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Dissertations / Theses on the topic 'Status epilepticu'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

GIOENI, DANIELA. "THE INFLUENCE OF ANESTHESIA IN THE CENTRAL NERVOUS SYSTEM STUDY." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/708703.

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Central nervous system is a complex machine; it is constituted by more or less 172 billions of cells divided between neurons and glia. This incredible number of cells, particularly neurons, are constantly connected, working 24 hours a day, never stopping. Their activity is maintained even during particular conditions such as sleep, pathological unconsciousness (coma) or general anesthesia. For all these peculiarities, since ancient times, man has devoted much effort to the study of the most fascinating organ of living beings (mammals in particular). Nowadays, thanks to the advance in medical technology, many tools are available to “look inside the brain”. Magnetic resonance imaging and, particularly, functional magnetic resonance imaging (fMRI) is a modern biomedical imaging method, which allows a non-invasive assessment of brain function. The detection of brain activity is based on the coupling between neuronal activity, energy consumption, and blood flow. Functional connectivity (FC) of brain regions is modulated in various central nervous system diseases, during sleeping and general anesthesia. Anesthesia during MRI procedures is commonly used in preclinical setting and, sometimes, is required also in clinical setting (uncollaborative patients, children, drugs induced-coma etc). The study of the relationship between anesthetics and FC presents a double value: allows to distinguish the alterations induced by anesthesia on FC, avoiding possible confounding elements, and permits an in depth investigation of drugs behaviour. For all these reasons, the main topic of this PhD dissertation is the relationship between anesthesia and central nervous system. We started from theoretical studies in healthy subjects and we arrived to clinical setting, describing the possible application of anesthetics drugs as a treatment of neurologic diseases. The first study included aims to describe the way in which dexmedetomidine and isoflurane modulate FC in guinea pigs. We analysed the characteristic of cortical, subcortical and cortico- subcortical connectivity under both drugs with resting state fMRI. The second study presented partial results of a more complex work concerning FC in rats under 4 different anesthetics protocols. Because in FC studies blood flow represents a crucial element we dedicated a part of the work to the study of haemodynamic alterations through the administration 3 of contrast medium. Dynamic Suceptibility Contrast MRI analysis allows the study of cerebral blood flow and cerebral blood volume of different brain anatomic regions under dexmedetomidine, isoflurane, midazolam-dexmedetomidine and midazolam-isoflurane. Finally, we moved to clinical setting to describe the successful treatment of 3 dogs suffering from idiopathic epilepsy presented in emergency department in a state of super refractory status epilepticus. They were treated successfully with a continuous infusion of dexmedetomidine and ketamine. In conclusion, taken together this thesis gives a little contribute to better understand anesthetics behavior at brain level. We believe that it is important to make a “rational choice” when we decide the anesthetic protocol for neuroimaging procedures (both in clinical and preclinical setting) and this “rational choice” could be make only if we have a widespread literature that describe the highest number of anesthetic protocol and their interaction on central nervous system. Finally, thanks to the continuous improvement of our understanding of anesthetics mechanism of action, especially from a molecular and functional point of view, is it possible to use different anesthetics as a therapy for different neurologic conditions, particularly the one based on neurotransmitters imbalance.
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2

Inoue, Yushi. "Ring chromosome 20 and nonconvulsive status epilepticus : A new epileptic syndrome." Kyoto University, 1998. http://hdl.handle.net/2433/182253.

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3

Damasceno, Patrícia Gomes. "O uso da vigabatrina como droga de adição no controle de crises epilépticas neonatais." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-25042018-143839/.

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Introdução: A vigabatrina (VGB - Gama-Vinil-GABA) é um fármaco que eleva os níveis de GABA no organismo, por inibição irreversível da GABA transaminase, cuja eficácia foi bem demonstrada no controle dos espasmos epilépticos em lactentes, especialmente na síndrome de West secundária à esclerose tuberosa. Há escassez de estudos clínicos evidenciando um possível papel deste fármaco no controle de crises epilépticas neonatais e pouco se sabe sobre o potencial impacto do seu uso nessa faixa etária, seus possíveis efeitos adversos, ou se sua introdução teria associações positivas com controle mais adequado das crises na evolução e melhor desenvolvimento neuropsicomotor da criança. A VGB foi introduzida em nosso serviço como terapia de adição para o controle de crises neonatais refratárias, há vários anos, instigando nossa impressão sobre a eficácia deste medicamento no período neonatal. Objetivos: Avaliar a efetividade do uso da VGB como adjuvante no controle das crises eletrográficas e eletroclínicas do período neonatal e seus efeitos sobre o padrão do eletroencefalograma (EEG); Avaliar a evolução clínica e eletrográfica das crianças durante seguimento ambulatorial; Pesquisar associação entre \"controle de crises neonatais com introdução de VGB\" e diversas características demográficas, clínicas e evolutivas destes recém nascidos; Quantificar e caracterizar a ocorrência de efeitos adversos precoces e durante o seguimento. Pacientes e métodos: Estudo transversal retrospectivo, envolvendo o levantamento dos prontuários de uma amostra de recém-nascidos que receberam VGB como tratamento para crises neonatais refratárias aos fármacos convencionais e status epilepticus, no período de janeiro de 2007 a março de 2014, no Serviço de Neonatologia e Terapia Intensiva Neonatal do HCFMRP-USP, mantendo seguimento ambulatorial por pelo menos 1 ano. Foram avaliados os dados demográficos, etiologia e semiologia clínico-eletroencefalográfica das crises, esquema terapêutico prescrito, indicação da introdução da VGB, tempo de internação e tempo para atingir o controle das crises, evolução clínica e eletrencefalográfica durante a internação e no seguimento ambulatorial, época da suspensão da VGB, além de seus efeitos adversos. Resultados: De 48 recém-nascidos avaliados, 34 (79,2 %) obtiveram controle de crises eletrográficas e/ou clínicas durante o período neonatal, havendo melhora no padrão eletrográfico após a introdução da VGB em 79%. Quanto aos critérios para sua indicação, 33,3% (16 indivíduos) iniciaram VGB devido a falha terapêutica no controle das crises com fenobarbital e/ou fenitoína; 27,1% (13 recém nascidos), pela presença de estado de mal epilético e, em 12 crianças (25%), por falha terapêutica do midazolam. Ao final do primeiro ano de vida, a atividade de base do EEG mostrou-se desorganizada em 58,1% (18 de 29 pacientes que o realizaram aos 12 meses de vida). No seguimento ambulatorial de 38 pacientes, algum grau de atraso do desenvolvimento neuropsicomotor foi detectado em 20 crianças (52,6%); 19 lactentes (39,5%) mantiveram o uso da VGB em politerapia, tendo 22 crianças (57,9%) evoluído com persistência das crises epilépticas. Já 37,8% (14 pacientes) enquadraram-se em um padrão de encefalopatia epiléptica, que correspondeu à síndrome de West em 13,9% (5 de 36 crianças). Quanto ao EEG realizado em 34 crianças nessa fase, 17,6% (6 casos) demonstraram a presença de hipsarritmia, enquanto anormalidades focais ou multifocais foram detectadas em 50% (17 lactentes). A taxa de óbito ao final do primeiro ano foi de 23,3% (10 de 43 crianças analisadas quanto a este dado). Não foi possível comprovar déficit visual relacionado diretamente ao uso da VGB. A variável \"controle de crises no período neonatal com o uso da VGB\" foi associada aos seguintes desfechos clínicos favoráveis: melhora no padrão eletrográfico (92,1%), proporção menor de crianças evoluindo para síndrome de West e outras encefalopatias epilépticas (71,9% não tiveram tal desfecho); menor frequência de hipsarritmia no EEG (92,9% sem hipsarritmia), maior alcance de desenvolvimento neuropsicomotor normal (56,2% com bom desenvolvimento neurológico), menor índice de óbito neonatal (97,4% vivos nesta fase) e durante os primeiros doze meses de vida (87,9%). Conclusão: Acreditamos que a VGB seja uma opção terapêutica efetiva e com adequada relação custo-benefício, a ser implementada no controle de crises epilépticas neonatais refratárias como fármaco adjuvante aos convencionais. Entretanto, estudos randomizados e controlados são necessários para confirmar sua eficácia quando comparada a outros medicamentos disponíveis para uso nesta população, bem como para avaliar seus possíveis efeitos adversos a longo prazo.
Introduction: Vigabatrin (VGB - Gama-Vinil-GABA) is an antiepileptic drug which increases systemic GABA levels by irreversibly inhibiting GABA transaminase, with well demonstrated efficacy in the control of infantile epileptic spasms, specially related to West syndrome due to tuberous sclerosis. Clinical studies demonstrating a possible role of VGB in the control of neonatal seizures are still very scarce and very little is known on the impact of its use at this early age, as well as on its possible side effects or eventual positive associations from its use with more adequate seizure control or better neuropsychomotor development in the outcome. VGB has been used in our service as an add-on therapy for refractory neonatal seizures arising the impression that this could be an effective antiepileptic medication in the neonatal period. Objectives: To evaluate the use of VGB as an add-on medication regarding its effectiveness for the control of neonatal electrographic and electroclinical seizures, as well as its effects over the EEG pattern; To evaluate clinical and electrographic evolution of the children in follow-up; To estimate VGB efficacy on the control of neonatal seizures in relation to the demographical and clinical characteristics of those newborns; To quantify and characterize the occurrence of early and late side effects of this medication along follow-up. Patients and methods: This is a transverse retrospective study carried out through charts analysis from a sample of newborns who received VGB as add-on medication for seizures and/or status epilepticus refractory to conventional drugs, from January 2007 through March 2014, at the Neonatal Intensive Care Service of HCFMRP-USP, keeping follow-up in our institution for at least 1 year. Demographical and etiological data were analyzed, as well as clinical-electrographical semiology, VGB prescription indication, therapeutic schedule, time to reach seizure control, clinical and electrographical evolution while in hospital and at the follow-up, age at VGB withdrawal, besides adverse effects. Results: Among 48 newborns evaluated, 34 (79.2%) reached control of electrographic and/or clinical seizures during neonatal period, with improvement of the EEG pattern after VGB introduction in 79%. As for drug introduction criteria, 33.3% (16 children) were started on VGB due to therapeutic failure of phenobarbital and/or phenytoin; 27.1% (13 newborns), due to status epilepticus and, in 12 babies (25%), due to therapeutic failure of midazolam. By the end of the first year of life, EEG background activity was disorganized in 58.1% (18 out of 29 children who had EEG registered at 12 month of life). Along the one year follow-up of 38 patients, 20 infants (52.6%) showed some degree of neurodevelopmental delay; 19 children (39.5%) remained on VGB in polytherapy, with seizure persistence in 22 (57.9%). Evolution to an epileptic encephalopathy was found in 14 kids (37.8%), with West Syndrome being characterized in 13.9% (5 out of 36 kids). As for the EEG carried out in 34 children at the follow-up, 17.6% (6 cases) showed hypsarrhythmia while focal or multifocal abnormalities were seen in 50% (17 infants). Up to 12 month of life, the death rate was 23.3% (10 out of 43 children evaluated for such endpoint). Visual deficit directly related to VGB use could not be determined. The variable \"seizure control during the neonatal period after VGB use\" was associated to the following endpoints: improvement of the EEG pattern (92,1% of children with seizure control after VGB), lower proportion of children evolving into West syndrome and other epileptic encephalopathies (71.9% did not show such endpoint), lower frequency of hypsarrhythmia in the EEG (92.9% without hypsarrhythmia), better milestones reached regarding neuropsychomotor development (56.2% with good neurological outcome), lower rate of neonatal death (97.4% alive by the end of neonatal period) and along the first year of life (87.9%). Conclusion: VGB is an effective therapeutic option with adequate cost-benefit relationship which should be implemented for the control of refractory neonatal seizures as add-on therapy to conventional drugs. However, controlled randomized studies are necessary to confirm such efficacy as compared to other drugs available for use in the neonatal period, as well as to evaluate its possible long term side effects.
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4

Walker, M. C. "The treatment of status epilepticus." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301305.

