Acute post-anoxic myoclonic status epilepticus is a well-defined entity, comprising mainly positive myoclonic jerks. However, there is limited literature on negative myoclonus in acute PABI. Negative myoclonus is a jerky, involuntary movement caused by a brief interruption of sustained muscle activity. It is well-described in chronic post-anoxic myoclonus (Lance Adams syndrome), leading to postural lapses. It can be of reticular or cortical origin.

This is a retrospective analysis of video-EEG and surface-electromyography (sEMG) recordings from the neck and bulbar muscles of three comatose patients with acute PABI. We measured the duration of EEG bursts, sEMG SPs, and EEG-SP latency.

All three patients had a generalized burst-suppression pattern on the EEG with brief sEMG SPs. In patients #1 and #2, all SPs were time-locked to EEG bursts, with the bursts preceding the SPs by an average latency of ~135ms and 124ms, respectively. The average SP duration was ~910ms and 852ms in patients #1 and 2, respectively. In patient #3, only ~31% of SPs were time-locked to EEG bursts. Interestingly, ~27% of SPs preceded the EEG bursts. The average SP duration was ~661ms.

Our study demonstrates the presence of quasi-periodic muscle SPs in acute PABI. We postulate that this finding is analogous to the ‘postural lapses’ seen in Lance-Adams syndrome. The generator can be cortical (as evidenced by preceding EEG bursts in patients #1 and 2) or reticular (patient #3). Covering the neck and bulbar muscles with sEMG electrodes provides a unique opportunity to study this phenomenon in comatose patients.