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Case Reports in Neurological Medicine
Volume 2017 (2017), Article ID 1471096, 7 pages
https://doi.org/10.1155/2017/1471096
Case Report

Acute Psychosis as Main Manifestation of Central Pontine Myelinolysis

1College of Osteopathic Medicine, Des Moines University, Des Moines, IA, USA
2Arizona College of Osteopathic Medicine, Midwestern University, Glendale, AZ, USA
3Baroda Medical College, Vadodara, Gujarat, India
4Department of Neurology, University of Illinois College of Medicine at Peoria, Peoria, IL, USA
5Illinois Neurological Institute, OSF St. Francis Medical Center, Peoria, IL, USA

Correspondence should be addressed to Hrachya Nersesyan

Received 26 November 2016; Revised 14 February 2017; Accepted 7 March 2017; Published 14 March 2017

Academic Editor: Mathias Toft

Copyright © 2017 Mangala Gopal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Central pontine myelinolysis (CPM) is an acute demyelinating neurological disorder affecting primarily the central pons and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy, and encephalopathy of various degrees; however, coma, “locked-in” syndrome, or death can occur in most severe cases. Rarely, CPM presents with neuropsychiatric manifestations, such as personality changes, acute psychosis, paranoia, hallucinations, or catatonia, typically associated with additional injury to the brain, described as extrapontine myelinolysis (EPM). We present a patient with primarily neuropsychiatric manifestations of CPM, in the absence of focal neurologic deficits or radiographic extrapontine involvement. A 51-year-old female without significant medical history presented with dizziness, frequent falls, diarrhea, generalized weakness, and weight loss. Physical examination showed no focal neurological deficits. Laboratory data showed severe hyponatremia, which was corrected rather rapidly. Subsequently, the patient developed symptoms of an acute psychotic illness. Initial brain magnetic resonance imaging (MRI) was unremarkable, although a repeat MRI two weeks later revealed changes compatible with CPM. This case demonstrates that acute psychosis might represent the main manifestation of CPM, especially in early stages of the disease, which should be taken into consideration when assessing patients with acute abnormalities of sodium metabolism.