Academic literature on the topic 'Epilepsis'
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Journal articles on the topic "Epilepsis"
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Rating, D. "SS-2-4 Therapeutic strategies in childhood epilepsis with special emphasis on intractable epilepsies in infants." Electroencephalography and Clinical Neurophysiology/Electromyography and Motor Control 97, no. 4 (September 1995): S67. http://dx.doi.org/10.1016/0924-980x(95)92659-a.
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Bahder, Brian W., Susan Halbert, De-Fen Mou, Ericka E. Helmick, Noemi Soto, Miriel Otero, and Alejandro E. Segarra. "Establishment of the Sea Grape Flatid, Petrusa epilepsis (Hemiptera: Fulgoroidea: Flatidae), in Florida." Florida Entomologist 101, no. 4 (December 1, 2018): 634. http://dx.doi.org/10.1653/024.101.0427.
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Anužytė, J. S., G. Rutkauskaitė, and R. Mameniškienė. "Tranzitorinė epilepsinė amnezija." Neurologijos seminarai 22, no. 77 (January 14, 2019): 213–18. http://dx.doi.org/10.29014/ns.2018.26.
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Tranzitorinė epilepsinė amnezija yra suaugusiųjų amžiuje prasidedančios temporalinės epilepsijos forma, kuri pasireiškia pasikartojančiais atminties sutrikimo epizodais. Pirmasis tranzitorinės epilepsinės amnezijos atvejis aprašytas daugiau kaip prieš šimtą metų, tačiau plačiau nagrinėti šį sutrikimą pradėta neseniai. Diagnozei patvirtinti taikomi 1998 m. suformuluoti kriterijai: 1) pasikartojantys liudininkų patvirtinti tranzitorinės amnezijos epizodai; 2) kitos pažinimo funkcijos epizodo metu nesutrikusios; 3) epilepsijos diagnozė paremta vienu ar daugiau iš pateiktų kriterijų: a) epilepsiforminis aktyvumas (EA) miego ir (arba) būdravimo elektroencefalogramoje (EEG); b) kiti epilepsijos priepuoliai (jeigu jų pradžia ir (ar) pasikartojimas yra susiję su tranzitorinės amnezijos epizodu); c) ryškus teigiamas vaistų nuo epilepsijos poveikis. Literatūroje nagrinėjami atvejai leidžia apibendrinti klinikinius simptomus: tranzitorine epilepsine amnezija suserga vidutinio amžiaus žmonės, dažniau – vyrai; amnezijos epizodai trumpi, linkę kartotis ir dažniau ištinka tik prabudus iš miego; atminties sutrikimui būdinga mišri anterogradinė ir retrogradinė amnezijos; 65 % pacientų amneziją lydi skonio ar kvapo haliucinacijos, déjà vu jausmas, trumpo nereagavimo epizodai, automatizmai; 43 % pacientų elektroencefalogramoje registruojami epilepsiforminiai potencialai temporalinėse skiltyse; įprastai tranzitorinės epilepsinės amnezijos priepuoliai nebesikartoja vartojant net mažas vaistų nuo epilepsijos dozes, tačiau tarp priepuolių gali išlikti paspartėjęs naujos informacijos užmiršimas, tolimos atminties praradimas ir topografinės atminties sutrikimas. Tranzitorinės epilepsinės amnezijos diferencinė diagnostika yra plati, neretai diagnozuojama netiksliai ir pavėluotai.
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Avanzini, Giuliano. "Do Seizures Promote Epileptogenesis and Cause Cognitive Decline?" European Neurological Review 9, no. 2 (2015): 120. http://dx.doi.org/10.17925/enr.2014.09.02.120.
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The assumption that repeated seizures may induce a progression of epilepsies towards an intractable condition and a cognitive decline does not hold true for idiopathic epilepsies but can only be considered for mesial temporal lobe epilepsy and epileptic encephalopathies. The available evidence leads to the conclusion that in most cases the epilepsy worsening and cognitive decline are due to the progression of the underlying pathology or to its interference with the developmental programme, the notable exception being the epileptic encephalopathies with continuous epileptic activity during sleep.
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Sukhov, A. A. "To the clinic "epilepsiae gastricae"." Neurology Bulletin XVIII, no. 1 (July 6, 2021): 177–84. http://dx.doi.org/10.17816/nb70828.
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Among the various forms of epileptic development, a clinical group of cases of epilepsy stands out, which some authors call epilepsia gastrica. The genesis and even the ethiology of this group is foggy, and only the clinical picture of epilepsy makes us agree to the temporary allocation of these cases to the epilepsia gastrica group.
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Matonytė, R., S. Ročka, and J. Grikinienė. "Vaikų epilepsijos gydymas kaliozotomija: du klinikiniai atvejai ir literatūros apžvalga." Neurologijos seminarai 24, no. 85 (December 29, 2020): 241–52. http://dx.doi.org/10.29014/ns.2020.32.
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Epilepsija yra viena iš dažniausių lėtinių vaikų ligų. Aktyvios vaikų epilepsijos paplitimas Lietuvoje, 2018 m. duomenimis, – 6,1/1000 vaikų. Nauji epilepsijos atvejai dažniausiai nustatomi vaikų arba vyresnių žmonių populiacijose. Epilepsija yra daugiaetiologinė liga ir pasireiškia labai įvairiais epilepsijos priepuoliais, kurių suvaldymas yra svarbiausias siekis gydant epilepsiją. Neslopinami priepuoliai gali sukelti vaiko kalbos, pažintinių funkcijų ir elgesio raidos sutrikimus – epilepsinę encefalopatiją. Veiksmingas epilepsijos gydymas vaikams ne tik pagerina sveikatos būklę, bet ir mažina socialinę atskirtį bei padeda integruotis į edukacinę veiklą. Tačiau, net ir anksti diagnozavus ligą ir paskyrus tinkamą gydymą vaistais nuo epilepsijos, epilepsijos priepuoliai išlieka 20-40 % sergančiųjų. Tokiems pacientams gali būti veiksmingas chirurginis epilepsijos gydymas – rezekcinės arba funkcinės (paliatyviosios) operacijos. Rezekcinis gydymas pagrįstas prielaida, kad epileptogeninės zonos pašalinimas apsaugo nuo priepuolių. Deja, kai kuriais atvejais epileptogeninė zona išlieka neaiški net ir po daugelio galvos smegenų tyrimų arba nesutampa su anatominio pažeidimo zona. Tokiu atveju rezekcinė operacija negali būti pritaikyta. Vienas iš veiksmingų sunkiai gydomos epilepsijos priepuolių kontrolės būdų yra paliatyvi chirurginė operacija – kaliozotomija (didžiosios smegenų jungties (corpus callosum) perpjovimas). Didžioji smegenų jungtis yra svarbiausia jungtis nerviniam impulsui plisti tarp abiejų smegenų pusrutulių, todėl jos atjungimas sutrikdo impulso plitimą tarp pusrutulių, taip sustabdydamas priepuolio generalizaciją. Klinikinių tyrimų duomenimis, kaliozotomija yra veiksminga iki 80-90 % operuotų pacientų – priepuoliai išnyksta arba reikšmingai sumažėja jų dažnis ir sunkumas. Aprašomi du pediatriniai pacientai, gydyti Vilniaus universiteto ligoninės Santaros klinikų Vaikų neurologijos ir neurochirurgijos skyriuose, kuriems buvo atlikta kaliozotomija ir palyginamos šių klinikinių atvejų išeitys su naujausių klinikinių tyrimų rezultatais.
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Shellhaas, Renée A., Courtney J. Wusthoff, Tammy N. Tsuchida, Hannah C. Glass, Catherine J. Chu, Shavonne L. Massey, Janet S. Soul, Natrujee Wiwattanadittakun, Nicholas S. Abend, and Maria Roberta Cilio. "Profile of neonatal epilepsies." Neurology 89, no. 9 (July 21, 2017): 893–99. http://dx.doi.org/10.1212/wnl.0000000000004284.
