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The generation mechanism of spike-and-slow wave discharges appearing on thalamic relay nuclei.

ABSTRACT: In this paper, we use a model modified from classic corticothalamic network(CT) to explore the mechanism of absence seizures appearing on specific relay nuclei (SRN) of the thalamus. It is found that typical seizure states appear on SRN through tuning several critical connection strengths in the model. In view of previous experimental and theoretical works which were mainly on epilepsy seizure phenomena appearing on excitatory pyramidal neurons (EPN) of the cortex, this is a novel model to consider the seizure observed on thalamus. In particular, the onset mechanism is different from previous theoretical studies. Inspired by some previous clinical and experimental studies, we employ the external stimuli voltage on EPN and SRN in the network, and observe that the seizure can be well inhibited by tuning the stimulus intensity appropriately. We further explore the effect of the signal transmission delays on seizures, and found that the polyspike phenomenon appears only when the delay is sufficiently large. The experimental data also confirmed our model. Since there is a complex network in the brain and all organizations are interacting closely with each other, the results obtained in this paper provide not only biological insights into the regulatory mechanisms but also a reference for the prevention and treatment of epilepsy in future.

SUBMITTER: Hu B

PROVIDER: S-EPMC5862852 | biostudies-other | 2018 Mar

REPOSITORIES: biostudies-other

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The generation mechanism of spike-and-slow wave discharges appearing on thalamic relay nuclei.

Hu Bing B Guo Yu Y Shi Feng F Zou Xiaoqiang X Dong Jing J Pan Long L Yu Min M Zhou Chaowei C Cheng Zhang Z Tang Wanyue W Sun Haochen H Chen Luonan L

Scientific reports 20180321 1

In this paper, we use a model modified from classic corticothalamic network(CT) to explore the mechanism of absence seizures appearing on specific relay nuclei (SRN) of the thalamus. It is found that typical seizure states appear on SRN through tuning several critical connection strengths in the model. In view of previous experimental and theoretical works which were mainly on epilepsy seizure phenomena appearing on excitatory pyramidal neurons (EPN) of the cortex, this is a novel model to consi ...[more]

PMID: 29563579

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Project description:Generalized spike-wave discharges in idiopathic generalized epilepsy are conventionally assumed to have abrupt onset and offset. However, in rodent models, discharges emerge during a dynamic evolution of brain network states, extending several seconds before and after the discharge. In human idiopathic generalized epilepsy, simultaneous EEG and functional MRI shows cortical regions may be active before discharges, and network connectivity around discharges may not be normal. Here, in human idiopathic generalized epilepsy, we investigated whether generalized spike-wave discharges emerge during a dynamic evolution of brain network states. Using EEG-functional MRI, we studied 43 patients and 34 healthy control subjects. We obtained 95 discharges from 20 patients. We compared data from patients with discharges with data from patients without discharges and healthy controls. Changes in MRI (blood oxygenation level-dependent) signal amplitude in discharge epochs were observed only at and after EEG onset, involving a sequence of parietal and frontal cortical regions then thalamus (P < 0.01, across all regions and measurement time points). Examining MRI signal phase synchrony as a measure of functional connectivity between each pair of 90 brain regions, we found significant connections (P < 0.01, across all connections and measurement time points) involving frontal, parietal and occipital cortex during discharges, and for 20 s after EEG offset. This network prominent during discharges showed significantly low synchrony (below 99% confidence interval for synchrony in this network in non-discharge epochs in patients) from 16 s to 10 s before discharges, then ramped up steeply to a significantly high level of synchrony 2 s before discharge onset. Significant connections were seen in a sensorimotor network in the minute before discharge onset. This network also showed elevated synchrony in patients without discharges compared to healthy controls (P = 0.004). During 6 s prior to discharges, additional significant connections to this sensorimotor network were observed, involving prefrontal and precuneus regions. In healthy subjects, significant connections involved a posterior cortical network. In patients with discharges, this posterior network showed significantly low synchrony during the minute prior to discharge onset. In patients without discharges, this network showed the same level of synchrony as in healthy controls. Our findings suggest persistently high sensorimotor network synchrony, coupled with transiently (at least 1 min) low posterior network synchrony, may be a state predisposing to generalized spike-wave discharge onset. Our findings also show that EEG onset and associated MRI signal amplitude change is embedded in a considerably longer period of evolving brain network states before and after discharge events.

