Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/30974
Title: Interictal and seizure-onset EEG patterns in malformations of cortical development: A systematic review.
Austin Authors: Shakhatreh, Lubna;Janmohamed, Mubeen;Baker, Ana Antonic;Willard, Anna;Laing, Joshua;Rychkova, Maria;Chen, Zhibin;Kwan, Patrick;O'Brien, Terence J;Perucca, Piero 
Affiliation: Epilepsy Research Centre
Department of Medicine (The Royal Melbourne Hospital), The University of Melbourne, Melbourne, Australia
Neurology
Department of Neuroscience, The Central Clinical School, Monash University, Melbourne, Australia
Department of Neurology, The Royal Melbourne Hospital, Melbourne, Australia
Department of Neurology, Alfred Health, Melbourne, Australia
Issue Date: 19-Sep-2022
Date: 2022
Publication information: Neurobiology of disease 2022; 174: 105863
Abstract: Malformations of cortical development (MCDs) are common causes of drug-resistant epilepsy. The mechanisms underlying the associated epileptogenesis and ictogenesis remain poorly elucidated. EEG can help in understanding these mechanisms. We systematically reviewed studies reporting scalp or intracranial EEG features of MCDs to characterise interictal and seizure-onset EEG patterns across different MCD types. We conducted a systematic review in accordance with PRISMA guidelines. MEDLINE, PubMed, and Cochrane databases were searched for studies describing interictal and seizure-onset EEG patterns in MCD patients. A classification framework was implemented to group EEG features into 20 predefined patterns, comprising nine interictal (five, scalp EEG; four, intracranial EEG) and 11 seizure-onset (five, scalp EEG; six, intracranial EEG) patterns. Logistic regression was used to estimate the odds ratios (OR) of each seizure-onset pattern being associated with specific MCD types. Our search yielded 1682 studies, of which 27 comprising 936 MCD patients were included. Of the nine interictal EEG patterns, five (three, scalp EEG; two, intracranial EEG) were detected in ≥2 MCD types, while four (rhythmic epileptiform discharges type 1 and type 2 on scalp EEG; repetitive bursting spikes and sporadic spikes on intracranial EEG) were seen only in focal cortical dysplasia (FCD). Of the 11 seizure-onset patterns, eight (three, scalp EEG; five, intracranial EEG) were found in ≥2 MCD types, whereas three were observed only in FCD (suppression on scalp EEG; delta brush on intracranial EEG) or tuberous sclerosis complex (TSC; focal fast wave on scalp EEG). Among scalp EEG seizure-onset patterns, paroxysmal fast activity (OR = 0.13; 95% CI: 0.03-0.53; p = 0.024) and repetitive epileptiform discharges (OR = 0.18; 95% CI: 0.05-0.61; p = 0.036) were less likely to occur in TSC than FCD. Among intracranial EEG seizure-onset patterns, low-voltage fast activity was more likely to be detected in heterotopia (OR = 19.3; 95% CI: 6.22-60.1; p < 0.001), polymicrogyria (OR = 6.70; 95% CI: 2.25-20.0; p = 0.004) and TSC (OR = 4.27; 95% CI: 1.88-9.70; p = 0.005) than FCD. Different MCD types can share similar interictal or seizure-onset EEG patterns, reflecting common underlying biological mechanisms. However, selected EEG patterns appear to point to distinct MCD types, suggesting certain differences in their neuronal networks.
URI: https://ahro.austin.org.au/austinjspui/handle/1/30974
DOI: 10.1016/j.nbd.2022.105863
ORCID: 
Journal: Neurobiology of disease
PubMed URL: 36165814
Type: Journal Article
Subjects: Focal cortical dysplasia
Heterotopia
Interictal
Intracranial EEG
Malformations of cortical development
Polymicrogyria
Scalp EEG
Seizure-onset
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