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Objective:Although individual neonatal epilepsy syndromes are rare, as a group they represent a sizable subgroup of neonatal seizure etiologies. We evaluated the profile of neonatal epilepsies in a prospective cohort of newborns with seizures.Methods:Consecutive newborns with seizures were enrolled in the Neonatal Seizure Registry (an association of 7 US children's hospitals). Treatment and diagnostic testing were at the clinicians' discretion. Neonates with seizures related to epileptic encephalopathies (without structural brain abnormalities), brain malformations, or benign familial epilepsies were included in this analysis.Results:Among 611 consecutive newborns with seizures, 79 (13%) had epilepsy (35 epileptic encephalopathy, 32 congenital brain malformations, 11 benign familial neonatal epilepsy [BFNE], 1 benign neonatal seizures). Twenty-nine (83%) with epileptic encephalopathy had genetic testing and 24/29 (83%) had a genetic etiology. Pathogenic or likely pathogenic KCNQ2 variants (n = 10) were the most commonly identified etiology of epileptic encephalopathy. Among 23 neonates with brain malformations who had genetic testing, 7 had putative genetic etiologies. Six infants with BFNE had genetic testing; 3 had pathogenic KCNQ2 variants and 1 had a pathogenic KCNQ3 variant. Comorbid illnesses that predisposed to acute symptomatic seizures occurred in 3/35 neonates with epileptic encephalopathy vs 10/32 with brain malformations (p = 0.03). Death or discharge to hospice were more common among newborns with brain malformations (11/32) than those with epileptic encephalopathy (3/35, p = 0.01).Conclusions:Neonatal epilepsy is often due to identifiable genetic causes. Genetic testing is now warranted for newborns with epilepsy in order to guide management and inform discussions of prognosis.
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Stanojlovic, Olivera, and Dragana Zivanovic. "Experimental models of epilepsy." Medical review 57, no. 7-8 (2004): 359–62. http://dx.doi.org/10.2298/mpns0408359s.
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Introduction An epileptic seizure is a clinical event and epilepsy is rather a group of symptoms than a disease. The main features all epilepsies have in common include: spontaneous occurrence, repetitiveness, and ictal correlation within the EEG. Epilepsies are manifested with distinct EEG changes, requiring exact clinical definition and consequential treatment. Current data show that 1% of the world's population (approximately 50 million people) suffers from epilepsy, with 25% of patients being refractory to therapy and requiring search for new substances in order to decrease EEG and behavioral manifestations of epilepsies. Material and methods In regard to discovery and testing of anticonvulsant substances the best results were achieved by implementation of experi- mental models. Animal models of epilepsy are useful in acquiring basic knowledge regarding pathogenesis, neurotransmitters (glutamate), receptors (NMDA/AMPA/kainate), propagation of epileptic seizures and preclinical assessment of antiepileptics (competitive and non-competitive NMDA antagonists). Results and conclusions In our lab, we have developed a pharmacologic model of a (metaphit, NMDA and remacemide-cilastatin) generalized, reflex, and audiogenic epilepsy. The model is suitable for testing various anticonvulsant substances (e.g. APH, APV, CPP, Mk-801) and potential antiepileptics (e.g. DSIP, its tetra- and octaanalogues).
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Halász, Péter. "Are Absence Epilepsy and Nocturnal Frontal Lobe Epilepsy System Epilepsies of the Sleep/Wake System?" Behavioural Neurology 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/231676.
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System epilepsy is an emerging concept interpreting major nonlesional epilepsies as epileptic dysfunctions of physiological systems. I extend here the concept of reflex epilepsy to epilepsies linked to input dependent physiological systems. Experimental and clinical reseach data were collected to create a coherent explanation of underlying pathomechanism in AE and NFLE. We propose that AE should be interpreted as epilepsy linked to the corticothalamic burst-firing mode of NREM sleep, released by evoked vigilance level oscillations characterized by reactive slow wave response. In the genetic variation of NFLE the ascending cholinergic arousal system plays an essential role being in strong relationship with a gain mutation of the nicotinic acethylcholin receptors, rendering the arousal system hyperexcitable. I try to provide a more unitary interpretation for the variable seizure manifestation integrating them as different degree of pathological arosuals and alarm reactions. As a supporting hypothesis the similarity between arousal parasomnias and FNLE is shown, underpinned by overlaping pathomechanism and shared familiarity, but without epileptic features. Lastly we propose that both AE and NFLE are system epilepsies of the sleep-wake system representing epileptic disorders of the antagonistic sleep/arousal network. This interpretation may throw new light on the pathomechanism of AE and NFLE.
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Zubkov, Sarah, and Ruben Kuzniecky. "Genetic Advances in Epilepsy." US Neurology 11, no. 02 (2015): 96. http://dx.doi.org/10.17925/usn.2015.11.02.96.
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Approximately 40–70 % of all epilepsies are now estimated to have a genetic cause. Though most epilepsies are genetically complex, the past decade has seen an explosion of advances in genetic etiologies. Early gene discovery in epilepsy was limited to large families with milder, inherited monogenic epilepsies using linkage analysis. Newer techniques underlie the past decade’s accelerated gene discovery, especially in noninherited, severe epileptic encephalopathies, and have reinforced the diverse role of cellular functions that may be affected. This review examines recently discovered epilepsy genes and discusses the importance of a genetic diagnosis in patient care.
Dissertations / Theses on the topic "Epilepsis"
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Murai, Marcelo Jun. "Expressão e purificação de proteinas relacionadas a epilepsia." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316860.
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Orientador: Iscia Teresinha Lopes-CendesTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Os genes LGI1 e EFHC1 não codificam canais iônicos; entretanto, afetam indiretamente a corrente nesses canais em síndromes epilépticas determinadas geneticamente. O gene LGI1 (do inglês Leucine-rich, glioma inactivated gene 1) está relacionado à epilepsia parcial autossômica dominante com sintomas auditivos. Recentemente, observou-se a interação de LGI1 com ADAM22 em um complexo que possivelmente regula a transmissão sináptica. A forma mutante da LGI1 é incapaz de se ligar à ADAM22, o que fortalece a hipótese de um mecanismo relacionado à perda de função nesta síndrome epiléptica. O gene EFHC1 (do inglês EF-hand domain C-terminal containing 1) foi encontrado mutado em algumas famílias com epilepsia mioclônica juvenil. Células transfectadas com EFHC1 apresentam maior taxa de apoptose, o que indica uma possível participação em morte celular programada. Clonamos e expressamos as proteínas humanas LGI1 em sua forma inteira (AA 1-557) e a porção C-terminal (AA 224-557; LGI1C), também chamada de domínio epitempina; as formas N-terminal (AA 78-364; EFHC1N), que compreende dois domínios DM10, e C-terminal (AA 403-640; EFHC1C) de EFHC1, formada por um domínio DM10 e um EF-hand putativo. Diversas fusões foram testadas com a proteína LGI1, seja inteira (GST, Trx, SUMO), seja a porção C-terminal (GST, Trx, NusA, MBP e SUMO), em diferentes cepas de Escherichia coli. Obteve-se proteína solúvel com NusALGI1C e MBP-LGI1C; entretanto, só foi possível a captura por cromatografia de afinidade à amilose com a fusão à MBP, na presença ou não da chaperonina GroEL. Apesar do protocolo de purificação de MBP-LGI1C ter sido estabelecido, a clivagem da cauda não foi eficiente, além de apresentar baixo rendimento. Espalhamento de luz dinâmico e SAXS mostraram que a proteína fusionada apresentava-se em um estado de forte agregação. As porções N- e C-terminal de EFHC1 foram clonadas com a fusão SUMO, apresentando alta solubilidade em bactéria. Essas construções foram capturadas em cromatografia de afinidade a níquel e submetidas à clivagem da cauda: obteve-se rendimento próximo de 100% com EFHC1C, enquanto que com a EFHC1N não houve reação. EFHC1C clivada foi separada da cauda e passou por mais um passo de purificação, para polimento. Espectroscopia de dicroísmo circular mostrou que esta porção é composta principalmente por a-hélices e a temperatura de transição foi determinada em 54,5ºC, na presença ou ausência de agente redutor DTT, indicando alta estabilidade. Espalhamento de luz dinâmico e SAXS mostraram que a proteína está monodispersa e modelagem computacional econstituindo o envelope da EFHC1C por SAXS indica uma forma prolata. Em relação à EFHC1N, observou-se a presença de duas populações distintas de proteínas por SAXS e por filtração em gel
Abstract: Non-ion channel genes, as LGI1 and EFHC1, have been shown to indirectly affect ion channel currents in genetically determined epilepsy syndromes. LGI1 (Leucine-rich, glioma inactivated gene 1) is linked to a rare form of partial epilepsy (autosomal dominant partial epilepsy with auditory features, ADPEAF). Recently, LGI1 protein was associated with ADAM22 in a complex that regulates synaptic transmission. The mutated form of LGI1 is incapable of binding to ADAM22, leading to a loss of function mechanism causing ADPEAF. EFHC1 is mutated in some families with juvenile myoclonic epilepsy (JME). It has been observed that EFHC1 transfected cells have a higher rate of apoptosis; therefore, it seems that EFHC1 protein could be involved in programmed cell death. We have successfully cloned and expressed the full form (AA 1-557) and C-terminal epitempin domain of human LGI1 (AA 224-557); and the N-terminus (AA 78-364; named EFHC1N), comprasing two DM10 domains in tandem, and the C-terminus portion of human EFHC1 (AA 403-640; named EFHC1C), comprising one DM10 domain and the EF-hand motif. Several fusion constructs were tested with full LGI1 (GST, Trx and SUMO) and C-terminal half (GST, Trx, NusA, MBP and SUMO) in different Escherichia coli strains. Soluble protein was obtained with NusA-LGI1C and MBP-LGI1C, but only MBP-LGI1C was captured by affinity amilose in the presence or absence of chaperonine GroEL. Despite the fact that we suceffuly established a purification protocol for MBP-LGI1C, tag cleavage presented low yield. Dinamic light scattering and SAXS showed that LGI1C fused to MBP was strongly aggregated. Furthermore, the N- and C-terminal of EFHC1 were cloned with SUMO fusion and showed high solubility in bacteria. These constructions were captured by nickel affinity chromatography and submitted to cleavage reaction. Near complete cleavage was achieved with EFHC1C, but no cleavage was obtained with EFHC1N. SUMO tag was separeted from EFHC1Cand a final purification step was performed. Circular dichroism spectroscopy showed that EFHC1C is composed mainly by a-helices and transition temperature in the presence or absence of reducing agent DTT was 54.5ºC, indicating high stability. Dynamic light scattering and SAXS showed that EFHC1C is in a monodisperse state and presents a prolate shape. EFHC1N presents two different populations of proteins, as determined by SAXS and size exclusion chromatography
Doutorado
Genetica Animal e Evolução
Doutor em Genetica e Biologia Molecular
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Loofbourrow, Rebecca L. "The Indiana Village for Epileptics, 1907-1952 the Van Nuys years /." Thesis, Connect to resource online, 2008. http://hdl.handle.net/1805/1868.
