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(064) A Case of Misdiagnosed Catatonia in Systemic Lupus Erythematosus


Jaime Thomas, DO – PGY-3 Resident, Albert Einstein Medical Center

Inder Kalra, MD – Consultant Psychiatrist, Albert Einstein Healthcare Network


Presenting Author: Jaime Thomas, DO, Albert Einstein Medical Center
Co-Author: Inder Kalra, MD, Albert Einstein Healthcare Network



Catatonia is a condition with a collection of symptoms characterized by disturbances in motor behavior due to neurotransmitter dysfunction. Generally, the presentation of catatonia is quickly diagnosable by psychiatrists due to its overt and unique presentation in patients with psychiatric disorders. However, similar appearing presentations secondary to other medical conditions are also seen, and when found are common in neurological disorders. Systemic lupus erythematosus (SLE) is an autoimmune disorder that can cause inflammation in multiple organs of the body including the central nervous system (CNS). Progressive SLE can lead to many neuropsychiatric symptoms in patients. This case discusses the recognition and management of symptoms given the overlap of presentation and the use of a dopamine agonist, Sinemet (Carbidopa-Levadopa).

Case Description

A previously healthy 15 year old Cambodian female presented to the hospital with fatigue, intermittent fevers, and progressive weakness. Lab testing showed positive antibodies revealing SLE. Due to progressing blurry vision and diagnosis of chorioretinitis, a steroid implant was placed in her left eye. Post-operatively, she developed catatonia symptoms of posturing, mutism, immobility, negativism, hypomimia, and rigidity. Intensive treatments for SLE were initiated and Ativan and Amantadine were started to manage what was thought to be catatonia. She had partial response to symptoms. There were concerns of SLE affecting the CNS leading to Parkinson like extra-pyramidal symptoms. A trial of Sinemet was initiated with improved response in symptoms.


Catatonia symptoms develop due to dysfunction of neurotransmitters. These neurochemical abnormalities include low GABA activity in the frontal cortex, low dopamine (D2) activity in the basal ganglia, and high glutamate activity (NMDA) in the parietal cortex. CNS lupus can lead to Parkinson like symptoms from decreased dopamine that present similarly as catatonia. Treatment with Amantadine which has dopamine agonistic activity, aids in neuro-recovery in TBI and catatonia. Sinemet is a precursor to dopamine that crosses the blood brain barrier and acts as dopamine in the brain. With this patient, Ativan and Amantadine showed partial response, and trial with Sinemet showed improved response. This case presents challenges in recognition and management of catatonia in the context of a neurological disorder and highlights the utility of Sinemet in this setting.

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