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5

Alotaibi, Khalid Nijr. "Convulsive status epilepticus in children." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/38829/.

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Convulsive status epilepticus (CSE) is an emergency condition associated with mortality and morbidity. It is commonly treated with antiepileptic drugs (AEDs), but these may cause serious adverse events and even death in children. Research on their effectiveness for CSE, and related adverse events in children remains limited. The primary aim of this research was thus to evaluate the effectiveness and safety of AEDs in treating acute tonic-clonic seizure including convulsive status epilepticus (CSE). Two systematic reviews and meta-analyses were conducted to address these aims. The first evaluated the effectiveness of AEDs in children with acute tonic-clonic seizures including (CSE). The second evaluated the safety of AEDs in this population. The systematic review of AED effectiveness identified 20 studies published between 1946 and April 2015. It showed that buccal midazolam was more effective than rectal diazepam for treating acute tonic-clonic seizures including CSE in children, and was associated with a lower recurrence rate. Lorazepam and diazepam were equally effective in terminating seizures, but for lorazepam, intravenous administration was more effective than the buccal, sublingual or intranasal routes. Intravenous valproate appeared to be more effective than intravenous phenytoin and phenobarbital; however, the difference was not significant. The systematic review of AED safety for children with acute tonic-clonic seizures identified 25 studies, published between 1946 and April 2015. These studies were predominantly randomised controlled trials and of these 19 studies reported more than one adverse event, while 6 reported none. A total of 203 adverse events were documented, most commonly respiratory depression (101 children), mainly after treatment with diazepam (46 children). The rates of respiratory depression with buccal midazolam and rectal diazepam were similar (3.0% and 3.3%, respectively). Compared to intravenous diazepam, intravenous lorazepam was associated with less respiratory depression. No child suffered respiratory depression associated with intravenous valproate treatment, compared to one child with intravenous phenobarbital. When looking at all adverse events, intravenous valproate was significantly safer than intravenous phenobarbital. Respiratory depression was not noted in children who received intravenous levetiracetam; however, all levetiracetam studies identified in this review were cohort and non-comparative. In conclusion, in the treatment of acute tonic-clonic seizures (including CSE), buccal was the best administration route for children admitted to the emergency department. Intravenous lorazepam treatment was associated with less respiratory depression than intravenous diazepam. Where IV access was practicable, intravenous lorazepam was the drug of choice. More randomised control trials are needed to evaluate the effectiveness and safety of AEDs as a second-line treatment.
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6

Lankinen, M. (Markus). "Ensihoitolääkäritoiminnan vaikutus status epilepticus -potilaiden hoitoon." Master's thesis, University of Oulu, 2018. http://jultika.oulu.fi/Record/nbnfioulu-201806132563.

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Tiivistelmä. Pitkittynyt epilepsiakohtaus on hengenvaarallinen tila, jonka hoito suositusten mukaisesti on kolmiportaista. Kolmiportaisen hoidon toteutumiselle oman haasteensa tuo lääkkeiden heikko säilyvyys, jolloin sairaalan ulkopuolella potilaita hoitavat ensihoitolääkärit eivät voi noudattaa hoitosuosituksia. Tämän tutkimuksen tarkoituksena oli selvittää, miten ensihoitolääkäreiden hoito sairaalan ulkopuolella vaikuttaa potilaiden hoitoon kokonaisuudessa Oulun yliopistollisen sairaalan alueella. Tutkimusryhmään kerättiin vuosilta 2011–2012 ensihoitolääkärin hoitamat potilaat, joiden luokse hätäkeskus oli lähettänyt ensihoitolääkärin pitkittyneen kouristuskohtauksen takia hälytyskoodilla 722B ja ensihoitolääkäri oli saattanut potilaan Oulun yliopistolliseen sairaalaan. Lisäksi huomioitiin muutamat verrokkiryhmästä löytyneet aluesairaalasta lääkärin saattamina yliopistolliseen sairaalaan saapuneet potilaat. Kokonaisuudessaan tutkimusryhmään päätyi 30 lääkärin saattamaa potilasta. Verrokkiryhmä koostui Oulun yliopistollisen sairaalan ensiapupoliklinikalla vuonna 2012 hoidetuista potilaista, joiden diagnoosiksi oli todettu ICD-10 järjestelmän mukaan G41 epileptinen sarjakohtaus. Verrokkiryhmään ei hyväksytty potilaita, jotka olivat tulleet sairaalaan lääkärin saattamina. Verrokkiryhmään päätyi 19 potilasta. Lapset rajattiin kokonaan tutkimuksen ulkopuolelle. Tutkimus on taannehtiva tapaus-verrokkitutkimus. Tärkeimpänä tutkimustuloksena todettiin ensihoitolääkärien hoitamilla potilailla vähemmän uusiutuneita kohtauksia. Lisäksi ensihoitolääkärin intuboimat potilaat saivat todennäköisemmin keuhkokuumeen kuin sairaalassa intuboidut. Sairaalassa intuboiduilla potilailla oli pitempi kokonaishoitoaika kuin ensihoitolääkärin intuboimilla tai ilman intubaatiota hoidetuilla potilailla.
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Othman, Jalal. "Der therapierefraktäre Status Epilepticus : Prädiktoren, Therapie, Prognose /." Berlin : Mensch-und-Buch-Verl, 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=013087340&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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8

Zimmermann, Romina. "Status epilepticus und epileptische Anfälle beim Hund." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-111701.

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Rußmann, Vera Franziska Agnes. "Untersuchungen in einem Post-Status epilepticus-Modell." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-148708.

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10

Towne, Alan R. "Outcomes of Status Epilepticus in the Elderly." VCU Scholars Compass, 2007. http://hdl.handle.net/10156/2076.

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11

Martinos, M. M. "The consequences of convulsive status epilepticus in children." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1310261/.

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Convulsive status epilepticus (CSE) is the most common neurological emergency in childhood. Approximately half of new CSE cases occur in children with no perceptible neurological priors (Chin et al., 2006). Prolonged febrile seizures (PFS), a type of CSE that occurs in neurologically normal children, have been retrospectively linked to temporal lobe epilepsy with hippocampal sclerosis. Imaging studies have revealed hippocampal abnormalities soon after PFS, yet, no neuropsychological study to date has investigated these children close to the time of insult. The present thesis investigated the effects of CSE on child development within a month of the incident and, subsequently, a year onwards. The first aim of this thesis was to investigate the effects of CSE on developmental functions using standardized assessments. The second aim was to examine children with PFS for signs of hippocampal dysfunction close to the time of incident. We hypothesized that aetiology would largely influence outcome in our CSE cohort, and, that children with PFS would reveal deficits in a delayed recognition paradigm that is thought to tap onto hippocampal processes. Eighty children were seen a mean of 38 days following CSE (34 PFS) and 50 children (24 PFS) were re-assessed a year onwards. At baseline neuropsychological impairments were evident in children following CSE associated with a PFS, as well as, children following CSE associated with other aetiologies (non-PFS), albeit, these were more pronounced in the non-PFS group. Moreover, in line with our hypothesis, the PFS group revealed deficits in a task of incidental recognition memory alluding to the presence of hippocampal dysfunction in this group. A year onwards deficits were still apparent in the two patient groups, although, the PFS group had shown some improvement on a number of measures. The implications of these findings for our understanding of CSE are discussed in this thesis.
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12

Matzen, Julia. "Untersuchungen zur Epileptogenese nach experimentellem Status epilepticus in vivo." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972578579.

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Choy, M. "MRI investigations into the pilocarpine model of status epilepticus." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444175/.

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Status epilepticus (SE) is a medical neurological emergency and may cause brain injury associated with epilepsy and cognitive decline. Evidence suggests that the hippocampus is particularly vulnerable to injury from SE and that the resulting hippocampal injury has been hypothesised to continue to evolve on to mesial temporal sclerosis associated temporal lobe epilepsy (MTS-TLE). This form of epilepsy is particularly difficult to treat with current medical therapies, and thus it is the most common epilepsy that requires surgical intervention. Therefore understanding the relationships between SE, hippocampal injury and MTS-TLE may provide the basis for development of novel therapies for treating post-SE injury. Clinical magnetic resonance imaging (MRI) studies have indicated that the hippocampus is injured following SE, but whether this injury will progress on to MTS-TLE remains unclear. To facilitate research, experimental models have been developed for investigating SE and its sequelae. Therefore, this study used the pilocarpine rat model for investigating SE and its related injury with multi-parametric MRI. The first part of this work investigated post-SE pathology with MRI and results indicate a characteristic injury profile for various brain regions injured by SE. Analysis of the hippocampus indicated a peak response 2 days following the insult showed a striking relationship to the degree of later injury, suggesting that imaging during the early period may predict later outcome. To investigate this response further, a combination of MRI and proteomic analysis was used and protein changes were identified. The second part of this study consisted of developing a method for imaging the onset and evolution of SE, and results suggest that limited perfusion may contribute to the hippocampal vulnerability to prolonged seizures. This work has identified an early MRI biomarker of later injury, and possible protein substrates for interventional therapy. Furthermore, evidence for the selective vulnerability to SE was found.
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Yoong, M. "Convulsive status epilepticus : prolonged childhood seizures and their consequences." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1353705/.

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Convulsive Status Epilepticus (CSE) is the most common medical neurological emergency in children. Prolonged seizures are associated with brain injury in both animal models and humans and there is concern about longer term outcomes. A qualitative difference between prolonged and shorter seizures is apparent, but information about the longer term prognosis of CSE remains scarce. Retrospective studies have linked the commonest form of childhood CSE, prolonged febrile seizures (PFS), and temporal lobe epilepsy due to mesial temporal sclerosis (TLE-MTS). This study aimed to prospectively follow a population-representative cohort of children following CSE and look for signs of evolving MTS or other brain injury. Magnetic resonance imaging (MRI) was used to visualise underlying brain abnormalities and identify early signs of injury. To investigate the longitudinal evolution of any injury, MRI investigations were repeated at 6 and 12 months post-CSE and the child’s clinical status monitored throughout. 31.2% of children had an abnormal MRI scan post-CSE. Most of these abnormalities pre-dated the episode of CSE and no clinically significant abnormalities were found in children with PFS. Mean hippocampal volumes were only reduced in the group of children with symptomatic CSE; however 20-30% of all children showed loss of hippocampal volume during the year following CSE. This could represent a precursor to TLE-MTS. Further abnormalities were shown on diffusion tensor imaging in children with PFS. Hippocampal mean diffusivity did not show the usual age dependency and widespread reductions in fractional anisotropy were seen across major white matter tracts. These reductions were apparent at 1 and 6 months post-PFS, but resolved by 1 year. These findings form important evidence that children with non-PFS CSE are also at risk of long-term hippocampal damage and that children with PFS appear to have extensive extra-hippocampal abnormalities. These will be further explored in the body of this thesis.
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Bankstahl, Jens P. "Untersuchungen von Mechanismen der Pharmakoresistenz in Status epilepticus-Modellen /." Giessen : DVG-Service, 2008. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016985795&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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16

Hamil, Nicola Elizabeth. "The neuromodulatory role of adenosine A1 receptors in status epilepticus." Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526032.

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Nocent, Deborah P. "An in vitro model of status epilepticus, kindling and neuroprotection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0016/MQ48493.pdf.

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18

Phillips, Kristin. "The effects of hypothermia on status epilepticus-induced acquired epilepsy." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2544.

