Abstracts

Post-hypoxic myoclonus is a common and challenging complication of cardiac arrest¹. In the intensive care unit (ICU), abnormal movements prompt rapid treatment. While this may prevent further neuronal injury, it also carries the risks of excess sedative and antiseizure medication with variable benefit.

Neurophysiology can offer objective markers of myoclonus origin and treatment responsiveness. In particular, EEG source localization can distinguish cortical from subcortical generators. We aim to broaden the use of EEG voltage potentials to underscore its value in post-hypoxic care. We present key EEG features that can be identified on a standard monitoring page, offering a practical bedside tool for targeted management.

We compared neurophysiological signals in two pediatric cases of post-hypoxic myoclonus:

1. Cortical case: A 5-month-old infant developed myoclonus within 24 hours of non-traumatic cardiac arrest. We extracted referential EEG epochs time-locked to myoclonic jerks (verified by EMG artifact on the ECG lead), marked and signal-averaged each spike, and computed a single moving dipole solution in Curry 9 using the patient’s 3D brain model.
2. Subcortical case: A 10-year-old boy developed refractory myoclonus within 48 hours following a non-traumatic cardiac arrest. We identified vertex-positive EEG epochs, averaged them, and performed single dipole fitting in Curry 9 with the patient-specific 3D model.

• Cortical myoclonus: Prominent left parietal negativity with contralateral positivity over the right hemisphere. Source localization placed a dipole in the left parietal cortex, oriented radially outward, confirming a cortical generator (Figure 1).
• Subcortical myoclonus: Prominent positivity at Cz. Dipole fitting localized a deep, midline source in the pontomesencephalic region, vector directed inferiorly toward the brainstem consistent with a subcortical generator (Figure 2).

Our analysis shows that routine EEG, when interpreted with voltage topography and dipole orientation, can reliably distinguish cortical from subcortical post-hypoxic myoclonus. This highlights different pathophysiologic mechanisms with therapeutic implications: cortical myoclonus, driven by focal cortex hyperexcitability, often responds to GABAergic or antiseizure medications to diminish disabling jerks and facilitate rehabilitation, whereas subcortical myoclonus often signals diffuse anoxic injury involving deep brain structures, carries a poor prognosis and is often refractory to treatment².

By equipping ICU teams with this tool, we can minimize unnecessary sedation, improve prognostic accuracy, and individualize treatment according to underlying pathophysiology.