Dissertations / Theses on the topic 'Migraine with aura'
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Di, Domenico Chiara. "A mathematical model for migraine aura." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amslaurea.unibo.it/12350/.
Full textMayer, Lisa, and Lisa Mayer. "Molecular Mechanisms in Pathophysiology of Migraine Aura." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625087.
Full textMenon, Saraswathy. "Migraine Molecular Genetic and Pharmacogenetic Studies." Thesis, Griffith University, 2011. http://hdl.handle.net/10072/365218.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Gasparini, Claudia Francesca. "Identification of Migraine Susceptibility Genes: Candidate Gene Studies." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/367879.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Science, Environment, Engineering and Technology
Full Text
GUERMONPREZ, PASCAL. "Possibilites de traitement homeopathique des migraines avec aura." Lille 2, 1990. http://www.theses.fr/1990LIL2M064.
Full textRoos-Araujo, Deidré. "Investigation of Xq chromosomal variation in relation to migraine." Thesis, Queensland University of Technology, 2019. https://eprints.qut.edu.au/128579/1/__qut.edu.au_Documents_StaffHome_StaffGroupH%24_halla_Desktop_Deidr%C3%A9%20Roos-Araujo%20Thesis.pdf.
Full textMaher, Bridget Helen. "Identification of X-Linked Genes in Migraine: Fine Mapping and Candidate Gene Studies." Thesis, Griffith University, 2012. http://hdl.handle.net/10072/367770.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Curtain, Robert, and n/a. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p." Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070810.132610.
Full textCurtain, Robert. "Candidate Gene Analysis of Migraine Susceptibility Regions on Chromosome 1q and 19p." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365960.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Sandweiss, Alexander J., Karissa E. Cottier, Mary I. McIntosh, Gregory Dussor, Thomas P. Davis, Todd W. Vanderah, and Tally M. Largent-Milnes. "17-β-Estradiol induces spreading depression and pain behavior in alert female rats." IMPACT JOURNALS LLC, 2017. http://hdl.handle.net/10150/627061.
Full textKallela, Mikko. "Clinical characteristics and pathophysiological mechanisms of familial migraine with and without aura." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kallela/.
Full textDhifallah, Sandra. "Étude fonctionnelle de mutations des canaux sodiques potentiel-dépendants Nav1.1 et Nav1.2 : corrélation phénotype/génotype et mise en évidence d’un mécanisme spécifique pour les troubles du spectre de l’autisme." Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://www.theses.fr/2020COAZ6004.
Full textThe genes encoding for the voltage-gated sodium channels (Nav) expressed in the central nervous system are the target of numerous mutations leading to various phenotypes. The aim of my work is to understand why mutations in the same gene can lead to distinct pathologies in order to consider the development of new therapeutic approaches. The SCN1A gene encoding for the Nav1.1 channels, mainly expressed in GABAergic interneurons (GABA IN), is the target of mutations responsible for epileptic syndromes and familial hemiplegic migraine (FHM-3), a rare form of migraine with aura. The mutations responsible for epilepsy have been shown to cause a loss of function, which leads to hypoexcitability of GABA IN and subsequently to the network hyperexcitability. At the opposite, the mutations responsible for MHF-3 showed a gain of function and hyperexcitability of GABA IN which can lead to the cortical spreading depression, a pathological mechanism of migarine. In particular, the functional study of the L1649Q mutation showed that the mutation leads to an important decrease of the current density (loss of function). Analysis of the biophysical properties of the mutated channels after partial recovery of the current density showed that the overall effect of the mutation is a gain of function, consistent with an hyperexcitability of GABA IN (Cestele and al. 2013 PNAS). In order to identify if other FHM-3 mutations share the same mechanism (loss / gain of function), the first part of my thesis aimed to characterize a new mutation responsible for MHF-3, L1670W. This mutation leads to a defect in the Nav1.1 channels expression at the membrane but after partial recovery of the current density, the mutation induces a clear gain of function of Nav1.1 channels. These results showed that the L1670W mutation, like the L1649Q mutation, leads to a defect in the Nav1.1 channels expression at the membrane and a gain in function, thus reinforcing the hypothesis that this mechanism could be generalized to other mutations responsible for MHF-3. The SCN2A gene encodes for the α subunit of Nav1.2 channels mainly expressed in excitatory neurons. Mutations in the SCN2A gene are responsible for different pathologies such as benign epilepsies, epileptic encephalopathies and autism spectrum disorder (ASD). To date, the detailed mechanisms responsible for these different pathologies remain unclear. In