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Dataset of EEG power integral, spontaneous recurrent seizure and behavioral responses following combination drug therapy in soman-exposed rats.

ABSTRACT: This article investigated the efficacy of the combination of antiepileptic drug therapy in protecting against soman-induced seizure severity, epileptogenesis and performance deficits. Adult male rats with implanted telemetry transmitters for continuous recording of electroencephalographic (EEG) activity were exposed to soman and treated with atropine sulfate and the oxime HI-6 one minute after soman exposure and with midazolam, ketamine and/or valproic acid 40 min after seizure onset. Rats exposed to soman and treated with medical countermeasures were evaluated for survival, seizure severity, the development of spontaneous recurrent seizure and performance deficits; combination anti-epileptic drug therapy was compared with midazolam monotherapy. Telemetry transmitters were used to record EEG activity, and a customized MATLAB algorithm was used to analyze the telemetry data. Survival data, EEG power integral data, spontaneous recurrent seizure data and behavioral data are illustrated in figures and included as raw data. In addition, edf files of one month telemetry recordings from soman-exposed rats treated with delayed midazolam are provided as supplementary materials. Data presented in this article are related to research articles "Rational Polytherapy in the Treatment of Cholinergic Seizures" [1] and "Early polytherapy for benzodiazepine-refractory status epilepticus [4].

SUBMITTER: Lumley LA

PROVIDER: S-EPMC6820070 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Dataset of EEG power integral, spontaneous recurrent seizure and behavioral responses following combination drug therapy in soman-exposed rats.

Lumley Lucille A LA Rossetti Franco F de Araujo Furtado Marcio M Marrero-Rosado Brenda B Schultz Caroline R CR Schultz Mark K MK Niquet Jerome J Wasterlain Claude G CG

Data in brief 20191008

This article investigated the efficacy of the combination of antiepileptic drug therapy in protecting against soman-induced seizure severity, epileptogenesis and performance deficits. Adult male rats with implanted telemetry transmitters for continuous recording of electroencephalographic (EEG) activity were exposed to soman and treated with atropine sulfate and the oxime HI-6 one minute after soman exposure and with midazolam, ketamine and/or valproic acid 40 min after seizure onset. Rats expos ...[more]

PMID: 31687442

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Project description:Background and objectiveEpilepsy is one of the most common neurological disorders, whose development is typically detected via early seizures. Electroencephalogram (EEG) is prevalently employed for seizure identification due to its routine and low expense collection. The stochastic nature of EEG makes manual seizure inspections laborsome, motivating automated seizure identification. The relevant literature focuses mostly on supervised machine learning. Despite their success, supervised methods require expert labels indicating seizure segments, which are difficult to obtain on clinically-acquired EEG. Thus, we aim to devise an unsupervised method for seizure identification on EEG.MethodsWe propose the first fully-unsupervised deep learning method for seizure identification on raw EEG, using a variational autoencoder (VAE). In doing so, we train the VAE on recordings without seizures. As training captures non-seizure activity, we identify seizures with respect to the reconstruction errors at inference time. Moreover, we extend the traditional VAE training loss to suppress EEG artifacts. Our method does not require ground-truth expert labels indicating seizure segments or manual feature extraction.ResultsWe implement our method using the PyTorch library and execute experiments on an NVIDIA V100 GPU. We evaluate our method on three benchmark EEG datasets: (i) intracranial recordings from the University of Pennsylvania and the Mayo Clinic, (ii) scalp recordings from the Temple University Hospital of Philadelphia, and (iii) scalp recordings from the Massachusetts Institute of Technology and the Boston Children's Hospital. To assess performance, we report accuracy, precision, recall, Area under the Receiver Operating Characteristics Curve (AUC), and p-value under the Welch t-test for distinguishing seizure vs. non-seizure EEG windows. Our approach can successfully distinguish seizures from non-seizure activity, with up to 0.83 AUC on intracranial recordings. Moreover, our algorithm has the potential for real-time inference, by processing at least 10 s of EEG in a second.ConclusionWe take the first successful steps in deep learning-based unsupervised seizure identification on raw EEG. Our approach has the potential of alleviating the burden on clinical experts regarding laborsome EEG inspections for seizures. Furthermore, aiding the identification of early seizures via our method could facilitate successful detection of epilepsy development and initiate antiepileptogenic therapies.

