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Готові списки джерел за темами / Experimental epilepsy

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Добірка наукової літератури з теми "Experimental epilepsy"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Experimental epilepsy"

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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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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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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Дисертації з теми "Experimental epilepsy"

1

Bukataru, Y. S. "Non-genetic experimental models of epilepsy." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18492.

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2

FALCICCHIA, Chiara. "BDNF delivery strategies in an experimental model of temporal lobe epilepsy." Doctoral thesis, Università degli studi di Ferrara, 2015. http://hdl.handle.net/11392/2388988.

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Neurotrophic factors (NTFs) have been reported to play opposite, pro- and/or anti-epileptic effects in experimental models. Some NTFs favor epileptogenesis or progression of epilepsy whereas others oppose these processes. Still other NTFs, including Brain-Derived Neurotrophic Factor (BDNF), can exert both positive and negative effects. Moreover, BDNF has been clearly shown to be involved in all the cellular and tissue changes that occur during epileptogenesis. To get further insight in the involvement of BDNF in epilepsy and, on this basis, to develop new therapeutic strategies, there is a need to develop new, advanced tools for the modulation of the BDNF signal within defined brain regions. Therefore, the aim of this thesis was to develop new delivery systems to block or to enhance the BDNF signal. Specifically, the thesis deals the investigation of the validity of BDNF as a therapeutic target, using advanced tools to down regulate BDNF expression (Herpes simplex virus-1 based amplicon vectors) and to continuously secrete it [encapsulated cell biodelivery (ECB) devices]. Two amplicon-based silencing strategies have been developed. The first, antisense (AS), targets and degrades the cytoplasmic mRNA pool of BDNF, whereas the second, based on the convergent transcription (CT) technology, directly represses the BDNF gene. In vitro (cell lines) and in vivo (stereotaxic injection in the epileptic hippocampus) experiments demonstrated a reliable effect of amplicon vectors in knocking down gene expression. However, whereas the CT-BDNF strategy proved effective only in vitro, the AS-BDNF amplicon vector proved effective both in vitro and in vivo, knocking down efficiently BDNF protein levels in the injected hippocampus at different time points. The antisense strategy seems therefore a better choice for silencing BDNF expression in vivo. For a prolonged administration of BDNF, BDNF-producing cells encapsulated in ECB devices have been tested in a rat model of Temporal Lobe Epilepsy. These devices, implanted bilaterally in the hippocampus of chronically epileptic animals, proved capable to significantly decrease the frequency of spontaneous generalized seizures. These new tools and experiments help to further elucidate the role of BDNF in epilepsy and provide an initial proof-of-concept for a new, promising therapeutic approach.

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3

Yaghouby, Farid. "EXPERIMENTAL-COMPUTATIONAL ANALYSIS OF VIGILANCE DYNAMICS FOR APPLICATIONS IN SLEEP AND EPILEPSY." UKnowledge, 2015. http://uknowledge.uky.edu/cbme_etds/32.

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Epilepsy is a neurological disorder characterized by recurrent seizures. Sleep problems can cooccur with epilepsy, and adversely affect seizure diagnosis and treatment. In fact, the relationship between sleep and seizures in individuals with epilepsy is a complex one. Seizures disturb sleep and sleep deprivation aggravates seizures. Antiepileptic drugs may also impair sleep quality at the cost of controlling seizures. In general, particular vigilance states may inhibit or facilitate seizure generation, and changes in vigilance state can affect the predictability of seizures. A clear understanding of sleep-seizure interactions will therefore benefit epilepsy care providers and improve quality of life in patients. Notable progress in neuroscience research—and particularly sleep and epilepsy—has been achieved through experimentation on animals. Experimental models of epilepsy provide us with the opportunity to explore or even manipulate the sleep-seizure relationship in order to decipher different aspects of their interactions. Important in this process is the development of techniques for modeling and tracking sleep dynamics using electrophysiological measurements. In this dissertation experimental and computational approaches are proposed for modeling vigilance dynamics and their utility demonstrated in nonepileptic control mice. The general framework of hidden Markov models is used to automatically model and track sleep state and dynamics from electrophysiological as well as novel motion measurements. In addition, a closed-loop sensory stimulation technique is proposed that, in conjunction with this model, provides the means to concurrently track and modulate 3 vigilance dynamics in animals. The feasibility of the proposed techniques for modeling and altering sleep are demonstrated for experimental applications related to epilepsy. Finally, preliminary data from a mouse model of temporal lobe epilepsy are employed to suggest applications of these techniques and directions for future research. The methodologies developed here have clear implications the design of intelligent neuromodulation strategies for clinical epilepsy therapy.

