Medication-induced neurotoxicity is a clinically significant complication in oncology, affecting both the central and peripheral nervous systems and frequently intersecting with critical care management. Neurotoxic risk arises from multiple therapeutic classes, including chemotherapeutic agents, immunotherapies, immunosuppressants, and supportive medications such as antiepileptic drugs and opioids, with incidence shaped by treatment exposure, pharmacogenomic factors, and comorbid organ dysfunction. Across cancer therapies, neurologic toxicities range from mild and transient symptoms to severe, potentially life-threatening complications, depending on the specific agent and exposure. Immune checkpoint inhibitors and CAR T-cell therapies have introduced distinct immune-mediated syndromes that require early recognition and coordinated multidisciplinary management. Additional contributors, including antiepileptic and opioid therapies, may further complicate neurologic assessment and function, particularly in the setting of polypharmacy and organ dysfunction. Early recognition, systematic neurologic assessment, and individualized dose modification remain central principles of prevention and management. Future priorities include the development of predictive biomarkers, risk-stratified monitoring frameworks, and targeted neuroprotective strategies to reduce long-term neurologic morbidity in this growing and vulnerable population.

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Medication-Induced Neurotoxicity in Critically Ill Cancer Patients

  • Aileen H. Hsi,
  • Monica E. Loghin

摘要

Medication-induced neurotoxicity is a clinically significant complication in oncology, affecting both the central and peripheral nervous systems and frequently intersecting with critical care management. Neurotoxic risk arises from multiple therapeutic classes, including chemotherapeutic agents, immunotherapies, immunosuppressants, and supportive medications such as antiepileptic drugs and opioids, with incidence shaped by treatment exposure, pharmacogenomic factors, and comorbid organ dysfunction. Across cancer therapies, neurologic toxicities range from mild and transient symptoms to severe, potentially life-threatening complications, depending on the specific agent and exposure. Immune checkpoint inhibitors and CAR T-cell therapies have introduced distinct immune-mediated syndromes that require early recognition and coordinated multidisciplinary management. Additional contributors, including antiepileptic and opioid therapies, may further complicate neurologic assessment and function, particularly in the setting of polypharmacy and organ dysfunction. Early recognition, systematic neurologic assessment, and individualized dose modification remain central principles of prevention and management. Future priorities include the development of predictive biomarkers, risk-stratified monitoring frameworks, and targeted neuroprotective strategies to reduce long-term neurologic morbidity in this growing and vulnerable population.