Project description:Epileptic seizures result in pronounced over-expression of neuropeptide Y (NPY). In vivo and in vitro studies revealed that NPY exerts potent anticonvulsive actions through presynaptic Y2 receptors by suppressing glutamate release from principal neurons. We now investigated whether seizure-induced over-expression of NPY contributes to epileptic tolerance induced by preceding seizures. We used a previously established animal model based on selective inhibition of GABA release from parvalbumin (PV)-containing interneurons in the subiculum in mice. The animals present spontaneous recurrent seizures (SRS) and clusters of interictal spikes (IS). The frequency of SRS declined after five to six weeks, indicating development of seizure tolerance. In interneurons of the subiculum and sector CA1, SRS induced over-expression of NPY that persisted there for a prolonged time despite of a later decrease in SRS frequency. In contrast to NPY, somatostatin was not overexpressed in the respective axon terminals. Contrary to interneurons, NPY was only transiently expressed in mossy fibers. To demonstrate a protective function of endogenous, over-expressed NPY, we injected the selective NPY-Y2 receptor antagonist JNJ 5207787 simultaneously challenging the mice by a low dose of pentylenetetrazol (PTZ, 30 or 40 mg/kg, i.p.). In control mice, neither PTZ nor PTZ plus JNJ 5207787 induced convulsions. In mice with silenced GABA/PV neurons, PTZ alone only modestly enhanced EEG activity. When we injected JNJ 5207787 together with PTZ (either dose) the number of seizures, however, became significantly increased. In addition, in the epileptic mice CB1 receptor immunoreactivity was reduced in terminal areas of basket cells pointing to reduced presynaptic inhibition of GABA release from these neurons. Our experiments demonstrate that SRS result in overexpression of NPY in hippocampal interneurons. NPY overexpression persists for several weeks and may be related to later decreasing SRS frequency. Injection of the Y2 receptor antagonist JNJ 5207787 prevents this protective action of NPY only when release of the peptide is triggered by injection of PTZ and induces pronounced convulsions. Thus, over-expressed NPY released "on demand" by seizures may help terminating acute seizures and may prevent from recurrent epileptic activity.

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Project description:C57BL/6J mice exposed to eight flurothyl-induced generalized clonic seizures exhibit a change in seizure phenotype following a 28-day incubation period and subsequent flurothyl rechallenge. Mice now develop a complex seizure semiology originating in the forebrain and propagating into the brainstem seizure network (a forebrain→brainstem seizure). In contrast, this phenotype change does not occur in seizure-sensitive DBA/2J mice. The underlying mechanism(s) was the focus of these studies.DBA2/J mice were exposed to eight flurothyl-induced seizures (1/day) followed by 24-hour video-electroencephalographic recordings for 28-days. Forebrain and brainstem seizure thresholds were determined in C57BL/6J and DBA/2J mice following one or eight flurothyl-induced seizures, or after eight flurothyl-induced seizures, a 28-day incubation period, and final flurothyl rechallenge.Similar to C57BL/6J mice, DBA2/J mice expressed spontaneous seizures. However, unlike C57BL/6J mice, DBA2/J mice continued to have spontaneous seizures without remission. Because DBA2/J mice do not express forebrain→brainstem seizures following flurothyl rechallenge after a 28-day incubation period, this indicated that spontaneous seizures were not sufficient for the evolution of forebrain→brainstem seizures. Therefore, we determined whether brainstem seizure thresholds were changing during this repeated-flurothyl model and whether this could account for the expression of forebrain→brainstem seizures. Brainstem seizure thresholds were not different between C57BL/6J and DBA/2J mice on day one or on the last induction seizure trial (day eight). However, brainstem seizure thresholds did differ significantly on flurothyl rechallenge (day 28) with DBA/2J mice showing no lowering of their brainstem seizure thresholds.These results demonstrated that DBA/2J mice exposed to the repeated-flurothyl model develop spontaneous seizures without evidence of seizure remission and provide a new model of epileptogenesis. Moreover, these findings indicated that the transition of forebrain ictal discharge into the brainstem seizure network occurs due to changes in brainstem seizure thresholds that are independent of spontaneous seizure expression.

Dataset Information

Dataset of EEG power integral, spontaneous recurrent seizure and behavioral responses following combination drug therapy in soman-exposed rats.

Publications

Dataset of EEG power integral, spontaneous recurrent seizure and behavioral responses following combination drug therapy in soman-exposed rats.

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