Abstract
BACKGROUND: Catatonia, including malignant catatonia, is a severe neuropsychiatric condition historically associated with schizophrenia or schizoaffective disorder. However, recent diagnostic frameworks, such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) and the International Classification of Diseases, 11th Revision (ICD-11), offer a broader understanding. These systems classify catatonia not as a standalone diagnosis but as a specifier that may occur alongside various psychiatric disorders, including schizophrenia spectrum disorders, mood disorders, neurodevelopmental disorders, or medical conditions. Although electroconvulsive therapy (ECT) and benzodiazepines are considered gold standard treatments for catatonia, many healthcare settings lack access to ECT, and certain physical conditions make ECT relatively contraindicated or a high-risk option. Guanfacine, a central adrenergic α2A receptor agonist, has a similar mechanism of action as the sedative dexmedetomidine, which has shown efficacy in treating catatonia. However, the effectiveness of guanfacine in this context has not been tested. CASE PRESENTATION: We report five cases of catatonia (including malignant catatonia) associated with schizophrenia or schizoaffective disorder. These cases were treated either in a psychiatric hospital or an outpatient clinic, both of which lacked access to ECT. Extended-release formulation of guanfacine was administered alongside temporary benzodiazepine use, and treatment outcomes were observed. All five patients were in syndromal remission from catatonia following treatment that included guanfacine in combination with other pharmacological interventions. Mild to moderate side effects were observed. These included dizziness and fatigue in one patient, and hypotension and bradycardia in two others. All adverse effects resolved with dose reduction. Complications of catatonia included impaired oral intake requiring nutritional support in two patients and urinary catheterization due to immobility in two patients. CONCLUSIONS: These findings suggest that guanfacine may serve as a safe and effective alternative to ECT for catatonia in settings where ECT is unavailable or relatively contraindicated. The clinical courses also suggest that dysfunction of the central noradrenergic system may contribute to the pathophysiology of catatonia, and that guanfacine's selective α2A adrenoceptor modulation may play a role in symptom improvement. Further research is needed to validate these findings and clarify the underlying mechanisms.