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4

Giussani, Giorgia. "Observational and experimental studies on the diagnosis and outcome of epilepsy and epileptogenic conditions : investigating the static and dynamic phenotype of epilepsy." Thesis, Open University, 2018. http://oro.open.ac.uk/53914/.

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Different studies spanning the diagnosis, the outcome and the treatment of the disease have been performed to investigate the spectrum of epilepsy. The topics were: 1. The differential diagnosis between epilepsy and another common clinical condition (PNES); 2. The verification if epilepsy could be a marker of genetic diseases characterized by intellectual disability and behavioural abnormalities (idic(15) syndrome); 3.The assessment of the long-term outcome of the disease to identify different prognostic patterns; 4.The investigation of the frequency and clinical features of drug-resistant epilepsy (DRE) with reference to the number of antiepileptic drugs (AEDs). In 1/3 of cases a confident diagnosis of PNES/ES can be established by epileptologists on video data only. Compared to epileptologists, psychiatrists demonstrated to be less accurate in diagnosing PNES but more attuned to capture the subtleties of human behaviour. Investigating the patients and their witnesses using ad-hoc structured questionnaires, some variables were highly predictive of PNES diagnosis. These instruments may be useful clinical tools in settings not offering the facilities for a correct diagnosis and in cases where video-EEG monitoring has failed. In the study on the characterisation of idic(15) syndrome, epilepsy was used as disease tracer. It was found to be one of the few symptoms with satisfactory agreement but not a marker of this genetic syndrome. To verify if the epilepsy course and treatment response is static or dynamic, a population based-study in a well-defined area of Italy was performed. DRE patients (1/6 patients with active epilepsy in the general population) can reach 2-year remission (24.9 %) at 20 years and also early terminal remission (1.3%). AEDs given at diagnosis are retained in the majority of cases and the withdrawal can be predicted by age at diagnosis, sex, disease characteristics and varies among drugs.

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5

Pereira, Pedro Miguel Miranda Sousa Gonçalves. "Severity and extent of tissue damage in human and experimental temporal lobe epilepsy." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2007. http://hdl.handle.net/10216/7259.

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6

Pereira, Pedro Miguel Miranda Sousa Gonçalves. "Severity and extent of tissue damage in human and experimental temporal lobe epilepsy." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2007. http://hdl.handle.net/10216/7259.

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7

Bumanglag, Argyle V. "INJURY-INDUCED HIPPOCAMPAL EPILEPTOGENESIS IN EXPERIMENTAL MODELS OF TEMPORAL LOBE EPILEPSY IN THE RAT." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/146070.

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The mechanism by which brain injuries cause temporal lobe epilepsy is unknown. Suspected epileptogenic insults include neuron loss and secondary processes triggered by injury. Difficulties in determining which abnormalities precede the onset of seizures, and could play a causal epileptogenic role, have been a major obstacle to progress. Chemoconvulsant-induced status epilepticus in animals has been widely used to induce epilepsy experimentally, but it has been impossible to determine when epileptogenesis occurs because early seizures could be the result of residual drug. As an alternative to chemoconvulsants, perforant pathway stimulation-induced status epilepticus was used to produce limited brain injury and to initiate hippocampal epileptogenesis. Continuous video monitoring and granule cell layer recording determined the latencies to hippocampal epileptiform events and clinical seizures. Spontaneous hippocampal epileptiform discharges and behavioral seizures were recorded during the first three days post-injury, indicating that hippocampal epileptogenesis is a rapid process coincident with neuron loss, and that the short latency to clinical epilepsy might be due to damage to all brain regions that normally act as barriers to seizure spread. To test this hypothesis, a less injurious stimulation paradigm was developed. Histological analysis confirmed neuronal injury mainly limited to the hippocampus and entorhinal cortex. Continuous monitoring after twenty-four hours of stimulation revealed that whereas spontaneous hippocampal granule cell population spikes and focal epileptiform discharges were coincident with initial neuron loss, the latency to the first clinical behavioral seizure was 14-35 days. Early focal seizures were associated with brief granule cell layer epileptiform discharges that lasted 34.7 ± 3.0 seconds, whereas generalized motor seizures were associated with longer granule cell layer epileptiform discharges 126.0 ± 12.8 seconds in duration. These results indicate that hippocampal epileptogenesis is an immediate network defect coincident with initial neuron loss, rather than with delayed secondary processes, and that the "latent period," when one exists, may represent a "kindling" process in which initially focal seizures slowly overcome undamaged barriers to seizure spread. The finding that hippocampal epileptogenesis develops coincident with the initial injury, rather than with slower secondary processes, suggests that neuroprotection in the immediate post-injury period may be the most effective anti-epileptogenic strategy.

