The Default Mode Network and Altered Consciousness in Epilepsy

Abstract

Abstract. The default mode network has been hypothesized based on the observation that specific regions of the brain are consistently activated during the resting state and deactivated during engagement with task. The primary nodes of this network, which typically include the precuneus/posterior cingulate, the medial frontal and lateral parietal cortices, are thought to be involved in introspective and social cognitive functions. Interestingly, this same network has been shown to be selectively impaired during epileptic seizures associated with loss of consciousness. Using a wide range of neuroimaging and electrophysiological modalities, decreased activity in the default mode network has been confirmed during complex partial, generalized tonic-clonic, and absence seizures. In this review we will discuss these three seizure types and will focus on possible mechanisms by which decreased default mode network activity occurs. Although the specific mechanisms of onset and propagation differ considerably across these seizure types, we propose that the resulting loss of consciousness in all three types of seizures is due to active inhibition of subcortical arousal systems that normally maintain default mode network activity in the awake state. Further, we suggest that these findings support a general "network inhibition hypothesis," by which active inhibition of arousal systems by seizures in certain cortical regions leads to cortical deactivation in other cortical areas. This may represent a push-pull mechanism similar to that seen operating between cortical networks under normal conditions.

Modulation of Intrinsic Brain Activity by Electroconvulsive Therapy in Major Depression

“…These results confirm a previous report of normalized RSFC of right hippocampus with ECT, though our methodological approaches differed (33). PCC and precuneus share direct anatomical connections with the hippocampus (34; 35), and together with medial PFC form the default mode RSN widely implicated in self-referential processing and depression (36–38), and aspects of epilepsy (39). The hippocampus is also a key structure in the pathophysiology of seizure disorders (e.g., temporal lobe epilepsy) (40), perhaps indicating that this structure is vulnerable to (and may even help to propagate) seizure activity elicited during ECT.…”

“…Epilepsy research suggests these regions are impacted during seizures (63). Notably, the cerebellum exhibits increased activity during post-ictal phase (i.e., a period of altered consciousness following a seizure) (39; 63), and may influence thalamocortical circuits to aid in seizure termination and suppression (39; 64). In our study, functional plasticity in the cerebellum and other regions exhibiting ΔECT effects in the absence of ΔMD effects may reflect nonspecific physiological effects of seizure-related processes.…”

Neuromagnetic high-frequency oscillations correlate with seizure severity in absence epilepsy

“…The default mode network has been hypothesized on the basis of the observation that specific regions of the brain are consistently activated during the resting state but deactivated when engaged with tasks (Danielson et al, 2011). This network is assumed to be selectively impaired during epileptic seizures associated with loss of consciousness, such as absence seizures.…”

The epileptogenic network: the relationship between resting state and pre-spike related perturbations

“…Also, Takaya et al (2006) demonstrated prefrontal hypometabolism and hypo-function in patients with intractable MTLE who also showed cognitive impairment (Takaya et al, 2006). Reduced connectivity in the DMN in MTLE patients has been also correlated with loss of consciousness (Cauda et al, 2009, Danielson et al, 2011.…”

“…Although most RSNs connectivity studies in MTLE patients aimed to understand the cognitive deficiencies often reported in those patients (Cataldi et al, 2013), some of these networks have been shown to be highly affected during rest (Maneshi et al, 2014, seizures (Danielson et al, 2011) and inter-ictal spikes (Laufs et al, 2007b, Fahoum et al, 2012.…”