Neurodevelopment in new-onset juvenile myoclonic epilepsy over the first 2 years

Objective Adults with juvenile myoclonic epilepsy (JME) have subtle brain structural abnormalities in the frontothalamocortical network, poorer cognitive function, and worse long‐term social outcomes, even when their seizures are controlled and/or remitted. The natural history of JME and development...

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Veröffentlicht in:Annals of neurology 2014-11, Vol.76 (5), p.660-668
Hauptverfasser: Lin, Jack J., Dabbs, Kevin, Riley, Jeffrey D., Jones, Jana E., Jackson, Daren C., Hsu, David A., Stafstrom, Carl E., Seidenberg, Michael, Hermann, Bruce P.
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Sprache:eng
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Zusammenfassung:Objective Adults with juvenile myoclonic epilepsy (JME) have subtle brain structural abnormalities in the frontothalamocortical network, poorer cognitive function, and worse long‐term social outcomes, even when their seizures are controlled and/or remitted. The natural history of JME and development of abnormalities in brain structure and cognition from epilepsy onset has not been studied. Methods The maturational trajectories of cognitive and brain development were prospectively compared between 19 children with new‐onset JME in the first 2 years after diagnosis and 57 healthy controls. Results Cognitive abilities of children with JME were similar to or worse than healthy controls at baseline but failed to reach the competence level of healthy controls at follow‐up across most of the tested cognitive abilities. Abnormal patterns of brain development, as assessed by magnetic resonance imaging studies, were evident in children with JME and included attenuation of age‐related decline in cortical volume, thickness, and surface area compared to typically developing children. The altered brain developmental trajectory in the JME group was evident in higher‐association frontoparietotemporal brain regions (p < 0.05, corrected for multiple comparisons). Interpretation Children with JME have abnormal structural brain development and impaired cognitive development early in the course of their epilepsy. Ann Neurol 2014;76:660–668
ISSN:0364-5134
1531-8249
DOI:10.1002/ana.24240