Abstract
Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V1a receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.
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References
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The authors warmly thank Mark Nunn (mark.nunn@gmail.com) for correcting the English.
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Bérenger Largeau conceived the idea, wrote the manuscript, and performed the selection and summary of published literature on the relationship between PRES and AVP. Olivier Le Tilly, Bénédicte Sautenet, Charlotte Salmon Gandonnière, Chantal Barin-Le Guellec, and Stephan Ehrmann helped to design, write, and revise the paper.
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Largeau, B., Le Tilly, O., Sautenet, B. et al. Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?. Mol Neurobiol 56, 6792–6806 (2019). https://doi.org/10.1007/s12035-019-1553-y
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DOI: https://doi.org/10.1007/s12035-019-1553-y