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Journal articles on the topic 'Experimental epilepsy'

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Author: Grafiati

Published: 11 March 2023

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1

Tanaka, Tatsuya, Kiyotaka Hashizume, Atsushi Sawamura, Katsunari Yoshida, Hiroshige Tsuda, Akira Hodozuka, and Hirofumi Nakai. "Basic Science and Epilepsy: Experimental Epilepsy Surgery." Stereotactic and Functional Neurosurgery 77, no. 1-4 (2001): 239–44. http://dx.doi.org/10.1159/000064621.

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2

Stanojlovic, Olivera, and Dragana Zivanovic. "Experimental models of epilepsy." Medical review 57, no. 7-8 (2004): 359–62. http://dx.doi.org/10.2298/mpns0408359s.

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Introduction An epileptic seizure is a clinical event and epilepsy is rather a group of symptoms than a disease. The main features all epilepsies have in common include: spontaneous occurrence, repetitiveness, and ictal correlation within the EEG. Epilepsies are manifested with distinct EEG changes, requiring exact clinical definition and consequential treatment. Current data show that 1% of the world's population (approximately 50 million people) suffers from epilepsy, with 25% of patients being refractory to therapy and requiring search for new substances in order to decrease EEG and behavioral manifestations of epilepsies. Material and methods In regard to discovery and testing of anticonvulsant substances the best results were achieved by implementation of experi- mental models. Animal models of epilepsy are useful in acquiring basic knowledge regarding pathogenesis, neurotransmitters (glutamate), receptors (NMDA/AMPA/kainate), propagation of epileptic seizures and preclinical assessment of antiepileptics (competitive and non-competitive NMDA antagonists). Results and conclusions In our lab, we have developed a pharmacologic model of a (metaphit, NMDA and remacemide-cilastatin) generalized, reflex, and audiogenic epilepsy. The model is suitable for testing various anticonvulsant substances (e.g. APH, APV, CPP, Mk-801) and potential antiepileptics (e.g. DSIP, its tetra- and octaanalogues).

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3

Gomes, Tâmara Kelly de Castro, Suzana Lima de Oliveira, and Raul Manhães de Castro. "Malnutrition and experimental epilepsy." Journal of Epilepsy and Clinical Neurophysiology 17, no. 1 (2011): 24–29. http://dx.doi.org/10.1590/s1676-26492011000100006.

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INTRODUCTION: Disturbances in intrauterine environment can have harmful effects on the fetus and pathological consequences persisting throughout adolescence and adulthood. Protein restriction during the prenatal period has a significant impact on growth and development of the central nervous system. Food restriction increases the risk of neurological disorders such as epilepsy. OBJECTIVE: To relate the programming model by malnutrition and its implications in experimental epilepsy. Material and methods: There has been research papers published in the databases Medline, PubMed, CAPES journals, ScienceDirect and Scielo. The keywords selected for the study included epilepsy, Status Epilepticus, pilocarpine, malnutrition, programming. RESULTS AND DISCUSSION: Several studies in animal models or humans highlights the possible adverse effects of malnutrition at the onset of epileptic seizures. The vulnerability immunological, biochemical and electrolyte abnormalities and hypoglycemia may be the factors responsible for the intensification of the epileptogenic process in malnourished individuals. CONCLUSION: Malnutrition negatively changes the epileptogenic circuitry.

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4

Moshe, S. L., E. F. Sperber, L. L. Brown, A. Tempel, and J. N. D. Wurpel. "Experimental epilepsy: developmental aspects." Cleveland Clinic Journal of Medicine 56, Supplement (January 1, 1989): S—92—S—99. http://dx.doi.org/10.3949/ccjm.56.s1.92.

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5

Bambal, Gönül. "Models of experimental epilepsy." Journal of Clinical and Experimental Investigations 2, no. 1 (March 1, 2011): 118–23. http://dx.doi.org/10.5799/ahinjs.01.2011.01.0047.

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6

Garcia Garcia, M. E., I. Garcia Morales, and J. Matías Guiu. "Experimental models in epilepsy." Neurología (English Edition) 25, no. 3 (April 2010): 181–88. http://dx.doi.org/10.1016/s2173-5808(10)70035-3.

