Postictal Generalized EEG Suppression Research Articles

Postictal generalized EEG suppression

To determine the consistency and facilitating cofactors of postictal generalized EEG suppression (PGES) of >20 seconds after convulsive seizures (CS), a suggested predictor of sudden unexpected death in epilepsy risk. We retrospectively reviewed video-EEG data of people with ≥2 recorded CS. Presence and duration of PGES were assessed by 2 independent observers blinded to patient status. Intraindividual consistency of PGES >20 seconds was determined and correlations with clinical characteristics were analyzed after correction for individual effects and the varying number of seizures. One hundred fifty-four seizures in 59 people were analyzed. PGES >20 seconds was found in 37 individuals (63%) and 57 (37%) of CS. The proportion of persons in whom PGES occurred consistently (presence or absence of PGES >20 seconds in all CS) was lower in those with more CS. PGES of >20 seconds was more frequent in seizures arising from sleep (odds ratio 3.29, 95% confidence interval 1.21-8.96) and when antiepileptic medication was tapered (odds ratio 4.80, 95% confidence interval 1.27-18.14). Apparent PGES consistency was less frequent in people with more CS recorded, suggesting that PGES is an inconsistent finding in any one individual. Thus, we believe that PGES >20 seconds is not a reliable predictor of sudden unexpected death in epilepsy. Sleep and antiepileptic drug reduction appear to facilitate the occurrence of PGES.

Periictal autonomic dysfunction and generalized postictal EEG suppression in convulsive seizures arising from sleep and wakefulness

Sleep appears to be an independent risk factor of sudden unexpected death in epilepsy (SUDEP). We retrospectively determined the periictal electrophysiological characteristics of nocturnal and diurnal generalized convulsive seizures (GCSs) in 109 patients. Our data showed that preictal heart rate (HR) was significantly lower in 46 patients with nocturnal GCSs than in 63 patients with diurnal GCSs (p=0.002). However, there was no significant difference in postictal HR and respiratory rate (RR), total seizure duration, total convulsive phase, tonic phase, and clonic phase. Meanwhile, postictal generalized EEG suppression (PGES) was observed in 52.4% of the patients with diurnal GCSs and 67.4% of the patients with nocturnal GCSs. Duration of PGES was 38.2±17.3s in patients with diurnal GCSs and 49.5±21.7s in patients with nocturnal GCSs. There was also no significant difference in the prevalence (p=0.118) and duration (p=0.044, Bonferroni-corrected significant level: α=0.00625) of PGES in the two patient groups. Therefore, there is no clear evidence to attribute the SUDEP risk associated with sleep to postictal autonomic dysfunction and PGES, as compared to wakefulness.

Characteristics of postictal generalized EEG suppression in children

Although the pathophysiologic mechanism of sudden unexpected death in epilepsy (SUDEP) is unknown, autonomic dysfunction is thought to be the most likely. It has been hypothesized that respiratory depression resulting in SUDEP may be secondary to postictal generalized electroencephalography suppression (PGES). We sought to determine the characteristics of PGES in children. This included whether PGES was associated with ictally mediated autonomic changes and potential increased risk of SUDEP. Children admitted to our Pediatric Epilepsy Monitoring Unit between 3/2009 and 10/2011 were prospectively recruited. Clinical and electrophysiological data from children with PGES were compared to those without PGES. Data included the occurrence of peri-ictal tachycardia, bradycardia, and hypoxemia. Potential SUDEP risk was assessed using SUDEP-7 Inventory scores. Thirty seven children with 168 seizures were analyzed. PGES was observed following 27/168 (16.1%) seizures in 12/37 (32.4%) children. Only primary and secondarily generalized tonic clonic seizures were marked by PGES. PGES was significantly associated with peri-ictal tachycardia (p=0.019) and hypoxemia (p=0.005). Children with PGES had significantly higher SUDEP-7 Inventory scores than those without PGES (4.2 ± 1.3 versus 2.8 ± 1.4, p=0.007). SUDEP-7 scores were not significantly different between children with and without peri-ictal tachycardia (3.4 ± 1.3 versus 2.5±1.6, p=0.12), bradycardia (4 ± 2 versus 2.9 ± 1.4, p=0.45), or hypoxemia (3.4 ± 1.5 versus 2.4 ± 1.3, p=0.051). Based on our data, PGES is not rare in children. Children with PGES may be at greater risk for SUDEP as measured by the SUDEP-7 Inventory.

Postictal generalized EEG suppression is not associated with periictal cardiac autonomic instability in people with convulsive seizures

Postictal generalized EEG suppression (PGES) seems to be a pathophysiologic hallmark in ictal recordings of sudden unexpected death in epilepsy (SUDEP). It has recently been suggested that presence and duration of PGES might be a predictor of SUDEP risk. Little is known about the etiology of PGES. We conducted a retrospective case-control study in 50 people with convulsive seizures (CS) recorded on digital video-electroencephalography (EEG). One CS per individual was reviewed for presence and duration of PGES by two independent observers: Preictal and postictal heart rate (HR) (1 min before seizure onset and 1, 3, 5, 15, and 30 min after seizure end) and frequency domain measures of heart rate variability (HRV), including the ratio of low frequency (LF) versus high frequency (HF) power, were analyzed. The relationship between PGES and periictal autonomic changes was evaluated, as well as its association with several clinical variables. Thirty-seven individuals (74%) exhibited PGES and 13 (26%) did not. CS resulted in a significant increase of periictal HR and the LF/HF ratio. PGES was associated with neither periictal HR (mean HR difference between PGES+ and PGES- seizures: -2 beats per minute [bpm], 95% confidence interval [CI] -10 to +6 bpm) nor HRV change. There was no association between the duration of PGES and periictal HR change. People with PGES were more likely to be asleep before seizure onset (odds ratio [OR] 4.7, 95% CI 1.2-18.3) and had a higher age of onset of epilepsy (median age 15 vs. 4 years). PGES was not associated with substantial changes in measures of cardiac autonomic instability but was more prevalent in CS arising from sleep.

