Secondary to breakdown of blood-brain barrier, leakage of (normally excluded) intravascular proteins and fluid into the cerebral interstitial space.

Primarily affects
white matter.

Seen around tumours, abscesses.

Can occur in late stages of cerebral ischaemia due to ischaemic damage to cerebral vessels.

Posterior reversible encephalopathy syndrome (PRES) is a type of vasogenic oedema which often arises secondary to malignant hypertension.

Altitude sickness (high altitude cerebral oedema (HACE)).

Seen on MRI as elevated apparent diffusion coefficient (ADC) (i.e. increased water diffusion).
Responds to dexamethasone therapy.

Increase in intracellular fluid in glia (particularly astrocytes) and neurons due to failure of cellular metabolism (ATP-dependent ion channels). Predominantly affects
grey matter.

Commonest cause is early cerebral ischaemia (failure of oxygen delivery to brain tissue), for example stroke; near drowning; cardiac arrest; carbon monoxide poisoning.

Drugs and toxins, for example hepatic encephalopathy (secondary to elevated ammonia); isoniazid.

Seen on MRI as reduced ADC (decreased water diffusion).
Not helped by dexamethasone.

Secondary to obstructive hydrocephalus which causes transependymal bulk flow of CSF from ventricle into adjacent white matter.

Oedema predominantly affects periventricular white matter.
Remember: Vasogenic and not cytotoxic oedema is helped by dexamethasone therapy.
Prevention of normal skull growth (children):

Multisutural synostosis (premature fusion of skull sutures), for example Crouzon’s syndrome.
Pathology/Pathogenesis
Monro–Kellie doctrine:
Remember: The cranial compartment (the skull) is of a fixed volume. Any increase in volume of one of the intracranial contents (blood (intravascular or haematoma), CSF or brain tissue (oedema/tumour/abscess)) must be compensated by a decrease in another.
- In normal circumstances, small increases in volume of contents are initially accommodated by the following: