Simultaneous EEG‐fMRI in drug‐naive children with newly diagnosed absence epilepsy

Abstract

SUMMARYPurpose: In patients with idiopathic generalized epilepsy (IGE), blood oxygen level dependent (BOLD) EEG during functional MRI (EEG-fMRI) has been successfully used to link changes in regional neuronal activity to the occurrence of generalized spike-and-wave (GSW) discharges. Most EEG-fMRI studies have been performed on adult patients with long-standing epilepsy who were on antiepileptic medication. Here, we applied EEG-fMRI to investigate BOLD signal changes during absence seizures in children with newly diagnosed childhood absence epilepsy (CAE). Methods: Ten drug-naive children with newly diagnosed CAE underwent simultaneous EEG-fMRI. BOLD signal changes associated with ictal EEG activity (i.e., periods of three per second GSW) were analyzed in predefined regions-of-interests (ROIs), including the thalamus, the precuneus, and caudate nucleus. Results: In 6 out of 10 children, EEG recordings showed periods of three per second GSW during fMRI. Three per second GSW were associated with regional BOLD signal decreases in parietal areas, precuneus, and caudate nucleus along with a bilateral increase in the BOLD signal in the medial thalamus. Taking into account the normal delay in the hemodynamic response, temporal analysis showed that the onset of BOLD signal changes coincided with the onset of GSW. Discussion: In drug-naive individuals with CAE, ictal three per second GSW are associated with BOLD signal changes in the same striato-thalamocortical network that changes its regional activity during primary and secondary generalized paroxysms in treated adults. No BOLD signal changes in the striato-thalamo-cortical network preceded the onset of three per second GSW in unmediated children with CAE.

The Default Mode Network and Altered Consciousness in Epilepsy

“…Most decreases during absence seizures occur >7 s after electrographic seizure onset [4,28]. Archer et al [3] reported significant SWD-related deactivation of the posterior cingulate, and BOLD signal decreases have also been reported in the parietal cortex [5,28,53], precuneus [53], caudate nucleus [53], cingulate gyrus [5,28], basal ganglia [5], and posterior temporal cortices [28]. CBF measurements have also confirmed that decreases occur in the same regions showing negative BOLD responses [33].…”

“…Aghakhani et al [1] were able to capture robust thalamic involvement during SWD in idiopathic generalized epilepsy using 1.5T fMRI, and Laufs et al [39] reported posterior thalamic activation at 3T. Robust thalamic involvement has also been reported during seizures in childhood absence epilepsy [4,5,53]. Other areas of activation include midfrontal regions [5,28] and the insulae [28].…”

What do patients with epilepsy tell us about language dynamics? A review of fMRI studies

“…For instance, it is not completely clear how changes in the hemodynamic response function (HRF) are affected by the ongoing subcritical epileptic activity, as suggested by several studies (Baumgartner et al, 1998;Federico et al, 2005;Mäkiranta et al, 2005;Hawco et al, 2007;Moeller et al, 2008). The HRF in epileptic seizures may have different shapes and higher variability compared with the HRF for exogenous stimuli and may be slower for negative than for positive blood oxygenation level-dependent (BOLD) signals (Bagshaw et al, 2004).…”

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

“…As mentioned above, a bilaterally present, hyperexcitable, focal area within the deep layers (V and VI) of the perioral somatosensory cortex (S1po) has been identified as the seizure onset zone (Meeren et al, 2002;Polack et al, 2007) or rather near in the S2 or insular cortex (Zheng et al, 2012) and the necessity of this focal area(s) for SWD generation has been validated by several independent research groups exploiting different experimental techniques (for review see (van Luijtelaar and Sitnikova, 2006). It can be noted, that such a focal cortical onset zone, although not located within the somatosensory cortex, but rather in fronto-temporal cortical regions, has also been identified in children with absence epilepsy in several EEG, MEG (magnetoencephalogram) and EEG-fMRI studies (Holmes et al, 2004;Moeller et al, 2008;Westmijse et al, 2009). …”