Abstracts

Rationale: Seizures are known to occur in anti-NMDA receptor (NMDAR) encephalitis. In the largest case series to date (Dalmau, 2008) involving 100 subjects, 76 suffered from clinical seizures, but documented epileptic activity was present in only 21 patients. At the same time, co-existence of dyskinesias in this disorder can be interpreted as seizures, leading to use of antiepileptic drug therapy which may not be completely justified. In this case series of anti-NMDAR encephalitis subjects, we aimed to (a) characterize and correlate seizure semiology with electroencephalogram (EEG) and (b) determine if the dyskinesias were seizures. Methods: A retrospective review of all anti-NMDAR encephalitis patients admitted to the National Neuroscience Institute from 2009 - 2012 was performed. All patients had confirmatory evidence of anti-NMDAR antibodies in the serum and/or cerebrospinal fluid (assays done at Oxford Radcliffe Hospitals, UK). Their demographic profile, tumour presence / absence, seizure semiology, EEG findings, and types of dyskinesias recorded during EEG sessions are described. Results: Ten patients were identified during this study period. The mean (SD) age was 26.2 (±10.6) years; all were female. Four had ovarian teratomas; six were tumour-negative. The mean (SD) number of EEG recordings was 4.3 (±2.1) per patient, with a range from 2 to 8. Electrographic seizures were recorded in three patients on day 53, day 2 and day 6 of their disease course respectively; all EEGs fulfilled Young's criteria for EEG seizures. One EEG showed 13Hz alpha activity maximum over the left frontal region evolving to 9Hz alpha activity, with the patient manifesting complex partial seizures in the form of right gaze deviation and right head turn. The second patient's EEG showed 11 Hz alpha activity over the right frontal region, evolving to 2Hz right frontal delta activity with no clinical manifestations. A third EEG showed repeated runs of generalized 2Hz rhythmic delta activity lasting 10-20 seconds, with each run followed by a period of generalized attenuation; the patient was stuporous and unresponsive during the EEG. One patient in this case series with neither clinical nor EEG seizures had right occipital sharp waves. In contrast, oro-lingual-facial dyskinesias were captured during the EEG recordings of seven patients, and were not associated with any change in the EEG pattern. Conclusions: Complex partial seizures are common in anti-NMDAR encephalitis, and can occur both early and late in the disease course. Multiple EEGs are often obtained for these patients. Unlike the faciobrachial dystonic seizures described in association with LGI1-antibody limbic encephalitis, the seizures in anti-NMDA encephalitis do not appear to have a stereotypical semiology nor ictal EEG pattern, though our sample size is small. Oro-lingual-facial dyskinesias, which characterise anti-NMDAR encephalitis and which are sometimes mistaken for seizures, do not appear to be epileptiform in nature.