Extreme delta brush (EDB), a unique EEG pattern characterized by generalized rhythmic delta with superimposed fast sharp activity, has been observed in 30% of patients with anti-NMDAR encephalitis. Questions have arisen about the specificity of EDB for anti-NMDAR encephalitis. We have compared the clinical seizures and EEG changes of two epilepsy patients related to anti-NMDAR encephalitis and lupus cerebritis.

Patient A: A 19-year old female with anti-NMDAR encephalitis related to ovarian teratoma developed psychiatric and behavioral changes and subsequent complex motor seizures (dystonic, choreoathetoid, and myoclonic movements in face, body and extremities) and status epilepticus. EEG demonstrated ictal EDBs with generalized high amplitude 1-2 Hz rhythmic slowing and superimposed low amplitude 15-25 Hz sharp components. She responded to aggressive AED treatments despite poor neurological recovery.

Patient B:  A 20-year old female with intractable motor seizures (spreading dystonia and myoclonus from trunk to extremities and face, ictal cry and postictal psychosis), visual hallucinations, neurocognitive decline and hematuria. Her epilepsy was related to SLE after excluding other causes including anti-NMDAR encephalitis. Ictal EEG showed stereotyped delta brush-like (DBL) patterns with generalized high amplitude 1-2 Hz rhythmic slowing superimposed by low amplitude 8-10 Hz sharp components that evolved to dominant repetitive sharp waves. She responded well to combined AEDs and immune suppressants.

Ictal delta brush were the major EEG findings for both patients with similar cortical regions involved in epileptogenesis. While the delta components were the same in both cases, the superimposed brushes were different. Generations of these EEG and clinical changes require active interactions between cortical and subcortical structures. Although uncertain, the delta activity may indicate nonspecific recruitment of subcortical structures by epileptogenic network. Meanwhile, the brushes may reflect distinct pathologies in the epileptogenic cortices. This observation may support specific correlation between EDB and anti-NMDAR encephalitis.