Expanding Horizons Beyond Autoimmune Encephalitis: Extreme Delta Brush Signifying a Toxidrome
Shaifali Arora1, Christopher Sanfilippo1, Mikayla Spott2, LeeAnn Chang1, James Valeriano3
1Allegheny General Hospital, 2Drexel University College of Medicine, 3Allegheny Neurological Associates
Objective:
NA
Background:
Extreme delta brush (EDB) is a distinct EEG pattern characterized by rhythmic delta activity with superimposed bursts of rhythmic beta frequency activity in the 20-30 hertz range. This pattern has been associated with autoimmune encephalitis, specifically NMDA receptor (NMDA-R) encephalitis and one case of dipeptidyl-peptidase–like protein 6 (DPPX) antibody–associated encephalitis. Our case, to the best of our knowledge, represents the first instance of EDB in a patient who did not have either of these encephalitides. Instead, the patient’s toxicologic exposure implicates NMDA-R physiology as a potential mechanism of EDB. 
Design/Methods:
NA
Results:

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. 

Conclusions:

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. 

 

10.1212/WNL.0000000000210387
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