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DOI 10.1016/j.clinph.2024.11.010

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2024

Repetitive muscle silent periods in acute post-anoxic brain injury: A novel phenotype of negative myoclonus.

Salehizadeh Saeideh, Hakami Suhailah, Shrestha Ramesh, Fotedar Neel

СтатьяКлинический случайПеревод пока не подготовлен

Аннотация

OBJECTIVE

To report a novel phenotype of negative myoclonus in acute post-anoxic brain injury (PABI).

METHODS

We performed a retrospective analysis of 18-channel video-EEG and surface-EMG (sEMG) recordings of three patients with PABI. sEMG electrodes were placed on the neck, bulbar and arm muscles.

RESULTS

All three patients had whole body tonic posturing with intermittent brief relaxation. In patients #1 and #2, a generalized EEG burst-suppression was present. Repetitive silent periods (SPs) were noted in the sEMG channels, time-locked to EEG bursts. The bursts preceded the SPs by 135 ms and 124 ms, respectively. The average SP duration was 910 ms and 852 ms in patients #1 and 2, respectively. Patient #3 had a generalized background suppression pattern and average SP duration of 272.5 ms. The SP recruitment pattern in patient #1 was rostro-caudal whereas patient #3 had a variable recruitment pattern.

CONCLUSION

Acute post-anoxic negative myoclonus can be detected in comatose patients with sEMG electrodes. The muscle SPs produce intermittent relaxation of the tonic posturing. The putative generator can be cortical or reticular, similar to Lance-Adams syndrome.

SIGNIFICANCE: We describe a novel phenotype of negative myoclonus in acute PABI. We also describe the EEG and sEMG characteristics and the localization of the putative generator.

Для цитирования: Salehizadeh Saeideh, Hakami Suhailah, Shrestha Ramesh, Fotedar Neel. Repetitive muscle silent periods in acute post-anoxic brain injury: A novel phenotype of negative myoclonus.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2024. DOI: 10.1016/j.clinph.2024.11.010.

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