Background
COVID-19 appears to directly and indirectly affect the central nervous system (CNS)(Helms 2020), and various mechanisms have been proposed regarding CNS inflammation and alteration of neurotransmission which could predispose patients to catatonia (Gouse 2020). We describe a case of catatonia precipitated by COVID-19 infection.
Case
A 48-year-old female with cerebral palsy, mild intellectual disability, and epilepsy was hospitalized for COVID-19 and with corticosteroid treatment and supportive care, and was neurovegetative at discharge. Withdrawal progressed to development of immobility, combativeness, impulsivity, and perseveration, prompting re-hospitalization. She was treated 10 years prior for perceived seronegative encephalitis and catatonia requiring electroconvulsive therapy (ECT). Based on this history, our team obtained MRI brain, CSF infectious and autoimmune/paraneoplastic studies, as well as EEG. Neurologic, metabolic, and infectious workups was solely remarkable for mild encephalopathy with focal bi-occipital dysfunction. Initial Bush-Francis Catatonia Rating Scale (BFCRS) score was 8 (including neurovegetative symptoms, rigidity, occasional combativeness). Prior to admission olanzapine for baseline behavioral management was held. BFCRS score fluctuated to 15 (including hyperkinetic episodes, verbigeration, grasp reflex), and lorazepam challenge only decreased BFCRS score to 13. Concurrent with uptitration of lorazepam, ECT was initiated. Given slow response and sub-therapeutic ECT seizures, augmentation with memantine was also initiated. The patient was discharged one month later with BFCRS score of 5 and guardian impression of patient behavioral baseline on a regimen of lorazepam 8 mg TID, memantine 10 mg BID, and resumed prior to admission olanzapine 2.5 mg at bedtime.
Discussion
This patient met clinical criteria for catatonia based on her clinical signs and symptoms, as well as response to catatonia treatment (lorazepam, ECT, memantine). Neurovegetative catatonia symptoms were present on discharge from COVID-19 hospitalization, with progression to more uniquely catatonic symptoms in the weeks after discharge. Given negative workup for alternative medical causes and no mood or psychotic episodes preceding catatonia, we concluded that catatonia was precipitated by COVID-19 in the setting of brain vulnerability to catatonia. Current literature describes at least 14 cases of COVID-19-induced catatonia, the majority of which responded well to catatonia-targeted therapies. (e.g. Gouse 2020; Deocleciano 2020), and one of which also occurred in the context of baseline intellectual disability (Deocleciano 2020).
Conclusions
Although hypoactive delirium is much more prevalent in COVID-19 hospitalizations, consult psychiatrists must maintain diagnostic vigilance for infrequent precipitation of catatonia in these cases, especially in the setting of predisposing risk factors.
References
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1.
Helms J, et al. “Neurologic Features in Severe SARS-CoV-2 Infection.” NEJM 2020; 382: 2268-2270.
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2.
Gouse BM, et al. Catatonia in a hospitalized patient with COVID-19 and proposed immune-mediated mechanism. Brain Behav Immun 2020;89:529–30.
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3.
Deocleciano de Araujo C, et al. Life-Threatening Catatonia Associated with Coronavirus Disease 2019. Psychosomatics. 2020;EPub Oct 22.