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sleepA Case of Catatonia Nearly Mistaken for Hepatic Encephalopathy

A Case of Catatonia Nearly Mistaken for Hepatic Encephalopathy

elder woman sick in bed with husband looking on

We admitted a 49-year-old woman with hypertension and cirrhosis secondary to nonalcoholic steatohepatitis with altered mental status. The patient’s family described a progressive decline in her ability to perform activities of daily living, interaction with others, speech, and motor function over 2 weeks. She was previously fully mobile and was currently bedbound. Her speech had deteriorated to mumbling that only her husband could understand. She was able to communicate with her family by answering dichotomous questions through blinking. Her sleep pattern was normal. There were no other ongoing neurological or infective symptoms.

On examination, the patient was alert, orientated, and followed commands through blinking. She was minimally communicative, with severely dysarthric speech. Her neck was supple, and examination of her cranial nerves was unremarkable. There was no jaundice, ascites, or asterixis. She had reduced motor strength across all muscle groups and the weakness appeared to be effort dependent. Her tone, sensation, and reflexes were normal, with a negative Babinski sign. The patient had a normal complete blood count and basic metabolic panel. Her total bilirubin was elevated at 3.0 mg/dL (range 0.2-1.2 mg/dL), but her liver transaminases, prothrombin time, and ammonia level were within normal limits. Urine drug screen, urinalysis, chest X-ray study, and venous blood gas were unremarkable. A computed tomography head scan was negative for acute pathology. An ultrasound of her liver showed known cirrhosis without ascites or portal vein thrombosis. Magnetic resonance imaging of her head and cerebrospinal fluid analysis were unrevealing.

On the wards, she showed no improvement with lactulose therapy. We initiated antiviral therapy for possible viral encephalitis, but this was ineffective. We administered an electroencephalogram, vitamin B12, thyroid-stimulating hormone, ceruloplasmin, treponemal immunoglobulin G, and tickborne panel, each of which were within normal limits. We obtained further collateral history, revealing a previous major depressive episode in her youth. There was no other past psychiatric history. We initiated a lorazepam challenge to evaluate for possible catatonia. The patient’s eye contact, speech, motor delay, and interaction with family improved over the course of several days. After 1 week of continuous improvement, the patient self-discharged against medical advice.

To read this article in its entirety please visit our website.

-Kevin G. Buell, MBBSa, S.B. Kiser, MD, MPHa, Eduard E. Vasilevskis, MD, MPHb,c

This article originally appeared in the June 2019 issue of The American Journal of Medicine.

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