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Status epilepticus (SE) is a type of neurological injury characterized by continuous seizure activity and can lead to molecular and pathophysiological alterations leading to plasticity changes. SE can lead to the development of AE by the process of epileptogenesis, which is a phenomenon that describes the transformation of normal brain tissue into a hyperexcitable neuronal population. It has been demonstrated both in vivo and in vitro that calcium (Ca2+) dynamics are severely altered during and after SE, and these changes play a major role in the progression of epileptogenesis. It has also been reported that preventing the rise in intracellular Ca2+ ([Ca2+]i) immediately following injury (the Ca2+ plateau) prevents the plasticity changes and ultimate development of epilepsy. Currently, there are no treatments available that can be administered following an injury to prevent the development of AE. Therefore it is clinically important to develop a therapy that can be administered after an injury to block epileptogenesis. Hypothermia is a potential therapeutic intervention. Hypothermia is used clinically to provide neuroprotection following various neurological insults such as stroke and traumatic brain injury (TBI). However, no studies have been performed to evaluate the therapeutic potential of hypothermia following SE. Hypothermia provides protection via multiple mechanisms, one of which includes modulating excitotoxic neurotransmission. It is believed to reduce Ca2+ influx by reducing NMDA receptor activation. It is unclear how hypothermia affects Ca2+ through other modes of entry. This dissertation evaluates the effects of hypothermia on the Ca2+ plateau and demonstrates the novel finding that hypothermia induced post-SE blocks the development of the Ca2+ plateau and reduces the development of AE.
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19

Nocent, Deborah P. (Deborah Patricia) Carleton University Dissertation Psychology. "An In vitro model of status epilepticus: kindling and neuroprotection." Ottawa, 1999.

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20

Rezende, Gustavo Henrique de Souza e. "Neuroplasticidade induzida pelo "status epilepticus" em ratos normonutridos e desnutridos." Universidade Federal de Minas Gerais, 2006. http://hdl.handle.net/1843/MBSA-6W7G2H.

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Neonatal undernutrition plays a significant role on morphology and physiology of the developing central nervous system (CNS), leading, frequently, to permanent alterations. These alterations are highly injurious when occur in the period of neurogenesis, including axonal sprouting. To investigate the effect of neonatal undernutrition onneuroplasticity of the CNS, promoted by the status epilepticus provoked by pilocarpine,four groups of Wistar rats wereused.Wellnourished group (WNG) fed ad libitum lab chow diet supplemented with 25% dog food; Undernourished group fed 60% of the amount o diet consumed by WNG; The wellnourished and undernourished groups were subdivided: one wellnourished group (WNGP) and one undernourished group (UNGP), at 45 days of life, were submitted to status epilepticus by pilocarpine induction (320mg/kg i.p.) 30 minutes after the administration of methyl-scopolamine (1,0 mg/kg i.p.). After 90 minutes in status epilepticus, the seizures were aborted with Diazepam NQTM(20 mg/kg). The control groups (WNG and UNG) had the same treatment, but saline injection replaced pilocarpine. After a recovery period, the animals were filmed daily for a period of 6 hours. At 120 days of life electroencephalography was registered and then the rats were sacrificed to measure DNA, proteins, glutamate release from hippocampus and Neo-Timm staining of the hippocampus granule cells sprouting. No difference was observed in the latenc y of the beginning of the spontaneous recurrent seizures (SRS), neither in the daily quantity of seizures between the WNGP and UNGP. However, it was observed longer lasting time of the SRS in the WNGP when compared to UNGP, but this difference was not observed for epileptiform EEG-register in thisgroups. The WNG and UNG did not present SRS. The food restriction model used decreased body mass from 7th day of life and brain mass at the sacrifice. No differences were found in the amount of proteins and DNA content in samples from hippocampus tissues of WNG and UNG controls or pilocarpine-treated. The amount of glutamate released, stimulated by K+, was greater in the hippocampus slices of WNGPthan in others studied groups. Also, it was found higher intensity of the mossy fibers sprouting of the granule cells of the hippocampus in WNGP than in the UNGP,assessed by Neo-Timm. The WNG and UNG groups did not present sprouting. The results indicate decreased neuroplasticity, due to nutritional insult, in the epilepsy model promoted by systemic injection of pilocarpine.Key words: Under-nutrition, neuroplasticity, sprouting and epilepsy.
A desnutrição neonatal exerce significativo efeito sobre a morfologia e fisiologia do sistema nervoso central em desenvolvimento, conduzindo, freqüentemente, a alterações permanentes. Esses efeitos são altamente danosos quando ocorrem em períodos de neurogênese, inclusive no brotamento axonal. Para investigar o efeito da desnutrição neonatal sobre a neuroplasticidade no Sistema Nervoso Central, induzida pelo status epilepticus, provocado pela pilocarpina, foram utilizados quatro grupos de ratos Wistar. Grupo normonutrido (GN), alimentado ad libitum com ração de biotério suplementada com 25% de ração para cães; Grupo desnutrido (GD), alimentado com 60% da quantidade de dieta ingerida pelo grupo GN. Os grupos, normonutrido e desnutrido, foram subdivididos: Um grupo (GNP) e um desnutrido (GDP), aos 45 dias de idade os animais foram submetidos ao status epilepticus induzido pela pilocarpina (320 mg/kg ip), 30 minutos após a administração de metil-escopolamina (1,0 mg/kg i.p.). Após um período de noventa minutos em status epilepticus, a crise foi abortada com Diazepam NQ (20mg/kg). O controle do grupo normonutrido (GN) e desnutrido (GD) teve o mesmo tratamento, com injeção de salina ao invés de pilocarpina. Após um período de recuperação os animais foram filmados diariamente por um período de 6 horas. Aos 120 dias de vida dados eletroencefalográficos foram registrados e então os ratos foram sacrificados para determinação de DNA, proteínas, liberação de glutamato do hipocampo e coloração por Neo-Timm do brotamento de células granulares do hipocampo. Não se observou diferença na latência do aparecimento de crises recorrentes espontâneas (CRE) e na quantidade diária de crises entre os grupos GNP e GDP. No entanto, observou-se maior tempo de duração das CRE no grupo GNP quando comparado ao GDP, mas essa diferença não foi observada quando comparado o tempo de registro-EEG epileptiforme nestes grupos. Os grupos GN e GD não apresentaram CRE. O modelo de restrição alimentar utilizado promoveu diminuição da massa corporal a partir do 7º dia de vida e da massa do cérebro, avaliada no sacrifício. Não foram encontradas diferenças nas quantidades de proteínas e DNA nas amostras de tecidos hipocampais nos grupos normonutridos e desnutridos, controles ou tratados com pilocarpina. A quantidade de glutamato (GLU) liberado, estimulada por K+, foi maior em fatias de hipocampo do grupo GNP, em relação aos demais grupos. Da mesma maneira foi encontrada maior intensidade de brotamento das fibras musgosas das células granulares do hipocampo no grupo GNP em relação ao grupo GDP, avaliado pelo Neo-Timm. Os grupos GN e GD não apresentaram brotamento axonal. Tais achados indicam uma neuroplasticidade diminuída pelo insulto nutricional no modelo de epilepsia promovido por injeção sistêmica de pilocarpina.
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Müller, Pricila Tolio. "EFEITO DO N-METIL-D-ASPARTATO (NMDA) EM CAMUNDONGOS SUBMETIDOS A MODELO DE EPILEPSIA POR PILOCARPINA." Universidade Franciscana, 2018. http://www.tede.universidadefranciscana.edu.br:8080/handle/UFN-BDTD/610.

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Epilepsy is characterized by a cerebral disorder with interruptions, recurrent and unpredictable of normal brain function. Glutamate is the major excitatory neurotransmitter in the brain and is involved in the mechanism of status epilepticus - a prolonged and self-sustaining seizure. The drug N-methyl-D-aspartate (NMDA) is a synthetic excitotoxin that acts as a specific agonist for the NMDA receptor subtype of glutamate. Pre- and post-conditioning strategies provide a proposal for molecular mechanisms responsible for endogenous neuronal protection. The aim of the study is evaluating the effect of NMDA in different doses against damage following status epilepticus induced by pilocarpine in animal model of epilepsy. For this purpose, 210 adult male mice (60 days, 30-40 g) Swiss albino were treated intraperitoneally with pilocarpine (100 mg/kg every 20 min up to a maximum of 300 mg/kg) evoking status epilepticus. All animals were exposed to behavioral tasks for motor evaluation (locomotion, balance, motor coordination) and memory, followed by evaluation of cellular viability at 30 days post-pilocarpine. The pilocarpine death in approximately 40% of the mice during 24 hours. Treatment with lower doses of NMDA (18 mg/kg) prolonged survival time without change the outcome. The other NMDA doses also had no significant effect on the number of deaths. The status epilepticus caused reduction of the locomotor activity of the mice, an effect reversed by treatment with NMDA 37 mg/kg. The pilocarpine group mice did not show expressive cognitive deficit during acquisition of memory, however reduced evocation. Cellular viability assessed 30 days after status epilepticus indicated damage by MTT test, but not by propidium iodide. Only the 18 mg/kg NMDA reduced damage. It is concluded that the dose 18 mg/kg NMDA induced neuroprotection in surviving animals. The cellular mechanisms of NMDA-induced tolerance remain unknown, but the present study reinforces the dual NMDA effect, since the same dose that increased the mortality rate was able to reduce cellular damage.
A epilepsia é caracterizada por uma desordem cerebral com interrupções, recorrentes e imprevisíveis da função cerebral normal. O glutamato é o principal neurotransmissor excitatório no cérebro e está envolvido no mecanismo de status epilepticus - estado de mal epiléptico, convulsões espontâneas. O fármaco N-metil-D-aspartato (NMDA) é uma excitotoxina sintética que age como agonista específico do subtipo de receptor NMDA do glutamato. As estratégias de pré- e pós-condicionamento fornecem uma nova proposta de mecanismos moleculares responsáveis pela proteção neuronal endógena. Diante do exposto, neste trabalho avaliamos o efeito do NMDA em diferentes doses contra danos decorrentes do status epilepticus induzido por pilocarpina em modelo animal de epilepsia. Para tal, foram utilizados 210 camundongos machos adultos (60 dias, 30-40g) da linhagem albino Swiss que foram tratados pela via intraperitoneal com pilocarpina (100 mg/kg a cada 20 min até o máximo de 300 mg/kg) para a indução do status epilepticus. Todos os animais foram submetidos a tarefas comportamentais para avaliação motora (locomoção, equilíbrio, coordenação motora) e memória, seguidas de avaliação de viabilidade celular em 30 dias pós-pilocarpina. O modelo de epilepsia induzido por pilocarpina induziu morte de aproximadamente 40% dos animais em 24 horas. O tratamento com a menor doses de NMDA (18 mg/kg) aumentou o período de sobrevivência dos animais, mas não modificou o desfecho. As demais doses de NMDA também não tiveram efeito significativo no número total de mortes. O status epilepticus causou redução da atividade locomotora dos camundongos, efeito revertido pelo tratamento com NMDA 37 mg/kg. O grupo pilocarpina não demonstrou expressivo déficit cognitivo na aquisição da memória, mas sim na evocação. A avaliação tardia, aos 30 dias, da viabilidade celular indicou efeito danoso da pilocarpina no teste do MTT, com proteção significativa de NMDA 18 mg/kg. Conclui-se que o NMDA na dose de 18 mg/kg nos animais sobreviventes induziu neuroproteção. Os mecanismos celulares da tolerância induzida por NMDA permanecem desconhecidos, mas o presente estudo reforça a função dual do NMDA, pois a mesma dose que aumentou a taxa de mortalidade foi capaz de reduzir o dano celular.
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22

Chin, Richard Frank Michael. "The North London convulsive STatus EPilepticus in childhood Surveillance Study - NLSTEPSS." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444569/.

