Revision 49 for 'Posterior reversible encephalopathy syndrome'All Revisions
Posterior reversible encephalopathy syndrome
Posterior reversible encephalopathy syndrome (PRES), also known as hypertensive encephalopathy, is a neurotoxic state 3 that occurs secondary to the inability of posterior circulation to auto-regulate in response to acute changes in blood pressure. Hyperperfusion with resultant disruption of the blood brain barrier results in vasogenic oedema, but no infarction, most commonly in the parieto-occipital regions.
It should not be confused with chronic hypertensive encephalopathy, also know as hypertensive microangiopathy, which results in microhemorrhages in the basal ganglia, pons and cerebellum.
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.
- severe hypertension
- haemolytic uraemic syndrome (HUS)
- thrombocytopaenic thromboic purpura (TTP)
- systemic lupus erythematosus (SLE)
- drug toxicity
- bone marrow or stem cell transplantation
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.
Parenchymal infarctions and hemorrhage are associated with PRES in respectively 10-25% and 15% of cases.
Affected regions are hypoattenuating.
- T1: hypo intense in affected region(s)
- C+ (Gd): patchy variable enhancement
- T2: hyperintense in affected region(s)
- DWI: usually normal
- ADC: signal increased in affected regions due to increased diffusion
- GRE: may show hypointense signal in cases of haemorrhage
General imaging differential considerations include: