Risk factors for postictal generalized EEG suppression in generalized convulsive seizure: A systematic review and meta-analysis

Abstract

Background and purposePostictal generalized EEG suppression (PGES) has been suggested as a pathophysiological hallmark for sudden unexpected death in epilepsy (SUDEP). We aimed to characterize the clinical determinants for PGES occurrence after generalized convulsive seizures (GCS). MethodsWe systematically searched Pubmed, Embase and Medline databases up to 30 August 2021. Eligibility screening, data extraction, and quality assessment of the retrieved articles were conducted by two independent reviewers. Studies reporting potential risk factors of PGES occurrence in GCS were included for subsequent meta-analysis and PGES was defined as a generalized EEG attenuation of any duration >1s below 10μV, immediately or within 30s after an ictal EEG pattern has terminated. A fixed-effects model was applied when the heterogeneity is low (I2 values < 50%). Otherwise, a random-effects model was used (I2 values ≥ 50%). We assessed the odds ratio (OR) as outcome measure for dichotomous variables and the STD Mean Difference (SMD) for continuous variables. The Begg test and the Egger test was applied in the assessment of publication bias. ResultsA total of 15 relevant studies were identified, enrolling 2057 GCSs. The incidence of PGES in GCS from 15 studies varied from 23% to 86%. The longer tonic phase duration (SMD, 0.26; 95%CI, 0.13 to 0.39; p < 0.001), sleep state at GCS onset (OR,1.63; 95%CI, 1.24 to 2.16; p = 0.001), older age of epilepsy onset (SMD, 0.48; 95%CI, 0.21 to 0.75; p = 0.001), the presence of postictal immobility (OR, 78.05; 95%CI, 32.31 to 188.53; p < 0.001) and oxygen desaturation nadir (SMD, -0.54; 95%CI, -0.76 to -0.33; p < 0.001) showed significant association with the likelihood of having PGES in GCS, but not total seizure duration (SMD, -0.06; 95%CI, -0.20 to 0.08; p = 0.385), tonic-clonic duration (SMD, -0.12; 95%CI, -0.26 to 0.01; p = 0.071), clonic phase duration (SMD, -0.09; 95%CI, -0.27 to 0.08; p = 0.293), epilepsy duration of patients (SMD, -0.09; 95%CI, -0.27 to 0.08; p = 0.293) or lack of early O2 administration (OR, 1.59; 95%CI, 0.80 to 3.17; p = 0.184). ConclusionThe current study informed that PGES is common after GCS. Early identification should be considered among individuals with GCS at high risk of PGES through clinical screening. Further studies with larger sample size are required for individualized evaluation of the risk of PGES in GCS and more effort is needed to further evaluate the risk of SUDEP.