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Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?

  • Bérenger LargeauEmail author
  • Olivier Le Tilly
  • Bénédicte Sautenet
  • Charlotte Salmon Gandonnière
  • Chantal Barin-Le Guellec
  • Stephan Ehrmann
Article

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.

Keywords

Leukoencephalopathy syndrome Hypertensive encephalopathy Antidiuretic hormone Neurological adverse drug reactions Blood-brain barrier 

Notes

Acknowledgments

The authors warmly thank Mark Nunn (mark.nunn@gmail.com) for correcting the English.

Authors’ Contributions

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.

Compliance with Ethical Standards

Competing Interests

The authors declare that they have no conflict of interest.

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© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.CHRU de Tours, Laboratoire de Biochimie et Biologie MoléculaireToursFrance
  2. 2.Université de Tours, Université de Nantes, INSERM, Methods in patients-centered outcomes and health research (SPHERE) - UMR 1246, CHRU de Tours, Service de Néphrologie-Hypertension artérielle, Dialyses et Transplantation RénaleToursFrance
  3. 3.CHRU de Tours, Service de Médecine Intensive RéanimationToursFrance
  4. 4.Université de Tours, Université de Limoges, INSERM, Individual profiling and prevention of risks with immunosuppressive therapies and transplantation (IPPRITT) - UMR 1248, CHRU de Tours, Laboratoire de Biochimie et Biologie MoléculaireToursFrance
  5. 5.Université de Tours, INSERM, Centre d’étude des pathologies respiratoires (CEPR) - UMR 1100, CHRU de Tours, Service de Médecine Intensive Réanimation, CIC 1415, réseau CRICS-TRIGGERSEPToursFrance

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