A 48-year-old male with a history of migraines, hypertension, attention deficit disorder, anxiety, and opioid use disorder presented to the emergency department after being found unresponsive. Upon arrival, the patient was stuporous, unable to consistently follow commands, and had rotary nystagmus. Initial blood tests, labs, and head CT were unremarkable. Urine drug screen was positive for benzodiazepines, which was consistent with the patient’s prescribed chlordiazepoxide for anxiety. Also, the patient was known to be using protonitazene (a synthetic opioid compound) along with an unidentified gray powder. The patient was admitted for suspected overdose. However, his presentation did not fit any toxidrome associated with his known medications.   

Neurology was consulted due to persistent encephalopathy and absence of a clear toxidrome. EEGs indicated severe generalized encephalopathy and was characterized by a pattern consistent with EDB. The patient was treated with high-dose steroids for possible autoimmune encephalitis until encephalitis panels resulted negative. He returned to his baseline neurologic status a week after admission and was discharged home. 

We propose the cause of EDB in this case was a toxicologic exposure to an unidentified substance. While the primary relevance of EDB is its association with NMDA-R encephalitis, we suggest it may also serve as a diagnostic marker for other conditions including toxicological exposures.