Neurotoxicity Syndromes

The grounding supports toxic exposure as the cause, including biologic, chemical, and pharmaceutical agents. It also specifically includes neurotoxicity associated with chemotherapy and with CAR T-cell therapy, where immune effector cell-associated neurotoxicity syndrome is described as a treatment-related toxicity.

The literature grounding indicates that mechanisms vary by toxic exposure, but it specifically highlights cytokine-mediated neurotoxicity in CAR T-cell therapy. In that setting, systemic and possibly local cytokine release acts on the central nervous system, and reactive astrocyte activation with neurotoxic phenotypes, complement components, and chemokines is also described as a mechanism relevant to neuroinflammation.

Exposure to toxic substances is the core risk factor, including biologic, chemical, and pharmaceutical agents. For CAR T-cell-associated neurotoxicity, higher pretreatment tumor burden is associated with more severe adverse events.

Management is described at the modality level as prevention and treatment of toxic exposure-related neurologic injury, including supportive and preventive approaches for chemotherapy-induced peripheral neuropathy. For CAR T-cell-associated neurotoxicity, the literature emphasizes prevention and management strategies for immune effector cell-associated neurotoxicity syndrome, but the supplied grounding does not support naming specific drug classes beyond that general category.