Background Incident catatonia in older adults with chronic psychosis may signal underlying organic pathology rather than primary psychiatric exacerbation. We describe three patients with different vulnerability profiles. Methods This retrospective series reviews the clinical course, psychopharmacological triggers, neuroimaging (MRI, 18F-FDOPA, 18F-FDG, tau and 18F-Florbetaben PET) and outcomes of three elderly men with long-standing psychosis and incident catatonia. Results Case 1 (67) developed catatonia after an antipsychotic rechallenge unmasking presynaptic dopaminergic denervation, and required maintenance electroconvulsive therapy (m-ECT). Case 2 (70) had recurrent catatonia after clozapine withdrawal and a lorazepam taper; amyloid PET was positive only within the reported gray zone, with unremarkable tau, FDOPA and FDG PET, so no biomarker supported neurodegeneration; he also required m-ECT. Case 3 (64) developed akinetic catatonia after benzodiazepine cessation amid severe cerebrovascular disease, remitting with pharmacotherapy alone. Conclusions Late-onset catatonia in chronic psychosis may reflect unrecognized brain pathology. What distinguished these courses was not which pathology was present but whether the vulnerability had stabilized: a static deficit with a reversible precipitant remitted on pharmacotherapy, whereas advancing or unidentified deficits required m-ECT. Misreading catatonia caused harm in both directions: antipsychotic escalation, and withdrawal of a benzodiazepine that was containing it. These observations are hypothesis-generating.
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Virotjanakood et al. (2026) studied this question.
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