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Absence Seizure

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M. S. Bruno – One of the best experts on this subject based on the ideXlab platform.

Gilles Van Luijtelaar – One of the best experts on this subject based on the ideXlab platform.

  • methods of automated Absence Seizure detection interference by stimulation and possibilities for prediction in genetic Absence models
    Journal of Neuroscience Methods, 2016
    Co-Authors: Gilles Van Luijtelaar, A E Hramov, Annika Luttjohann, Vladimir V Makarov, Vladimir A Maksimenko, A A Koronovskii
    Abstract:

    Abstract Background Genetic rat models for childhood Absence epilepsy have become instrumental in developing theories on the origin of Absence epilepsy, the evaluation of new and experimental treatments, as well as in developing new methods for automatic Seizure detection, prediction, and/or interference of Seizures. Method Various methods for automated off and on-line analyses of ECoG in rodent models are reviewed, as well as data on how to interfere with the spike-wave discharges by different types of invasive and non-invasive electrical, magnetic, and optical brain stimstimulation. Also a new method for Seizure prediction is proposed. Results Many selective and specific methods for off- and on-line spike-wave discharge detection seem excellent, with possibilities to overcome the issue of individual differences. Moreover, electrical deep brain stimstimulation is rather effective in interrupting ongoing spike-wave discharges with low stimulation intensity. A network based method is proposed for Absence Seizures prediction with a high sensitivity but a low selectivity. Solutions that prevent false alarms, integrated in a closed loop brain stimstimulation system open the ways for experimental Seizure control. Conclusions The presence of preictal cursor activity detected with state of the art time frequency and network analyses shows that spike-wave discharges are not caused by sudden and abrupt transitions but that there are detectable dynamic events. Their changes in time-space-frequency characteristics might yield new options for Seizure prediction and Seizure control.

  • dynamics of networks during Absence Seizure s on and offset in rodents and man
    Frontiers in Physiology, 2015
    Co-Authors: Annika Luttjohann, Gilles Van Luijtelaar
    Abstract:

    Network mechanisms relevant for the generation, maintenance and termination of spike-wave discharges (SWD), the neurophysiological hallmark of Absence epilepsy, are still enigmatic and widely discussed. Within the last years, however, improvements in signal analytical techniques, applied to both animal and human fMRI, EEG, MEG, and ECoG data, greatly increased our understanding and challenged several, dogmatic concepts of SWD. This review will summarize these recent data, demonstrating that SWD are not primary generalized, are not sudden and unpredictable events. It will disentangle different functional contributions of structures within the cortico-thalamo-cortical system, relevant for the generation, generalization, maintenance, and termination of SWD and will present a new “network based” scenario for these oscillations. Similarities and differences between rodent and human data are presented demonstrating that in both species a local cortical onset zone of SWD exists, although with different locations; that in both some forms of cortical and thalamic precursor activity can be found, and that SWD occur through repetitive cyclic activity between cortex and thalamus. The focal onset zone in human data could differ between patients with varying spatial and temporal dynamics; in rats the latter is still poorly investigated.

  • application of adaptive nonlinear granger causality disclosing network changes before and after Absence Seizure onset in a genetic rat model
    Journal of Neuroscience Methods, 2014
    Co-Authors: M V Sysoeva, Evgenia Sitnikova, I V Sysoev, B P Bezruchko, Gilles Van Luijtelaar
    Abstract:

    Abstract Background Advanced methods of signal analysis of the preictal and ictal activity dynamics characterizing Absence epilepsy in humans with Absences and in genetic animal models have revealed new and unknown electroencephalographic characteristics, that has led to new insights and theories. New method Taking into account that some network associations can be considered as nonlinear, an adaptive nonlinear Granger causcausality approach was developed and applied to analyze cortico-cortical, cortico-thalamic and intrathalamic network interactions from local field potentials (LFPs). The outcomes of adaptive nonlinear models, constructed based on the properties of electroencephalographic signal and on statistical criteria to optimize the number of coefficients in the models, were compared with the outcomes of linear Granger causcausality. Results The nonlinear adaptive method showed statistically significant preictal changes in Granger causcausality in almost all pairs of channels, as well as ictal changes in cortico-cortical, cortico-thalamic and intrathalamic networks. Current results suggest rearrangement of interactions in the thalamo-cortical network accompanied the transition from preictal to ictal phase. Comparison with existing method(s) The linear method revealed no preictal and less ictal changes in causality. Conclusions Achieved results suggest that this proposed adaptive nonlinear method is more sensitive than the linear one to dynamics of network properties. Since changes in coupling were found before the Seizure-related increase of LFP signal amplitude and also based on some additional tests it seems likely that they were not spurious and could not result from signal to noise ratio change.

Arnaldo E. Negrón – One of the best experts on this subject based on the ideXlab platform.

  • gabaergic neurotransmission in the c57bl 10 sps sps mouse mutant a model of Absence Seizures
    Experimental Neurology, 1991
    Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. Bruno
    Abstract:

    Abstract The C57BL 10 , sps sps mouse mutant displays generalized Absence Seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the Absence-like Seizures in C57BL 10 , sps sps mice.

  • GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of Absence Seizures.
    Experimental neurology, 1991
    Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. Bruno
    Abstract:

    Abstract The C57BL 10 , sps sps mouse mutant displays generalized Absence Seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the Absence-like Seizures in C57BL 10 , sps sps mice.

Gaoxiang Ouyang – One of the best experts on this subject based on the ideXlab platform.

Mayra L. Cordero – One of the best experts on this subject based on the ideXlab platform.

  • gabaergic neurotransmission in the c57bl 10 sps sps mouse mutant a model of Absence Seizures
    Experimental Neurology, 1991
    Co-Authors: J G Ortiz, Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. Bruno
    Abstract:

    Abstract The C57BL 10 , sps sps mouse mutant displays generalized Absence Seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the Absence-like Seizures in C57BL 10 , sps sps mice.

  • GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of Absence Seizures.
    Experimental neurology, 1991
    Co-Authors: Arnaldo E. Negrón, A.p. Thomas, H. Heimer, J. A. Moreira, Mayra L. Cordero, J. Aranda, M. S. Bruno
    Abstract:

    Abstract The C57BL 10 , sps sps mouse mutant displays generalized Absence Seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca2+-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the Absence-like Seizures in C57BL 10 , sps sps mice.