Baclofen toxicity mimicking brain death in severe traumatic brain injury: the critical role of brainstem reflex assessment

ABSTRACT

Baclofen toxicity may cause profound neurological depression even at therapeutic doses when blood-brain barrier (BBB) integrity is compromised, as occurs in severe traumatic brain injury (TBI). We report a 65-year-old man who sustained severe TBI after a two-meter fall, underwent decompressive craniectomy, and was managed with multimodal sedation including midazolam. Oral baclofen was initiated for ventilator asynchrony. On day 5, he developed fixed pupils and absent corneal and oculovestibular reflexes with preservation of the cough reflex, raising concern for death by neurologic criteria (DNC). Reversible confounders had been excluded. Following discontinuation of both agents, brainstem reflexes recovered within 24 hours and electroencephalography confirmed preserved cerebral activity. This case illustrates that baclofen neurotoxicity in the setting of BBB disruption can mimic clinical features of DNC. Reflex dissociation, particularly preserved cough reflex, may help distinguish pharmacological suppression from irreversible injury. Determination of DNC must not be initiated until all toxic and sedative confounders are excluded.