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Kinjo, Erika Reime. "Conexinas na epilepsia experimental induzida por pilocarpina: abordagem molecular e eletrofisiológica." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-19032012-142510/.

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Este estudo teve como objetivo avaliar a expressão hipocampal de proteínas e de RNAm das Cx43 e Cx36 no modelo de epilepsia do lobo temporal (ELT) induzido por pilocarpina. Além disso, os efeitos do bloqueador de canais de junções comunicantes (CJC), carbenoxolona (CBX), foram avaliados por eletrofisiologia durante o período de status epilepticus. Os dados referentes à Cx43 demonstraram redução dos níveis proteicos no período latente (p<0,05) e aumento no período crônico do modelo (p<0,01). Os níveis de RNAm de Cx43 não sofreram alterações. Tanto os níveis proteicos quanto os de RNAm de Cx36 não se alteraram. Os dados eletrofisiológicos mostraram redução da potência na banda de frequência entre 15 e 30 Hz no eletrocortigrama, além de redução da amplitude relativa dos potenciais epileptiformes. Foi observado ainda que o grupo tratado com CBX passou a apresentar períodos flat antecipadamente. Os dados deste estudo sugerem um importante papel dos CJC na ELT induzida por pilocarpina, contribuindo para o conhecimento da regulação destes canais na epilepsia.
In this study, the hippocampal protein and mRNA levels of Cx43 and Cx36 were investigated in the pilocarpine model of temporal lobe epilepsy (TLE). In addition, the effects of a gap junction (GJ) blocker (carbenoxolone-CBX) on pilocarpine-induced status epilepticus (SE) were also evaluated by electrophysiological recordings. Our results on Cx43 showed reduction of protein levels in the latent period (p<0.05) and increase in the chronic period of the model (p<0.01), whereas no changes were observed in the mRNA levels. Both protein and mRNA levels of Cx36 showed no changes. The electrophysiological recordings indicated that CBX promoted a marked reduction of power in the 15-30 Hz electrocorticographic frequency. Decrease in the amplitude of the epileptiform potentials was also seen, in addition to anticipation of occurrence of flat periods in the group treated with CBX. Data obtained from this study suggest an important role for GJ channels in the pilocarpine-induced TLE, contributing to a greater understanding of the regulation of these channels in the epilepsy.

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9

Nicholls, Briony Rachel. "An investigation into the long-term effects of experimental limbic epilepsy of exploratory behaviour of rats." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240652.

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10

Okuma, Chihiro. "Studies on mechanisms of antiepilepsy and antiobesity in experimental animal models." Kyoto University, 2016. http://hdl.handle.net/2433/215225.

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Книги з теми "Experimental epilepsy"

1

D, Schmidt Dieter M., Morselli Paolo Lucio, World Health Organization, International League against Epilepsy, and Workshop on Intractable Epilepsy (1985 : Saint-Germain-en-Laye, France), eds. Intractable epilepsy: Experimental and clinical aspects. New York: Raven Press, 1986.

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2

Alain, Malafosse, ed. Idiopathic generalized epilepsies: Clinical, experimental and genetic aspects. London: John Libbey, 1994.

