22. Etiologies of Posterior Reversible Encephalopathy Syndrome and Forms of Osmotic Demyelination Syndrome

  1. Edward M. Manno MD, FCCM, FAAN, FAHA
  1. J. Javier Provencio MD

Published Online: 11 APR 2012

DOI: 10.1002/9781118297162.ch22

Emergency Management in Neurocritical Care

Emergency Management in Neurocritical Care

How to Cite

Provencio, J. J. (2012) Etiologies of Posterior Reversible Encephalopathy Syndrome and Forms of Osmotic Demyelination Syndrome, in Emergency Management in Neurocritical Care (ed E. M. Manno), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781118297162.ch22

Editor Information

  1. Neurological Intensive Care Unit Cleveland Clinic Cleveland, OH, USA

Author Information

  1. Cerebrovascular Center, Cleveland Clinic, Cleveland, OH, USA

Publication History

  1. Published Online: 11 APR 2012
  2. Published Print: 11 MAY 2012

Book Series:

  1. Neurology in Practice

Book Series Editors:

  1. Robert A. Gross and
  2. Jonathan W. Mink

Series Editor Information

  1. Department of Neurology, University of Rochester Medical Center, Rochester, NY, USA

ISBN Information

Print ISBN: 9780470654736

Online ISBN: 9781118297162

SEARCH

Keywords:

  • etiologies of PRES and ODS forms;
  • syndrome of PRES and ODS;
  • PRES, treating the disorder as toxic, in ameliorating cause;
  • PRES in multitude of disease processes;
  • nonhypertensive causes of PRES, considered;
  • second mainstay of therapy, hypertension control;
  • ODS, inability of brain to adjust osmolarity changes;
  • ODS, better prevented, than treated;
  • aggressive potassium replacement, in ODS prevention

Summary

The syndromes of reversible encephalopathy (PRES) and osmotic demylination (ODS) have little in common save their clumsy definitions and their preventable ability to cause harm. In this chapter, we will discuss the mechanisms, new insights, prevention, and treatment of these two syndromes. PRES was long thought to be the result of hypertension overwhelming the ability of the blood–brain barrier to contain intravascular water, but a recent rethinking has led to a more nuanced understanding of the syndrome. It now seems that a number of brain toxic phenomena can predispose patients to PRES. Treatment remains blood pressure control and removal of obvious toxins when possible. ODS, on the other hand, is due to a rapid correction of hyponatremia in patients who have largely expended their ability to regulate brain osmolarity. The treatment remains careful management of sodium repletion in susceptible patients.