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Convulsive status epilepticus (CSE) is the most common medical neurological emergency in childhood. To ultimately improve the management of CSE, an understanding of its incidence, aetiology, seizure types, treatment and outcome in the general childhood population is required. Using emerging techniques for systematic reviews in observational studies, a systematic review of the epidemiology of status epilepticus was conducted. All eligible studies were based on predominantly or exclusively adult populations. The data from these studies suggest that the epidemiology of CSE in childhood differs from that in adults. Thus, an epidemiological study on CSE in a paediatric population was required. The North London convulsive STatus EPilepticus in childhood Surveillance Study (NLSTEPSS), a prospective study, is the first such study. In NLSTEPSS, children with CSE were identified through a multi-tiered notification system. Data were collected using a standard questionnaire and capture-recapture was used to assess ascertainment. The incidence of CSE in childhood is 18-20/100,000/year (95% CI 17- 23/100,000/yr), with a higher incidence amongst non-white children, children of lower socioeconomic status and younger children. Lack of prehospital treatment, and treatment with more than 2 doses of benzodiazepines independently increase the likelihood of CSE lasting longer than 60 minutes. A third of children with CSE are not given prehospital treatment and only 21% of those treated are given adequate initial doses. Treatment with more than 2 doses of benzodiazepines is associated with respiratory depression. Intravenous lorazepam may be better first line therapy than rectal diazepam and intravenous phenytoin may be better second line therapy than rectal paraldehyde. CSE lasting longer than 60 minutes and CSE associated with respiratory depression independently increase the likelihood of admission to paediatric intensive care (PICU). Thus, strategies to reduce those factors may reduce admissions to PICU. On the basis of the data from NLSTEPSS, treatment guidelines for CSE in childhood may need to be revised and a new treatment guideline is proposed.
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Scott, Rodney Craig. "Childhood status epilepticus : structural consequences and assessment of a novel treatment." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325323.

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24

Steinbrenner, Lara Mirja [Verfasser]. "Antiepileptogenese nach experimentellem Status epilepticus : Evaluation der Hypothermie / Lara Mirja Steinbrenner." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1075757185/34.

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Barbosa, Geraldo. "Preservação das funções executivas em ratos expostos ao Status Epilepticus neonatal." Universidade Presbiteriana Mackenzie, 2017. http://tede.mackenzie.br/jspui/handle/tede/3377.

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Universidade Presbiteriana Mackenzie
Status Epilepticus (SE) is a transient occurrence of signs and / or symptoms due to excessive neuronal activity or abnormal synchrony in the brain. The transient term is used as a time path for the beginning and end of the crisis. The neonatal crisis is the most frequent manifestation of neurological dysfunction in the newborn, with a higher incidence in the first year of life, and presents risk of death, neuronal injury, neuronal death, neural network alterations or neurological and cognitive impairment of long depending on the type and duration of the crisis. However, about 40-50% of affected children develop normally. Studies in animal models demonstrate that neonatal seizures in rodents produce long-term neurological adverse effects such as: deficits in learning, visuospatial memory, impairment in cognitive exibility, autistic behavior, characterized by low preference for social novelty, discrimination deficit social and anxious type behavior. Based on the set of changes triggered by neonatal seizures in rodents, the model may be useful for inves- tigating the relationship between seizures in early development and executive functions. Thus, this project intends to evaluate behaviors related to the executive functions of animals that were exposed to neonatal SE. Male Wistar rats at the ninth day of life (P9) were submitted to SE by the administration of pilocarpine (350 mg / kg, ip) and controls received 0.9% saline (0.1 mL / 10 g). In P60 the animals were evaluated by the following paradigms: the operant conditioning box and the T. maze. The sample was composed of 25 animals, 11 controls and 14 experimental. These tests evaluate: visuospatial associative learning, memory consolidation, working memory, persevering behavior, inhibitory control and behavioral exibility. The data suggest that the experimental group in the operant conditioning box showed no impairment in visuospatial associative learning, that there was memory consolidation, did not present perseverant behavior, impairment in working memory and persevering behavior. In the T-maze, the experimental group maintained their working memory, reference memory and motivation, and it showed no impairment in behavioral exibility. The data suggest that a single neonatal SE episode does not impact associative learning, long-term memory, working and reference memories, and behavioral exibility.
O Status Epilepticus (SE) é u ama ocorrência transitória de sinais e ou sintomas devido a atividade neuronal excessiva ou sincronia anormal no cérebro. O termo transitório é usado como demarcador de tempo, para início e fim da crise. A crise neonatal constitui-se a mais frequente manifestação de disfunção neurológica no recém-nascido, com maior incidência no primeiro ano de vida, e apresenta risco de morte, lesão neuronal, morte neuronal, alterações de redes neuronais ou prejuízos neurológicos e cognitivos de longo prazo dependendo do tipo de duração da crise. Entretanto, cerca de 40%-50% das crianças afetadas se desenvolvem normalmente. Estudos em modelos animais demonstram que as convulsões neonatais em roedores produzem efeitos adversos neurológicos de longo prazo, tais como: déficits na aprendizagem, memória visuo-espacial, prejuízo na flexibilidade cognitiva, comportamento autista, caracterizado pela baixa preferência pela novidade social, déficit de discriminação social e comportamento tipo ansioso. Com base no conjunto de alterações desencadeadas pelas crises neonatais em roedores, o modelo pode ser útil para a investigação da relação entre as convulsões no início do desenvolvimento e as funções executivas. Assim, este projeto pretende avaliar comportamentos relacionados às funções executivas de animais que foram expostos ao SE neonatal. Ratos Wistar machos ao nono dia de vida (P9) foram submetidos ao SE pela administração da policarpina (350 mg/kg, ip) e os controles receberam salina 0,9% (0,1 mL/10 g). Em P60 os animais foram avaliados pelos seguintes paradigmas: a caixa de condicionamento operante e o labirinto em T. A amostra foi composta por 25 animais, 11 controles e 14 experimentais. Estes testes avaliam: aprendizagem associativa visuo-espacial, consolidação da memória, memória de trabalho, comportamento perseverante, controle inibitório e flexibilidade comportamental. Os dados sugerem que o grupo experimental, na caixa de condicionamento operante, não exibiu prejuízo na aprendizagem associativa visuo-espacial, que houve a consolidação da memória, não apresentou comportamento perseverante, prejuízo na memória de trabalho e nem comportamento perseverante. No labirinto em T o grupo experimental mantiveram preservadas a memória de trabalho, a memória de referência e motivação, e não exibiram prejuízo na flexibilidade comportamental. Os dados sugerem que um único episódio SE neonatal não impacta a aprendizagem associativa, a memória de longo prazo, as memórias de trabalho e de referência e a flexibilidade comportamental.
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26

Stoll, Jana [Verfasser]. "Management des Status epilepticus im Kindesalter unter besonderer Berücksichtigung des infektassoziierten Status epilepticus ohne Erregernachweis im Liquor bei Kindern und Jugendlichen in Deutschland : zwei deutschlandweite Erhebungen / Jana Stoll." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/109818517X/34.

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27

Stephens, Michelle Lee. "GLUTAMATE REGULATION IN THE HIPPOCAMPAL TRISYNAPTIC PATHWAY IN AGING AND STATUS EPILEPTICUS." UKnowledge, 2009. http://uknowledge.uky.edu/gradschool_diss/736.

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A positive correlation exists between increasing age and the incidence of hippocampal-associated dysfunction and disease. Normal L-glutamate neurotransmission is absolutely critical for hippocampal function, while abnormal glutamate neurotransmission has been implicated in many neurodegenerative diseases. Previous studies, overwhelmingly utilizing ex vivo methods, have filled the literature with contradicting reports about hippocampal glutamate regulation during aging. For our studies, enzyme-based ceramic microelectrode arrays (MEA) were used for rapid (2 Hz) measurements of extracellular glutamate in the hippocampal trisynaptic pathway of young (3-6 months), late-middle aged (18 mo.) and aged (24 mo.) urethane-anesthetized Fischer 344 rats. Compared to young animals, glutamate terminals in cornu ammonis 3 (CA3) showed diminished potassium-evoked glutamate release in aged rats. In late-middle aged animals, terminals in the dentate gyrus (DG) showed increased evoked release compared to young rats. The aged DG demonstrated an increased glutamate clearance capacity, indicating a possible age-related compensation to deal with the increased glutamate release that occurred in late-middle age. To investigate the impact of changes in glutamate regulation on the expression of a disease process, we modified the MEA technology to allow recordings in unanesthetized rats. These studies permitted us to measure glutamate regulation in the hippocampal formation without anesthetic effects, which showed a significant increase in basal glutamatergic tone during aging. Status epilepticus was induced by local application of 4-aminopyridine. Realtime glutamate measurements allowed us to capture never-before-seen spontaneous and highly rhythmic glutamate release events during status epilepticus. A significant correlation between pre-status tonic glutamate and the quantity of status epilepticus-associated convulsions and glutamate release events was determined. Taken together, this body of work identifies the DG and CA3 as the loci of age-associated glutamate dysregulation in the hippocampus, and establishes elevated levels of glutamate as a key factor controlling severity of status epilepticus in aged animals. Based upon the potential ability to discriminate brain areas experiencing seizure (i.e. synchronized spontaneous glutamate release) from areas not, we have initiated the development of a MEA for human use during temporal lobe resection surgery. The final studies presented here document the development and testing of a human microelectrode array prototype in non-human primates.
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28

Wang, Li Racine Ronald J. "Expression of EphA receptors and ligands in rat brain following status epilepticus." *McMaster only, 2006.

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29

Magalhães, Diogo Filipe Domingues. "Clínica de animais de companhia." Master's thesis, Universidade de Évora, 2021. http://hdl.handle.net/10174/29285.

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O presente relatório foi elaborado no âmbito do estágio curricular, parte do Mestrado Integrado em Medicina Veterinária da Universidade de Évora, e encontra-se dividido em duas partes. A primeira parte trata a casuística acompanhada durante o estágio, que foi realizado no Hospital Veterinário do Baixo Vouga de 1 de Setembro de 2019 a 29 de Fevereiro de 2020. A segunda parte corresponde a uma monografia sobre o tema “Ataques epileptiformes em cães num contexto de emergências”, complementada com a apresentação de um caso clínico acompanhado durante o estágio. Os ataques epileptiformes prolongados ou frequentes como é o caso de status epilepticus e ataques epileptiformes em cluster são emergências neurológicas que podem ser fatais. Estas situações requerem uma abordagem terapêutica imediata e dinâmica, sendo importante investigar a etiologia após controlo do ataque epileptiforme e estabilização do paciente; Small Animal Practice Abstract: This report was prepared under the frame of the curricular traineeship, as part of the Integrated Master in Veterinary Medicine of the University of Évora, and is divided in two parts. The first part deals with the case load followed up during the traineeship, which took place at the Hospital Veterinário do Baixo Vouga from September 1st 2019 to February 29th 2020. The second part corresponds to a monography on the subject “Seizures in dogs in an emergency context”, complemented with the presentation of a clinical case followed during the internship. The long or frequent seizures such as status epilepticus and cluster seizures are neurological emergencies which can be deadly. These situations require an immediate and dynamic therapeutic approach, along with the importance of investigating their etiology after controlling the seizures and stabilizing the patient.
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Vescovi, Mathias. "Die Inzidenz des Status epilepticus bei Erwachsenen in Mittelhessen eine bevölkerungsbezogene, prospektive Studie /." [S.l.] : [s.n.], 2003. http://archiv.ub.uni-marburg.de/diss/z2003/0287/.

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Raith, Karina. "Kontinuierliche EEG Überwachung für die Therapie von Hunden und Katzen im Status epilepticus." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-122812.

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Seeger, Natalie. "Prüfung des Erythropoetin-mimetischen Peptids pHBSP in einem chronischen Post-Status-Epilepticus-Modell." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-133891.

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Michler, Christina. "Evaluierung von Radiopharmaka zur bildgebenden Darstellung der Pharmakoresistenz in einem Status epilepticus-Modell." Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-154628.

