(014) Fighting the Fire: Anti-Inflammatory Effects of Aripiprazole as Mechanism for Improvement in Medical Catatonia?

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Introduction: Disorders of central nervous system inflammation have a strong association with catatonia. We ‎present a case of a patient with multiple sclerosis who presented with new onset psychosis and catatonia secondary ‎to an MS exacerbation. Her psychiatric symptoms quickly improved after addition of aripiprazole to her ‎benzodiazepine regimen. Postulated mechanisms include dopamine agonism and anti-inflammatory action.‎

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Case: Ms. M was a 49-year-old female. Her medical history was significant for MS, multinodular goiter, and ‎marijuana use. She had no psychiatric history. She had achieved a masters-level education and maintained ‎employment. She presented due to mania and psychosis with sudden onset. Brain imaging demonstrated three ‎lesions consistent with active demyelination. She was treated with high dose steroids.‎

On psychiatric evaluation, she was diagnosed with severe major depressive disorder with psychotic features and ‎catatonia. Catatonia was felt to most likely be secondary to her MS exacerbation. The patient was started on ‎lorazepam, 2 mg every 4 hours. After completion of steroids, she was transferred to an inpatient psychiatric facility. ‎She was re-admitted to a neurologic service after sustaining a fall.‎

After patient was transferred back to neurology for further evaluation of autoimmune encephalitis. Our psychiatry ‎consult service continued the lorazepam that was started at the outside hospital. Her presentation was noticeable for ‎psychotic symptoms, specifically persecutory and nihilistic delusions. Quetiapine was briefly introduced but ‎discontinued due to worsening of catatonic symptoms. We decided on a trial of aripiprazole 2.5 mg nightly. The next ‎day, the patient showed a marked improvement in her spontaneity, and was less focused on her delusions. She ‎tolerated dose increases up to 7.5 mg daily, with reduction in her Bush-Francis Catatonia Rating Scale and ‎improvement in her symptoms. The patient was then transferred to an inpatient psychiatric facility, where she began ‎electroconvulsive treatments. She underwent six treatments. Her aripiprazole was increased to target residual ‎psychotic symptoms. She was discharged on 15 mg daily.‎

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Discussion: Ms. M's symptoms showed marked improvement after aripiprazole. Though the pathophysiology ‎of catatonia isn't completely understood, hypo-dopaminergia in the striatum is thought to play a key role(1). ‎Aripiprazole has several interesting properties, including dopamine agonism and anti-inflammatory action(2). ‎Neuroinflammation may have a significant contribution to catatonic presentations, and deserves further study(3).‎

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References: ‎
‎1. Beach, S. R., Luccarelli, J., Praschan, N., Fusunyan, M., & Fricchione, G. L. (2023). Molecular and immunological origins ‎of catatonia. Schizophrenia Research.‎
‎2. Juncal-Ruiz, M., Riesco-Dávila, L., de la Foz, V. O. G., Martínez-Garcia, O., Ramírez-Bonilla, M., Ocejo-Viñals, J. G., ... ‎& Crespo-Facorro, B. (2018). Comparison of the anti-inflammatory effect of aripiprazole and risperidone in 75 drug-‎naïve first episode psychosis individuals: A 3 months randomized study. Schizophrenia research, 202, 226-233.‎
‎3. Rogers, J. P., Pollak, T. A., Blackman, G., & David, A. S. (2019). Catatonia and the immune system: a review. The ‎Lancet Psychiatry, 6(7), 620-630.‎