(PO-069) (PO-069) A Case of Post-COVID Catatonia Partially Refractory to IV Lorazepam

Background
COVID-19 has been associated with a variety of neuropsychiatric sequelae, including catatonia. The mechanism of this complication remains poorly understood, with no consensus on the most appropriate therapeutic approach. To our knowledge, there are only eight prior reports of catatonia occurring in this context. We report on the case of a man who presented with post-COVID catatonia that was refractory to standard treatments.  
 
Case
Mr. J is a 22-year-old man with history of depression and mild COVID-19 infection who presented to our Hospital in March 2021. Over the previous several months, he had been neglecting his grooming and hygiene, exhibited poor oral intake, exhibited staring and intermittent mutism. Before admission, treatment with perphenazine and quetiapine resulted in increased muscle rigidity and abnormal involuntary movements. On admission, SARS-CoV-2 PCR was positive, and he had elevation of muscle (CPK) and liver enzymes. An MRI of the brain was unremarkable.  The Bush-Francis catatonia rating scale (BFCRS) score was 27 and intravenous lorazepam was initiated and titrated up to 3 mg every 6 hours. Memantine was added as adjunct treatment. Bupropion hydrochloride was added to target depressive symptoms. The patient’s health care proxy did not consent to electroconvulsive therapy (ECT) and he was discharged after successful transition to oral agents. His discharge BFCRS score was 8. Treatment with nine sessions of bilateral ECT was eventually administered two months following discharge due to persistent symptoms of catatonia, with patient achieving full resolution and returning to baseline level of functioning.
 
Discussion
Catatonia associated with COVID-19 infection has been described^1,2,3,4 with lorazepam as first line of treatment with mixed results. ECT remains the standard of care for the management of refractory cases⁴, however, it may not be readily available in certain clinical situations. Catatonia in the setting of COVID-19 may be associated with an increase in pro-inflammatory mediators² leading to altered GABA-ergic transmission and a hypodopaminergic state. As in more typical presentations, avoiding antipsychotic agents remains an important consideration to prevent the development of malignant catatonia.

Conclusion
Consultation-liaison psychiatrists are increasingly managing neuropsychiatric sequelae of COVID-19, including catatonia. Knowing how to readily recognize it and prevent and/or efficiently treat its complications, even when ECT is not available, is imperative.  Further research is needed to understand its underlying mechanism and treatment.
 
References
 
1. Caan M, Lim C, Howard M. A case of catatonia in a man with COVID-19. Psychosomatics. 2020;61(5):556-560
2. Gouse B, Spears W, Nieves A, et al. Catatonia in a hospitalized patient with COVID-19 and proposed immune-mediated mechanism. Brain Behav Immun. 2020;89:529-530
3. Scheiner NS, Smith AK, Wohlleber M, Malone C, Schwartz AC. COVID-19 and Catatonia: A Case Series and Systematic Review of Existing Literature. J Acad Consult Liaison Psychiatry. 2021;S2667-2960(21)00077-X
4. Austgen G, Meyers MS, Gordon M, Livingston R. The Use of Electroconvulsive Therapy in Neuropsychiatric Complications of Coronavirus Disease 2019: A Systematic Literature Review and Case Report. J Acad Consult Liaison Psychiatry. 2021;S2667-2960(21)00127-0
5. Bush G, Fink M, Francis A, et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatrica Scandinavica. 1996; 93:129-136