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

Abstract

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.

Case report: Invasive neuromonitoring in status epilepticus induced hypoxic ischemic brain injury

“…To the best of our knowledge, this is the first case report using INM to guide management in refractory intracranial hypertension in a patient with SE-induced diffuse cerebral edema, in the absence of other primary ABI, and to survive it with a good neurologic outcome. In the setting of SE following ABI due to other primary causes such as intraparenchymal hemorrhage, cardiac arrest, SAH, and TBI, we found case reports of the use of INM showing brain hypoxia, increased ICP ( 8 , 9 , 11 ), hyperemia ( 9 , 10 ), and cerebral metabolic crisis ( 9 , 11 ). While these studies demonstrate the effects of seizures on cerebral physiology, these patients had concomitant primary ABI as a cause of seizures, therefore many of the physiological changes were attributable to their primary ABI rather than effects of seizures alone.…”

“…Intracranial hypertension, metabolic crisis and hypoxic-ischemic brain injury (HIBI) have been described in SE patients. However, literature is primarily focused on SE that occurs following other primary forms of acute brain injury (ABI) such as intraparenchymal hematoma, cardiac arrest, subarachnoid hemorrhage (SAH), or traumatic brain injury (TBI), which in itself may impact pathophysiology of RSE ( 8–11 ). We found limited literature on development of DCE ( 1 ) in patients with SE without other primary forms of ABI, and no literature on the use of invasive neuromonitoring (INM) to guide clinical care of these patients.…”