After cardiac arrest, global hypoxic-ischaemic brain injury can cause myoclonus, electrographic seizures, non-convulsive status epilepticus and a range of other abnormal EEG patterns. Interpreting these findings requires both seizure expertise and careful neurological prognostication.
Why seizures can occur after cardiac arrest
During cardiac arrest the brain is deprived of oxygen and blood flow. Even after circulation returns, delayed cellular injury can continue.
Acute cortical injury can produce seizures and other epileptiform EEG patterns.
Clinical movements can be misleading
Myoclonus after cardiac arrest can be epileptic, non-epileptic or part of a mixed electroclinical picture.
Visual observation alone cannot reliably determine whether repetitive movements represent cortical seizures.
EEG is central
Continuous EEG can identify electrographic seizures, non-convulsive status and the evolution of the background rhythm.
Timing matters because EEG patterns can change substantially during the first hours and days after resuscitation.
Seizures are only one part of the EEG
Suppression, burst-suppression, periodic discharges, reactivity and background continuity all contribute information.
No single EEG feature should be used in isolation to make major prognostic decisions.
Treatment remains an area of uncertainty
Definite electrographic seizures and status epilepticus are usually treated, but the benefit of aggressively suppressing every rhythmic or periodic pattern after cardiac arrest remains uncertain.
This is particularly important for patterns on the ictal-interictal continuum.
Prognostication must be multimodal
Modern post-cardiac-arrest prognostication combines the clinical examination with EEG, imaging, biomarkers and, in selected settings, somatosensory evoked potentials.
Sedation, temperature management and other confounders must be considered before interpreting neurological findings.
Recovery is not determined by one EEG label
Historically, some post-anoxic seizure and myoclonus patterns were regarded as uniformly fatal. More recent literature has documented exceptions and emphasises greater caution.
Treatment and prognosis should therefore be individualised and based on the complete clinical picture.
Related reading
Sources and further reading
- The evolving role of EEG in postarrest care — 2024
- EEG reactivity in neurological prognostication after cardiac arrest — 2024
- The role of EEG and evoked potentials after cardiac arrest
- Nonconvulsive status epilepticus following cardiac arrest
Evidence checked: September 2026.