Posterior reversible encephalopathy syndrome (PRES) is an acute neurological disorder of vascular origin characterized by seizure, headache, encephalopathy, visual disturbances, focal neurological signs, and distinct neuroimaging features such as vasogenic edema, usually on the bilateral parieto-occipital region. 1,2 It occurs in the context of renal failure, autoimmune disorder, cytotoxic drug usage, eclampsia, and preeclampsia. 1 Two theories are most widely accepted to explain pathogenesis. One of the theories is the rapid development of hypertension to the level where autoregulation fails leading to hyperperfusion, vascular leakage, and finally vasogenic edema. Edema is due to the extravasation of plasma proteins and macromolecules through disrupted tight junctions. The other theory suggests PRES is due to endothelial dysfunction due to exogenous (like in immunosuppressive and cytotoxic drugs) and endogenous (like in eclampsia and sepsis) factors. The circulating toxins cause vascular leakage, edema, and release of vasoactive and immunogenic substances. 2,3 Posterior reversible encephalopathy syndrome following administration of cytotoxic agents like calcineurin inhibitors, tyrosine kinase inhibitors, oxaliplatin, bevacizumab, and 5-FU has been