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Antiepileptic Drug of Levetiracetam Decreases Centrotemporal Spike-Associated Activation in Rolandic Epilepsy

The objective was to study the modulation effects of levetiracetam on the fMRI activation/deactivation patterns associated with centrotemporal spikes (CTS) in Rolandic epilepsy. Forty patients with Rolandic epilepsy, including levetiracetam-medicated patients (n = 20) and drug-naive patients (n = 20...

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Detalles Bibliográficos
Autores principales: Zhang, Qirui, Yang, Fang, Hu, Zheng, Xu, Qiang, Bernhardt, Boris C., Quan, Wei, Li, Qian, Zhang, Zhiqiang, Lu, Guangming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6277790/
https://www.ncbi.nlm.nih.gov/pubmed/30542255
http://dx.doi.org/10.3389/fnins.2018.00796
Descripción
Sumario:The objective was to study the modulation effects of levetiracetam on the fMRI activation/deactivation patterns associated with centrotemporal spikes (CTS) in Rolandic epilepsy. Forty patients with Rolandic epilepsy, including levetiracetam-medicated patients (n = 20) and drug-naive patients (n = 20), were studied. Single and sequential hemodynamic response functions-based EEG-fMRI analysis was performed to detect dynamic activation/deactivation associated with CTS. Comparisons of spatiotemporal features of activation/deactivation were performed between the two groups. Both the groups (CTS were detected in 12 cases of levetiracetam-medicated group, and 11 cases of drug-naive group) showed CTS-associated activation in the Rolandic cortex, whereas activation strength, time-to-peak delay, and overall activation were diminished in the levetiracetam-medicated group. Moreover, the drug-naive group showed deactivation in the regions engaged in higher cognition networks compared with the levetiracetam-medicated group. Levetiracetam inhibits CTS-associated activation intensity and alters the temporal pattern of this activation in the epileptogenic regions, and it also affects the brain deactivation related to higher cognition networks. The findings sheds a light on the pharmocological mechanism of levetiracetam therapy on Rolandic epilepsy.