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7

Jafarian, Maryam, Mohammad Esmaeil Alipour, and Fariba Karimzadeh. "Experimental Models of Absence Epilepsy." Basic and Clinical Neuroscience Journal 11, no. 6 (November 1, 2020): 715–26. http://dx.doi.org/10.32598/bcn.11.6.731.1.

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Introduction: Absence epilepsy is a brief non-convulsive seizure associated with sudden abruptness in consciousness. Because of the unpredictable occurrence of absence seizures and the ethical issues of human investigation on the pathogenesis and drug assessment, researchers tend to study animal models. This paper aims to review the advantages and disadvantages of several animal models of nonconvulsive induced seizure. Methods: The articles that were published since 1990 were assessed. The publications that used genetic animals were analyzed, too. Besides, we reviewed possible application methods of each model, clinical types of seizures induced, purposed mechanism of epileptogenesis, their validity, and relevance to the absence epileptic patients. Results: The number of studies that used genetic models of absence epilepsy from years of 2000 was noticeably more than pharmacological models. Genetic animal models have a close correlation of electroencephalogram features and epileptic behaviors to the human condition. Conclusion: The validity of genetic models of absence epilepsy would motivate the researchers to focus on genetic modes in their studies. As there are some differences in the pathophysiology of absence epilepsy between animal models and humans, the development of new animal models is necessary to understand better the epileptogenic process and, or discover novel therapies for this disorder.

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8

Cole-Edwards, Kasie K., and Nicolas G. Bazan. "Lipid Signaling in Experimental Epilepsy." Neurochemical Research 30, no. 6-7 (June 2005): 847–53. http://dx.doi.org/10.1007/s11064-005-6878-4.

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9

Reddy, Sandesh, Iyan Younus, Vidya Sridhar, and Doodipala Reddy. "Neuroimaging Biomarkers of Experimental Epileptogenesis and Refractory Epilepsy." International Journal of Molecular Sciences 20, no. 1 (January 8, 2019): 220. http://dx.doi.org/10.3390/ijms20010220.

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This article provides an overview of neuroimaging biomarkers in experimental epileptogenesis and refractory epilepsy. Neuroimaging represents a gold standard and clinically translatable technique to identify neuropathological changes in epileptogenesis and longitudinally monitor its progression after a precipitating injury. Neuroimaging studies, along with molecular studies from animal models, have greatly improved our understanding of the neuropathology of epilepsy, such as the hallmark hippocampus sclerosis. Animal models are effective for differentiating the different stages of epileptogenesis. Neuroimaging in experimental epilepsy provides unique information about anatomic, functional, and metabolic alterations linked to epileptogenesis. Recently, several in vivo biomarkers for epileptogenesis have been investigated for characterizing neuronal loss, inflammation, blood-brain barrier alterations, changes in neurotransmitter density, neurovascular coupling, cerebral blood flow and volume, network connectivity, and metabolic activity in the brain. Magnetic resonance imaging (MRI) is a sensitive method for detecting structural and functional changes in the brain, especially to identify region-specific neuronal damage patterns in epilepsy. Positron emission tomography (PET) and single-photon emission computerized tomography are helpful to elucidate key functional alterations, especially in areas of brain metabolism and molecular patterns, and can help monitor pathology of epileptic disorders. Multimodal procedures such as PET-MRI integrated systems are desired for refractory epilepsy. Validated biomarkers are warranted for early identification of people at risk for epilepsy and monitoring of the progression of medical interventions.

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10

Rubio, Carmen, Moises Rubio-Osornio, Socorro Retana-Marquez, Marisol Lopez, Veronica Custodio, and Carlos Paz. "In Vivo Experimental Models of Epilepsy." Central Nervous System Agents in Medicinal Chemistry 10, no. 4 (December 1, 2010): 298–309. http://dx.doi.org/10.2174/187152410793429746.

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11

Luijtelaar, Gilles van, Mehrnoush Zobeiri, Annika Lüttjohann, and Antoine Depaulis. "Experimental Treatment Options in Absence Epilepsy." Current Pharmaceutical Design 23, no. 37 (February 9, 2018): 5577–92. http://dx.doi.org/10.2174/1381612823666171017170226.

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12

Gonzàlez-Darder, José M., Efrain Gómez-Cárdenas, Maribel Guerrero, Dolores Segura-Pastor, and José L. Gil-Salú. "Intrathecal Antiepileptic Drugs in Experimental Epilepsy." Stereotactic and Functional Neurosurgery 57, no. 3 (1991): 147–55. http://dx.doi.org/10.1159/000099566.

