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Central Pontine Myelinolysis: A Case Study Cover
Open Access
|Jan 2018

Abstract

Central Pontine Myelinolysis (CPM) commonly presents as a complication of treatment in patients with profound life threatening hyponatraemia. It occurs when the sodium level is corrected too rapidly. Hyponatraemia should never be corrected at a rate greater than 8-10mmol/L of sodium per day. Rapid correction causes extracellular tonicity and will continue to drive water out of the brain’s cells leading to cellular dysfunction.

Frequent clinical signs include dysphagia, dysarthria, diplopia and acute para/quadraparesis. Patients can also experience locked in syndrome, where cognitive function is intact but all muscles are paralysed with the exception of eye blinking.

CPM gets its name as it occurs when cell dysfunction causes destruction of the myelin sheath of nerve cells in the brain stem, more specifically the pons. It is associated with poor prognosis and prevention is of primary importance.

Freddy is a 35 year old freelance graphic designer, fitness instructor and ultra-marathon runner. In October 2011 he competed in the Sahara Marathon in Morocco, a 6 day 255km ultra-marathon. At the end of the third day Freddy was found collapsed and vomiting. He was confused and was suffering severe leg cramps. The next morning Freddy suffered a single convulsive episode and was subsequently transferred to a hospital in Egypt.

DOI: https://doi.org/10.21307/ajon-2017-108 | Journal eISSN: 2208-6781 | Journal ISSN: 1032-335X
Language: English
Page range: 15 - 19
Published on: Jan 3, 2018
Published by: Australasian Neuroscience Nurses Association
In partnership with: Paradigm Publishing Services
Publication frequency: 2 issues per year

© 2018 Leigh Arrowsmith, Christopher Tolar, published by Australasian Neuroscience Nurses Association
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.