Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiological entity associated with nonspecific neurological symptomatology (headache, seizures, confusion, impaired level of consciousness, stroke-like symptoms, visual disturbances, coma) associated with distinct precipitants (moderate to severe arterial hypertension, eclampsia or pre-eclampsia, immunosuppressor agents in the context of systemic chemotherapy or solid-organ and bone marrow transplantation, septicemia, chronic renal failure and dialysis, autoimmune conditions, e.g., systemic lupus erythematosus and Henoch-Schönlein purpura, hemolytic uremic syndrome) [1,2]. Haemorrhage occurs in 5-17% of cases [2-4]. The pathophysiology behind hemorrhagic PRES remains controversial but has been associated with two mechanisms: the first supports that severe hypertension leads to hyperperfusion with failed autoregulation, with subsequent blood–brain barrier breakthrough and extravasation of fluid, resulting in vasogenic brain oedema, potentially containing blood. Yet, PRES develops also in patients with normal or mildly increased systematic blood pressure. The second hypothesis states that PRES results from endothelial cell injury and dysfunction, secondary to systemic toxicity mediated by intense cytokine response (IL-1, IL6, TNF-a), causing secondary ischemia and hypoperfusion, which may account for the watershed pattern occasionally observed [1,2,4]. Typical imaging findings of PRES consist of diffuse, bilateral and symmetrical hyperintensities on T2 and FLAIR images in parietooccipital and posterior frontal subcortical and deep white matter. Asymmetrical lesions are observed in 28% of cases. Lesions can also affect the temporal lobes, the superior frontal sulcus and, less commonly, brainstem, cerebellum and basal ganglia [1,3]. Three types of haemorrhage have been identified as having similar incidences according to the literature: focal petechial haemorrhage (<5 mm), intra-parenchymal hematomas and subarachnoid sulcal haemorrhage [1,2]. The risk of hemorrhagic transformation is greater in patients who have undergone allogeneic bone marrow transplants or organ transplants, as well as in patients taking anticoagulants [1,2]. The rate of haemorrhage is independent of the toxic levels of blood pressure [2,3]. In most cases of uncomplicated with haemorrhage PRES, both clinical symptoms and neuroimaging findings regress with the removal of the causative factors (during the first 1-2 weeks), while complete resolution occurs in the first month [2]. Cases of haemorrhage are associated with permanent neurologic sequelae, while the risk of fatal outcome is high. Immediate recognition and correction of the condition that provokes PRES is the best way to treat the disorder and prevent haemorrhage.