Autonomic changes with seizures correlate with postictal EEG suppression

Sudden unexpected death in epilepsy (SUDEP) poses a poorly understood but considerable risk to people with uncontrolled epilepsy. There is controversy regarding the significance of postictal generalized EEG suppression as a biomarker for SUDEP risk, and it remains unknown whether postictal EEG suppression has a neurologic correlate. Here, we examined the profile of autonomic alterations accompanying seizures with a wrist-worn biosensor and explored the relationship between autonomic dysregulation and postictal EEG suppression. We used custom-built wrist-worn sensors to continuously record the sympathetically mediated electrodermal activity (EDA) of patients with refractory epilepsy admitted to the long-term video-EEG monitoring unit. Parasympathetic-modulated high-frequency (HF) power of heart rate variability was measured from concurrent EKG recordings. A total of 34 seizures comprising 22 complex partial and 12 tonic-clonic seizures from 11 patients were analyzed. The postictal period was characterized by a surge in EDA and heightened heart rate coinciding with persistent suppression of HF power. An increase in the EDA response amplitude correlated with an increase in the duration of EEG suppression (r = 0.81, p = 0.003). Decreased HF power correlated with an increase in the duration of EEG suppression (r = -0.87, p = 0.002). The magnitude of both sympathetic activation and parasympathetic suppression increases with duration of EEG suppression after tonic-clonic seizures. These results provide autonomic correlates of postictal EEG suppression and highlight a critical window of postictal autonomic dysregulation that may be relevant in the pathogenesis of SUDEP.

Postictal generalized EEG suppression is linked to seizure‐associated respiratory dysfunction but not postictal apnea

The relationship of postictal generalized electroencephalography (EEG) suppression (PGES) with sudden unexpected death in epilepsy (SUDEP) is controversial. It has been suggested that PGES is associated with respiratory inhibition leading to SUDEP, but the relationship between PGES and respiratory depression is unknown. Respiratory rate and amplitude of airflow increase following seizures but there is persistent hypercapnia and hypoxemia. To determine whether seizures with PGES result in respiratory dysfunction, we analyzed respiratory parameters recorded during video-EEG telemetry in patients with localization-related epilepsy. Secondarily generalized convulsive seizures (GC) with PGES on scalp EEG or bilateral postictal attenuation (BA) on intracranial recordings were compared to GC without PGES/BA. Oxygen desaturation nadir and duration, end-tidal CO(2) (ETCO(2) ), apnea duration, and duration of the seizure and of the convulsive component were compared in GC with or without PGES/BA. There was no significant difference between GC with (n = 30) or without PGES/BA (n = 72) for total seizure duration or duration of the convulsion. GC with PGES/BA had a mean oxygen desaturation nadir of 68.8 ± 11.8% (71.5, 43-88) (mean ± standard deviation [median, range]) that was lower (p = 0.002) than seizures without PGES/BA (76.31 ± 10.17% [79, 42-93]). The duration of desaturation was significantly longer and peak ETCO(2) higher in GC with PGES/BA. There was no difference in apnea duration. Apnea did not start during PGES/BA and did not typically extend into the postictal period in GC with or without PGES/BA. PGES is not associated with postictal central apnea but is more likely related to the severity of seizure-associated intrinsic pulmonary dysfunction.

Retrospective audit of postictal generalized EEG suppression in telemetry

Sudden unexpected death in epilepsy (SUDEP) has on rare occasions occurred during electroencephalography (EEG) telemetry, and in such cases postictal EEG suppression (PI EEG-SUP) was frequently observed. More recently a retrospective case-control study reported this pattern as a risk factor for SUDEP. We retrospectively audited frequency and electroclinical features of this pattern as well as immediate management following tonic-clonic seizures during telemetry. Forty-eight patients with tonic-clonic seizures were identified from 470 consecutive EEG-videotelemetry reports. Thirteen patients (27%) with PI EEG-SUP (mean duration 38.1 s, range 6-69 s, median 38 s) were compared to 12 randomly selected controls. One seizure was analyzed per individual. Those with PI EEG-SUP were significantly more likely to be motionless after the seizure and have simple nursing interventions performed (suction, oxygen administration, placed in recovery position, vital signs checked). This pattern is relatively common and requires further study as a potential marker for increased mortality in epilepsy.

Postictal Generalized EEG Suppression and Sudden Unexplained Death in Epilepsy

Does electrocerebral suppression lead to central apnea and fatal respiratory failure in patients with epilepsy? To explore this important issue, researchers conducted a case-control study, comparing 10 patients with confirmed sudden unexplained death in epilepsy (SUDEP) who had undergone video electroencephalography (EEG) monitoring and 30 matching control patients who had at least one seizure recorded during monitoring. The cases included one patient who …