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Thesis (M.A.)--Indiana University, 2008.Title from screen (viewed on August 28, 2009). Department of History, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): William Schneider. Includes vita. Includes bibliographical references (leaves 93-98).
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Oliveira, Gisele Ramos de. "ImportÃncia da anÃlise da frequÃncia cardiÃca na diferenciaÃÃo de eventos epilÃpticos e nÃo epilÃpticos." Universidade Federal do CearÃ, 2006. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=562.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorAs convulsÃes dialÃpticas tÃm como principais alteraÃÃes ictais as alteraÃÃes de consciÃncia que sÃo independentes das manifestaÃÃes ictais no eletroencefalograma. Essa classificaÃÃo de convulsÃes epilÃpticas foi proposta por LÃders et al em 1998 e tem como base exclusivamente a semiologia ictal. O presente estudo avalia um total de 59 eventos dialÃpticos de 27 pacientes. Os eventos foram retrospectivamente avaliados e classificados em: crises dialÃpticas parciais complexas, crises dialÃpticas parciais simples, e eventos dialÃpticos nÃo epilÃpticos. à de amplo conhecimento que a regulaÃÃo cardiovascular à uma funÃÃo da atividade neuronal no cÃrtex cerebral, na amÃgdala e na formaÃÃo reticular do bulbo e que a ativaÃÃo seletiva dos centros cardÃacos nessas Ãreas produz aumento ou diminuiÃÃo da freqÃÃncia cardÃaca. Esse estudo analisou as alteraÃÃes da freqÃÃncia cardÃaca 1 hora antes, durante e 1 hora depois de cada evento dialÃptico. Foi observado que a freqÃÃncia cardÃaca do perÃodo basal era semelhante nos grupos de crises parciais complexas e de crises nÃo epilÃpticas. TambÃm foi observado que a freqÃÃncia cardÃaca basal està aumentada no grupo de pacientes com crises parciais simples (P<0,05). Por sua vez, a freqÃÃncia cardÃaca no perÃodo ictal nÃo aumentou no grupo de crises nÃo epilÃpticas, bem como no grupo de crises parciais simples. Foi observado um aumento da freqÃÃncia cardÃaca (taquicardia) em cada crise dialÃptica parcial complexa (P<0,05), com o retorno da freqÃÃncia cardÃaca aos nÃveis basais no perÃodo pÃs ictal. Esses achados indicam que a taquicardia mediada por vias centrais à uma caracterÃstica das crises dialÃpticas parciais complexas. Na segunda parte do estudo, foram analisada as alteraÃÃes da freqÃÃncia cardÃaca induzidas pelo movimento em crises epilÃpticas e nÃo epilÃpticas. Foi demonstrado que em nenhuma crise nÃo epilÃptica moderada houve um aumento da freqÃÃncia cardÃaca durante a fase ictal acima de 39,3%, comparando-se com a freqÃÃncia cardÃaca do perÃodo basal. NÃo houve aumento da freqÃÃncia cardÃaca em nenhuma crise nÃo epilÃptica leve acima de 16,3% durante a fase ictal, bem como nenhuma crise parcial simples apresentou um aumento da FC acima de 20,6%, comparando-se com o perÃodo basal. Foi verificado que a utilizaÃÃo de uma escala para gradaÃÃo da quantidade de movimento pode ser usada como ferramenta na verificaÃÃo de uma tendÃncia de alteraÃÃo da freqÃÃncia cardÃaca de acordo com a quantidade de alteraÃÃo de movimento. Assim, a anÃlise da freqÃÃncia cardÃaca pode ser usada como critÃrio para exclusÃo de eventos psicogÃnicos
Dialeptic seizures are characterized by ictal loss of consciouness, that is independent of the EEG correlate. This classification of epileptic seizures is based only on ictal semiology and was proposed by LÃders et al in 1998. We studied 59 dialeptic events of 27 patients. The events were retrospectively analyzed and classified in: dialeptic complex partial seizures, dialeptic simple partial seizures and dialeptic non epileptic events. It is well known that cardiovascular regulation is a function of neuronal activity in the cerebral cortex, amygdala, and reticular formation in the medulla, and that selective activation of cardiac centers in theses areas is responsible for changes in the heart rate. Our study analyzed the heart rate changes 1 hour prior, during and 1 hour after each dialeptic event. It was shown that the heart rate of the basal period was similar in the complex partial seizures group and in the non epileptic group. The basal heart rate was increased in the simple partial seizures group (P<0.05). The ictal heart rate did not increase in the non epileptic group, as well as in the simple partial seizures group. We showed an increase in the heart rate in each dialeptic complex partial seizure (P<0.05), and the heart rate returned to normal in the post-ictal period. Our study showed that central mediated tachycardia is a feature of dialeptic complex partial seizures. In the second part of our study, the heart rate changes secondary to movement in epileptic and non epileptic seizures were analyzed. It was shown that none of the moderate non epileptic seizures had an increase in the ictal heart rate above 39.3% when compared to the heart rate in the basal period. There wasnât any heart rate increase in any of the mild non epileptic seizures greater than 16.3% in the ictal period. None of the simple partial seizures showed heart rate increase above 20.6% of the basal period. We showed that a scale for movement quantification allow us to show a tendency of heart rate changes secondary to different degrees of body movement. Therefore, heart rate analysis can be used as an additional criterion for exclusion of psychogenic events
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Teocchi, Marcelo Ananias 1980. "Expressão hipocampal de genes envolvidos em vias de apoptose em pacientes com epilepsia do lobo temporal." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310396.
