The pathogenic hallmarks are failure of cerebral autoregulation and the development of vasogenic oedema.
The posterior regions of the brain may be more susceptible to failed autoregulation due to relatively less sympathetic innervation.
Endothelial damage with blood–brain barrier disruption lead to fluid and protein transudation.
Focal vasoconstriction may cause cerebral infarcts. [1, 3, 5]
