J-LSMS 2018 | Archive | Issues 1 to 4

JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY

Central Pontine Myelinolysis in a Patient with Schizophrenia

Carine Nzodom, MD

Central pontinemyelinolysis (CPM) was first described in 1959. Since then, many case reports and case series have been published about this topic. According to literature, the most common predisposing factor is hyponatremia and the most common presentation is encephalopathy. Unfortunately, the appropriate treatment of hyponatremiadoesnot prevent this condition.The standardmethodof diagnosis is brainMagnetic resonance imaging (MRI).The typical radiological findings are hyperintense lesions in the central pons or associated extra pontine structures. Understanding the pathophysiology and recognizing the symptoms for CPM help identify the disease and therefore decrease its morbidity and mortality.

INTRODUCTION

Department (ED) after being found down in his apartment for an unknown period. He was intubated at the scene by EMS. His home medication regimen consisted of olanzapine 20mg HS and hydrochlorothiazide/Lisinopril 25/20 mg daily. On arrival to the hospital, he had a temperature of 94.6 degrees F and blood pressure of 110/99mmHg. He was very lethargic but responsive to sternal rub. Initial lab findings showed sodium of less than 100 mEq/L (Normal=136-144 mEq/L), potassium of 2.7 mEq/L (Normal= 3.7-5.2 mEq/L), CPK of 12, 785 unit/l (Normal=22-198U/L), Urine Osmolality of 417, SerumOsmolality 206mOsm/kg (Normal=275- 295mosm/kg), Urine NA< 20 (Normal=40-220 mEq/L/day). Computted tomography (CT) scan of the head showed chronic ischemic changes, chest X-ray was otherwise unremarkable. His electrocardiography (ECG) was significant for bradycardia at 58 beats per minute. His hyponatremia was believed to be a result of intravascular volume depletion due his antihypertensive agents as evidenced by the urine osmolality and urine sodium. There was no evidence to indicate SIADH. By hospital day four, he could open his eyes and follow some commands, and was stepped down to the medical floor from the intensive care unit (ICU). His sodium had corrected to 121 and his clinical status continued to improve but not his mental state. On the same day, psychiatry was consulted by the internal medicine team to evaluate for agitation. The team wondered if his presentation was due to schizophrenia or any other psychiatric conditions. The psychiatry consult team found the patient lethargic with a shifting sensorium as well as fluctuation of attention and concentration. The consult team diagnosed the patient with delirium secondary to his metabolic disturbance and restarted him on his nightly dose of Zyprexa as well as prns to manage his agitation. Four days after being stepped down, he became hypoverbal, unable to follow commands, and developed new onset dysphagia. Following a staffing that included the psychiatry consultants, a brain MRI was ordered which showed osmotic demyelination syndrome with central

Central pontine myelinolysis is a condition most often associated with rapid correction of hyponatremia and consists of dysarthria, dysphagia, oculomotor dysfunction, and variable degrees of quadriparesis. It was first described in 1959 by Adams et al. in malnourished and alcoholic patients. Since then, several psychiatric illnesses and many neuropsychiatric medications have been associated with hyponatremia and CPM as a potential complication of treating this electrolyte disorder. Multiple case reports and case series have been published documenting hyponatremia resulting in CPM in patients with schizophrenia, anorexia, and primary psychogenic

polydipsia. Among patients with chronic mental illness, 10–25% may have primary polydipsia, increasing the risk of hyponatremia and premature death. The most typical presentation involves the symmetrical butterfly-shaped area of demyelination within the central pons viewed on neuroimaging. The clinical manifestations of this condition vary based on the affected region of the brain. The mortality rate in CPM is reportedly between 5 - 10%. 1 There is no specific treatment for CPM so prevention as well as recognition are the key to minimizing morbidity and mortality.

CASE

A 56-year-old African American male with a history schizophrenia and hypertension was admitted to the Emergency

J La State Med Soc VOL 170 MARCH/APRIL 2018 43

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