Automated Detection of Postictal Generalized EEG Suppression

Summary Objective: The dynamics of the postictal period, which may demonstrate such dramatic clinical phenomena as focal neurological deficits, prolonged coma and immobility, and even sudden death, are poorly understood. We sought to classify and characterize postictal phases of bilateral tonic-clonic seizures based on EEG criteria and associated clinical features. Methods: We performed a detailed electroclinical evaluation of the postictal period in a series of 31 bilateral tonic-clonic seizures in 16 patients undergoing epilepsy surgery evaluations for focal pharmacoresistant epilepsy with intracranial electrodes and time-locked video. Results: The postictal EEG demonstrated three clearly differentiated phases: attenuation, a burst-attenuation pattern, and a return to continuous background, with abrupt, synchronized transitions between phases. Postictal attenuation was common, occurring in 84% of seizures in 94% of patients in this study. There was increased power in gamma frequencies (> 25 Hz) during postictal attenuation periods relative to preictal baseline in 88% of seizures demonstrating the attenuation pattern (N=25 seizures, p<0.002). Such increases were seen in more than 90% of channels in 13 seizures (52%), and fewer than 10% of channels in three seizures (12%). Postictal immobility was seen in 87% of seizures, with either a flaccid (58%) or rigid/dystonic (29%) appearance. Clinical motor manifestations, including focal dystonic posturing, automatisms, head and eye deviation, and myoclonic jerking, continued or emerged within the first minute following seizure termination in 48% of seizures, regardless of EEG appearance. Significance: Intracranial postictal attenuation, which may be diffuse or focal, is so common that it should be regarded as an ubiquitous feature of bilateral tonic-clonic seizures, rather than an unusual event. The prominence of high frequency activity coupled with emerging clinical features, including rigid immobility and semiologies such as automatisms, during the postictal period support the presence of ongoing seizure-related neuronal activity in unrecorded brain regions.

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“…These factors likely contribute to the limited inter-reader reliability of PGES. 30 A combined approach may be preferred for future studies.…”

Section: Discussionmentioning

confidence: 99%

Postictal clinical and electroencephalographic activity following intracranially recorded bilateral tonic–clonic seizures

et al. 2018

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“…Presence and duration of postictal generalized EEG suppression (PGES) 20 were determined by a validated automated EEG suppression detection tool 21 and supplemented by visual analysis by 2 epilepsy neurophysiologists when the tool gave no solution. Presence and duration of postictal EEG burst suppression were also determined.…”

Section: Cardiorespiratory Monitoring and Veeg Monitoringmentioning

confidence: 99%

Postconvulsive central apnea as a biomarker for sudden unexpected death in epilepsy (SUDEP)

et al. 2019

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ObjectiveTo characterize peri-ictal apnea and postictal asystole in generalized convulsive seizures (GCS) of intractable epilepsy. MethodsThis was a prospective, multicenter epilepsy monitoring study of autonomic and breathing biomarkers of sudden unexpected death in epilepsy (SUDEP) in patients ≥18 years old with intractable epilepsy and monitored GCS. Video-EEG, thoracoabdominal excursions, nasal airflow, capillary oxygen saturation, and ECG were analyzed. ResultsWe studied 148 GCS in 87 patients. Nineteen patients had generalized epilepsy; 65 had focal epilepsy; 1 had both; and the epileptogenic zone was unknown in 2. Ictal central apnea (ICA) preceded GCS in 49 of 121 (40.4%) seizures in 23 patients, all with focal epilepsy. Postconvulsive central apnea (PCCA) occurred in 31 of 140 (22.1%) seizures in 22 patients, with generalized, focal, or unknown epileptogenic zones. In 2 patients, PCCA occurred concurrently with asystole (near-SUDEP), with an incidence rate of 10.2 per 1,000 patient-years. One patient with PCCA died of probable SUDEP during follow-up, suggesting a SUDEP incidence rate 5.1 per 1,000 patient-years. No cases of laryngospasm were detected. Rhythmic muscle artifact synchronous with breathing was present in 75 of 147 seizures and related to stertorous breathing (odds ratio 3.856, 95% confidence interval 1.395-10.663, p = 0.009). ConclusionsPCCA occurred in both focal and generalized epilepsies, suggesting a different pathophysiology from ICA, which occurred only in focal epilepsy. PCCA was seen in 2 near-SUDEP cases and 1 probable SUDEP case, suggesting that this phenomenon may serve as a clinical biomarker of SUDEP. Larger studies are needed to validate this observation. Rhythmic postictal muscle artifact is suggestive of post-GCS breathing effort rather than a specific biomarker of laryngospasm.

