Topography of generalized periodic epileptiform discharges in postanoxic nonconvulsive status epilepticus

Abstract

SummaryWe studied slow (≤2.5 Hz) nonevolving generalized periodic epileptiform discharges (GPEDs) in the electroencephalogram (EEG) of comatose patients after cardiac arrest (CA) in search of evidence that could assist early diagnosis of possible hypoxic nonconvulsive status epilepticus (NCSE) and its differentiation from terminal brain anoxia (BA), which can present with a similar EEG pattern. We investigated the topography of the GPEDs in the first post‐CA EEGs of 13 patients, using voltage‐mapping, and compared findings between two patients with NCSE and GPEDs > 2.5 Hz (group 1), and 11 with GPEDs ≤ 2 Hz, of whom six had possible NCSE (group 2) and five had terminal BA (group 3). Voltage mapping showed frontal maximum for the negative phase of the GPEDs in all patients of groups 1 and 2, but not in any of the patients of group 3, who invariably showed maximization of the negative phase posteriorly. Morphology, amplitude, and duration of the GPEDs varied across the groups, without distinctive features for possible NCSE. These findings provide evidence that, in hypoxic coma after CA with slow GPEDs, anterior topography of the maximum GPED negativity on voltage mapping may be a distinctive biomarker for possible NCSE contributing to the coma.

Concepts in Periodic Discharges: A Descriptive Study

“…18 Continuous bedside EEG monitoring proved a valuable tool in the detection and follow-up of an electrographic status or a nonconvulsive status epilepticus. 18,19 Immediate treatment with antiepileptics decreased the extent of neuronal damage, reduced the frequency of seizures, and prevented the development of pharmacoresistance. 18,19 In our study, 16% patients underwent cardiopulmonary resuscitation following cardiac arrest.…”

“…18,19 Immediate treatment with antiepileptics decreased the extent of neuronal damage, reduced the frequency of seizures, and prevented the development of pharmacoresistance. 18,19 In our study, 16% patients underwent cardiopulmonary resuscitation following cardiac arrest. Cerebral hypoxia was associated with evolving generalized periodic discharges and a nonconvulsive status epilepticus.…”

“…Cerebral hypoxia was associated with evolving generalized periodic discharges and a nonconvulsive status epilepticus. 18,19 Nonconvulsive status epilepticus contributed to progressive neuronal injury, cerebral ischemia, and irreversible neuronal damage. 18,19 This cycle of inevitable consequences was enhanced by a glutamate mediated excitotoxicity that resulted in the production of generalized periodic discharges.…”

“…18,19 Nonconvulsive status epilepticus contributed to progressive neuronal injury, cerebral ischemia, and irreversible neuronal damage. 18,19 This cycle of inevitable consequences was enhanced by a glutamate mediated excitotoxicity that resulted in the production of generalized periodic discharges. 9 Metabolic derangements resulted in microstructural changes, stimulation of postsynaptic receptors, impaired clearance of neurotransmitters, endothelial, and microglial activation.…”

“…9 Metabolic derangements resulted in microstructural changes, stimulation of postsynaptic receptors, impaired clearance of neurotransmitters, endothelial, and microglial activation. 18,19 During an electrical status epilepticus, there was increased energy consumption by the hyperactive neurons resulting in a loss of neuronal integrity. [18][19][20] Thus, cerebral hypoxia increased the metabolic demands in a compromised brain leading to neuronal exhaustion, synaptic failure, and irreversible brain death.…”