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EEG–fMRI study on the interictal and ictal generalized spike-wave discharges in patients with childhood absence epilepsy

Authors :
Dezhong Yao
Qifu Li
Qiyong Gong
Cheng Luo
Ling Liu
Hongru Xu
Tianhua Yang
Li He
Dong Zhou
Zhiping Yao
Source :
Epilepsy Research. 87:160-168
Publication Year :
2009
Publisher :
Elsevier BV, 2009.

Abstract

Summary Background Absence epilepsy is characterized clinically by the impairment of consciousness and 3 Hz generalized spike-wave discharges (GSWDs) on EEG. Clinical absence can be observed with ictal GSWDs, but interictal GSWD bursts are usually clinically silent. Simultaneous EEG and blood-oxygen-level-dependent (BOLD) functional MRI (EEG–fMRI) has been successfully used to link the changes in regional neuronal activity to the occurrence of GSWDs. Methods We used EEG–fMRI to investigate and compare the BOLD signal changes during interictal and ictal GSWDs in patients with childhood absence epilepsy (CAE). Results Fifteen drug-naive children with newly diagnosed CAE were studied using continuous EEG–fMRI. BOLD signal changes associated with interictal (nine sessions with six patients) and ictal (eight sessions with six patients) GSWDs were analyzed at the individual and group levels. GSWDs were associated with widespread and symmetrical deactivation in the cortex and caudate nucleus with a frontal maximum, and predominant activation in the thalamus bilaterally during ictal GSWDs and in the cortex during interictal GSWDs. The BOLD response was characterized by a higher statistical significance and a more widespread extent at the time of the ictal GSWDs as compared to the time of interictal GSWDs. Conclusions Both interictal and ictal GSWDs in patients with CAE are associated with BOLD signal changes in the basal ganglia–thalamocortical loop. Ictal GSWDs showing predominant thalamic activation and widespread cortical deactivation might cause a complete suspension of the normal brain's default state and manifest clinically as abrupt loss of consciousness (absence seizures).

Details

ISSN :
09201211
Volume :
87
Database :
OpenAIRE
Journal :
Epilepsy Research
Accession number :
edsair.doi.dedup.....db5a4aba742a519235a9587133a468db
Full Text :
https://doi.org/10.1016/j.eplepsyres.2009.08.018