Circuits generating secondarily generalized seizures

Brodovskaya, Anastasia

doi:10.1016/j.yebeh.2019.106474

Cited by 26 publications

(27 citation statements)

References 41 publications

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“…The pathophysiology of FBTCS is understood to involve disrupted network interactions between different brain areas. Local ictal discharges bilaterally propagate to brainstem motor areas via the corpus callosum to trigger the tonic–clonic phase 20,21 . Motor areas project excitatory activity to the thalamic nuclei and subcortical structures.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have suggested that impairments in specific brain regions support FBTCS, after finding disrupted structure and function in circuits mediated by thalamus and basal ganglia 6,12–18 . It has also been suggested that FBTCS have a different mechanism to primary generalized seizures, with more complex patient‐specific spread 10,19–23 . There is a need to investigate the full complexity of brain networks, 24 beyond the canonical thalamocortical pathways, 12 to delineate networks underlying FBTCS.…”

Section: Introductionmentioning

confidence: 99%

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Focal to bilateral tonic–clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy

et al. 2021

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Objective Our objective was to identify whether the whole‐brain structural network alterations in patients with temporal lobe epilepsy (TLE) and focal to bilateral tonic–clonic seizures (FBTCS) differ from alterations in patients without FBTCS. Methods We dichotomized a cohort of 83 drug‐resistant patients with TLE into those with and without FBTCS and compared each group to 29 healthy controls. For each subject, we used diffusion‐weighted magnetic resonance imaging to construct whole‐brain structural networks. First, we measured the extent of alterations by performing FBTCS‐negative (FBTCS−) versus control and FBTCS‐positive (FBTCS+) versus control comparisons, thereby delineating altered subnetworks of the whole‐brain structural network. Second, by standardizing each patient's networks using control networks, we measured the subject‐specific abnormality at every brain region in the network, thereby quantifying the spatial localization and the amount of abnormality in every patient. Results Both FBTCS+ and FBTCS− patient groups had altered subnetworks with reduced fractional anisotropy and increased mean diffusivity compared to controls. The altered subnetwork in FBTCS+ patients was more widespread than in FBTCS− patients (441 connections altered at t > 3, p < .001 in FBTCS+ compared to 21 connections altered at t > 3, p = .01 in FBTCS−). Significantly greater abnormalities—aggregated over the entire brain network as well as assessed at the resolution of individual brain areas—were present in FBTCS+ patients (p < .001, d = .82, 95% confidence interval = .32–1.3). In contrast, the fewer abnormalities present in FBTCS− patients were mainly localized to the temporal and frontal areas. Significance The whole‐brain structural network is altered to a greater and more widespread extent in patients with TLE and FBTCS. We suggest that these abnormal networks may serve as an underlying structural basis or consequence of the greater seizure spread observed in FBTCS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Focal to bilateral tonic–clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy

et al. 2021

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“…37 Given that the motor cortex projects to the thalamus, corpus callosum, and striatum, it also receives projections from the thalamus. 38 Deep brain stimulation of the subthalamic nucleus and anterior thalamus has been reported to affect motor cortex excitability in Parkinson's disease or epilepsy. 24,39 These findings imply that subcortical structures, including the thalamus, striatum, and corpus callosum, may affect motor cortex hyperexcitability in BTCS.…”

Section: Discussionmentioning

confidence: 99%

Cortical Excitability in Temporal Lobe Epilepsy with Bilateral Tonic-Clonic Seizures

Yin

Yang

et al. 2020

Can. J. Neurol. Sci.

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Objective: We investigated motor cortical excitability (CE) in unilateral temporal lobe epilepsy (TLE) and its relationship to bilateral tonic-clonic seizure (BTCS) using paired-pulse transcranial magnetic stimulation (TMS). Methods: In this cross-sectional study, we enrolled 46 unilateral TLE patients and 16 age-and sex-matched healthy controls. Resting motor thresholds (RMT); short-interval intracortical inhibition (SICI, GABAA receptor-mediated); facilitation (ICF, glutamatergic-mediated) with interstimulus intervals (ISIs) of 2, 5, 10, and 15 ms; and long-interval intracortical inhibition (LICI, GABAB receptor-mediated) with ISIs of 200–400 ms were measured via paired-pulse TMS. Comparisons were made between controls and patients with TLE, and then among the TLE subgroups (no BTCS, infrequent BTCS and frequent BTCS subgroup). Results: Compared with controls, TLE patients had higher RMT, lower SICI and higher LICI in both hemispheres, and higher ICF in the ipsilateral hemisphere. In patients with frequent BTCS, cortical hyperexcitability in the ipsilateral hemisphere was found in a parameter-dependent manner (SICI decreased at a stimulation interval of 5 ms, and ICF increased at a stimulation interval of 15 ms) compared with patients with infrequent or no BTCS. Conclusions: Our results demonstrate that motor cortical hyper-excitability in the ipsilateral hemisphere underlies the epileptogenic network of patients with active BTCS, which is more extensive than those with infrequent or no BTCS.

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“…This FCD pattern has been argued to represent an acquired post-natal reorganizational dysplasia, impairing normal maturation, likely to be both aetiologically and temporally linked with the development of HS, although its functional significance remains unclear ( Thom et al, 2009 ). The superficial cortical layers are highly relevant to seizure propagation through extensive cortical-cortical networks and generation of slow rhythms ( Halgren et al, 2018 ) ; discharges from the superficial cortex spread over a larger area than deeper cortex ( Serafini et al, 2015 ), recruitment of layer II/III neurones plays a critical role in seizure spread ( Brodovskaya and Kapur, 2019 ) and activation of cAMP-response element binding protein, a neuronal activity biomarker, was recently shown only in layer II neurones of epilepsy surgical resections ( De Santis et al, 2020 ). There is also a body of evidence of the integral role of astroglia and glial-neuronal interactions in the pathophysiology of epilepsy ( Patel et al, 2019 ) which are less explored in the superficial cortex.…”

Section: Introductionmentioning

confidence: 99%

Glial regenerative cell types in the superficial cortex in cortical dysplasia subtypes

et al. 2021

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Circuits generating secondarily generalized seizures

Cited by 26 publications

References 41 publications

Focal to bilateral tonic–clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy

Focal to bilateral tonic–clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy

Cortical Excitability in Temporal Lobe Epilepsy with Bilateral Tonic-Clonic Seizures

Glial regenerative cell types in the superficial cortex in cortical dysplasia subtypes

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