Higher-order thalamic nuclei facilitate the generalization and maintenance of spike-and-wave discharges of absence seizures

Atherton, Zoe; Nagy, Olivér; Barcsai, Lívia; Sere, Péter; Zsigri, Nikolett; Földi, Tamás; Gellért, Levente; Berényi, Antal; Crunelli, Vincenzo; Lőrincz, Magor L.

doi:10.1016/j.nbd.2023.106025

Cited by 3 publications

(2 citation statements)

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“…Recent studies emphasized the contribution of the visual network to the formation of GSWDs. A rodent model of genetic absences has revealed temporary desynchronization in cortical areas, such as the primary visual cortex, during spike-wave activity [44]. A clinical EEG/fMRI study on IGEs noted a decrease in synchrony of the occipital cortex during the GSWDs [45].…”

Section: Discussionmentioning

confidence: 99%

The Pre-Interictal Network State in Idiopathic Generalized Epilepsies

Pitetzis,

Frantzidis,

Psoma

et al. 2023

Brain Sciences

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Generalized spike wave discharges (GSWDs) are the typical electroencephalographic findings of Idiopathic Generalized Epilepsies (IGEs). These discharges are either interictal or ictal and recent evidence suggests differences in their pathogenesis. The aim of this study is to investigate, through functional connectivity analysis, the pre-interictal network state in IGEs, which precedes the formation of the interictal GSWDs. A high-density electroencephalogram (HD-EEG) was recorded in twenty-one patients with IGEs, and cortical connectivity was analyzed based on lagged coherence and individual anatomy. Graph theory analysis was used to estimate network features, assessed using the characteristic path length and clustering coefficient. The functional connectivity analysis identified two distinct networks during the pre-interictal state. These networks exhibited reversed connectivity attributes, reflecting synchronized activity at 3–4 Hz (delta2), and desynchronized activity at 8–10.5 Hz (alpha1). The delta2 network exhibited a statistically significant (p < 0.001) decrease in characteristic path length and an increase in the mean clustering coefficient. In contrast, the alpha1 network showed opposite trends in these features. The nodes influencing this state were primarily localized in the default mode network (DMN), dorsal attention network (DAN), visual network (VIS), and thalami. In conclusion, the coupling of two networks defined the pre-interictal state in IGEs. This state might be considered as a favorable condition for the generation of interictal GSWDs.

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Section: Discussionmentioning

confidence: 99%

The Pre-Interictal Network State in Idiopathic Generalized Epilepsies

Pitetzis,

Frantzidis,

Psoma

et al. 2023

Brain Sciences

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“…Notwithstanding, the rodent thalamic posterior nucleus may be one of the key thalamic hubs in view of its critical involvement in pre-and post-ictal activity (Lüttjohann and Pape, 2019). Notably, TC neurons in intralaminar thalamic nuclei show a similar decrease in total firing as that of first-order thalamic nuclei during ASs but present two patterns of ictal burst firing: one with a transient increase in bursts at seizure-onset and one with a sustained increase in burst firing that lasts for the duration of the seizure (Atherton et al, 2023). Moreover, it is interesting to note that extracellular alkalosis elicits ASs by activating intralaminar thalamic, but not cortical and first-order thalamic neurons of WAG/Rij rats (Salvati et al, 2022b), a finding of key clinical significance since hyperventilation is a trigger of ASs in many CAE patients.…”

Section: Cellular Activity In the Neocortex And Thalamus During Assmentioning

confidence: 99%

Corticothalamic Network Abnormalities Underlying Absence Seizures

Leresche,

Crunelli

2023

The Cerebral Cortex and Thalamus

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Absence seizures (ASs) are genetic generalized seizures and one of the critical neurological phenotypes that originate from abnormalities in corticothalamic (CT) networks. Genetic analyses of cohorts with only ASs have identified 2p16.1 and 2q22.3 as significant loci and a few genes related to intrinsic and synaptic membrane channels. In normal animals, the genetic mutation of a single voltage- or ligand-gated channel in a single cortical or thalamic neuronal population can lead to spontaneous ASs. The electrographic activity of ASs invariably initiates from a localized cortical area, but the full expression of these seizures’ clinical symptoms requires interactions between cortical and thalamic networks. In contrast to focal and other genetic generalized seizures, the ictal activity of cortical and thalamic neurons during ASs is predominantly characterized by a decreased, but highly synchronized firing, with individual neurons often showing a different firing pattern from one seizure to the next. The high remittance rate of children with ASs indicates that CT networks, and/or their modulatory inputs from the basal ganglia and brainstem, have the inherent capacity to compensate for the developmental abnormalities that lead to ASs, but the mechanisms of remittance have not been investigated since all available models lack this feature of human ASs.

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