Project description:BackgroundContinuous spike-wave during slow wave sleep syndrome (CSWS) and Landau-Kleffner syndrome (LKS) are two epileptic encephalopathies that present with neurocognitive regression, aphasia, and clinical seizures, typically presenting in children around five years of age. The pathophysiology of these conditions is not completely understood. Some studies suggest a common origin for both. No systematic reviews have assessed the efficacy of pharmacological interventions for these conditions.ObjectivesTo assess the benefit and adverse effects of pharmacological interventions for the treatment of CSWS and LKS.Search methodsOn 8 September 2020, we searched the Cochrane Register of Studies (CRS Web) and MEDLINE Ovid (1946 to September 04, 2020). We applied no language restrictions. CRS Web includes randomised or quasi-randomised, controlled trials from CENTRAL, PubMed, Embase, ClinicalTrials.gov, and the World Health Organization International Clinical Trials Registry Platform.Selection criteriaRandomised controlled trials, quasi-randomised controlled trials, and cluster-randomised trials comparing antiepileptic drugs alone, or with steroids or intravenous immunoglobulins, or both versus other antiepileptic drugs, or placebo, or no treatment, administered to children with CSWS and LKS. We planned to compare treatments for the two conditions separately.Data collection and analysisTwo review authors independently assessed studies identified by the search strategy for inclusion. The primary outcomes considered in this review were neuropsychological-neurolinguistic functions.Main resultsOur search strategy yielded 18 references. Two review authors independently assessed all references. We did not find any completed studies to include. We identified one ongoing trial, which was terminated because of lack of enrolment.Authors' conclusionsThere was no evidence from trials to support or refute the use of pharmacological treatment for continuous spike-wave during slow wave sleep syndrome or Landau-Kleffner syndrome. Well-designed randomised controlled trials are needed to inform practice.

Project description:IntroductionDifferent studies have investigated by means of EEG-fMRI coregistration the brain networks related to generalized spike-and-wave discharges (GSWD) in patients with idiopathic generalized epilepsy (IGE). These studies revealed a widespread GSWD-related neural network that involves the thalamus and regions of the default mode network. In this study we investigated which brain regions are critically involved in the termination of absence seizures (AS) in a group of IGE patients.MethodsEighteen patients (6 male; mean age 25 years) with AS were included in the EEG-fMRI study. Functional data were acquired at 3T with continuous simultaneous video-EEG recording. Event-related analysis was performed with SPM8 software, using the following regressors: (1) GSWD onset and duration; (2) GSWD offset. Data were analyzed at single-subject and at group level with a second level random effect analysis.ResultsA mean of 17 events for patient was recorded (mean duration of 4.2 sec). Group-level analysis related to GSWD onset respect to rest confirmed previous findings revealing thalamic activation and a precuneus/posterior cingulate deactivation. At GSWD termination we observed a decrease in BOLD signal over the bilateral dorsolateral frontal cortex respect to the baseline (and respect to GSWD onset). The contrast GSWD offset versus onset showed a BOLD signal increase over the precuneus-posterior cingulate region bilaterally. Parametric correlations between electro-clinical variables and BOLD signal at GSWD offset did not reveal significant effects.ConclusionThe role of the decreased neural activity of lateral prefrontal cortex at GSWD termination deserve future investigations to ascertain if it has a role in promoting the discharge offset, as well as in the determination of the cognitive deficits often present in patients with AS. The increased BOLD signal at precuneal/posterior cingulate cortex might reflect the recovery of neural activity in regions that are "suspended" during spike and waves activity, as previously hypothesized.

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The generation mechanism of spike-and-slow wave discharges appearing on thalamic relay nuclei.

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The generation mechanism of spike-and-slow wave discharges appearing on thalamic relay nuclei.

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