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Orientador: Lília Freire Rodrigues de SouzaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A epilepsia do lobo temporal associada à esclerose hipocampal [ELT(EH)] é o tipo mais comum de epilepsia focal que causa crises refratárias. A morte neuronal na EH pode ser desencadeada por danos excitotóxicos e citocinas específicas. Pesquisas em modelos experimentais de crises convulsivas ressaltaram a citocina pleiotrópica fator de necrose tumoral (TNF) como um importante efetor/mediador de neuroinflamação e morte celular. Além disso, esses modelos sugeriram que o TNF possa ter uma ação dicotômica por meio de seus dois receptores: ativação da morte celular programada (via TNFRSF1A) ou atuação na sobrevivência celular (via TNFRSF1B), através do fator nuclear kappa B (NFkB). Klotho (KL), originalmente identificada como uma proteína antienvelhecimento, tem se destacado como um importante hormônio regulador de cálcio e fósforo. Sua função cerebral é desconhecida; porém, camundongos knockout para Kl apresentam características que remetem ao envelhecimento humano, com neurodegeneração e redução de sinapses no hipocampo. Em modelos de doença renal crônica e colite, foi comprovado que o TNF inibe KL através do NFkB. Nosso objetivo é identificar alvos críticos na epileptogênese e na fisiopatologia molecular da ELT(EH). Avaliamos a expressão relativa do RNAm de cinco genes-alvo: TNF, TNFRSF1A, TNFRSF1B, NFKB1 e KL. A expressão gênica foi avaliada em amostras de tecido hipocampal de 14 pacientes com ELT(EH) e comparadas com cinco amostras de controles post mortem. Além disso, ambos os receptores do TNF foram analisados nas amostras hipocampais por imuno-histoquímica. Todos os cinco genes avaliados apresentaram expressão significantemente alterada nos pacientes com ELT(EH) (P<0,05). A expressão de ambos os receptores foi constatada nos tecidos dos pacientes. Este é o primeiro estudo a relacionar KL e epilepsia. Nossos dados reforçam o componente inflamatório da EH e sugerem que o TNF possa inibir a expressão de KL no hipocampo dos pacientes. A repressão de KL abre novas frentes de pesquisa que podem contribuir para a compreensão da complexa fisiopatologia da ELT(EH). Além disso, uma vez que TNF, TNFRSF1A e NFKB1 são protagonistas na via extrínseca da apoptose, concluímos que a sinalização do TNF participe criticamente da neurodegeneração hipocampal associada à ELT. Existem controvérsias sobre o papel do TNFRSF1B. Sua ativação pode estar relacionada a mecanismos de sobrevivência, hipótese corroborada pela concomitante hiperexpressão de NFKB1; todavia, já foi demonstrado que o TNFRSF1B pode reforçar a ação do TNFRSF1A. Apresentamos evidências de que KL e a sinalização do TNF constituem um importante eixo para estudos farmacológicos, especialmente em relação aos benefícios de uma terapia anti-inflamatória nesses pacientes
Abstract: Temporal lobe epilepsy associated with hippocampal sclerosis [TLE(HS)] is the most common form of focal epilepsy that causes refractory seizures. Neuronal death in HS can be triggered by excitotoxic damage and specific cytokines. Previous research in seizure models indicates that the pleiotropic cytokine tumor necrosis factor (TNF) as an important effector/mediator of neuroinflammation and cell death. Through its two receptors, TNF can play a dichotomous role in animal seizures: programmed cell death activation (via TNFRSF1A) or cell survival actuation (via TNFRSF1B), through the nuclear factor kappa B (NFkB) activation. Klotho (KL), originally identified as an antiaging protein, is emerging as an important calciophosphoregulatory hormone. Its cerebral function is unclear; however, the Kl knockout mouse exhibits a phenotype resembling human aging presenting neural degeneration and a reduction of synapses in the hippocampus. Studies have demonstrated that TNF downregulates KL through NFkB in animal models of chronic kidney disease and colitis. Our aim is to identify critical targets in epileptogenesis to clarify the molecular pathophysiology in TLE(HS). We evaluated the relative mRNA expression of five target genes: TNF, TNFRSF1A, TNFRSF1B, NFKB1 and KL. Gene expression was performed in resected hippocampal tissue samples from 14 TLE(HS) patients and compared to five post mortem controls. Moreover, an immunohistochemistry assay was done to verify the activation of both TNF receptors in patient and control tissues. We found that all target genes were differentially regulated in the TLE(HS) patients (P<0.05). Both TNF receptors were clearly activated in patient's tissues. This is the first study relating KL to epilepsy. Our data corroborates the prominent role of inflammation in HS and suggests that TNF might affect KL expression in hippocampus. As a multifunctional protein, KL downregulation in TLE(HS) patients opens several possible avenues of research that will help us to understand the complex pathophysiology in HS. Furthermore, since TNF, TNFRSF1A and NFKB1 are key factors in the death receptor signaling canonical pathway, we conclude that TNF signaling plays a crucial role in TLE hippocampal neurodegeneration. There is still some controversy on TNFRSF1B role. Its augmentation could be related to a survival mechanism because the concomitant NFKB1 upregulation; however, it has already been demonstrated that TNFRSF1B may reinforce TNFRSF1A action. Our evidence reveals KL and the TNF pathway as an important axis for pharmacological studies regarding the benefits of an anti-inflammatory therapy in these patients
Doutorado
Saude da Criança e do Adolescente
Doutor em Ciências
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Fonseca, Viviane de Carvalho. "Alterações da substância branca de pacientes com epilepsia parcial secundária à displasia cortical focal = estudo de imagem por tensor de difusão com análise voxel-a-voxel." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309288.
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Orientador: Fernando CendesDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A epilepsia parcial secundária a displasia cortical focal (DCF), comumente se origina nos primeiros anos de vida, entretanto, alguns casos podem apresentar início após os 40 anos. Atualmente, a DCF é identificada em 20 - 25% de pacientes com epilepsia parcial extratemporal e aproximadamente 76% dos pacientes supostamente apresentam epilepsia refratária à medicação. Trata-se de uma malformação do desenvolvimento cortical (MDC), identificada por uma diferenciação anormal do córtex e neurônios displásicos na substância branca (SB). O exame de imagem por tensor de difusão (DTI) tem a capacidade de descrever a integridade da SB, através da quantificação da difusão e orientação das moléculas de água nos tecidos de forma não invasiva, podendo detectar anormalidades no tecido cerebral em estágios precoces em relação ao exame convencional de imagem por RM ponderado em T1 ou T2. Com o objetivo de detectar alterações microestruturais no tecido cerebral, utilizamos o exame de DTI para investigar a SB desses pacientes. Para isso, utilizamos uma medida de direcionamento da difusão, conhecida como anisotropia fracional (AF), que representa a orientação do eixo das estruturas dos feixes de fibras ao longo do qual as moléculas de água se movem de modo preferencial, indicando mudanças da microestrutura tissular. Foram analisados 53 sujeitos, sendo 22 pacientes e 31 indivíduos saudáveis. Todos os pacientes tinham diagnóstico clínico e eletroencefalográfico de epilepsia extratemporal (lobo frontal) secundária a provável DCF. Processamos o DTI com os programas: MRIcroN, FSL e TBSS (Tract-based Spatial Statistics). A comparação entre o grupo de pacientes e grupo controle foi realizada usando two-sample teste-t, com nível de significância de p <0,05. Identificamos áreas com redução da FA, nos lobos frontal, parietal, temporal e occipital, sendo elas: fórceps menor à direita (p=0,032), fórceps menor à esquerda (p=0,042), giro do cíngulo à esquerda (p=0,048), trato córtico-espinhal direito e esquerdo (p=0,022), fascículo fronto-occipital inferior direito (p=0,022), fascículo longitudinal superior e inferior esquerdo (p=0,034), radiação talâmica anterior à direita (p=0,034) e fascículo uncinado à esquerda (p=0,042). Nossos resultados mostraram um padrão extenso de anormalidades estruturais em regiões da SB que se estendem além do foco epileptogênico (lobo frontal), provavelmente decorrente da cronicidade da epilepsia. É possível que essas alterações sejam secundárias às descargas epilépticas muito freqüentes, associadas à generalização e bissincronia secundária
Abstract: Epilepsy secondary to FCD usually begins early in life, however, some cases may have onset after 40 years. Currently FCD has been identified in 20-25% of patients with extratemporal epilepsy and approximately 76% of patients with epilepsy refractory to antiepileptic drug treatment. FCD is a malformation of cortical development (MCD), identified by an abnormal differentiation of cortex and dysplastic neurons on the white matter. Diffusion tensor imaging (DTI) has a powerful ability to describe white matter integrity, through the quantification of the spread and direction of water molecules in tissues noninvasively, which can detect the abnormalities of the brain tissue in an earlier stage than conventional T2- or T1-weighted MRI. Aiming to detect microstructural changes in brain tissue, we used DTI to investigate the WM these patients. For this, we used a measure of diffusion direction, known as fractional anisotropy (FA), which represents the axis orientation of the structures of the fiber bundles along which the water molecules move preferentially, indicating changes in tissue microstructure. We analyzed 53 subjects, 22 patients and 31 healthy individuals. All the patients had clinical and EEG diagnosis of extratemporal epilepsy (frontal lobe), probably secondary to FCD. To process the DTI we used the following softwares: MRIcroN, FSL, TBSS. The comparison between the patients group and control group was performed using two-sample t-test, and the level of significance was set at <0.05. FA reduction in patients were identified in the frontal, parietal, temporal and occipital lobes, which were: right forceps minor (p =0.032), left forceps minor (p = 0.042), left cingulum (p = 0.048), right and left corticospinal tracts (p = 0.022), inferior right fronto-occipital fasciculus (p = 0.022),right and left superior longitudinal fasciculus (p = 0.034), right anterior thalamic radiation (p = 0.034) and the left uncinate fasciculus (p = 0,042). Our results showed a widespread pattern of WM micro structural abnormalities extending beyond the ictal onset zone (frontal lobe), probably due to the epilepsy chronicity. It is possible that this damage is secondary to persistent epileptic discharges with frequent generalization and secondary bilateral synchrony
Mestrado
Ciencias Biomedicas
Mestre em Ciências Médicas
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Gonçalves, Eleonora Borges. "Transtornos depressivos em pacientes com epilepsia do lobo temporal mesial, refratários às drogas antiepiléticas." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309277.