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3

G, Bazán Nicholás, ed. Lipid mediators in ischemic brain damage and experimental epilepsy. Basel: Karger, 1990.

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4

Vohora, Divya, ed. Experimental and Translational Methods to Screen Drugs Effective Against Seizures and Epilepsy. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1254-5.

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5

Corcoran, Michael E., and Gordon Campbell Teskey. Kindling: An Inquiry into Experimental Epilepsy. Oxford University Press, 2004.

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6

Shaikh, Mohd Farooq, Ayanabha Chakraborti, Annamaria Vezzani, and Jafri Malin Abdullah, eds. Experimental Models of Epilepsy and Related Comorbidities. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-843-1.

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7

Shaikh, Mohd Farooq, Teresa Ravizza, Jafri Malin Abdullah, Ayanabha Chakraborti, and Terence John O’Brien, eds. Experimental & Clinical Epilepsy and Related Comorbidities. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-146-6.

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8

(Editor), Devin K. Binder, and Helen E. Scharfman (Editor), eds. Recent Advances in Epilepsy Research (Advances in Experimental Medicine and Biology). Springer, 2004.

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9

Schmidt, Dieter. Intractable Epilepsy: Experimental and Clinical Aspects (L.E.R.S. Monograph Series, Vol 5/Order No 1684). Raven Pr, 1987.

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10

Vohora, Divya. Experimental and Translational Methods to Screen Drugs Effective Against Seizures and Epilepsy. Springer, 2022.

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Частини книг з теми "Experimental epilepsy"

1

Bengzon, J., and O. Lindvall. "Transplantation in Experimental Epilepsy." In Restoration of Brain Function by Tissue Transplantation, 39–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77718-9_5.

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2

Lunardi, G., P. Mainardi, V. Rubino, M. Fracassi, F. Pioli, S. Cultrera, and C. Albano. "Tryptophan and Epilepsy." In Advances in Experimental Medicine and Biology, 101–2. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_15.

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3

Reschke, Cristina R., and David C. Henshall. "microRNA and Epilepsy." In Advances in Experimental Medicine and Biology, 41–70. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22671-2_4.

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4

Halász, Péter, and György Rásonyi. "Neuroprotection and Epilepsy." In Advances in Experimental Medicine and Biology, 91–109. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8969-7_6.

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5

Zavala-Tecuapetla, Cecilia, and Luisa Rocha. "Experimental Models to Study Pharmacoresistance in Epilepsy." In Pharmacoresistance in Epilepsy, 185–97. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6464-8_12.

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6

Leppik, Ilo E. "Intractable Epilepsy in Adults." In Advances in Experimental Medicine and Biology, 1–7. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1335-3_1.

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7

Carlen, Peter L., Marc R. Pelletier, Aviv Ouanounou, Michael Tymianski, and Liang Zhang. "Neuroprotective Strategies in Epilepsy." In Advances in Experimental Medicine and Biology, 209–24. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-1335-3_19.

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8

Ono, Tomonori, and Aristea S. Galanopoulou. "Epilepsy and Epileptic Syndrome." In Advances in Experimental Medicine and Biology, 99–113. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-0653-2_8.

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9

Zheng, Fang. "TRPC Channels and Epilepsy." In Advances in Experimental Medicine and Biology, 123–35. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1088-4_11.

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Katona, István. "Cannabis and Endocannabinoid Signaling in Epilepsy." In Handbook of Experimental Pharmacology, 285–316. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20825-1_10.

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Тези доповідей конференцій з теми "Experimental epilepsy"

1

D., Chavan M., Karamthoti M. B., and Kurra S. B. "Na+-K+-2Cl– Cotransport Inhibitors and their Effect on Induced Seizure Tests in Experimental Models." In 20th Joint Annual Conference of Indian Epilepsy Society and Indian Epilepsy Association. Thieme Medical and Scientific Publishers Private Ltd., 2018. http://dx.doi.org/10.1055/s-0039-1694864.