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Bankstahl, Jens P. [Verfasser]. "Untersuchungen von Mechanismen der Pharmakoresistenz in Status-epilepticus-Modellen / vorgelegt von Jens P. Bankstahl." Gießen : DVG-Service, 2008. http://d-nb.info/997441909/34.

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Rennebaum, Florian [Verfasser]. "Klinische Merkmale und peri-iktale MRT-Befunde bei Patienten im Status epilepticus / Florian Rennebaum." Ulm : Universität Ulm, 2017. http://d-nb.info/1137557664/34.

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Wang, Xiaolan. "Neuropharcological and kinetic correlates of antiepileptic drugs in an animal model of 'status epilepticus'." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405880.

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Sartori, César Renato 1973. "Atividade fisica e neuroproteção em camundongos adultos após indução de status epilepticus por pilocarpina." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314234.

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Orientador: Francesco Langone
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O modelo de epilepsia induzida por pilocarpina em camundongos reproduz a Epilepsia do Lobo Temporal (ELT) em humanos. Animais submetidos à indução de status epilepticus apresentam alterações comportamentais, eletroencefalográficas e lesão neuronal compatíveis com esta condição. Estudos recentes relatam relevantes efeitos positivos da prática de atividade física sobre o sistema nervoso tanto em humanos como em modelos animais. Dentre estes efeitos figuram o aumento da sobrevivência neuronal e da resistência cerebral a diferentes insultos, promoção da angiogênese, estímulo da neurogênese, fortalecimento da potenciação de longa duração no hipocampo, melhora da aprendizagem e memória e contribuição para a manutenção da função cognitiva durante o envelhecimento. Todos estes efeitos conferem à atividade física um grande potencial neuroprotetor. Além disso, foram relatados benefícios decorrentes desta intervenção ambiental diretamente em pacientes com epilepsia e em animais submetidos à epilepsia induzida. Contudo, não há dados na literatura sobre o possível efeito neuroprotetor da atividade física no modelo de epilepsia induzida por pilocarpina em camundongos. Assim sendo, o presente estudo teve por objetivo investigar os efeitos da atividade física voluntária crônica sobre a perda neuronal no hipocampo e suas conseqüências na função mnemônica de camundongos submetidos a este modelo experimental. Trinta e dois camundongos Swiss foram divididos em quatro grupos experimentais (n=8): Saudável Sedentário (SS), Saudável Corredor (SC), Epiléptico Sedentário (ES) e Epiléptico Corredor (EC). Quarenta e oito horas após a indução do status epilepticus, ou sua simulação, foi proporcionado aos animais dos grupos corredores (SC e EC) o acesso a uma roda de atividade instalada em suas respectivas gaiolas por um período de 28 dias. Após este período os animais foram testados no labirinto aquático de Morris para avaliação da memória de referência espacial. Ao final dos testes os animais foram perfundidos com paraformaldeído (4% em tampão fosfato) e os cérebros removidos e processados para inclusão em parafina. Foram então obtidos cortes frontais do cérebro (8µm) para avaliação da extensão da lesão tecidual (coloração de Nissl), da presença de neurônios em degeneração (Fluoro Jade B) e da proliferação celular (PCNA) na formação hipocampal dorsal. Os animais dos grupos SS e SC não apresentaram lesão neuronal ou neurodegeneração, como esperado; também não diferiram entre si na proliferação celular e no teste de memória de um modo geral. Os animais dos grupos ES e EC apresentaram lesão neuronal e neurodegeneração, não sendo constatadas diferenças entre sedentários e corredores. Por outro lado, os animais ES revelaram maior proliferação celular comparados aos EC. Os animais do grupo EC apresentaram desempenho significativamente melhor nos testes de memória quando comparados aos animais ES. Assim, nossos dados revelaram que, a despeito de não ter ocorrido proteção contra lesão histológica, a atividade física melhorou significantemente o desempenho dos animais submetidos ao status epilepticus no teste do labirinto aquático de Morris, indicando que mesmo após lesão neurológica a atividade física promove melhora funcional. Acreditamos que tal melhora pode ser atribuída a mecanismos moleculares relacionados à plasticidade neuronal, que não foram identificados pelas técnicas utilizadas no presente estudo
Abstract: Pilocarpine-induced epilepsy in mice is an experimental model of the Temporal Lobe Epilepsy (TLE). Status epilepticus determined by pilocarpine adminstration leads to behavioral and electroencephalographic changes and neuronal damage similar to those observed in TLE. Recently, it has been shown that physical activity exerts neuroprotective effects, such as increase in neuronal survival, angiogenesis and neurogenesis; resistance to brain injuries, strengthening of the long term potentiation (LTP), improvement of memory and learning; and preservation of cognitive function during aging process. Particularly, physical activity also plays a positive role in epileptic patients and animals. However, there are no reports regarding the neuroprotective action of physical activity on the pilocarpine model of epilepsy in mice. In the present work, we studied the effects of the voluntary physical activity on hippocampal neuronal loss and mnemonic function of mice after the pilocarpine-induced status epilepticus. Thirty-two Swiss mice were assigned to four experimental groups (n=8): Normal Sedentary (NS), Normal Runner (NR), Epileptic Sedentary (ES) and Epileptic Runner (ER). Forty-eight hours after the status epilepticus or its simulation the animals of the runner groups (NR, ER) had access to a running wheel for 28 days. After that, the mice were submitted to the Morris Water Maze test for the evaluation of the spatial memory. Finally, the mice were perfused with paraformaldehyde (4% in phosphate buffer), the brains were dissected and processed for paraffin embedding. Frontal sections (8mm) were serially cut and used for analysis of histologic damage (Nissl staining), degenerating neurons (Fluoro Jade B) and cell proliferation (immunohistochemistry for PCNA) of the dorsal hippocampal formation. Mice of the NS and NR groups showed neither neuronal damage nor neurodegeneration. In addition, these groups were similar to each other in the Morris Water Maze test and exhibited comparable immunostainig patterns for PCNA. In contrast to the previous groups, in ES and ER groups neuronal damage and neurodegeneration were observed and equivalent. However, cell proliferation was higher in ES than in ER. Animals of the ER group had better performance in the Morris Water Maze test compared to ES mice. In conclusion, our results show that physical activity improved significantly the spatial memory of mice that had status epilepticus induced by pilocarpine, despite of having not changed the morphological evidence of neuronal damage. We believe that such improvement might be attributed to molecular mechanisms related to neuronal plasticity, which were not identified by the techniques we used in the present investigation
Mestrado
Fisiologia
Mestre em Biologia Funcional e Molecular
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38

Nogueira, Rita Maria Dantas. "Marinobufogenin-induced status epilepticus, a substance isolated from Bufo paracnemis Lutz 1925 parotoids glands." Universidade Federal do CearÃ, 2000. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=56.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
FundaÃÃo de Amparo à Pesquisa do Estado do CearÃ
O principal enfoque desta pesquisa direcionou-se no sentido de isolar uma substÃncia com forte poder convulsivante, presente nas secreÃÃes obtidas das glÃndulas parotÃides do sapo Bufo paracnemis, Lutz, determinar sua estrutura quÃmica e realizar estudos farmacolÃgicos centrais deste composto. AtravÃs de processos de fracionamento, utilizando o sistema de cromatografia lÃquida de alta eficiÃncia (HPLC), acoplado a uma coluna preparativa C-18 de fase reversa (shim-pack prep. ODS 2,5 x 30 cm), obtivemos essa substÃncia pura em grandes quantidades. Sua estrutura quÃmica foi elucidada atravÃs da tÃcnica de RessonÃncia MagnÃtica Nuclear. Trata-se de um esterÃide cardiotÃnico, um BufadienolÃdeo, contendo um anel esterÃide clÃssico, acoplado a um grupo lactÃnico, denominado Marinobufogenina (14beta -15beta - epoxi - 3beta - 5beta-dihidroxi - 20, 22 - bufadienolÃdeo). Nossos resultados, baseados em anÃlise comportamental e eletrogrÃfica, mostraram efeitos centrais induzidos pela administraÃÃo sistÃmica de Marinobufogenina em ratos e em camundongos. Os animais apresentaram severos efeitos neutÃxicos, tais como movimentos circulares, automatismos gustatÃrios, taquipnÃia, clonias de cabeÃa e de patas, tremores, convulsÃes tÃnico-clÃnicas generalizadas, status epilepticus e morte. A DL50 de Marinobufogenina foi de 10,5 Â1,5 mg/kg para camundongos e de 25,0  2,0 mg/kg para ratos, ambos por via intraperitoneal. A administraÃÃo de Marinobufogenina tambÃm foi efetiva atravÃs de outras vias (subcutÃnea, oral, endovenosa, intramuscular). A forte atividade convulsivante dessa substÃncia à dose-dependente e doses de 5,0 mg/kg para camundongos e de 20,0 mg/kg para ratos , ambos por via intraperitoneal, jà evidenciam alteraÃÃes comportamentais que evoluem para convulsÃes tÃnico-clÃnicas generalizadas, acompanhadas do registro eletroencefalogrÃfico que apresenta descargas epilÃpticas no cÃrtex e hipocampo. Marinobufogenina induziu o aparecimento de crises convulsivas culminando em status epilepticus que persistiu por mais de uma hora. Observou-se uma reduÃÃo das convulsÃes em aproximadamente 80% dos animais tratados com Diazepam (10,0 e 12,5 mg/kg, i.p.), enquanto no registro eletroencefalogrÃfico as crises epilÃpticas permaneceram em alguns dos animais submetidos a esse tratamento. O Fenobarbital (50 mg/kg, i.p.) nÃo bloqueou as crises comportamentais induzidas por Marinobufogenina . A FenitoÃna foi capaz de reverter as convulsÃes tÃnico-clÃnicas generalizadas em todos os animais do grupo, sugerindo uma aÃÃo atravÃs de envolvimento na alteraÃÃo de cÃtions monovalentes. Estudos bioquÃmicos e eletrofisiolÃgicos mais aprofundados deverÃo ser realizados para confirmar essa hipÃtese. Nossos resultados sugerem que a Marinobufogenina pode constituir-se numa ferramenta farmacolÃgica para o desenvolvimento de um modelo experimental de epilepsia, uma vez que preencheu requisitos importantes, tais como : i) demonstrou a presenÃa de atividade epileptiforme nos registros eletroencefalogrÃficos; ii) as crises convulsivas foram bloqueadas por anticonvulsivantes como o Diazepam e FenitoÃna, requisito essencial para a avaliaÃÃo do efeito de novas drogas a serem utilizadas no tratamento da epilepsia.
The main focus of this research was the isolation of a substance with a strong convulsant action from the secretions of the toad Bufo paracnemis, Lutz, parotid glands, determination of its chemical structure and its behavioral and electrographic effects on central nervous system. This substance was purified in large amounts using a reverse-phase high-performance liquid chromatography (HPLC), with a C-18 preparative column (shim-pack prep. ODS 2,5 x 30 cm). Its chemical structure was elucidated using high resolution Nuclear Magnetic Resonance analysis, allowing its identification as a steroid of the bufodienolide type, already known in the literature as Marinobufagin (14beta-15beta-epoxy-3beta,5beta-dihidroxy-20,22-bufadienolide). Our results based on behavioral and electrographic analysis showed central effects induced by systemic administration of Marinobufagin in rats and mice. The animals presented severe neurotoxic effects as circle-like movements, tachypnea, mild tremor of the head , a whole body tremor , myoclonic movements of the fore or hindlimbs, tonic-clonic seizures and death. Marinobufagin DL50 was 10.5 Â l.5 mg/kg for mice and 25.0 Â 2.0 mg/kg for rats, both through intraperitoneal injection. This strong convulsant activity is dose-dependent and 5.0 mg/kg doses for mice and 20.0 mg/kg for rats, both intraperitoneal (IP), already showed behavioral changes that evolved to generalized tonic-clonic seizures. Marinobufagin induced seizures that ended up in status epilepticus that lasted more than an hour. Seizures decreased in almost 80% of the animals treated with Diazepan (10.0 and 12.5 mg/kg, IP) even though some of these animals continued to show seizures in the electrographic recordings. Phenobarbital didnât block seizures induced by Marinobufagin. Phenitoin was able to block generalized tonic-clonic seizures in all animals of the group, suggesting an action involving changes in monovalent cations. Our results suggest that Marinobufagin could represent a pharmacological tool for the development of an epilepsy experimental model, since it had fulfilled the following requirements: i) showed epileptiform activity in electrographic recordings; ii) seizures were blocked by anticonvulsant drugs such as Diazepan and Phenitoin, an essential requirement for the evaluation of the effects of new drugs to be used in epilepsy treatment.
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39

Pacifico, Ana Miriã. "Avaliação da expressão gênica do sistema ocitocinérgico em ratos expostos ao status epilepticus neonatal." Universidade Presbiteriana Mackenzie, 2016. http://tede.mackenzie.br/jspui/handle/tede/2964.

