Objective: Describe parkinsonism after B-cell maturation antigen (BCMA)-targeted chimeric antigen receptor (CAR) T-cell therapy for treatment of multiple myeloma.

Background: BCMA-targeted CART-cell therapy effectively treats relapsed and refractory multiple myeloma^1,2. Up to 5% of patients develop movement and neurocognitive neurotoxicity, including parkinsonism with severe functional impairment^3,4. Data describing this phenomenon’s clinical presentation and treatment response are limited^5–8.  Consequently, adequate description of phenomenology and treatment strategies is vital.

Method: We present a case series of patients with BCMA CAR-T cell therapy induced parkinsonism at Weill Cornell Medicine.

Results: 4 patients with parkinsonism following BCMA-directed CAR T-cell therapy (ages between 62-74 years, 2 men and 2 women) were identified. Three received Ciltacabtagene autoleucel (two men ages 62 and 69, and one woman age 65), and one woman (age 74) received Idecabtagene Vicleucel. The average time to the development of parkinsonism was 25.5 ± 3.5 days. The average MDS-UPDRS part III score at time of initial movement disorder examination (average 354.7 ± 182.6 and 330.7 ± 180.2 days from the time of infusion and parkinsonism onset, respectively) was 63.3 ± 4.7. The dominant symptoms were bradykinesia (MDS-UPDRS part III sub-scores 2-4/4), rigidity (2-3/4), and gait abnormalities (2-4/4). Tremor sub-scores were 1/4 or lower. Dopamine transporter scans were obtained in the male patients and were normal. Non-contrast brain MRI obtained in the 62-year-old male and 65-year-old female demonstrated unremarkable basal ganglia.  An FDG PET scan was obtained for the 65-year-old female and showed unilaterally decreased tracer uptake in basal ganglia.  All patients were given carbidopa/levodopa 25/100 with doses ranging from 600-2000 mg per day. Amantadine (200-300mg/day) and Ropinirole (4-6mg/day) were prescribed to 3 of 4 patients with total Levodopa Equivalent Dose of 960-1220. None of the patients reported improvement in their parkinsonism since starting therapy.

Conclusion: BCMA-targeted CAR-T cell therapy-induced parkinsonism is a devastating adverse event with limited treatment response based on the available data and as seen in our small series. Further large-scale studies are needed to adequately characterize the phenomenology, radiographic findings, and treatment response.

References: 1. Cordas dos Santos, D. M. et al. A systematic review and meta-analysis of nonrelapse mortality after CAR T cell therapy. Nat. Med. 30, 2667–2678 (2024).
2. Jagannath, S. et al. Long-Term (≥5-Year) Remission and Survival After Treatment With Ciltacabtagene Autoleucel in CARTITUDE-1 Patients With Relapsed/Refractory Multiple Myeloma. J. Clin. Oncol. 43, 2766–2771 (2025).
3. Graham, C. E. et al. Non-ICANS neurological complications after CAR T-cell therapies: recommendations from the EBMT Practice Harmonisation and Guidelines Committee. Lancet Oncol. 26, e203–e213 (2025).
4. Cohen, A. D. et al. Incidence and management of CAR-T neurotoxicity in patients with multiple myeloma treated with ciltacabtagene autoleucel in CARTITUDE studies. Blood Cancer J. 12, 32 (2022).
5. Van Oekelen, O. et al. Neurocognitive and hypokinetic movement disorder with features of parkinsonism following BCMA-targeting CAR-T cell therapy. Nat. Med. 27, 2099–2103 (2021).
6. Couturier, A. et al. Parkinson‐like neurotoxicity in female patients treated with idecabtagene‐vicleucel. HemaSphere 8, e131 (2024).
7. Ellithi, M. et al. Neurotoxicity and Rare Adverse Events in BCMA-Directed CAR T Cell Therapy: A Comprehensive Analysis of Real-World FAERS Data. Transplant. Cell. Ther. 31, 71.e1-71.e14 (2025).
8. Schneider, S., Aamodt, W. W., Pruitt, A. A. & Berger, J. R. Parkinsonism Associated with Anti-B-Cell Maturation Antigen Chimeric Antigen Receptor T-Cell Therapy. Mov. Disord. Clin. Pract. 11, 1625–1628 (2024).

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