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13

Banach, Monika, Elwira Gurdziel, Marian Jędrych, and Kinga K. Borowicz. "Melatonin in experimental seizures and epilepsy." Pharmacological Reports 63, no. 1 (January 2011): 1–11. http://dx.doi.org/10.1016/s1734-1140(11)70393-0.

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14

Czuczwar, Stanisław J., and Kinga K. Borowicz. "Polytherapy in epilepsy: the experimental evidence." Epilepsy Research 52, no. 1 (November 2002): 15–23. http://dx.doi.org/10.1016/s0920-1211(02)00181-x.

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15

Rolston, John D., Sharanya Arcot Desai, Nealen G. Laxpati, and Robert E. Gross. "Electrical Stimulation for Epilepsy: Experimental Approaches." Neurosurgery Clinics of North America 22, no. 4 (October 2011): 425–42. http://dx.doi.org/10.1016/j.nec.2011.07.010.

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16

MAMELI, P., O. MAMELI, E. TOLU, F. MELIS, M. CARIA, D. GIRAUDI, and G. PADUA. "Cardio-arrhythmogenic trigger in experimental epilepsy." Journal of Molecular and Cellular Cardiology 19 (1987): S55. http://dx.doi.org/10.1016/s0022-2828(87)80173-6.

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17

Hughes, John R. "Intractable epilepsy: experimental and clinical aspects." Electroencephalography and Clinical Neurophysiology 67, no. 1 (July 1987): 96. http://dx.doi.org/10.1016/0013-4694(87)90170-2.

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18

Shiragapur, Bahubali, Nishikant Surwade, Aishwarya Nair, Shefali Singh, and Priya Choudhary. "Experimental Study on Detection of Epilepsy." HELIX 9, no. 3 (June 30, 2019): 5052–56. http://dx.doi.org/10.29042/2019-5052-5056.

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19

Bertorelli, R., M. Adami, and E. Ongini. "The Mongolian gerbil in experimental epilepsy." Italian Journal of Neurological Sciences 16, no. 1-2 (March 1995): 101–6. http://dx.doi.org/10.1007/bf02229081.

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20

Oommen, Joseph, Martha Morrell, and Robert S. Fisher. "Experimental electrical stimulation therapy for epilepsy." Current Treatment Options in Neurology 7, no. 4 (July 2005): 261–71. http://dx.doi.org/10.1007/s11940-005-0036-9.

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21

ScorzaI, Carla A., Roberta M. Cysneiros, Ricardo M. Arida, Vera C. Terra, Hélio R. Machado, Antonio-Carlos G. de Almeida, Esper A. Cavalheiro, and Fulvio A. Scorza. "Alcohol consumption and sudden unexpected death in epilepsy: experimental approach." Arquivos de Neuro-Psiquiatria 67, no. 4 (December 2009): 1003–6. http://dx.doi.org/10.1590/s0004-282x2009000600008.

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Using the pilocarpine model of epilepsy, we investigated the effects of alcohol consumption on the frequency of seizures in animals with epilepsy as well the underlying a possible association between alcohol intake and sudden unexpected death in epilepsy (SUDEP) occurrence. Rats were divided randomly into two groups: (A) rats with epilepsy and (B) rats with epilepsy that received a daily dose of ethanol solution (350 mg kg-1, i.p.) for 30 days. The basal frequency of seizures observed in the A and B groups during the first 30 days were 3.4±1.5 and 3.2±1.9 seizures per week per animal, respectively. In B group, it was observed a significant seizure increase (11.6±5.3) during the first 2 weeks of alcohol administration and quite interesting, one rat died suddenly after a generalized tonic-clonic seizure during this period. We concluded in our experimental study that exist a possible association between alcohol abuse and SUDEP occurrence.

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22

Debski, K. J., N. Ceglia, A. Ghestem, A. I. Ivanov, G. E. Brancati, S. Bröer, A. M. Bot, et al. "The circadian dynamics of the hippocampal transcriptome and proteome is altered in experimental temporal lobe epilepsy." Science Advances 6, no. 41 (October 2020): eaat5979. http://dx.doi.org/10.1126/sciadv.aat5979.