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Fundo Mackenzie de Pesquisa
Experimental studies show evidence that rats subjected to neonatal seizures have morphological and cognitive changes, also exhibiting autistic behavior characterized by low preference for social novelty, social discrimination deficits and behavior type anxious. However, the mechanisms that account for these changes are not yet known. Several lines of evidence show that Oxytocin (OT) is present in key regions for social recognition, such as the medial amygdala and the hippocampus. We postulate that the deficiency in signaling mediated by OT on neural network related to the social brain responds by impaired sociability and increased emotionality subsequent neonatal seizure. This study aims to assess the social recognition memory and gene expression of OT and its receptor (OTR) in animals with neonatal status epilepticus. Wistar rats were adult males submitted to status epilepticus on the ninth day of life (P9) the administration of pilocarpine (350 mg / kg, ip) and the controls received saline 0.9% (0.1 ml / 10 g). In P90 social memory was evaluated by habituation/deshabituation paradigm. At the end of behavioral testing, the animals were anesthetized and decapitated to remove the structures of study (amygdala, hippocampus, and hypothalamus). Thereafter it was performed gene expression analysis of oxytocin and its receptor in the aforementioned tissues by real-time PCR. In social memory test experimental animals had shorter social research, injury indicative of the motivation system / reward and loss of habituation / deshabituation, suggesting impairment in social recognition memory. The gene expression of oxytocin did not differ between the groups in the analyzed structures, but there was a small decrease in gene expression of oxytocin receptor in the hippocampus. Thus concludes the neonatal status epilepticus in rats produces memory deficits in social recognition and motivation /mesolímibic reward systems. This work demonstrated that animals subjected to neonatal status epilepticus have reduced exploration of social novelty, suggesting impairment in motivation system / mesolimbic reward and social recognition memory that may be related to reduced expression of oxytocin receptors in the hippocampus.
Estudos experimentais mostram evidências de que ratos adultos submetidos às convulsões neonatais apresentam mudanças morfológicas e cognitivas, exibindo também comportamento autista caracterizado pela baixa preferência pela novidade social, déficit de discriminação social e comportamento tipo ansioso. Porém, os mecanismos que respondem por estas alterações ainda não são conhecidos. Várias evidências demonstram que a ocitocina (OT) está presente em regiões importantes para reconhecimento social, tais como a amígdala medial e o hipocampo. Postulamos que a deficiência na sinalização mediada pela OT na rede neural relacionada com o cérebro social responda pelo prejuízo na sociabilidade e pelo aumento da emocionalidade subsequente à convulsão neonatal. Este trabalho tem como objetivo avaliar a memória de reconhecimento social e a expressão gênica da OT e do seu receptor (OTR) em animais submetidos ao status epilepticus neonatal. Foram utilizados ratos Wistar machos adultos submetidos ao status epilepticus no nono dia de vida (P9) pela administração da pilocarpina (350 mg/kg, ip) e os controles receberam salina 0.9% (0,1 mL/10 g). Em P90 foi avaliada a memória social pelo paradigma de habituação/desabituação. Ao fim dos testes comportamentais, os animais foram anestesiados e decapitados para a retirada das estruturas de estudo (amígdala, hipocampo, e hipotálamo). Posteriormente foi realizada a análise da expressão gênica da ocitocina e seu receptor nos tecidos citados, por meio da PCR em tempo real. No teste de memória social os animais experimentais apresentaram menor tempo de investigação social, indicativo de prejuízo no sistema de motivação/recompensa e prejuízo de habituação/desabituação, sugestivo de prejuízo na memória de reconhecimento social. A expressão gênica da ocitocina não diferiu entre os grupos nas estruturas analisadas, mas observou-se uma pequena redução na expressão gênica do receptor de ocitocina no hipocampo. Com isso conclui-se o status epilepticus neonatal em ratos produz déficit na memória de reconhecimento social e do sistema de motivação / recompensa mesolímibico. O presente trabalho mostrou que animais submetidos ao status epilepticus neonatal apresentam redução da exploração da novidade social, sugestivo de prejuízo no sistema de motivação/recompensa mesolímbico e da memória de reconhecimento social que pode estar relacionada a redução da expressão dos receptores da ocitocina no hipocampo.
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40

Bessa, Rafael dos Santos de. "Din?mica do status epilepticus em dois modelos animais de epilepsia do lobo temporal." PROGRAMA DE P?S-GRADUA??O EM NEUROCI?NCIAS, 2016. https://repositorio.ufrn.br/jspui/handle/123456789/24080.

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A epilepsia do lobo temporal (ELT) ? a forma mais frequente de epilepsia em adultos, caracterizada clinicamente por um quadro progressivo de crises epil?pticas com foco no lobo temporal, em particular no hipocampo. Dentre os modelos animais, os mais utilizados na investiga??o dos mecanismos fisiopatol?gicos desta condi??o geram crises recorrentes espont?neas atrav?s da indu??o inicial de um estado convulsivo sustentado (status epilepticus, SE) ? por administra??o do agonista glutamat?rgico ionotr?pico, ?cido ca?nico (AC) ou do agonista colin?rgico muscar?nico, pilocarpina (PILO). Entretanto, o uso de inje??es sist?micas e a falta de controle preciso sobre a dura??odo SE geram alta mortalidade, morte celular dispersa e grande variabilidade comportamental durante a fase cr?nica da epilepsia, o que difere em v?rios aspectos do quadro humano. A nosso ver, este padr?o decorre da a??o sist?mica da droga e da dificuldade de controlar a atividade eletrogr?fica/tempo de SE a que cada animal ? submetido, influenciando a din?mica da epileptog?nese. Portanto, este projeto teve como objetivo gerar modelos de ELT por infus?o intra-hipocampal de AC e PILO em ratos e analisar seus comportamentos e atividade eletrofisiol?gica durante o SE. Vale ressaltar que ainda n?o h? estudos eletrofisiol?gicos aprofundados sobre o modelo de PILO intra-hipocampal. Para isto, implantamos feixes de microeletrodos bilateralmente no hipocampo e unilateralmente no c?rtex pr?-frontal medial (CPFm), junto a uma c?nula no hipocampo ventral para infus?o de AC ou PILO. Ap?s a indu??o do SE analisamos a progress?o comportamental e eletrofisiol?gica dos animais. O SE foi bloqueado ap?s 2h por um coquetel anti-convulsivante mais potente do que o utilizado na maioria dos estudos atuais e os animais foram acompanhados por registros cont?nuos de v?deo-EEG sincronizado por at? 72h. Sete dias ap?s o SE, os animais foram sacrificados e seus c?rebros retirados para verifica??o histol?gica da posi??o da c?nula e eletrodos. Os registros de v?deo e de EEG foram analisados por inspe??o visual e t?cnicas de an?lise de s?ries temporais. Nossos resultados mostraram que os animais PILO apresentam 1a crise comportamental com menor lat?ncia do que os animais tratados com AC, por?m com severidade mais vari?vel (AC: 90% animais classe 1 vs. PILO: 50% animais ?classe 3, escala de Racine). Animais PILO tamb?m tiveram menor n?mero de comportamentos do tipo wet-dog shakes que os animais AC, associado a um in?cio de SE precoce comparado aos animais AC. Do ponto de vista eletrofisiol?gico, observamos oscila??es de alta frequ?ncia (>150 Hz), comumente observadas na fase cr?nica da epilepsia, logo ap?s a inje??o de ambos convulsivantes (15-40 min antes do in?cio do SE) concomitante ?s primeiras crises eletrogr?ficas. Por fim, identificamos que o SE em ambos modelos exibe uma organiza??o modular da atividade parox?stica com v?rios n?veis de ritmicidade sobrepostos. Nossos resultados indicam uma maior epileptogenicidade da PILO em rela??o ao AC e, que estas drogas produzem SE com din?micas distintas. Pudemos observar uma composi??o com m?dulos de oscila??es sobrepostas repetidos periodicamente, m?dulos de hipersincronia sem oscila??es acopladas e segmentos de atividade ass?ncrona. Nossos dados ressaltam a import?ncia do registro eletrogr?fico durante o SE para melhor controlar as respostas individuais durante este per?odo.
Temporal lobe epilepsy (TLE) is the most common form of epilepsy in adults. It is characterized by a progressive occurrence of epileptic seizures originating in the temporal lobe, particularly in the hippocampal formation (mesial TLE). Among the animal models used to investigate the physiopathological mechanisms of TLE, the most used are those that lead to spontaneous seizures after an initial insult, such as a prolonged convulsive state (status epilepticus, SE). This condition can be induced by the administration of the glutamatergic agonist, kainic acid (KA) or the cholinergic agonist, pilocarpine (PILO). However, the use of systemic injections and the lack of electrophysiological monitoring during SE lead to high mortality rates, widespread cell death and high behavioral variability during the chronic phase of epilepsy, which differs in several aspects from the human condition. These effects are mainly due to the lack of electrographic control of SE duration and the dynamics of the epileptogenesis process during the weeks following SE. Therefore, this project aimed to generate two animal models of TLE by intra-hippocampal injections of KA or PILO, and then, to analyze their behavioral and electrographic progression during SE. It is important to notice that no electrophysiological study has investigated the SE dynamics in animals infused with PILO into hippocampus so far. For that, we implanted two bundles of microelectrodes in the hippocampus bilaterally, one bundle in the medial prefrontal cortex and a cannula above the intermediate hippocampus for KA or PILO infusion. Following SE induction, we analyzed the behavioral and electrophysiological evolution of KA and PILO animals. SE was blocked after 2h by the injection of an anti-convulsant cocktail and the animals were continuously monitored by video-EEG for up to 72h. Seven days after SE, animals underwent euthanasia and had the brains removed for histological localization of cannula and electrodes. Video and EEG recordings were analyzed by visual inspection and spectral decomposition. Our results showed that PILO animals had shorter latency for first behavioral seizure than KA rats after drug injection. However, seizure severity showed higher variability among PILO rats (PILO: 50% animals had class 3 or higher vs. KA: 90% animals had class 1; Racine?s scale). PILO animals had a reduced number of wet-dog shake behaviors and shorter latency to SE onset as compared to KA rats. Electrophysiologically, we observed that high frequency oscillations (>150 Hz) occurred short after the injection of both drugs (15-40min before SE onset), as opposed to what is commonly reported to occur during the chronic phase of epilepsy in rodents. They were usually found within the first electrographic seizures. Finally, we have identified a distinct modular organization of paroxystic activity during the SE in each group, which consisted of blocks of nested rhythms. These findings thus suggest that PILO is more epileptogenic that KA and that these drugs produce distinct SE dynamics, which seem to be organized as periodically repeating modules of nested oscillations, modules of hyper synchrony with no nested oscillations and segments of asynchronous activity. Our data emphasizes the importance to conduct electrophysiological recordings during SE induction in order to better control individual brain responses. This can reduce variability during epileptogenesis and produce a more homogeneous model of chronic epilepsy.
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41

Oliveira, Diogo Losch de. "Efeitos comportamentais e neuroquímicos do status epilepticus induzido por LiCI-pilocarpina em ratos jovens." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/15393.

