A case series of COVID-19-related catatonia: A focus on immunological and neural mechanisms

Abstract

COronaVIrus Disease 19 (COVID-19) has led to a global health crisis and dramatically changed people's lifestyles. Several neuropsychiatric complications, including catatonia, have been reported as either para- or post-infectious complications of COVID-19. We describe three cases of catatonia associated with COVID-19, presenting with distinct psychiatric histories and medical contexts.

Putative pathogenic mechanisms of COVID-19-related catatonia involve a combination of direct viral neuronal damage and neuroinflammation secondary to cytokine storm. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) can reach the central nervous system via axonal transport along sensory nerves or via haematogenous spread. The pathogenic pathways activated by viral infection may also affect neurotransmission in basal ganglia involving gamma-aminobutyric acid, dopamine, and glutamate systems. In some cases, COVID-19 can lead to anti-NMDA receptor encephalitis by activating mechanisms of molecular mimicry.

These cases highlight the importance of appropriate screening of neuropsychiatric manifestations after COVID-19 infection and early diagnosis of catatonia. Therapeutic strategies include the use of benzodiazepines and electroconvulsive therapy as first-line treatments for catatonia, despite some concerns related to poor response or medical complications of COVID-19 infections. Mounting evidence suggests that augmentation with a NMDA receptor antagonist is a useful therapeutic option, especially for treatment-resistant catatonia.