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  • Title: [Default mode network in childhood absence epilepsy by 3.0T magnetic resonance imaging].
    Author: Li Y, Wang E, Han X, Gao L, Zheng M, Zhang Y, Ren T, He G, Yan X, Zheng H, Xue Z.
    Journal: Zhonghua Yi Xue Za Zhi; 2014 Dec 09; 94(45):3540-4. PubMed ID: 25622829.
    Abstract:
    OBJECTIVE: To explore the default mode network (DMN) in childhood absence epilepsy (CAE) patients and examine their correlations between functional connectivity (FC) and clinical characteristics. METHODS: Fourteen CAE patients and 14 healthy volunteers were prospectively recruited from Henan Provincial People's Hospital from September 2012 to June 2014. FC in DMN of each group, between-group comparison of DMN FC and their relationships with clinical characteristics were respectively analyzed with 3.0T resting-state functional magnetic resonance imaging (fMRI) FC analysis seeding at bilateral precuneus/posterior cingulate cortex (PCC). RESULTS: Seeding at bilateral precuneus/posterior cingulate cortex (PCC), positive connection was found in bilateral angular gyrus, bilateral superior parietal gyrus, bilateral superior and middle frontal gyrus, bilateral superior medial frontal gyrus, bilateral middle temporal gyrus and bilateral superior and middle occipital gyrus in controls. However, positive connection in CAE patients was observed in bilateral superior parietal gyrus and bilateral superior occipital gyrus. Between-group analysis of DMN connectivity revealed a reduction of DMN FC in bilateral medial orbitofrontal cortex, bilateral anterior cingulate cortex, bilateral superior frontal gyrus, bilateral middle frontal gyrus and left caudate in CAE patients. Moreover, increased DMN FC was present in right paracentral lobule and right middle cingulate gyrus. FC between PCC and bilateral medial orbitofrontal cortex or bilateral superior/middle frontal gyrus correlated negatively with disease duration, but there was no correlation with seizure frequency or initial age. CONCLUSION: Brain's default mode network in childhood absence epilepsy is impaired, presumably, as a result of unconsciousness and cognitive impairment during absence seizure. Abnormal DMN activities may be a biomaker of disease progress in absence epilepsy.
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