Intracortical focal non-convulsive status epilepticus causing cerebral hypoxia and intracranial hypertension.

We describe the pathophysiological consequences and long-term neurological outcome of a patient with acute brain injury (ABI) in whom intracortical electroencephalography (iEEG) captured an episode of prolonged focal non-convulsive status epilepticus (NCSE) that remained undetectable on scalp electroencephalography. A 53-year-old right-handed woman was admitted to hospital due to a large frontal left intraparenchymal hematoma. Over two and a half days, we captured recurrent non-convulsive electrographic and electroclinical seizures compatible with the diagnosis of intracortical focal NCSE. The patient remained sedated and a burst-suppression pattern was obtained. We also performed invasive brain multimodality monitoring including iEEG and measurements of intracranial pressure (ICP), partial brain tissue oxygenation (PbtO2) and brain temperature. During non-convulsive electrographic and electroclinical seizures, the values of PbtO2 decreased and those of ICP increased. Six months later, brain MRI revealed encephalomalacia localized to the left paramedial fronto-basal region. The neuropsychological assessment carried out one year after the injury showed scores below average in verbal learning memory, motor dexterity and executive functions. In summary, iEEG is a feasible innovative invasive technique that may be used to record non-convulsive electrographic and electroclinical seizures which remain invisible on the surface. Intracortical focal NCSE causes metabolic changes such as reduced brain oxygenation and an increase in ICP that can further damage previously compromised brain tissue.