LAUSR

Posterior Reversible Encephalopathy Syndrome (PRES) was first described in 1996 in a case series of 15 patients. Initially, typical presenting symptoms of patients with PRES were seizures, visual disturbances, encephalopathy, and headache. Currently, the diagnosis is considered in patients with acute neurological symptoms in the context of blood pressure fluctuations, renal disease, (pre-)eclampsia, autoimmune disorders, and as a complication of medical treatment (e.g., immunosuppressive therapy) [1, 2]. Neuroimaging shows subcortical and cortical vasogenic edema usually symmetrically distributed in the parietal or occipital lobes. Other brain regions can be involved, mainly around the superior frontal sulcus or holohemispheric in the watershed areas. Although the edema is reversible, PRES can be complicated by cerebral ischemia and hemorrhage [2]. Several theories on the pathophysiological mechanism leading to cerebral edema exist. The first states that (rapidly rising) hypertension impairs the cerebral autoregulation causing hyperperfusion and breakdown of the blood–brain barrier. The second theory hypothesizes endothelial injury to arise from cytokine activation either in patients with autoimmune disorders or those treated with immunosuppressive or cytotoxic agents [1–4]. As a result of endothelial dysfunction, extravasation of plasma occurs, readily visible on magnetic resonance imaging (MRI) as vasogenic edema.