A Case of Malignant Catatonia Complicated by Seizures and Respiratory Failure Mimicking Autoimmune Encephalitis: A Diagnostic Challenge
Sarah Zubair1, Hesham Kelani2, Mohammad Jadidi2, Tarek Elshourbagy2, Noah George Anderson2, Oluwasina Williams2, Tariq Mu'amar1, Mohamed Sabra1, Nuveed Loqman1, Artem Sunik2, Moshe Mizrahi2, Lisa R. Merlin2, David P. Lerner2
1Brookdale Hospital at One Brooklyn Health, 2Neurology Department, SUNY Downstate Health Sciences University at One Brooklyn Health
Background:
Malignant catatonia is a rare, life-threatening neuropsychiatric emergency characterized by rigidity, autonomic instability, and altered mental status. It can closely resemble neuroleptic malignant syndrome, severe infection, or autoimmune encephalitis, often delaying diagnosis and treatment. Seizures are uncommon, occurring in fewer than 5% of cases. Electroconvulsive therapy (ECT) is considered the gold-standard treatment with high response rates, but recovery without ECT remains exceptional.
Design/Methods:
A 46-year-old woman with bipolar disorder presented with disorganized behavior, mutism, and psychomotor slowing. She was febrile, tachycardic, and exhibited generalized rigidity. Brain imaging was unremarkable. Cerebrospinal fluid analysis showed elevated protein and albumin without inflammatory markers, and autoimmune and paraneoplastic panels were negative. Abdominal imaging revealed a chronic hydrosalpinx, further complicating the differential diagnosis. Despite treatment with benzodiazepines and dantrolene, the patient developed recurrent fevers, autonomic instability, and seizure-like activity. Continuous EEG confirmed right temporo-occipital focal seizures with diffuse cerebral dysfunction. She required intubation, valproic acid loading, and intensive care management. Over several weeks, her rigidity and autonomic symptoms improved with clonazepam titration. She was successfully extubated and discharged in stable condition without neurological deficits.
Results:
This case underscores the diagnostic complexity of malignant catatonia, particularly when seizures are present. After excluding infectious, autoimmune, and structural causes, abrupt cessation of olanzapine was identified as the most likely precipitant, leading to dopaminergic and GABAergic imbalance. Clinical recovery following benzodiazepine escalation rather than dantrolene highlights the central role of GABAergic modulation in treatment.
Conclusions:
Malignant catatonia can mimic several medical and neurological conditions, complicating diagnosis. This case illustrates that, even in the absence of ECT, timely recognition, sustained benzodiazepine therapy, and comprehensive supportive care can achieve full recovery and prevent life-threatening complications.
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