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Orientador: Fernando CendesTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Objetivos: Avaliar os transtornos depressivos em comorbidade com a epilepsia do lobo temporal (ELT), em pacientes com crises refratárias às drogas antiepilépticas (DAEs). Pacientes e métodos: Realizamos um estudo transversal, entrevistando e coletando informações dos prontuários de pacientes que procuraram atendimento no Ambulatório de epilepsia de difícil controle do HC-UNICAMP. A população foi de adultos, com idade igual ou maior de 24 anos, em acompanhamento no HC-UNICAMP, com diagnóstico de ELT refratária, em uso adequado da medicação instituída e ausência de rebaixamento intelectual, demência ou problemas de linguagem. Os pacientes foram submetidos a uma entrevista psiquiátrica semiestruturada, o que conferiu diagnóstico segundo a Classificação Internacional de Doenças (CID-10)-OMS. Aplicamos os seguintes instrumentos: (1) Mini Entrevista Neuropsiquiátrica Internacional (MINI) e (2) Inventário de Depressão de Beck (IDB). Resultados: Foram incluídos 40 pacientes com idade de 24-60 anos, trinta e um dos 40 pacientes (77,5%) apresentaram transtornos depressivos: 14 (45,2 %) com distimia, 11 (35,5%) com transtorno depressivo recorrente e 6 (19,3%) com transtorno bipolar, na ocasião depressivo. Dois (5%) apresentaram transtorno misto de ansiedade e depressão. Os outros 7 pacientes (15%) apresentaram eventuais manifestações de depressão e ansiedade, sem constituírem um diagnóstico de depressão, sendo um deles com transtorno orgânico de ansiedade. Apenas 8 dos 31 pacientes (25,8%) receberam tratamento antidepressivo satisfatório prévio. A duração da epilepsia apresentou uma tendência a ser maior nos pacientes com transtorno depressivo (p=0.10); não houve associação entre depressão e frequência de crises. Conclusões: Este trabalho confirma que o transtorno depressivo é frequente e subdiagnosticado em pacientes com ELTM refratária às DAEs. A duração da epilepsia apresenta uma tendência a ser maior nos pacientes deprimidos. Não houve associação entre depressão e frequência de crises
Abstract: Objectives: To assess depressive disorders in patients with temporal lobe epilepsy (TLE), refractory to antiepileptic drugs (AEDs). Patients and methods: We performed a cross-sectional study, interviewing and collecting information from records of patients who sought treatment at the Epilepsy Clinic of the HC-UNICAMP. The population consisted of adults aged greater than 24 years followed at UNICAMP, diagnosed with refractory TLE, in appropriate use of AEDs and lack of established mental retardation, dementia or language problems. Patients underwent a semi-structured psychiatric interview, which gave diagnosis according to the International Classification of Diseases (CID-10) - WHO. We applied the following instruments: (1) Mini International Neuropsychiatric Interview (MINI) and (2) the Beck Depression Inventory (BDI). Results: There were 40 patients aged 24-60 years. Thirty-one of these (77.5%) had depressive disorders: 14 (45.2%) with dysthymia, 11 (35.5%) with recurrent depressive disorder and 6 (19.3%) with bipolar disorder who had depression at the time of evaluation. Two (5%) had mixed anxiety disorder and depression. The other 7 patients (15%) showed signs of depression and anxiety, without imposing a diagnosis of depression, one of them with organic anxiety disorder. Only 8 of the 31 patients (25.8%) had received prior satisfactory antidepressant treatment. The duration of epilepsy tended to be higher in patients with depressive disorder (p = 0.10). There was no association between depression and seizure frequency. Conclusions: This study confirms that depressive disorder is common and underdiagnosed in patients with TLE refractory to AEDs. The duration of epilepsy had a tendency to be higher in depressed patients. There was no association between depression and seizure frequency
Doutorado
Neurologia
Doutora em Ciências Médicas
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Jörninge, Fridha. "Psykiatrivård och epilepsi i Sverige : Skildrat genom Ebba Ramsays epilepsisjukhus Vilhelmsro." Thesis, Uppsala universitet, Historiska institutionen, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-210681.
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The purpose of this essay was to investigate and compare the treatment of patients at Vilhelmsro’s hospital for children with epilepsy in Jönköping, Sweden, to the treatment of mentally deficient patients in Sweden during the 19th and 20th century. To fulfill the purpose of this investigation the administrative and medicinal archive at Jönköping’s county hospital Ryhov, and the provincial archives in Vadstena were used. The basis and the results of the investigation were drawn from studying and analyzing patient records, seizure books and enrollment charts of discharged patients, dated from 1928 to 1939. The investigation shows that although the treatment of patients at Vilhelmsro share a lot of fundamental values with the treatment of mentally deficient patients at mental institutions around Sweden at that time, such as correctness of behavior in order to fit into the norms of society, the hospital’s main concern was to educate and care for the children with epilepsy in hopes of adapting into society. This was not always possible, and the care at Vilhelmsro mainly had three outcomes which consisted of either being discharged due to recovery from illness, being discharged into the care of a more severe care facility or death from severe seizures. The hospital did concern itself with making sure that the children were molded into fitting into society’s interests and behavior and unfortunately this might have taken away from the actual medical care.
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Oliveira, Elton Pallone de. "Estudo crítico dos modelos experimentais em epilepsia espontânea do tipo ausência." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-24052011-135103/.
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A epilepsia é uma das afecções neurológica mais comum na população mundial. Trata-se de uma condição crônica altamente incapacitante que acomete indivíduos de ambos os sexos e de todas as faixas etárias, com um discreto predomínio em homens e, maior freqüência em crianças abaixo de dois anos e idosos acima de 65 anos. As conseqüências de morbidade e mortalidade desta patologia repercutem negativamente na sociedade e, conseqüentemente na economia global. Estima-se que de 60 a 100 milhões de pessoas ao redor do mundo apresentaram alguma condição epiléptica durante suas vidas. Segundo alguns autores a incidência da epilepsia varia de 11 a 131/100 mil habitantes por ano e a prevalência de 1,5 a 30/1000 habitantes por ano, sendo que os maiores valores encontram-se nos países em desenvolvimento, particularmente na America Latina e na África. As epilepsias generalizadas idiopáticas (EGI) constituem-se cerca de um terço de todas as formas de epilepsias e são 15 a 20% mais freqüentes em relação aos demais tipos de epilepsia. As EGI do tipo ausência, as quais são estritamente relacionadas à faixa etária infantil e adolescente podem muitas vezes (2,8 5,7% dos casos) afetar pacientes com idade superior a 15 anos. A fisiopatologia, assim como, as causas reais da ocorrência e/ou recorrência das crises de ausência na idade adulta não estão completamente esclarecidos e se representam um importante desafio para os epileptologistas. As epilepsias generalizadas idiopáticas (EGIs), (etiologia genética) são classificadas em: a) crises de ausência típicas, b) crises de ausência atípicas, c) crises de ausência com fatores especiais, d) crises mioclônicas, e) crises mioclônicas atônicas, f) crises mioclônicas tônicas, g) crises clônicas, h) crises tônicas e, i) crises atônicas. O tratamento e comumente farmacológico e as crises são controladas na maioria dos casos, no entanto, cerca de um terço dos pacientes são refratários às drogas anticonvulsivantes. Tendo como principal finalidade a elucidação de mecanismos básicos e, auxílio no desenvolvimento de abordagens terapêuticas eficazes para esses pacientes, pesquisadores do mundo inteiro dedicam muitos esforços para o desenvolvimento de modelos experimentais capazes de mimetizar o fenômeno que se pretende reproduzir. Dentre os principais modelos experimentais em EGIs, pode-se citar: (1) o modelo de epilepsia generalizada induzida por penicilina em gatos; (2) modelos de investigação da bicuculina; (3) indução por estimulação elétrica; (4) ratos geneticamente epilépticos de Strasbourg (GAERS); (5) cepa WAG/Rij; (6) modelo do gama-hidroxibutirato (GHB) e (7) os camundongos mutantes. Tais modelos experimentais têm provido meios para que os pesquisadores possam avaliar e quantificar adequadamente as alterações neuronais que ocorrem durante os processos epileptógenos tanto in vitro ou in vivo, possibilitando importantes avanços no desenvolvimento de novas abordagens terapêuticas e, melhora na qualidade de vida de portadores de epilepsiaEpilepsy is a very commom neurological disorders in world population. It is a chronicle condition highly disabling that affects both genera male and female independent of your age with a soft predominance in men and is more frequent in child under 2 years old and adult above 65 years old. The morbidity and mortality consequences of this disorder have many negative repercussions at society and global economy consequently. It is estimated about 60 to 100 millions of people around the world present any epileptic condition during their lives. According some researchers the epilepsy incidence varies about 11 to 131/100 thousand habitants for year and the prevalence between 1.5 to 30/1000 habitants for year, about this statics the higher values are found in developing countries, Latin America and Africa particularly. The Idiopathic Generalized Epilepsy (IGE) are about a third of all others kinds of epilepsies and are 15 to 20% more frequent tha n others types of epilepsies. The absences IGEs are strictly related with childhood and adolescence age group and sometimes can affect patients (2.8 5.7 of cases) with age higher than 15 years old. The physiopathology as the real causes of to occur and to reoccur of absences crises in adult age are not completely enlightened and represent a important challenge to epileptlogists. The IGEs (genetic etiology) are classified in: a) typical absence seizures, b) atypical absence seizures, c) absence seizures with special factors, d) mioclonics seizures, f) tonic mioclonic seizures, g) clone seizures, h) tonic seizures and i) atonic seizures. The treatment commonly is pharmacologic and seizures are controlled in major parts of cases although about a third of patients are refratory to anticonvulsants drugs. Having as principal finality the elucidation of basic mechanisms and help of development of effectiv e therapeutical approaches to these patients, researchers around the world spend many efforts to develop experimental models able to reproduce the phenomena that want to reproduce. Among the principal experimental models of IGEs, it is possible to cite: (1) the general epilepsy model induced by penicillin in cats; (2) the models of investigation of bicuculin; (3) induction by electrical stimulation; (4) Genetic Absence Epilepsy Rats of Strasbourg (GAERS); (5) cepa WAG/Rij; (6) the model of gamma-hydroxybutyric (GHB) and (7) mutant rats. These experimental models have promoted ways to researchers can to evaluate and quantify adequately the neuronal alterations that occur during epileptigenes process both in vitro or in vivo, making possible important advances in development of new therapeutical approaches and improvement in quality of life of epilepsy carriers
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Flores, Juan Antonio Castro. "Amigdalo-hipocampectomia transtemporal, utilizando acesso mínimo (key-hole): avaliação da técnica cirúrgica e dos resultados." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-11012018-091356/.