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Gene and protein expressions display circadian oscillations, which can be disrupted in diseases in most body organs. Whether these oscillations occur in the healthy hippocampus and whether they are altered in epilepsy are not known. We identified more than 1200 daily oscillating transcripts in the hippocampus of control mice and 1600 in experimental epilepsy, with only one-fourth oscillating in both conditions. Comparison of gene oscillations in control and epilepsy predicted time-dependent alterations in energy metabolism, which were verified experimentally. Although aerobic glycolysis remained constant from morning to afternoon in controls, it increased in epilepsy. In contrast, oxidative phosphorylation increased in control and decreased in epilepsy. Thus, the control hippocampus shows circadian molecular remapping, which is altered in epilepsy. We suggest that the hippocampus operates in a different functioning mode in epilepsy. These alterations need to be considered when studying epilepsy mechanisms, designing drug treatments, and timing their delivery.

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23

Xu, Guixing, Fang Xiao, Hua Liu, and Donghua Zheng. "Analysis of the effect of sodium valproate sustained release tablets on epilepsy control and cognitive improvement in elderly patients." International Journal of Advances in Medicine 7, no. 5 (April 23, 2020): 845. http://dx.doi.org/10.18203/2349-3933.ijam20201623.

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Background: To study the effect of sodium valproate sustained release tablets on epilepsy control and cognitive function improvement in elderly patients.Methods: Study was conducted from January 2018 to December 2019, the elderly epilepsy patients admitted in our center were prospectively collected and divided into experimental group and control group according to the method of random number table. The experimental group was treated with sodium valproate sustained-release tablets, and the control group was treated with carbamazepine tablets. The epilepsy control rate and cognitive function improvement of the two groups were observed.Results: total of 71 patients entered the study, including 36 in the experimental group and 35 in the control group; the epilepsy control rate (p = 0.03) and the improvement of cognitive function (p = 0.01) in the experimental group were better than those in the control group.Conclusions: Sodium valproate sustained-release tablets can improve the epilepsy control rate and cognitive function of elderly epilepsy patients, but it needs further large samples and external data validation.

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24

Sills, Graeme J. "Seizures Beget Seizures: A Lack of Experimental Evidence and Clinical Relevance Fails to Dampen Enthusiasm." Epilepsy Currents 7, no. 4 (July 2007): 103–4. http://dx.doi.org/10.1111/j.1535-7511.2007.00189.x.

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Three Brief Epileptic Seizures Reduce Inhibitory Synaptic Currents, GABAACurrents, and GABAA-Receptor Subunits. Evans MS, Cady CJ, Disney KE, Yang L, LaGuardia JJ. Epilepsia 2006;4710):1655–1664. PURPOSE: Cellular mechanisms activated during seizures may exacerbate epilepsy. γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in brain, and we hypothesized that brief epileptic seizures may reduce GABA function. METHODS: We used audiogenic seizures (AGSs) in genetically epilepsy-prone rats (GEPRs) to investigate effects of seizures on GABA-mediated inhibition in the presence of epilepsy. GEPRs are uniformly susceptible to AGSs beginning at 21 postnatal days. AGSs are brief convulsions lasting 20 s, and they begin in inferior colliculus (IC). We evoked three seizures in GEPRs and compared the results with those in seizure-naive GEPRs and nonepileptic Sprague-Dawley (SD) rats, the GEPR parent strain. RESULTS: Whole-cell recording in IC slices showed that GABA-mediated monosynaptic inhibitory postsynaptic currents (IPSCs) were reduced 55% by three brief epileptic seizures. Whole-cell recording in IC neuronal cultures showed that currents elicited by GABA were reduced 67% by three seizures. Western blotting for the alpha1 and alpha4 subunits of the GABAA receptor showed no statistically significant effects. In contrast, three brief epileptic seizures reduced gamma2 subunit levels by 80%. CONCLUSIONS: The effects of the very first seizures, in animals known to be epileptic, in an area of brain known to be critical to the seizure network, were studied. The results indicate that even brief epileptic seizures can markedly reduce IPSCs and GABA currents and alter GABAA-receptor subunit protein levels. The cause of the reductions in IPSCs and GABA currents is likely to be altered receptor subunit composition, with reduced gamma2 levels causing reduced GABAA-receptor sensitivity to GABA. Seizure-induced reductions in GABA-mediated inhibition could exacerbate epilepsy.