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2

D., Chavan M., Karamthoti M. B. та Kurra S. B. "Peroxisome Proliferator Activated Receptor σ (pPARσ) Agonists and Their Role on Epilepsy-Induced Seizures: An Experimental Evaluative Study". У 20th Joint Annual Conference of Indian Epilepsy Society and Indian Epilepsy Association. Thieme Medical and Scientific Publishers Private Ltd., 2018. http://dx.doi.org/10.1055/s-0039-1694878.

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3

K., Saniya, Patil B. G., Madhavrao C., Prakash K. G., and Mythili Bai K. "Preclinical Screening of Antiepileptic Properties of Diltiazem in Chemically and Electrically Induced Battery of Seizures Tests in Laboratory Experimental Animal Models." In 20th Joint Annual Conference of Indian Epilepsy Society and Indian Epilepsy Association. Thieme Medical and Scientific Publishers Private Ltd., 2018. http://dx.doi.org/10.1055/s-0039-1694893.

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4

Sotelo, A., E. Guijarro, M. J. Garcia, and C. E. Vdzquez. "Epoch Parameterization by Gabor Atom Density in Experimental Epilepsy." In 2007 4th International Conference on Electrical and Electronics Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iceee.2007.4344973.

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5

Kutlu, F., and C. Kose. "Epileptic seizure detection from ECoG signals acquired with experimental epilepsy." In 2013 21st Signal Processing and Communications Applications Conference (SIU). IEEE, 2013. http://dx.doi.org/10.1109/siu.2013.6531296.

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6

Zocche Junior, Giovani, Isadora Ghilardi, Laura Provenzi, Gabriel Leal, Giulia Pinzetta, Nicole Becker, Vitoria Pimentel, et al. "Modulation of gene transcription promoted by mesenchymal stem cells on cation-chloride cotransporter NKCC1 in experimental epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.684.

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Анотація:

Introduction: temporal lobe epilepsy is a disorder in which synchronized and rhythmic neural firing causes spontaneous recurrent seizures (1). Refractoriness due to this condition reaches 30% of its carriers (2,3). The search for therapeutic alternatives to help cope with this disease are extremely important. Mesenchymal stem cells (MSCs) appear as a plausible treatment option, as they present a less invasive approach and due to their niche modulating character (4,5). Objectives: this study aimed to quantify the gene expression of cation-chloride cotransporter NKCC1 encoded by the SLC12A2 gene in the encephalic tissue of pilocarpine-induced epileptic rats (6,7). Design: experimental study, brain institute of Rio Grande do Sul. Methods: MSCs were obtained from the bone marrow of Wistar rats, cultured, and transplanted through intravenous injection into control and epileptic Wistar rats. The rats were divided between control group, MSCs treated group, and pilocarpine group, containing 8 individuals each (8). Expression analysis was performed using real-time polymerase chain reaction. Results: for both 1 day and 7 days post-transplantation, an increase in the NKCC1 expression in both control and epileptic treated groups as compared to its expression in untreated epileptic and control groups with special attention to the amygdala, the hippocampus and the prefrontal cortex. Conclusion: MSCs stimulated expression of NKCC1 in brain structures of rats induced by pilocarpine to epilepsy. This corroborates the hypothesis of neuroprotective effects and modulating properties of stem cells and may point to more mechanisms for investigating the functioning and collaboration of these cells as a treatment for epilepsy.

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7

Esser, Daniel, John Peters, Abby M. Grillo, Sarah J. Garrow, Tyler Ball, Robert Naftel, Dario J. Englot, et al. "Robotic Curvilinear Laser Thermal Therapy Probe for Transforamenal Hippocampotomy." In The Hamlyn Symposium on Medical Robotics: "MedTech Reimagined". The Hamlyn Centre, Imperial College London London, UK, 2022. http://dx.doi.org/10.31256/hsmr2022.52.

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Epilepsy affects an estimated one out of 150 people, with 30% of patients unresponsive to existing drug- based therapies for seizure management. Hippocampal resection can be a curative procedure for drug-resistant temporal lobe epilepsy [1], however, current rates of surgical resection are limited by perceived and real risks of undergoing neurosurgery [2]. Laser Interstitial Thermal Therapy (LITT) is a less invasive alternative to surgical resection, which heats brain tissue causing thermal necrosis [3]. Existing commercial LITT tools (Medtronic, Monteris) are straight probes which are inserted through the skull. Reaching deep brain targets such as the hippocampus requires traversing significant amounts of potentially eloquent brain tissue [3]. Deploying LITT using curved needles to avoid critical neural structures has been proposed and explored in simulation and computational design [4], [5], but has yet to be demonstrated experimentally. The purpose of this paper is to describe the first experimental prototype of a needle that can deliver LITT along a curved trajectory.

