brain gets squished, and will pop over rigid boundaries and out the small holes within the skull.

This is known as “herniating” the brain tissue. It can occur in numerous places within the skull depending on where the pressure is greatest. However, the most important herniation clinically occurs at the base of the skull where a hole known as the foramen magnum exists.

Intracranial volume compensatory changes explained by the Monro-Kellie hypothesis (MKH) occur in spontaneous intracranial hypotension (SIH) and may be seen on MR imaging ³⁾.

Many of the MRI abnormalities seen in intracranial hypotension or CSF volume depletion can be explained by the Monro-Kellie hypothesis. These abnormalities include meningeal enhancement, subdural fluid collections, engorgement of cerebral venous sinuses, prominence of the spinal epidural venous plexus, and enlargement of the pituitary gland ⁴⁾.

see Intracranial hypertension