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Convulsões prolongadas, status epilepticus (SE), durante o desenvolvimento cerebral podem afetar a estrutura e a função neuronal, levando a morte celular e alterações comportamentais na idade adulta. Nesta tese, investigamos os efeitos neuroquímicos e comportamentais, a curto e longo prazo, do SE induzido por LiCl-pilocarpina em animais jovens. O SE induzido por LiCl-pilocarpina reduz em 50% a atividade da Na+/K+ ATPase 1,5 h após a indução do insulto. Doze e vinte e quatro horas após a administração de pilocarpina, a atividade da Na+/K+ ATPase retornou aos níveis do controle. A diminuição da atividade da Na+/K+ ATPase foi acompanhada por uma diminuição significativa na captação de glutamato em concentrações fisiológicas (1 μM). No entanto, em concentrações elevadas (100 μM) não observou-se alteração da captação de glutamato. Nos animais tratados com LiCl-pilocarpina observou-se uma diminuição dos níveis de fosforilação das proteínas PKB e GKS-3β de 35,84% e 38,79%, respectivamente, 1,5 h após a indução do SE na região CA1 do hipocampo. No entanto, 24 h após a indução do SE, a fosforilação da PKB e GKS-3β retornaram aos níveis do controle. No giro denteado, observou-se uma redução de aproximadamente 30% nos níveis de fosforilação tanto da PKB e GKS-3β em 1,5 e 24 h após a indução do SE. Um elevado número de neurônios em degeneração foi observado 24 h após a indução do SE nas regiões CA1 e hilo do hipocampo. Na idade adulta, os animais tratados com LiCl-pilocapina apresentaram um severo déficit de memória-aprendizado na tarefa de esquiva inibitória, sendo que os animais que apresentaram menor latência para descida da plataforma apresentaram um maior escore para brotamento de fibras musgosas no hipocampo. No teste do claro-escuro, os animais submetidos ao SE retornaram menos e permaneceram menos tempo no compartimento claro quando comparados aos animais controles. Além disso, os animais tratados com LiCl-pilocarpina apresentaram elevados níveis da proteína S100B no líquor, bem como apresentaram uma correlação positiva entre o escore para brotamento de fibras musgosas e o imunoconteúdo de GFAP na região CA1. Portanto, nossos resultados mostraram que o SE induzido por LiCl-pilocarpina diminui a atividade da Na+/K+ ATPase, bem como a captação de glutamato em hipocampo 1,5 h após a indução do insulto. Estes efeitos foram acompanhados por uma diminuição da fosforilação das proteínas PKB e GKS-3β nas regiões CA1 e giro denteado, os quais podem estar relacionados com a morte neuronal observada 24 h após a indução do SE. Além disso, na idade adulta, o SE induzido aos 14 dias pós-natal induziu alterações no processo de memória-aprendizado e no comportamento emocional. As alterações comportamentais parecem estar relacionadas ao brotamento de fibras musgosas, visto que os animais que apresentaram déficit de memória na tarefa de esquiva inibitória e elevados níveis de ansiedade no teste claro-escuro apresentaram maior escore para brotamento de fibras musgosas no hipocampo. Além disso, os animais tratados com LiCl-pilocarpina apresentaram elevados níveis da proteína S100B no líquor bem como uma correlação positiva entre o imunoconteúdo de GFAP na região CA1 e o escore para brotamento de fibras musgosas, sugerindo uma resposta glial ao dano neuronal. Estes dados indicam que o status epilepticus induzido em períodos iniciais do desenvolvimento cerebral é danoso ao sistema nervoso central, alterando sua maturação e levando a alteração neuroquímicas, morfológicas e comportamentais na idade adulta.
Prolonged seizure activity, i.e. status epilepticus (SE), or repeated, brief seizures affect neuronal structure and function in the developing nervous system leading to neuronal death and behavioral impairment at adulthood. In this study, we investigated the short- and long-term effects of early-life LiCl-pilocarpine-induced SE on neurochemical and behavioral parameters. LiClpilocarpine- induced SE decreased Na+/K+ ATPase activity by 42% in hippocampal plasma membranes 1.5 h after SE induction when compared with control group. However, at 12 and 24 h after SE induction the activity of pump returned to control levels. At physiologic concentration of glutamate (1 μM), LiCl-pilocarpine treated animals showed decreased levels of glutamate uptake 1.5 h after SE induction. However, LiCl-pilocarpine-induced SE did not alter the glutamate uptake 12 and 24 h after SE induction. At higher concentration of extracellular glutamate (100 μM), no alterations were observed in glutamate uptake between control and LiCl-pilocarpine-induced SE groups in all times tested. LiCl-pilocarpine-induced SE decreased the phosphorylation of PKB by 35.84% and GSK-3β by 38.79% 1.5 h after SE induction in CA1 subfield. However, 24 h after LiCl-pilocarpine-induced SE the phosphorylation of PKB and GSK-3β returned to control levels. At dentate gyrus, the phosphorylation of PKB was reduced by 35.18% and 31.19% at 1.5 and 24 h after SE induction, respectively. GSK-3β phosphorylation was reduced by 38.05% and 33.12% at 1.5 and 24 h, respectively, after LiCl-pilocarpine administration. Twenty four h after SE, it was observed an increased number of degenerating neurons in the CA1 subfield and in the hilus. At adulthood, SE group presented an aversive memory deficit in an inhibitory avoidance task and the animals that presented lower latency to the step down showed a higher score for mossy fiber sprouting. In the light-dark exploration task, SE rats returned less and spent less time in the light compartment and present an increased number of risk assessment behavior (RA). There was a negative correlation between the time spent in the light compartment and the score for mossy fiber sprouting and a positive correlation between score for mossy fiber sprouting and number of RA. LiCl-pilocarpine-treated animals showed higher levels of S100B immunocontent in the CSF as well as a positive correlation between the score for sprouting and the GFAP immunocontent in the CA1 subfield, suggesting an astrocytic response to neuronal injury. Our results showed that early-life LiCl-pilocapine-induced SE reduce hippocampal Na+/K+ ATPase as well as glutamate uptake 1.5 h after SE induction. These effects were accompanied by a reduced phosphorylation of Akt and GSK- 3β at CA1 and dentate gyrus, which may be related to neuronal death observed 24 h after SE induction. Moreover, at adulthood the animals submitted to LiCl-pilocapine induced SE displayed memory impairment and increased anxiety-like behavior. The behavioral alterations appear to be associated with the mossy fiber sprouting, since the animals that presented impairment in the performance of inhibitory avoidance task and higher levels of anxiety in adulthood showed higher scores for mossy fiber sprouting in the hippocampus. Moreover, LiCl-pilocarpine-treated animals showed higher levels of S100B immunocontent in the CSF as well as a positive correlation between the score for mossy fiber sprouting and the GFAP immunocontent in the CA1 subfield, suggesting an astrocytic response to neuronal injury. These data indicate that LiCl-pilocarpine-induced SE early in life might harmfully affect brain maturation, leading to behavioral, morphological and neurochemical alterations in adulthood.
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42

Einhellig, Marion Franziska. "Semiologie des Status epilepticus (SE) unter Berücksichtigung der Ätiologie, der Statusdauer und der Elektroenzephalographie (EEG)." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145852.

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43

Kuk, Raafat. "Lestaurtinib (CEP-701) Potentiates the Anticonvulsant Effect of Phenobarbital against Kainic Acid-induced Status Epilepticus." Thesis, The University of Arizona, 2018. http://hdl.handle.net/10150/626859.

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44

Barbosa, Geraldo Henrique Lemos. "Avaliação do repertório comportamental TDAH-LIKE de ratos injetados com pilocarpina que desenvolveram Status Epilepticus." Universidade Presbiteriana Mackenzie, 2012. http://tede.mackenzie.br/jspui/handle/tede/1586.

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Made available in DSpace on 2016-03-15T19:39:56Z (GMT). No. of bitstreams: 1 Geraldo Henrique Lemos Barbosa.pdf: 744647 bytes, checksum: a447200460fcb4cfbb7a563e03f92252 (MD5) Previous issue date: 2012-08-16
Fundo Mackenzie de Pesquisa
Epilepsy is a multifactorial disease, multi-faceted, featuring different variations in severity from person to person, characterized by the emergence of spontaneous seizures due to neuronal hyperactivity. Among the epilepsies, temporal lobe epilepsy (TLE) is a very serious and common, comprising about 40% of all cases, often refractory to medication with a substantial impact on cognitive processes and behavior of the affected person. The ELT is characterized by the presence of complex partial seizures with onset in limbic structures, partially attributed to more frequent primary neuropathology, hippocampal sclerosis. This crisis can cause behavioral and cognitive impairments associated with psychiatric disorders, which Disorder Attention Deficit Hyperactivity Disorder (ADHD). In order to evaluate the locomotor activity and exploration in young rats subjected to status epilepticus. Male Wistar rats aged 25 days postnatal, received intraperitoneal injection of pilocarpine (350mg/kg). Control animals received saline. The model induced by pilocarpine was used in this study, given that their histological, biochemical, electrophysiological and behavioral reliably reproduce those found in human TLE. After induction by pilocarpine SE animals underwent behavioral tests that began five days after SE and were completed in 15 days. They were: the open field and elevated plus maze. The present study showed evidence that young animals subjected to status epilepticus exhibit moderate hyperactivity with increased emotionality in a threatening context. Hyperactivity was observed over time, when the animals were reintroduced to an environment with neutral context (open field) or immediately when exposed to a threatening environment (LCE). The results of this study argue for the simultaneous presence of ADHD in the model of TLE. Evidence shows that behavioral changes are manifested early, even before the installation of behavioral seizures. In this respect, it opens a window of opportunity to get early interventions that may minimize the deleterious consequences of seizures.
A epilepsia é uma doença multifatorial, multifacetada, que apresenta diferentes variações de gravidade de pessoa para pessoa, caracterizada pelo surgimento de crises espontâneas devido à hiperatividade neural. Dentre as epilepsias, a epilepsia do lobo temporal (ELT) é uma forma muito grave e comum, que compreende cerca de 40% de todos os casos, comumente refratária à medicação com um impacto substancial no processo cognitivo e no comportamento da pessoa afetada. A ELT é caracterizada pela presença de crises parciais complexas com início nas estruturas límbicas, parcialmente atribuídas à neuropatologia primária mais frequente, a esclerose hipocampal. Essa crise pode causar prejuízos cognitivos e comportamentais, associados a transtornos psiquiátricos, os quais o Transtorno do Déficit de Atenção e Hiperatividade (TDAH). Com objetivo de avaliar a atividade locomotora e exploratória em ratos jovens submetidos ao status epilepticus. Ratos Wistar machos com idade de 25 dias pós-natal, receberam injeção intraperitoneal de pilocarpina (350mg/kg). Animais controle receberam solução salina. O modelo de indução por pilocarpina foi utilizado nessa pesquisa, tendo em vista que suas características histológicas, bioquímicas, eletrofisiológicas e comportamentais reproduzem de forma fidedigna as encontradas na ELT em humanos. Após a indução ao SE por pilocarpina os animais foram submetidos a testes comportamentais que tiveram início 5 dias após o SE e foram concluídos em 15 dias. Foram eles: o campo aberto e o labirinto em cruz elevado. O presente trabalho mostrou evidências que animais jovens submetidos ao status epilepticus apresentam hiperatividade moderada com aumento da emocionalidade em um contexto ameaçador. A hiperatividade foi observada ao longo do tempo, quando os animais foram reapresentados a um ambiente com contexto neutro (campo aberto) ou imediatamente, quando expostos a um ambiente ameaçador (LCE). Os resultados observados neste estudo argumentam a favor da presença concomitante de TDHA no modelo de ELT. Mostra evidências que as alterações comportamentais se manifestam precocemente, antes mesmo da instalação das crises epilépticas comportamentais. Neste aspecto, abre-se uma janela de oportunidades para se buscar intervenções precoces que possam minimizar as consequências deletérias das crises convulsivas.
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45

Merrill, Elaine Alice. "A Mechanism-Based Model to Describe GABAA Receptor Trafficking and Benzodiazepine Pharmacoresistance during Status Epilepticus." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1347458024.