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“…There are discrepancies even amongst experts in PGES identification (Theeranaew et al, 2018). PGES duration was assessed automatically using a custom MATLAB (Mathworks) script and event-related spectral perturbation (ERSP) time-frequency spectral decompositions of the preictal, ictal, and post-ictal period in the MATLAB EEGlab toolbox (Swartz Center for Computational Neuroscience, San Diego, CA).…”

Section: Pges Determinationmentioning

confidence: 99%

Post-ictal generalized EEG suppression and seizure-induced mortality are reduced by enhancing dorsal raphe serotonergic neurotransmission

Petrucci

Joyal

et al. 2020

Preprint

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AbstractSudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. A proposed risk marker for SUDEP is the duration of post-ictal generalized EEG suppression (PGES). The mechanisms underlying PGES are unknown. Serotonin (5-HT) has been implicated in SUDEP pathophysiology. Seizures suppress activity of 5-HT neurons in the dorsal raphe nucleus (DRN). We hypothesized that suppression of DRN 5-HT neuron activity contributes to PGES and increasing 5-HT neurotransmission or stimulating the DRN before a seizure would decrease PGES duration. Adult C57BL/6 and Pet1-Cre mice received EEG/EMG electrodes, a bipolar stimulating/recording electrode in the right basolateral amygdala, and either a microdialysis guide cannula or an injection of adeno-associated virus (AAV) allowing expression of channelrhodopsin2 plus an optic fiber into the DRN. Systemic application of the selective 5-HT reuptake inhibitor citalopram (20 mg/kg) decreased PGES duration from seizures induced during wake (n = 23) and NREM sleep (n = 13) whereas fluoxetine (20 mg/kg) pretreatment decreased PGES duration following seizures induced from wake (n = 11), but not NREM sleep (n = 9). Focal chemical (n = 6) or optogenetic (n = 8) stimulation of the DRN reduced PGES duration following kindled seizures and reduced morality following maximal electroshock seizures (n = 6) induced during wake. During PGES, animals exhibited immobility and suppression of EEG activity that was reduced by citalopram pretreatment. These results indicate that 5-HT and the DRN may regulate PGES and seizure-induced mortality.Highlights-PGES consistently follows seizures induced by amygdala stimulation in amygdala-kindled mice.-Seizure-induced dysregulation of 5-HT neurotransmission from the dorsal raphe nucleus may contribute to PGES.-Systemic administration of 5-HT enhancing drugs and stimulation of the DRN reduces PGES duration.-PGES is associated with post-ictal immobility in kindled mice that can be reduced by pretreatment with citalopram.-Recovery of EEG frequencies to baseline occurs in a stepwise manner with the lowest frequencies recovering first.

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Automated Detection of Postictal Generalized EEG Suppression

Cited by 31 publications

References 23 publications

Postictal clinical and electroencephalographic activity following intracranially recorded bilateral tonic–clonic seizures

Postictal clinical and electroencephalographic activity following intracranially recorded bilateral tonic–clonic seizures

Postconvulsive central apnea as a biomarker for sudden unexpected death in epilepsy (SUDEP)

Post-ictal generalized EEG suppression and seizure-induced mortality are reduced by enhancing dorsal raphe serotonergic neurotransmission

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