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25

Méndez-Armenta, Marisela, Concepción Nava-Ruíz, Daniel Juárez-Rebollar, Erika Rodríguez-Martínez, and Petra Yescas Gómez. "Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/293689.

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Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

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26

Kubová, Hana, and Solomon L. Moshé. "Experimental Models of Epilepsy in Young Animals." Journal of Child Neurology 9, no. 1_suppl (October 1994): S3—S11. http://dx.doi.org/10.1177/0883073894009001031.

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Seizures occur more frequently early in life. Some of these early seizures may eventually become epilepsy. Others are reactive seizures due to excessive environmental stimuli that, in any other age group, might not have elicited a similar response. To understand the developmental aspects of seizures and epilepsy in humans, it is important to study these processes in animals of equivalent ages. In this paper, we describe several animal models of developmental seizures, including their electroclinical manifestations and their validity in respect to human epileptic syndromes. There are several factors that may account for the increased seizure susceptibility of the immature brain, including the delayed development of effective systems or synaptic networks that are involved in the suppression of seizures. A better insight of the basic pathophysiology of seizures as a function of age in animal models will lead to the development of new therapeutic approaches for the treatment of age-specific epileptic disorders in humans. (J Child Neurol 1994;9(Suppl):S3-S11).

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27

Orozco-Suarez, Sandra, Iris Feria-Romero, and Israel Grijalva. "Immunology and Epilepsy: Clinical and Experimental Evidence." Current Immunology Reviews 6, no. 3 (August 1, 2010): 185–94. http://dx.doi.org/10.2174/157339510791823691.

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28

Durand, Dominique. "Ictal Patterns in Experimental Models of Epilepsy." Journal of Clinical Neurophysiology 10, no. 3 (July 1993): 281–97. http://dx.doi.org/10.1097/00004691-199307000-00004.

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29

van Engelen, B. G., W. O. Renier, and C. M. Weemaes. "Immunoglobulin treatment in human and experimental epilepsy." Journal of Neurology, Neurosurgery & Psychiatry 57, Suppl (November 1, 1994): 72–75. http://dx.doi.org/10.1136/jnnp.57.suppl.72.

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30

Van Rijckevorsel, K., and M. Delire. "Immunoglobulin treatment in human and experimental epilepsy." Journal of Neurology, Neurosurgery & Psychiatry 59, no. 1 (July 1, 1995): 105. http://dx.doi.org/10.1136/jnnp.59.1.105-b.

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31

Czuczwar, Stanisław J. "Therapy of drug-resistant epilepsy – experimental clues." Pharmacological Reports 62 (September 2010): 20. http://dx.doi.org/10.1016/s1734-1140(10)71108-7.

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32

Kiessling, Marika, and Peter Gass. "Immediate Early Gene Expression in Experimental Epilepsy." Brain Pathology 3, no. 4 (October 1993): 381–93. http://dx.doi.org/10.1111/j.1750-3639.1993.tb00766.x.

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33

Mameli, P., O. Mameli, E. Tolu, G. Padua, D. Giraudi, M. A. Caria, and F. Melis. "Neurogenic Myocardial Arrhythmias in Experimental Focal Epilepsy." Epilepsia 29, no. 1 (February 1988): 74–82. http://dx.doi.org/10.1111/j.1528-1157.1988.tb05102.x.

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34

Pozo, M. A., N. Hernández-Martín, P. Bascuñana, R. Fernández de la Rosa, F. Gómez, E. D. Martín, and L. García-García. "Experimental models in the study of epileptogenesis." ANALES RANM 139, no. 139(02) (August 2022): 140–49. http://dx.doi.org/10.32440/ar.2022.139.02.rev04.