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46

Burman, Richard J. "Investigating excitatory GABAergic signalling & benzodiazepine resistance in an in vitro model of status epilepticus." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/27886.

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Status epilepticus (SE) describes a state of persistent seizures which are unrelenting. First- line treatment for status epilepticus uses a group of drugs, the benzodiazepines, that promote the action of the major inhibitory neurotransmitter within the brain, gamma (γ)-aminobutyric acid (GABA). In a subset of patients however, benzodiazepines prove to be ineffective in terminating SE. Previous data from in vitro models has demonstrated that during single seizures, instead of being inhibitory, activation of the GABAA receptor can have an excitatory effect on neurons. To date, it is unknown whether this shift in GABAergic function contributes to SE, nor how it may modulate the anticonvulsant properties of benzodiazepines. In this thesis I explore the role of excitatory GABAergic signaling in an in vitro model of SE and how this may affect the anticonvulsant efficacy of the benzodiazepine, diazepam. Firstly, I confirm that benzodiazepine-resistant SE is prevalent in a South African paediatric population. Secondly, consistent with its established mechanism of action, I show that diazepam enhances GABAAR synaptic currents. Thirdly, using the in vitro 0 Mg²⁺ model of status epilepticus I show that whilst early application of diazepam has anticonvulsant properties, this is lost when the drug is applied during prolonged epileptiform activity. Fourthly, to investigate this phenomenon I use optogenetic activation of GABAergic interneurons to show that interneurons can drive epileptiform discharges during SE-like activity in vitro. Finally, I confirm that during seizure-like events there is a transient shift in GABAergic signaling that is caused by activity driven changes in the transmembrane Cl⁻ gradient. This thesis provides insight into how excitatory GABAergic signaling during prolonged seizures may contribute towards benzodiazepine resistance in SE. I believe that these results are relevant for understanding of the pathophysiology of SE and may help inform optimal treatment protocols for this condition.
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47

Schmitt, Friedhelm C. [Verfasser]. "Über das wechselseitige Verhältnis von Status epilepticus und Körpertemperatur : eine tierexperimentelle Arbeit / Friedhelm C. Schmitt." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1029845220/34.

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48

Deng, Lucy. "Seizures following vaccination: risk, outcome and recurrence." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/27195.

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Background An adverse event following immunisation is any untoward medical occurrence that follows immunisation and does not necessarily have a causal relationship with the usage of the vaccine. Seizures, ranging from the common and mostly benign febrile seizure to the life-threatening status epilepticus, that occur following immunisation are considered adverse events following immunisation. Febrile seizures have been observed to occur in defined periods following vaccination when a fever is most likely to occur. The magnitude of risk attributed to specific vaccines varies, with no known increased risk seen for some vaccines. Status epilepticus, continuous seizure activity for 5 minutes or more without return of consciousness, or recurrent seizure activity without a return to baseline consciousness in between, has also been reported following vaccination, though the magnitude of attributable risk is unclear. Both seizure types are rare, but serious adverse events, that can follow and sometimes be triggered by immunisation. Because of the potential risk of neurodevelopmental sequalae, seizures can affect both provider and consumer confidence in vaccine safety and therefore immunisation coverage. Knowledge gaps on seizures following vaccination include their clinical severity, developmental outcomes, genetic risks and revaccination outcomes. In my thesis, I aimed to address these gaps to better inform immunisation providers about the risks and outcomes of these potentially serious adverse events following immunisation, to improve guidance on their assessment and management, and ultimately to improve parent and consumer confidence in vaccine safety. Febrile seizures following vaccination In this thesis, I set out to assess the clinical severity, neurodevelopmental outcome and genetic risk of febrile seizures following vaccination, to supplement the known attributable risk of febrile seizures following specific vaccines. Vaccine proximate seizures were defined as VPS was defined as a seizure within 14 days of a vaccination encounter, based on previous studies on the timing of fever and febrile seizures following specific vaccines. I examined the clinical severity of vaccine-proximate febrile seizures through a multi-site prospective cohort study. I discovered that febrile seizures most commonly occurred following the first dose of measles-containing vaccine, and were not clinically any different to febrile seizures due to another cause such as a viral illness. The only factor that prolonged hospitalisation in children with a vaccine-proximate febrile seizure was the presence of concomitant laboratory-confirmed infection. A subsequent prospective case-control study was conducted to assess developmental and behavioural outcomes, and to identify the presence of genetic variants in children with vaccine-proximate febrile seizures compared to children with non-vaccine-proximate febrile seizures and no history of seizures. Using standardised developmental tests administered by certified assessors blinded to the child’s medical history and standardised parent-completed questionnaires, this study found no increased risk of developmental or behavioural problems in children with vaccineproximate febrile seizures compared to children with non-vaccine-proximate seizures or no history of seizures. Genetic variants in the sodium channel gene, SCN1A, associated with a severe form of epilepsy were only identified in children with prolonged vaccine-proximate febrile seizures. Status epilepticus following vaccination Prior to this thesis, there were only case reports and case series on vaccine-proximate status epilepticus, presenting an incomplete and potentially biased picture of the risk and severity of vaccineproximate status epilepticus that may not be generalisable to the whole population. Using a retrospective, population-based, record-linked cohort linking birth, immunisation, hospitalisation and death data, I was able to determine that less than 4% of first episode status epilepticus in children was vaccine proximate. Similar to vaccine-proximate febrile seizures, status epilepticus was found to occur most commonly following the first dose of measles-containing vaccine, but at a rate 35 times lower than that of vaccine-proximate febrile seizure for the same risk window. There was no difference in clinical severity, measured by duration of hospitalisation, intensive care unit admission or death, between vaccine-proximate and non-vaccine-proximate status epilepticus cases. The predictor for ongoing seizures subsequent to the first status epilepticus was seizure onset prior to the status epilepticus episode. Importantly, vaccination uptake decreased following status epilepticus, regardless of the proximity of the status epilepticus episode to vaccination. These findings were confirmed in a second retrospective cohort study I conducted using medical record review to validate the findings from the larger population-based retrospective study that relied on hospital administrative data. The retrospective cohort study also found morbidity following vaccine-proximate status epilepticus was associated with the presence of an underlying genetic epilepsy, where the seizures are the result of a known or presumed genetic defect. Revaccination outcomes following vaccine-proximate seizures Following the identification of the risk and outcome of seizures following vaccination, the next logical clinical question to address was can these children safely proceed with subsequent vaccinations and, if so, how? I, therefore, examined the risk of seizure recurrence following revaccination in children with a previous vaccine-proximate seizure. Through a 5-year multi-site retrospective cohort study, I reviewed the clinical management and outcomes of children with a history of vaccine-proximate seizures who presented to a Specialist Immunisation Clinic, a specialist clinic at tertiary paediatric hospitals where children with a vaccine proximate seizure are provided specialised medical assessment and management for subsequent vaccinations. Vaccine-proximate seizure recurrence was found to be more likely in children with an underlying genetic epilepsy, in particular Dravet syndrome. Reassuringly, the risk of seizure recurrence decreased with the use of prophylactic benzodiazepine with vaccination in these children. Conclusions Vaccination is one of the most effective public health measures for reducing the burden of infectious diseases. However, the success of vaccination programs has been threatened by vaccine hesitancy, that is, the reluctance or refusal to vaccinate despite vaccine availability. Concerns regarding the safety of vaccines and their potential long-term neurological sequalae are amongst the complex reasons why people choose not to vaccinate. My doctoral research has contributed to vaccine safety knowledge globally, specifically in the understanding of seizures, specifically febrile seizures and status epilepticus, as severe acute neurological events following vaccination. In this thesis, I not only identified the children most at risk of neurological sequelae following a vaccine-proximate seizure, but also a revaccination management plan that would allow these children to continue vaccinations without placing them at risk of further vaccine-proximate seizures. These are children aged <12 months, whose underlying genetic epileptic encephalopathy is unmasked by a vaccination event. These children typically present with status epilepticus following vaccination, and are most likely to have further seizures with revaccination if it is given without additional precautions in the form of prophylactic benzodiazepine. My thesis finding highlights the importance of, and future work required to better understand, adversomics – the immunogenetics and immunogenomics of vaccine adverse events at the individual and population level, respectively – and its implications on vaccine safety, confidence and uptake. Finally, my thesis incorporates a variety of research methods, from retrospective record-linked cohort studies to examine whole-of-population risk, retrospective multi-site clinic-based cohort studies to examine detailed clinical management and outcomes, and prospective case-control studies to test hypotheses. I have demonstrated the unique contribution of each of these research methods and the strength in combining these to form a broader pharmacovigilance program of research that can help inform both risk and outcome at a population and individual level. By applying the doctoral research skills I have acquired, I aim to continue my work as a vaccine safety clinician researcher in the monitoring and investigation of vaccine safety signals for novel vaccines, including the multiple COVID-19 vaccines currently in early use globally, to ensure the continued safe and effective use of vaccines in the years to come.
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49

Pujar, S. "The status epilepticus in childhood outcomes study (STEPSOUT) : long-term mortality, neurological, cognitive and neuroimaging outcomes." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1485753/.

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Childhood convulsive status epilepticus (CSE) is associated with considerable short-term mortality and morbidity, but data on long-term outcomes are uncertain. In addition, while the current evidence suggests that prolonged febrile seizures (PFS) can result in acute hippocampal injury, whether this evolves into mesial temporal sclerosis (MTS) and cause temporal lobe epilepsy (TLE) in the long-term is uncertain. In the status epilepticus in childhood outcomes study (STEPSOUT), prospective follow-up of a previously identified unique population-based cohort was performed to investigate mortality, morbidity, and structural consequences within 10 years after childhood CSE. Data from STEPSOUT suggest that aetiology is the main determinant of long-term outcomes following CSE in childhood, and CSE characteristics including seizure duration did not affect outcomes. Mortality within 10 years after childhood CSE was 46 times higher than expected in the reference population, but was predominantly seen in children with pre-existing neurological impairments at CSE presentation and the cause of death was usually not seizure related. Similarly, the long-term outcome was generally less favourable for children who had epilepsy and/or neurological impairments at CSE presentation, but was surprisingly good for those who were neurologically normal prior to their initial CSE and survived beyond 30 days after CSE. Children with PFS had a generally favourable outcome, and only a small minority developed TLE and/or MTS. Neuroimaging data demonstrated little evidence of evolving MTS, but suggested that children with PFS may have a higher prevalence of hippocampal developmental malformations. In addition, widespread diffusion tensor imaging changes reflecting disruption of white matter microstructure were apparent in children with PFS. The novel findings in this work are in some instances, contrary to the long-standing perceptions/beliefs about childhood CSE. The implications of these findings for our understanding of the natural history and long-term prognosis after childhood CSE will be further explored in the body of this thesis.
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50

Haas, Carina [Verfasser]. "Veränderungen der Herzfrequenz und Reaktion auf eine Benzodiazepingabe als Prädiktoren beim nonkonvulsiven Status epilepticus / Carina Haas." Ulm : Universität Ulm. Medizinische Fakultät, 2015. http://d-nb.info/1079908900/34.

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