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<p>T cell–redirecting therapies directed against B-cell maturation antigen (BCMA) have revolutionized the treatment of relapsed or refractory multiple myeloma (MM). BCMA-directed CAR-T cell therapy has been reported to cause a parkinsonism-predominant neurotoxicity referred to as movement and neurocognitive toxicity (MNT). MNT is considered distinct from immune effector cell-associated neurotoxicity syndrome (ICANS) in terms of its clinical features and time to onset. However, MNT-like delayed-onset parkinsonism has not been well documented after BCMA-directed bispecific antibody (BsAb) therapy. We report the case of a woman with relapsed/refractory MM who developed parkinsonism following elranatamab. She experienced neither cytokine release syndrome nor ICANS. Beginning the day after the Week 7 dose, she developed bradykinesia, repeated falls, gait disturbance, and cognitive decline. Neurological examination revealed hypomimia, bradykinesia, upper extremity rigidity, postural instability, and a shuffling gait, consistent with parkinsonism. Brain MRI and dopamine transporter single-photon emission computed tomography findings showed no findings suggestive of degenerative Parkinson’s disease. Her symptoms gradually improved after discontinuation of elranatamab. This case highlights the possibility of delayed-onset parkinsonism with neurocognitive symptoms following treatment with a BCMA-directed BsAb. Clinicians should recognize the potential for delayed-onset parkinsonism and ensure close neurological monitoring in patients receiving these agents.</p>

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Delayed-onset parkinsonism possibly associated with elranatamab treatment for relapsed/refractory multiple myeloma: a case report of a poorly characterized neurological event

  • 期刊论文

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  • 发表日期：

    2026年7月7日

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  • Asuka Kono,
  • Yoshihiro Umezawa,
  • Kensuke Oshima,
  • Keisuke Tanaka,
  • Yuki Kobayashi,
  • Takehiko Mori,
  • Masahide Yamamoto

摘要

T cell–redirecting therapies directed against B-cell maturation antigen (BCMA) have revolutionized the treatment of relapsed or refractory multiple myeloma (MM). BCMA-directed CAR-T cell therapy has been reported to cause a parkinsonism-predominant neurotoxicity referred to as movement and neurocognitive toxicity (MNT). MNT is considered distinct from immune effector cell-associated neurotoxicity syndrome (ICANS) in terms of its clinical features and time to onset. However, MNT-like delayed-onset parkinsonism has not been well documented after BCMA-directed bispecific antibody (BsAb) therapy. We report the case of a woman with relapsed/refractory MM who developed parkinsonism following elranatamab. She experienced neither cytokine release syndrome nor ICANS. Beginning the day after the Week 7 dose, she developed bradykinesia, repeated falls, gait disturbance, and cognitive decline. Neurological examination revealed hypomimia, bradykinesia, upper extremity rigidity, postural instability, and a shuffling gait, consistent with parkinsonism. Brain MRI and dopamine transporter single-photon emission computed tomography findings showed no findings suggestive of degenerative Parkinson’s disease. Her symptoms gradually improved after discontinuation of elranatamab. This case highlights the possibility of delayed-onset parkinsonism with neurocognitive symptoms following treatment with a BCMA-directed BsAb. Clinicians should recognize the potential for delayed-onset parkinsonism and ensure close neurological monitoring in patients receiving these agents.