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Epilepsy is a chronic neurological disease characterized by spontaneous recurrently occurring epileptic seizures as a consequence of abnormal, excessive and synchronous neuronal activity in the brain. Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy in adults, being characterized by hippocampal sclerosis, reactive gliosis, neurodegeneration, and synaptic reorganization. Animal models of TLE based on the administration of convulsive agents trigger a status epilepticus (SE) that progresses towards the occurrence of spontaneous recurrent seizures. Among these models are those induced by the systemic administration of pilocarpine or by intrahippocampal injection of kainic acid, both being characterized by 3 clearly defined phases: (i) acute SE seizures; (ii) latent period and (iii) occurrence of recurrent spontaneous seizures. These models not only reproduce most of the neuropathological TLE features but also allow for the identification of biomarkers of epileptogenesis and potential pharmacological targets. The use of neuroimaging techniques such as positron emission tomography (PET) with the radiotracer 18F-Fluorodeoxyglucose (18F-FDG) identifies brain hypometabolism in the latent period that not only localizes the epileptic focus but is also an biomarker of early diagnosis. Other neuroimaging techniques allow for detecting, among others, biomarkers of neuroinflammation, alterations in the permeability of the blood-brain barrier and astrocytic activation, all of them associated with epileptogenesis. Finally, the use of chemogenetics through DREADDs (Designer Receptors Exclusively Activated by Designer Drugs) technology in murine models leads to targeted modulation of astrocytic activity, being a novel tool that considers the contribution of the astrocytes role in brain metabolic alterations in epileptogenesis.

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35

Balykova, O. P., N. P. Shikhanov, V. S. Inozemtseva, A. A. Sosunov, G. McKhann, and Yu A. Chelyshev. "Mechanisms of development of temporal lobe epilepsy: clinical and experimental studies." Neurology Bulletin XXXIV, no. 1-2 (April 15, 2002): 51–59. http://dx.doi.org/10.17816/nb87556.

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Among the many forms of epilepsy, one of the most studied is epilepsy of the temporal lobe (temporal lobe epilepsy) associated with the pathology of the limbic system, and especially the hippocampus. Sections of the limbic system are the source of epileptic seizures in this form of the disease, which is confirmed by electroencephalographic data, including those obtained using embedded electrodes [81], and the clinical effectiveness of surgery. Removal of certain parts of the medial temporal cortex, including part of the hippocampus, can heal or reduce the frequency and severity of seizures [92]. On the basis of structural changes, two main types of epilepsy of the temporal lobe are distinguished: 1) with the presence of a volumetric process (tumor, congenital pathology, blood vessel aneurysm, hemorrhage) affecting the limbic system; 2) without the presence of clearly verified volumetric changes in the medial temporal lobe [23]. In the latter case, the only structural manifestation of temporal lobe epilepsy is hippocampal sclerosis. The name reflects the most striking morphological manifestations of the disease - the loss of neurons primarily in the CA1 and CA3 zones of the horn of the ammonia and the development of replacement gliosis. Intravital brain imaging using functional positron emission tomography, magnetic resonance imaging, and magneto-encephalography confirms changes in the hippocampus in temporal lobe epilepsy, usually in the form of a decrease in its volume [60]. There is also a positive correlation between intravital structural and biochemical (in particular, the number of AMPA-A receptors and the intensity of absorption of F-fluoro-2-deoxy-D-glucose) changes in the sclerosed hippocampus and data from the study of surgical material [75].

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Avoli, M., G. G. C. Hwa, G. Kostopoulos, A. Olivier, and J. G. Villemure. "Electrophysiological Analysis of Human Neocortex In Vitro: Experimental Techniques and Methodological Approaches." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S4 (November 1991): 636–39. http://dx.doi.org/10.1017/s0317167100032856.

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ABSTRACT:In this review we summarize a number of technical and methodological approaches that have been used in our laboratory to study human brain slices maintained in vitro. The findings obtained in the course of these studies appear to be relevant in establishing he mechanisms that underlie physiological phenomena of the human brain such as synaptic plasticity or responses to neuroactive drugs. Moreover, these data are important for understanding certain fundamental mechanisms of epilepsy. In this respect, however, we aution that the mechanisms that apply to different forms of clinical epilepsy might be ifficult to find given the variability present in the pathogenesis of human epilepsy.

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Vogel, Stephan, Martin Kaltenhäuser, Cora Kim, Nadia Müller-Voggel, Karl Rössler, Arnd Dörfler, Stefan Schwab, Hajo Hamer, Michael Buchfelder, and Stefan Rampp. "MEG Node Degree Differences in Patients with Focal Epilepsy vs. Controls—Influence of Experimental Conditions." Brain Sciences 11, no. 12 (November 30, 2021): 1590. http://dx.doi.org/10.3390/brainsci11121590.

