Paroxysmal EEG pattern in a child with N-methyl-D-aspartate receptor antibody encephalitis.

A previously healthy 8-year-old male presented with cognitive regression, sleep disturbance, hallucinations, and severe attacks of agitation and oligoclonal bands in the cerebrospinal fluid. N-methyl-d-aspartate receptor (NMDAR) antibodies in serum and cerebrospinal fluid were detected 2 months after onset of symptoms. Bursts of agitation were initially considered to be epileptic leading to the administration of a high dose of benzodiazepines. Video-electroencephalography (EEG) failed to disclose any correlation between the episodes of agitation and paroxysmal rhythmic slow activity on EEG persisting throughout and after attacks of agitation. Clinical improvement and EEG normalization followed an initial plasma exchange performed 3 months after onset of disease. This particular paroxysmal EEG pattern in NMDAR antibody encephalitis suggests that it may result from the combination of reduced NMDAR function and major γ-aminobutyric acid (GABA)-ergic activation.