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8

Pinzetta, Giulia, Allan Alcará, Isadora Ghilardi, Vitoria Pimentel, Nicole Becker, Laura Provenzi, Gabriel Leal, Giovani Zocche, et al. "Modulation of the expression of the SLC12A2 gene that encodes the cationic co- transporter NKCC1 in epileptic animals treated with mesenchymal stem cells." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.689.

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Introduction: Temporal Lobe Epilepsy (TLE) can be identified by synchronized and rhythmic firing of neuronal populations that results in spontaneous and recurrent seizures in individuals affected by it1 . This type of epilepsy is clinically relevant because of its high incidence and refractoriness rate2,3. Thus, the search for therapeutic alternatives becomes important. Due to its benefits and less invasive administration, the mesenchymal stem cells (MSCs)4 appears as a possible therapeutic alternative, because can stimulate and provide a favorable niche for recovery based on their paracrine activities5 . Objectives: The present work aim to highlight the effect promoted by MSCs on the transcription of mRNA of the NKCC1 gene in the TLE induced by pilocarpine model in rats. NKCC1 plays a role in controlling the potential reversal of current and voltage signals executed by Gamma-aminobutyric acid receptors, contributing to inhibitory GABAergic efficacy6 . Design and setting: Experimental design was held at the Pontifical Catholic University of Rio Grande do Sul. Methods: Bone marrow cells were extracted from donor rats, then cultured and transplanted intranasally in animals induced to status epilepticus by pilocarpine7,11. Results: It was observed the ability of the MSCs to alter the amount of transcripts in the brain of the animals. When analyzing the stratified areas of the brain, an increase in NKCC1 expression12 was observed directly to the amygdalas and hippocampi, which are limbic lobe structures affected in epilepsy. Conclusion: MSCs had a modulatory function in the levels of gene expression of cation- chloride co-transporter NKCC1 during acute phase of epilepsy.

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9

Otte, W. M., R. M. Dijkhuizen, C. J. Stam, K. van der Marel, M. P. A. van Meer, M. A. Viergever, and K. P. J. Braun. "Spatiotemporal network alterations in experimental focal cortical epilepsy: MRI-based longitudinal functional connectivity and weighted graph analysis." In 2010 IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2010. http://dx.doi.org/10.1109/isbi.2010.5490129.

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10

Kim, Jung Hwan, Garrett Astary, Svetlana Kantorovich, Thomas H. Mareci, Paul R. Carney, and Malisa Sarntinoranont. "Voxelized 3D Computational Transport Model of Infusions Into the Ventral Hippocampus: Comparison With Experimental Studies." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53444.

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Convection enhanced delivery (CED) is a promising local delivery technique for overcoming the blood brain barrier (BBB) and treating diseases of the central nervous system (CNS). For CED, infusate is infused directly into brain tissue and the drug agent is spread through the extracellular space, which is considered highly tortuous porous media. Previous studies have indicated that the infusion of therapeutic agents into the hippocampus is a potential treatment method for epilepsy [1]. In this study, a 3D interstitial transport modeling approach is presented in which tissue properties and anatomical boundaries are assigned on a voxel-by-voxel basis using tissue alignment data from magnetic resonance (MR) diffusion tensor imaging (DTI). The developed model was used to predict CED transport in the ventral hippocampus and predicted tracer distributions were compared with experimental studies. In rat CED experiments, T1-weighted contrast-enhanced MR images were acquired to measure Gd-DTPA albumin tracer distributions after infusion into the ventral hippocampus. Similar infusate distribution patterns were obtained demonstrating the reliability and repeatability of this modeling scheme. Qualitative comparisons between predicted and measured distribution patterns, volumes and shapes were also conducted to determine the model’s proficiency.

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