order to elucidate the genotype/phenotype relationship, we studied the functional effects of 23 SCN2A mutants responsible for these different pathologies. Our results show that all the mutations responsible for ASD induce an important decrease (almost complete) of the current density while for the other pathologies the effects are heterogeneous. In order to reproduce the heterozygous conditions, we studied the co-expression of wild-type (WT) channels with each mutated channel. Our results showed a reduction in the WT channels current density only in the presence of channels carrying mutations responsible for ASD. Consequently, only the mutations responsible for ASD induce a negative dominance on WT channels. To determine whether this negative dominance mechanism is due to the interaction of α subunits described recently (Clatot et al., 2018 Nat Commun), we used different strategies to inhibit this interaction. The results obtained showed that the negative dominance effect of the mutants responsible for ASD is no longer observed when the interaction between the α subunits is inhibited. Therefore, our results allow us to describe for the first time that mutations in Na+ channels responsible for ASD act by a negative dominance mechanism, which is mediated by the interaction between WT and mutated channels
Zerimech, Sarah. "Dépression Corticale Envahissante : nouveau mécanisme d'initiation par hyperactivité des neurones GABAergiques, et stratégie pharmacologique pour la réduire." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR4032.
Full textCortical Spreading Depression is a wave of neuronal depolarization that spread slowly across cerebral cortex. It generates a rapid phase of neuronal hyperactivity, followed by a slower phase of electrical silence of cortical cells. It is possible to experimentally induce CSD on several animal models, in vivo or on neocortical slices, by focal application of Glutamate, Acetylcholine or highly concentrated KCl solution, or by electrical stimulation.CSD is widely studied as the pathophysiological mechanism of migraine with aura, but also ischemia. Studies of experimental CSD have shown involvement of numerous biological substances in the wave generation and propagation, including Potassium, Calcium, Glutamate, and other neurotransmitters. The pharmacological approach allows to identify actors of this electrical phenomenon: voltage gated channel, ionotropic glutamate receptors (NMDA & AMPRA-kainate), astrocytes and Na-K pumps.Familial Hemiplegic Migraine is a monogenic form of migraine with aura; the migraine attack is associated with variable motor disorders. Genetic mutations have been described leading to molecular dysfunctions. Nowadays three main forms of this pathology caused by three mutated genes, have been described and studied. FHM type 1 (Cav2.1 gain of function) and FH% type 2 (NaK ATPase pump loss of function) mouse models studies confirmed the important involvement of Glutamate and Potassium in CSD initiation.Type 3 of FHM is caused by Nav1.1 mutations, a voltage gated sodium channel that is widely expressed in GABAergic neurons in which they are essential for excitability. Our team showed on transfected neurons in culture that he mutation is a gain of function, leading to an increased neuronal excitability. However, the link between the mutation, cortical hyperexcitability and CSD facilitation or FHM phenotype, remains unknown.Our work hypothesis and the base of my research project, is that the increasing Nav1.1 channel or GABAergic neurons’ activity, triggers a cortical hyperexcitability and CSD. To confirm this hypothesis, my work required a ex vivo experimental approach, on acute neocortical slices of wild-type and transgenic mice, associated with extracellular electrophysiology, IOS imaging, pharmacology and/or optogenetics. Nav1.1 channel activation by a selective activator (spider toxin), or GABAergic neurons stimulation by optogenetics, can trigger CSD, validating our initial hypothesis and identify a new model of CSD.My work allow us to highlight and characterised a new model of CSD by GABAergic neuron hyperexcitability leading to an initial build up of extracellular potassium, that depolarizes and activates more and more excitatory neurons. This leads to a sustained potassium release until a critical threshold of CSD triggering.In a second time, my thesis work explored a pharmacologic modulation of network excitability, to find new elements that could decrease the CSD susceptibility. To do so, with the same experimental approach, I used a cholinergic agonist, Carbachol, known for modulation the network activity. The results showed that even if Carbachol increases network excitability, it inhibits CSD induction, likely through the muscarinic pathway.In conclusion, during my thesis I identified a new mechanism of CSD induction, and a une inhibitory pathway of CSD by cholinergic modulation
Ducros, Anne. "Migraine hémiplégique familiale : localisation d'un second gène sur le chromosome 1 et analyse des corrélations génotype-phénotype au sein de 21 familles." Montpellier 1, 1997. http://www.theses.fr/1997MON11118.
