| Early steroid escalation |
When neurologic decline is clinically meaningful, and alternative diagnoses have been addressed |
Best used as part of a workflow that includes neurology input, severity grading, and seizure exclusion when appropriate |
Consensus and review-level guidance (1–3) |
| Antiseizure therapy |
Treat witnessed or electrographic seizures; consider a lower threshold in clearly high-risk severe cases. |
The current included evidence does not support routine prophylaxis for all patients |
EEG series and review-level guidance (2, 3, 9, 10, 25) |
| Tocilizumab prophylaxis in bispecific programs |
Reasonable program-level strategy where step-up dosing logistics and prior institutional experience support it |
Needs integration with local pathways and continued neurologic vigilance because low event rates do not equal zero risk |
Real-world 119-patient cohort with low CRS and ICANS rates (13) |
| ICU transfer/continuous EEG |
Severe encephalopathy, coma, recurrent seizure concern, hemodynamic instability, or multi-organ toxicity |
Triggered escalation is more efficient than blanket ICU use |
Consensus workflow literature and adult EEG data (1, 9) |
| Late-syndrome surveillance and rescue |
Movement disorder or executive decline after BCMA-directed therapy should prompt renewed neurologic evaluation; rescue strategies may differ from classical early ICANS |
Delayed syndromes may not respond like typical dopaminergic disease; case literature supports alternative immunomodulatory approaches in selected settings. |
Cilta-cel MNT analyses and delayed rescue literature (17–20) |