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Drug-resistant epilepsy can be most limiting for patients, and surgery represents a viable therapy option. With the growing research on the human connectome and the evidence of epilepsy being a network disorder, connectivity analysis may be able to contribute to our understanding of epilepsy and may be potentially developed into clinical applications. In this magnetoencephalographic study, we determined the whole-brain node degree of connectivity levels in patients and controls. Resting-state activity was measured at five frequency bands in 15 healthy controls and 15 patients with focal epilepsy of different etiologies. The whole-brain all-to-all imaginary part of coherence in source space was then calculated. Node degree was determined and parcellated and was used for further statistical evaluation. In comparison to controls, we found a significantly higher overall node degree in patients with lesional and non-lesional epilepsy. Furthermore, we examined the conditions of high/reduced vigilance and open/closed eyes in controls, to analyze whether patient node degree levels can be achieved. We evaluated intraclass-correlation statistics (ICC) to evaluate the reproducibility. Connectivity and specifically node degree analysis could present new tools for one of the most common neurological diseases, with potential applications in epilepsy diagnostics.

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38

Orhan, DidemDeliorman, Mustafa Aslan, and Nilufer Orhan. "Effect of Gentiana olivieri on experimental epilepsy models." Pharmacognosy Magazine 7, no. 28 (2011): 344. http://dx.doi.org/10.4103/0973-1296.90419.

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39

Yakhin, F. A., E. N. Popova, and F. F. Yakhina. "Morphology of cerebral cortex vessels in experimental epilepsy." Kazan medical journal 78, no. 1 (February 15, 1997): 45–49. http://dx.doi.org/10.17816/kazmj81108.

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The reversible changes of cerebral cortex vessels prevail in cerebrovascular ischemia caused by unilateral ligation of the common carotid artery in rats. In bilateral ligation of the common carotid arteries, vertebral arteries, stenosis of ascending aorta the dystrophic vascular changes are manifested significantly. In postepileptic period in the presence of cerebrovascular disorders the dystrophic changes of cerebral cortex vessels prevail. In audiogenic epilepsies in the presence of renal hypertension and alimentary atherosclerosis the dystrophic changes of the vessels increase.

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40

Yang, Baowang, Jing Wang, and Ni Zhang. "Effect of nobiletin on experimental model of epilepsy." Translational Neuroscience 9, no. 1 (December 31, 2018): 211–19. http://dx.doi.org/10.1515/tnsci-2018-0031.

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AbstractBackgroundThe effects of nobiletin, a plant-derived flavonoid was examined against pentylenetetrazole (PTZ)-induced seizures. The study also aimed to assess whether nobiletin potentiated the effects of antiepileptic drug clonazepam (CZP).MethodsPTZ (92 mg/kg, subcutaneous) was used to induce seizures in mice. Treatment groups (n = 18/group) received nobiletin (12.5, 25, or 50 mg/kg) via oral gavage for 6 consecutive days and 45 min prior to PTZ injection. CZP (0.015-2.0 mg/kg) was administered 15 min prior to PTZ. Skeletal muscle strength was assessed by measuring grip strength and Chimney test was performed to study the motor performance in animals. TUNEL assay was done to study neuro-apoptosis. RT-PCR and Western blot analysis were performed for assessment of mRNA and protein expressions.ResultsNobiletin and CZP improved muscle strength and motor coordination and reduced seizure severity significantly. The administration of nobiletin and CZP, individually or in combination, downregulated seizure-induced increases in apoptotic cell count and apoptotic protein expression, modulated the expression of gamma-aminobutyric acid (GABA)A and glutamate decarboxylase 65 and restored the glutamate/GABA balance. Nobiletin and CZP administration significantly upregulated phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling.ConclusionNobiletin exerted protective effect against seizures by regulating signaling pathways associated with epileptogenesis and potentiated the effects of CZP.

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41

Rodin, E. "Paper Recordings of Ultrafast Frequencies in Experimental Epilepsy." Clinical EEG and Neuroscience 36, no. 4 (October 2005): 263–70. http://dx.doi.org/10.1177/155005940503600405.

