One of the possible mechanisms that may explain cognitive deficits associated with epileptiform activity is related to the interaction between the epileptic and cognitive networks. In that context, the interference of epileptic activity with the default mode network (DMN) has been investigated in detail. The DMN consisting of precuneus, retrosplenial cortex, and parietal and anterior medial frontal cortex, and is active in the resting brain with a high degree of functional connectivity (Raichle et al., 2001). It has been suggested that the DMN constitutes a necessary favorable neurometabolic environment for cognitive functions, represents a physiologic baseline for processes of attention and working memory, and supports dynamic integration of cognitive and emotional processing (Raichle & Mintun, 2006). Abnormal activity in the DMN and disturbed connectivity between the structures involved may influence task performance and contribute to pathogenesis of neuropsychiatric disorders such as attention-deficit/hyperactivity disorder, Alzheimer's disease, autism, schizophrenia, and depression (Eichele et al., 2008; Broyd et al., 2009). Moreover, altered activity in the DMN has been associated with fluctuations and disturbance of consciousness (Boly et al., 2008). It has been suggested that disruption of the resting state activity by pathologic processes (e.g., those that give rise to epileptic spike) may be related to alterations in cognitive function and that this may be a possible mechanism that underlies cognitive deficits in epilepsy (Gotman et al., 2005). Deactivations in the DMN have been described in awake patients with primary and secondary generalized paroxysms and absence seizures (Aghakhani et al., 2004; Gotman et al., 2005; Hamandi et al., 2006; Moeller et al., 2008a,b, 2010a,b). These DMN deactivations may reflect disturbance of awareness or consciousness (Gotman et al., 2005). The abnormal connectivity in the DMN has been observed in several epileptic disorders (Zhang et al., 2009, 2010), including typical EE such as continuous spikes and waves during slow sleep (CSWS) and Lennox-Gastaut syndrome (Siniatchkin et al., 2010; Pizoli et al., 2011; Moehring et al., 2013; Moehring J, Kroeher B, Galka A, von Ondarza G, Moeller F, Wolff S, Granert O, Jansen O, Boor R, Stephani U, Siniatchkin M, unpublished manuscript). However, the abnormal activity and connectivity in the DMN is only one explanation among others for mechanisms of EE. The disturbed connectivity in other cognitive networks in relation to epileptic activity has been described in several studies (Bettus et al., 2009). However, there is an urgent need for further studies on functional neuroimaging that should describe short-term and long-term impact of epileptic activity on cognitive networks, especially in the context of EE.