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Introdução: A esclerose mesial temporal é causa frequente das síndromes epilépticas focais. A ressecação cirúrgica das estruturas mesiais temporais é a melhor opção para seu tratamento. Objetivo: Apresentar uma técnica operatória para tratar a epilepsia temporal e os resultados da intervenção Casuística e Métodos: Estudo prospectivo envolvendo 120 doentes operados por um único neurocirurgião e em uma única instituição de saúde de 2006 a 2012 com a aplicação da técnica de amígdalo-hipocampectomia transtemporal com acesso mínimo (key-hole). Cinquenta e cinco por cento dos doentes era do sexo masculino. A cirurgia foi realizada à direita em 85% dos doentes. Resultados: As primeiras 70 cirurgias duraram, em média, 2,51 horas e as últimas 50 cirurgias 1,62 horas. Ocorreram complicações em 3,3% dos doentes operados. Cinco por cento dos doentes apresentou atrofia discreta do músculo temporal. De acordo com a Escala de Engel, no segundo ano do período pós-operatório, 71% dos doentes foram classificados como Classe I, 21%, como Classe II, e 6%, como Classe III. Conclusão: A técnica descrita é viável, reprodutível, segura e proporciona resultados satisfatóriosIntroduction: Temporal mesial sclerosis is a frequent cause of focal epilepsy. Surgical resection of the mesial temporal structures considered an effective method for its treatment. Objective: To describe a new operative technique for treatment of temporal epilepsy and the results of the procedure. Methods: prospective case-series in a single institution, by the same surgeon, from 2006 to 2012 envolving 120 patients underwent a minimally invasive keyhole transtemporal amygdalohippocampectomy. 55% of the patients were male and the operation was performed at the right side in 85% of them. Results: The first 70 surgeries had a mean surgical time of 2.51 hours, and the last 50 surgeries 1.62 hours. The morbidity rate was 3.3%. Mild temporal muscle atrophy was observed in 5% of the patients. At the second year follow-up 71% of the patients were classified according the Engel Outcome Scale as, Class I, 21%, as Class II and 6% as Class III. Conclusion: This new technique is feasible and reproducible and the clinical results were satisfactory
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Neri, Marina Liberalesso 1980. "Avaliação neuropsicológica de crianças com epilepsia rolândica = funções executivas." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309169.
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Orientadores: Marilisa Mantovani Guerreiro, Catarina Abrão GuimarãesTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A epilepsia benigna da infância com pontas centrotemporais (EBIPCT) ou rolândica (ER) é a forma mais freqüente de epilepsia na infância e é classificada como sendo focal, genética e de evolução benigna. Apesar de não haver déficit intelectual, essas crianças podem apresentar alterações cognitivas específicas. O presente estudo teve como objetivos: identificar e descrever alterações de funções executivas em crianças com ER e verificar a influência de variáveis clínicas da epilepsia nas funções executivas. Os participantes foram submetidos à aplicação de testes de funções executivas. Foram incluídas crianças com diagnóstico clínico e eletroencefalográfico de ER. A maioria dos pacientes estava controlada e muitos deles encontravam-se sem medicação. Os resultados obtidos foram comparados com os de um grupo de crianças de um grupo-controle (GC) constituído de indivíduos normais, com idade e nível sócio-educacional semelhantes ao das crianças com epilepsia. Os dados coletados nos dois grupos foram analisados e comparados através dos testes estatísticos: Mann-Whitney, teste Qui-quadrado e teste Exato de Fisher. Os resultados mostraram que quanto aos dados numéricos crianças com ER obtiveram pior desempenho em cinco das seis categorias consideradas do Wisconsin Card Sorting Test (WCST): nº de erros, nº de erros perseverativos, nº de respostas perseverativas, nº de categorias completadas e nº de fracassos em manter o set. Considerando-se resultados categóricos crianças com ER obtiveram pior desempenho no Trail Making Test (TMT) parte B, no Teste de fluência verbal FAS e em três categorias do WCST: nº de erros, nº de erros perseverativos e nº de respostas perseverativas. Em relação à variável idade de início da epilepsia, crianças com início mais precoce apresentaram pior desempenho em um dos instrumentos utilizados quando comparadas com crianças com início mais tardio da epilepsia; em relação às demais variáveis da epilepsia, não foi possível qualquer tipo de análise; quanto às variáveis das crises, não houve diferença nos resultados obtidos pelos pacientes divididos em grupos. Diante desses resultados concluímos que: as crianças com ER apresentaram déficit em funções executivas quando comparadas com o grupo-controle; a bateria utilizada mostrou-se adequada para detecção das disfunções apresentadas pelas crianças com ER; em relação à variável da epilepsia idade de início, crianças com início mais precoce apresentaram pior desempenho do que crianças com início mais tardio da epilepsia; em relação às demais variáveis da epilepsia e às variáveis das crises, não houve diferença entre os dois grupos. Assim, nosso estudo segue a linha de raciocínio de que o termo benigno deve ser usado com cautela uma vez que nossos pacientes apresentaram déficits neuropsicológicos em funções executivas, independentemente da fase ativa da epilepsia e do uso de medicações
Abstract: The benign childhood epilepsy with centrotemporal spikes (EBIPCT) or rolandic epilepsy (RE) is the most common type of childhood epilepsy and is considered to be a focal, genetic and benign epilepsy. Although there is no intellectual deficit, these children may have specific cognitive impairments. This study aimed: to identify and describe changes in executive functions in children with RE and to verify the influence of clinical variables of epilepsy in executive functions. Participants were evaluated with tests to assess executive functions. We included children with clinical and EEG features of RE. Most patients were controlled and several were without medication. The results were compared with those of a control group (CG) comprised of normal subjects with age and socioeconomic level similar to that of the RE group. The data collected from both groups were analyzed and compared using statistical tests: Mann-Whitney, Chi-square and Fisher exact tests. The results showed that concerning the numerical data, children with RE had the worst performance in five of the six categories of the WCST: number of errors, number of perseverative errors, number of perseverative answers, number of completed categories and number of failures to maintain the set. Considering categorical results, children with RE had worse performance in Trail Making Test part B, Verbal fluency test FAS and three categories of the WCST: number of errors, number of perseverative errors and number of perseverative answers. Concerning the variable age of onset of epilepsy, children with earlier onset of epilepsy had a worse performance in one of the tools when compared with children with later onset of epilepsy; the other variables of epilepsy did not allow any analysis; considering seizure variables, there was no difference between the two groups. We conclude that: children with RE showed deficits in executive functions when compared with the control group; the set of tests was adequate to detect the dysfunctions presented by children with RE; in relation to the variable age of onset of epilepsy, children with earlier onset had a worse performance than children with later onset of epilepsy; concerning other epilepsy and seizure variables, there was no difference between the two groups. Thus, our study is in keeping with the idea that the term benign should be cautiously used since our patients had neuropsychological deficits in executive functions regardless of the active phase of epilepsy and the use of medications
Doutorado
Ciencias Biomedicas
Doutor em Ciências Médicas
Books on the topic "Epilepsis"
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Epilepsia: Enfermedad sagrada del cerebro. México, D.F: Fondo de Cultura Económica, 1999.