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Digital EEG technology has facilitated the recording of fast activity above 50 Hz, but previous work carried out in this field is, commonly, no longer referred to in the literature. This paper presents a summary of our experience in experimental epilepsy when frequencies above 100 Hz were recorded. It was shown that conventional recordings (1–70 Hz) do not correlate with the onset of clinical seizures and can actually lead to misleading neurophysiologic conclusions. Ultrafast activity (100–1500 Hz), on the other hand, showed excellent correlation with clinical behavior and pointed to the low brainstem for the origin of nonfocal tonic-clonic seizures. In the animal analogue of absence seizures the cortex, including cingulate gyrus, thalamus, and cerebellum, showed greater involvement than other brain structures. Ultrafast activity has a very limited electrical field, and evoked responses remain restricted to the corresponding sensory pathways. Focal penicillin administration led not only to spike generation but also to associated ultrafast frequency bursts in that area. It appears likely that ultrafast burst activity may be a better marker for focal cortical epileptogenesis than spikes or sharp waves, which can be transmitted from a distance.

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Rijkers, Kim, Véronique M. P. Moers-Hornikx, Roelof J. Hemmes, Marlien W. Aalbers, Yasin Temel, Johan S. H. Vles, and Govert Hoogland. "Sustained Reduction of Cerebellar Activity in Experimental Epilepsy." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/718591.

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Clinical and experimental evidence suggests a role for the cerebellum in seizure control, while no data are available on cerebellar activity between seizures. We hypothesized that interictal regional activity of the deep cerebellar nuclei is reduced in epilepsy and tested this in an animal model by using ΔFosB and cytochrome oxidase (COX) (immuno)histochemistry. The expression of these two markers of neuronal activity was analysed in the dentate nucleus (DN), interpositus nucleus (IN), and fastigial nucleus (FN) of the cerebellum of fully amygdala kindled rats that were sacrificed 48 hours after their last seizure. The DN and FN of kindled rats exhibited 25 to 29% less ΔFosB immunopositive cells than their respective counterpart in sham controls (P<0.05). COX expression in the DN and FN of kindled animals was reduced by 32 to 33% compared to respective control values (P<0.05). These results indicate that an epileptogenic state is characterized by decreased activity of deep cerebellar nuclei, especially the DN and FN. Possible consequences may include a decreased activation of the thalamus, contributing to further seizure spread. Restoration of FN activity by low frequency electrical stimulation is suggested as a possible treatment option in chronic epilepsy.

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Steriade, Claude, Jacqueline French, and Orrin Devinsky. "Epilepsy: key experimental therapeutics in early clinical development." Expert Opinion on Investigational Drugs 29, no. 4 (March 30, 2020): 373–83. http://dx.doi.org/10.1080/13543784.2020.1743678.

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Mameli, O., M. A. Caria, A. Pintus, G. Padua, and S. Mameli. "Sudden death in epilepsy: An experimental animal model." Seizure 15, no. 5 (July 2006): 275–87. http://dx.doi.org/10.1016/j.seizure.2006.02.007.

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45

Matsui, Hideki, and Osanni Hatase. "Experimental epilepsy and immunosuppressants, FK506 and cyclosporin A." Japanese Journal of Pharmacology 67 (1995): 82. http://dx.doi.org/10.1016/s0021-5198(19)46296-3.

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Holt, Abbey B., and Theoden I. Netoff. "Computational modeling of epilepsy for an experimental neurologist." Experimental Neurology 244 (June 2013): 75–86. http://dx.doi.org/10.1016/j.expneurol.2012.05.003.

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47

Masserini, C., E. Rosina, F. Morosini, A. C. Altamura, C. L. Cazzullo, and L. Torcello. "Hyperbaric oxygen induced experimental epilepsy: the age factor." Italian Journal of Neurological Sciences 7, no. 3 (June 1986): 343–48. http://dx.doi.org/10.1007/bf02340873.

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Chen, Rong-Chi, Yn-Her Huang, and Shu-Wen How. "Systemic penicillin as an experimental model of epilepsy." Experimental Neurology 92, no. 3 (June 1986): 533–40. http://dx.doi.org/10.1016/0014-4886(86)90295-5.

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Legido, Agustín, and Christos D. Katsetos. "Experimental Studies in Epilepsy: Immunologic and Inflammatory Mechanisms." Seminars in Pediatric Neurology 21, no. 3 (September 2014): 197–206. http://dx.doi.org/10.1016/j.spen.2014.10.001.

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Vezzani, Annamaria, and Tiziana Granata. "Brain Inflammation in Epilepsy: Experimental and Clinical Evidence." Epilepsia 46, no. 11 (November 2005): 1724–43. http://dx.doi.org/10.1111/j.1528-1167.2005.00298.x.

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