This site is targeted at medical and radiology professionals, contains user contributed content and material that may be confusing to a lay audience. Use of this site implies acceptance of our Terms of Use.

Posterior reversible encephalopathy syndrome

Dr Henry Knipe and Dr Frank Gaillard et al.

Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic state that occurs secondary to the inability of posterior circulation to autoregulate in response to acute changes in blood pressure. Hyperperfusion with resultant disruption of the blood brain barrier results in vasogenic oedema, but not infarction, most commonly in the parieto-occipital regions.


PRES is also known as hypertensive encephalopathy or reversible posterior leukoencephalopathy.

The term PRES can be a misnomer as the syndrome can involve or extend beyond the posterior cerebrum. Furthermore, although most cases involve a resolution of changes with treatment of the precipitating cause and clinical recovery some patients can progress to develop permanent cerebral injury and be left with residual neurological defects.

It should not be confused with chronic hypertensive encephalopathy, also known as hypertensive microangiopathy, which results in microhemorrhages in the basal ganglia, pons and cerebellum.

Clinical presentation

Patients present with headache, seizures, encephalopathy and/or visual disturbance. 


The syndrome can be precipitated by various clinical settings. The mechanism is not well understood but is thought to be related to altered integrity of the blood brain barrier. Two main theories have been proposed:

  • high blood pressure: leads to loss of self-regulation, hyperperfusion with endothelial damage and vasogenic oedema
  • endothelial dysfunction: leads to vasoconstriction and hypoperfusion resulting in cerebral ischaemia and subsequent vasogenic oedema

Hypertension is not present or does not reach the upper limits to self-regulation (150-160 mmHg) in 25% of patients.


Radiographic features

Most commonly there is vasogenic oedema within the occipital and parietal regions (~95% of cases), perhaps relating to the posterior cerebral artery supply. The oedema is usually symmetrical. Despite being termed posterior, PRES can be found in a non posterior distribution, mainly in watershed areas, including within the frontal, inferior temporal, cerebellar and brainstem regions 2. Both cortical and subcortical locations are affected.

There are three main imaging patterns:

  1. holohemispheric at watershed zones
  2. superior frontal sulcus
  3. parieto-occipital dominance

Other uncommon patterns of PRES in <5% include: purely unilateral, or "central" (brainstem or basal ganglia lacking cortical or subcortical white matter involvement).

Parenchymal infarctions and haemorrhage are associated with PRES in respectively 10-25% and 15% of cases.


The affected regions, as outlined above, are hypoattenuating.


Signal characteristics of affected regions include:

  • T1: hypo intense in affected regions
  • T1 C+ (Gd): patchy variable enhancement. It can be seen in ~35% of patients, whether leptomeningeal or cortical pattern. 
  • T2:  hyperintense in affected regions
  • DWI: usually normal
  • ADC: signal increased in affected regions due to increased diffusion
  • GRE: may show hypointense signal in cases of haemorrhage
  • SWI: may show microhemorrhages in up to 50%

Differential diagnosis

General imaging differential considerations include:

Updating… Please wait.


Error Unable to process the form. Check for errors and try again.

Alert_accept Thank you for updating your details.