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Guberman, Alan. Essentials of clinical epilepsy. 2nd ed. Boston: Butterworth-Heinemann, 1999.
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Illinois. Dept. of Human Rights. An Employers guide to epilepsy. Chicago, Ill: Illinois Dept. of Human Rights, 1989.
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Shorvon, S. D. (Simon D.) and British Medical Association, eds. Understanding epilepsy. Poole: Family Doctor, 2009.
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The educator's guide to students with epilepsy. Springfield, Ill: Charles C. Thomas, 1995.
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Zarrina, Kurtz, ed. Special services for people with epilepsy in the 1970s. London: H.M.S.O., 1987.
Find full textBook chapters on the topic "Epilepsis"
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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Epilepsies: Temporal Lobe Epilepsy." In Imaging Brain Diseases, 1143–56. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_45.
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Ono, Tomonori, and Aristea S. Galanopoulou. "Epilepsy and Epileptic Syndrome." In Advances in Experimental Medicine and Biology, 99–113. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-0653-2_8.
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Cross, J. Helen. "Epilepsy and Epileptic Seizures." In Dietary Treatment of Epilepsy: Practical Implementation of Ketogenic Therapy, 11–18. West Sussex, UK: John Wiley & Sons, Ltd,., 2013. http://dx.doi.org/10.1002/9781118702772.ch2.
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Urbach, Horst, and Jörg Wellmer. "Epileptic Seizures and Epilepsy." In MRI in Epilepsy, 3–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/174_2012_556.
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Muro, Valeria M., and Mary B. Connolly. "Classifying Epileptic Seizures and the Epilepsies." In Epilepsy, 10–14. Oxford: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118456989.ch2.
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Lüders, H. O., and S. Noachtar. "Classification of Epileptic Seizures and Epilepsies." In Textbook of Stereotactic and Functional Neurosurgery, 2561–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-69960-6_152.
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Hakimian, Shahin. "Juvenile Myoclonic Epilepsy and Other Primary Generalized Epilepsies." In Epilepsy, 175–83. Oxford: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118456989.ch24.
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Lekka, Vasia. "Discovering Epilepsy and Epileptics in Victorian London." In Boston Studies in the Philosophy and History of Science, 71–112. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06293-8_4.
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Löscher, W. "Animal Models of Epilepsy and Epileptic Seizures." In Antiepileptic Drugs, 19–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60072-2_2.
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Glynn, Simon M., and John A. Detre. "Imaging Epilepsy and Epileptic Seizures Using fMRI." In fMRI, 177–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-34342-1_14.
Full textConference papers on the topic "Epilepsis"
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Saito, Takashi, Tomomi Ogawa, Takumi Yoshida, Kenyu Uehara, Hiroko Kadowaki, and Koji Mori. "Proposal of Indexes to Support Diagnosis of Epilepsy Symptom Using a Duffing Oscillator." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-70745.
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The misdiagnosis rate of epilepsy is said to keep high from 5% to 30% because of dependency upon an individual judgment by each medical doctor in diagnosis and a quantitative index seems necessary to manage diagnosis uncertainty. To detect some change appearing in brain waves, we focus on introducing a Duffing oscillator model, which could provide reasonably good predictions for the dynamics of neuronal groups. The aim of this paper is to discuss indexes for epilepsy diagnosis by representing characteristics of electroencephalogram (EEG) quantitatively using a Duffing oscillator model. The model parameters are directly identified to adapt the characteristics of the temporal EEG variation to dynamical properties of the model quantitatively. Therefore, in animal experiments, we obtained time histories of the EEG data changed from normal EEG to the epileptic EEG. As a result, it is found that the parameter values related to non-linearity are extremely reduced as the epileptic EEG progresses with time. On the other hand, the input signal strength in epileptic EEG is much bigger than that of normal as expected. Moreover, the directly identified exciting frequency and the eigenfrequency determined by the identified parameter exist in wider band than that of normal as the epileptic EEG progresses with time. The change of the EEG due to epileptic seizure could reflect on the model parameters and it is shown that the model parameters have the possibility to use as supporting index of diagnosis about epilepsy. As a result, the proposed method could be used to support the decline of misdiagnosis rate of epilepsy.
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SHishelova, A. YU, and K. S. Smirnov. "The role of social isolation in critical periods of early postnatal ontogenesis in the formation of epileptic activity of the brain and learning ability in adulthood." In Global science. Development and novelty. L-Journal, 2020. http://dx.doi.org/10.18411/gsdn-25-12-2020-03.
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The effect of complete social isolation in the critical periods of early postnatal ontogenesis on the learning and epileptic activity in Wag/Rij rats with a genetic predisposition to the absence epilepsy was studied. The different learning tasks with positive reinforcement (the Intellicage test) and punishment (the two-way active avoidance in the “shuttle box”) were used. It was found that a 3-hour daily social isolation of rat pups from the mother and siblings in early postnatal ontogenesis changes the learning ability and its connection with epileptic activity in adulthood depending on the period of isolation. The isolation from 2th to 8th postnatal day led to a decrease of epileptic activity and improved the learning with positive reinforcement in adult rats. The isolation from 9th to 15th postnatal day improved the learning a conditioned avoidance response with punishment and induced the interrelations between epileptic activity and the active avoidance learning. The isolation from 16th to 22th postnatal – 14 – Global science. Development and novelty day led to an improvement of positive reward-related learning and formation of the significant interactions between epileptic activity and the learning with positive and negative reinforcement.
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Uehara, Kenyu, and Takashi Saito. "Dependency ECoG Band Spectrum in Epileptic Discharges Upon Local Cooling Rate on Brain." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-72158.
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Focal brain cooling has recently drawn attention as a less-invasive treatment for intractable epileptic patients. The objective of this study is to investigate the dependence of brain cooling rate on epileptic discharges (EDs) suppression with experiments using four epilepsy model rat. EDs were induced by Penicillin G in anesthetized rat, and cooled to 16 °C under four different time conditions (30, 60, 100 and 200 second, respectively). The ECoG obtained from the experiments were sorted into frequency band components which have physiological significance. The results of frequency analyses confirmed that the suppression of EDs have a cooling rate dependency, and power of four frequency bands (delta, theta, alpha and beta waves) in EDs are smaller when the cooling rate is slower. Our results suggested that slower cooling on brain surface can effectively suppress EDs and rapid brain cooling is not necessarily the best way. This finding implied that there are optimum cooling condition depending on the degree of EDs or epileptic symptoms.
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Lara, Jéssica Naiara, Juliana Pereira Cardoso, Camila Raianna Justiniana Rocha, and Samyra Giarola Cecílio. "A INFLUÊNCIA DA BAIXA CONCENTRAÇÃO DE MAGNÉSIO EM DISTÚRBIOS NEUROLÓGICOS COMO A EPILEPSIA E ENXAQUECA." In II Congresso Brasileiro de Ciências Biológicas On-line. Revista Multidisciplinar Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1663.
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Introdução: O magnésio (Mg2+) é considerado o quarto cátion mais abundante em todo o corpo e o segundo cátion mais abundante na célula. Os íons Mg2+ são importantes para vários processos fisiológicos e são críticos para a regulação de diversas funções celulares, como ciclos metabólicos, vias de sinalização, controle de canais iônicos e outros. Dessa forma é indispensável uma boa regulação dos níveis Mg2+, contudo, na literatura, descrições mostram que a deficiência desse íon pode promover distúrbios neurológicos, como epilepsia e enxaqueca, que possuem o mesmo substrato neurobiológico. Objetivo: A proposta do presente estudo consistiu em uma revisão da literatura sobre a possível influência do magnésio na epilepsia e enxaqueca. Material e métodos: Foi realizado levantamento bibliográfico do período de 1970 a 2020 e foram utilizadas as palavras-chave “magnesium”, “migraine” e “epilepsy”. Resultados: De fato, alguns trabalhos mostram que a deficiência de Mg2+ está relacionada a epilepsia e a enxaqueca. As crises epilépticas podem ser uma manifestação da depleção de Mg2+, e alguns autores afirmam que após observações clínicas em humanos e o desenvolvimento de experimentos em animais, a redução do Mg2+ parece estar associada aos eventos epileptiformes. Outros autores notaram que a ausência de Mg2+, eventualmente, resulta em crises convulsivas em humanos e em tecido animal, promove atividades epileptiformes e a indução de ondas de depressão alastrante após estimulação repetitiva. Em pacientes com enxaqueca hemiplégica, foram coletadas amostras do líquor e, após análise, foi demonstrada uma redução significativa de Mg2+. Alguns autores demonstram que a administração de Mg2+ por via intravenosa se mostrou um medicamento eficiente, seguro e bem tolerado no tratamento de crises de enxaqueca. Além disso, trabalhos recentes afirmam que a enxaqueca se manifesta quando há uma redução de Mg2+ no líquido cefalorraquidiano e que esse cátion tem sido utilizado, com grande sucesso, na profilaxia e tratamento da enxaqueca. Conclusão: Nota-se que a deficiência de magnésio parece desempenhar um papel importante na fisiopatologia da enxaqueca e da epilepsia, portanto, mais estudos investigando sua influência nesses distúrbios neurológicos são necessários.
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Pereira, João Guilherme, Matheus de Freitas Oliveira Baffa, Fabrício Henrique Simozo, Luiz Otavio Murta Junior, and Joaquim Cezar Felipe. "On The Use of Machine Learning Algorithms to Classify Focal Cortical Dysplasia on MRI." In Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2021. http://dx.doi.org/10.5753/sbcas.2021.16063.
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Refractory epilepsy is a condition characterized by epileptic seizure occurrence which cannot be controlled with antiepileptic drugs. This condition is associated with an excessive neuronal discharge produced by a group of neurons in a certain epileptogenic zone. Focal Cortical Dysplasia (FCD), usually found in these zones, was detected as one of the main causes of refractory epilepsy. In these cases, surgical intervention is necessary to minimize or eliminate the seizure occurrences. However, surgical treatment is only indicated in cases where there is complete certainty of the FCD. In order to assist neurosurgeons to detect precisely these regions, this paper aims to develop a classification method to detect FCD on MRI based on morphological and textural features from a voxel-level perspective. Multiple classifiers were tested throughout the extracted features, the best results achieved an accuracy of 91.76% using a Deep Neural Network classifier and 96.15% with J48 Decision Tree. The set of evaluating metrics showed that the results are promising.
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Gao, Jianbo, and Jing Hu. "Fast Monitoring of Epileptic Seizures Based on Recurrence Time Analysis of EEGs." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6082.
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Epilepsy is one of the most common disorders of the brain. Currently, studies of epileptic seizures often involve tedious and time-consuming visual inspection of multi-channel long EEG data by medical experts. To better monitor seizures and make medications more effective, we propose a recurrence time based approach to characterize brain electrical activity. Unlike many other nonlinear methods, the proposed approach does not require that the EEG data be chaotic and/or stationary. It only contains a few parameters that are largely signal-independent, and hence, is very easy to use. The method detects epileptic seizures with accuracy close to 100% (when subclinical seizures are not counted) and false alarm rate per hour close to 0. Most critically, the method is very fast: with an ordinary PC (CPU speed less than 2 GHz), computation of the recurrence time from one channel EEG data of duration one hour with sampling frequency of 200 Hz takes about 1 minute CPU time. Therefore, with an ordinary PC, the method is able to process all 28 channels of 1-hour EEG data in about half an hour, and thus faster than the data being continuously collected. The method can also effectively monitor propagation of seizures in the brain. Therefore, it has the potential to be an excellent candidate for real-time monitoring of epileptic seizures in a clinical setting.
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Kutlu, F., and C. Kose. "Epileptic seizure detection from ECoG signals acquired with experimental epilepsy." In 2013 21st Signal Processing and Communications Applications Conference (SIU). IEEE, 2013. http://dx.doi.org/10.1109/siu.2013.6531296.
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Yucel, Zeynep, and A. Bulent Ozguler. "Detection of epilepsy seizures and epileptic indicators in EEG signals." In 2008 IEEE 16th Signal Processing, Communication and Applications Conference (SIU). IEEE, 2008. http://dx.doi.org/10.1109/siu.2008.4632759.
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Burns, Samuel P., Sabato Santaniello, William S. Anderson, and Sridevi V. Sarma. "State Dynamics of the Epileptic Brain." In ASME 2013 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/dscc2013-3708.
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Communication between specialized regions of the brain is a dynamic process allowing for different connections to accomplish different tasks. While the content of interregional communication is complex, the pattern of connectivity (i.e., which regions communicate) may lie in a lower dimensional state-space. In epilepsy, seizures elicit changes in connectivity, whose patterns shed insight into the nature of seizures and the seizure focus. We investigated connectivity in 3 patients by applying network-based analysis on multi-day subdural electrocorticographic recordings (ECoG). We found that (i) the network connectivity defines a finite set of brain states, (ii) seizures are characterized by a consistent progression of states, and (iii) the focus is isolated from surrounding regions at the seizure onset and becomes most connected in the network towards seizure termination. Our results suggest that a finite-dimensional state-space model may characterize the dynamics of the epileptic brain, and may ultimately be used to localize seizure foci.
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Chen, Yue, Megan E. Poorman, David B. Comber, E. Bryn Pitt, Cindy Liu, Isuru S. Godage, Hong Yu, William A. Grissom, Eric J. Barth, and Robert J. Webster. "Treating Epilepsy via Thermal Ablation: Initial Experiments With an MRI-Guided Concentric Tube Robot." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3408.
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Epilepsy is a prevalent neurological disorder affecting 65 million people globally [1]. Anti-epileptic medications fail to provide effective seizure control for 30% of patients, placing them at a 7–17% risk of Sudden Unexplained Death in Epilepsy and recurrent seizures. Surgical resection of the seizure focus is a potentially curative treatment for patients with seizures that electrophysiologically correlate to a focal lesion. For these patients, focal surgical resection can result in 60–70% seizure-freedom rates [2]. However, open resection carries the risk of cognitive impairment or focal neurologic deficit [3]. Recent innovations in MRI enable high resolution soft tissue visualization, and real-time temperature monitoring, making MR-guided ablation therapy a promising minimally invasive technique to restrict the tissue destruction to just the seizure focus. Commercial products (e.g., Visualase, Medtronic Inc.; ClearPoint, MRI Interventions Inc.; NeuroBlate, Monteris Inc.) have recently been introduced for MR-guided laser-based thermal ablation. These products require the physician drill a hole into the skull for ablation probe placement, and may not always be able to ablate the entire seizure focus when the structure has a curved shape (such as the hippocampus) [4]. Incomplete ablation of the seizure focus would lead to seizure recurrence. We have recently proposed concentric-tube steerable needles as a means to address these challenges [4–7]. They enable nonlinear trajectories and offer the potential to enter the brain through the patient’s cheek via a natural opening in the skull base (i.e. the foramen ovale). We have designed and fabricated an MR-compatible robotic system to provide high resolution actuation for helical needle deployment [5]. We have shown in simulation that the curved medial axis of hippocampus can be accessed via a helical needle that delivers the ablation probe into the brain [4]. These preliminary results suggest that MR-guided robotic transforamenal thermal therapy could potentially provide a less invasive approach for potentially curative epilepsy treatment. In this paper we present our first results delivering heat along curved paths in brain phantoms and imaging the resulting treatment zones using MRI.
Reports on the topic "Epilepsis"
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Stefanova, Irina, Rumyana Kuzmanova, Sevda Naydenska, and Katerina Stambolieva. Character of Epileptic Seizures and Electroencephalographic Changes in Patients with Epilepsy and Comorbid Diseases. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, July 2018. http://dx.doi.org/10.7546/crabs.2018.07.16.
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Carretón, María Carmen, and Ángeles Feliu Alabaladejo. El tratamiento de la epilepsia en la agenda de los medios para una comunicación afirmativa. The treatment of epilepsy in the media agenda to an affirmative communication. Revista Internacional de Relaciones Públicas, December 2011. http://dx.doi.org/10.5783/rirp-2-2011-13-237-261.
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Jiang, Huabei. Photoacoustic Imaging of Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada587641.
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Jiang, Huabei. Photoacoustic Imaging of Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada549242.
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Jiang, Huabei. Photoacoustic Imaging of Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada607157.
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Lin, Ching-Yi. Magnetic Stimulation and Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada611602.
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Jiang, Huabei. Photoacoustic Imaging of Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada613888.
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Jiang, Huabei. Photoacoustic Imaging of Epilepsy. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada576914.
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Carreton-Ballester, María Carmen, and Francisco Lorenzo-Sola. Niveles de responsabilidad de los medios en sus relaciones con las minorías. Epilepsia y autismo/Levels of responsibility of the media in their relations with minorities. Epilepsy and autismo. Revista Internacional de Relaciones Públicas, June 2018. http://dx.doi.org/10.5783/rirp-15-2018-12-215-236.
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Ugarnes, Gabriela. Actualización en el Diagnóstico y Tratamiento de la Epilepsia. Buenos Aires: siicsalud.com, February 2017. http://dx.doi.org/10.21840/siic/154124.
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