Full textReuter, Uwe. "Pathomechanismen der Migräne." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/13911.
Full textThe pathophysiological events which initiate a migraine attack are largely unknown. Cortical spreading depression (CSD) is supposed to be the pathophysiological correlate of the migraine aura. CSD is able to activate the ipsilateral trigeminal nerve system thereby leading to a series of events within meninges consistent with the notion of headache. In particular, CSD leads to a delayed increase of meningeal blood flow and the extravasation of plasma proteins. In an experimental animal model the infusion of glyceryl trinitrate causes delayed meningeal inflammation. The latter serves as the correlate of delayed migraine attacks after glyceryl trinitrate infusion in susceptible individuals. Protracted administration of sumatriptan and zolmitritpan does not alter the outcome in functional assays that are used to determine the efficacy of triptans. Moreover, the expression of serotonin (5-HT1) receptor mRNA is not significantly attenuated in tissues related to migraine pathophysiology. In summary, these studies shed light on the mechanism leading to migraine headache and thereby identify novel targets for the development of new anti-migraine drugs.
DâAlmeida, Josà Artur Costa. "Estudo da AÃÃo da Toxina BotulÃnica do tipo âAâ na profilaxia da MigrÃnea Sem Aura." Universidade Federal do CearÃ, 2004. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=283.
Full textEstuda atravÃs de ensaio duplo cego, controlado, randomizado o efeito da Toxina BotulÃnica do tipo A na profilaxia de crises de migrÃnea sem aura. A migrÃnea à um tipo comum de cefalÃia primÃria, benigna, episÃdica, e recorrente que se caracteriza por dor geralmente hemicrÃnica e pulsÃtil, e que à agravada pela atividade fÃsica. Existem outros sintomas associados como nÃuseas, fotofobia, fonofobia, ou irritabilidade. Na migrÃnea com aura podem tambÃm ocorrer alteraÃÃes neurolÃgicas motoras, sensitivas, ou visuais denominadas de aura. A migrÃnea, cuja fisiopatologia ainda nÃo à perfeitamente compreendida, seria o resultado de um processo patolÃgico complexo que envolveria o tronco cerebral e levaria à inflamaÃÃo local de vasos sangÃÃneos cranianos atravÃs da liberaÃÃo de neuropeptÃdeos vasoativos como SubstÃncia P (SP), Neurocinina A (NA), e PeptÃdio Relacionado ao Gene da Calcitonina (PRGC). Apesar das vÃrias opÃÃes terapÃuticas (analgÃsicos simples, antiinflamatÃrios hormonais e nÃo hormonais, triptanos, antipsicÃticos, derivados ergotamÃnicos, e opiÃides) para tratamento da crise ou para tratamento preventivo, somente cerca de um terÃo dos pacientes fica satisfeito com o tratamento. Foi observado que pacientes utilizando toxina botulÃnica para tratamento estÃtico de rugas da face ou distonias apresentavam uma reduÃÃo na quantidade de crises de migrÃnea. A toxina botulÃnica à uma potente neurotoxina produzida pela bactÃria Clostridium botulinum. A aÃÃo da toxina à impedir a liberaÃÃo de acetilcolina nos terminais nervosos. Ela tambÃm age inibindo a liberaÃÃo de neuropeptÃdeos vasoativos. O uso da toxina botulÃnica nos faria agir exatamente no cerne do processo fisiopatolÃgico da doenÃa. Com o objetivo de testar esse possÃvel efeito analgÃsico nos pacientes portadores de migrÃnea sem aura, realizou-se um estudo duplo-cego, controlado, e randomizado. Mediu-se o nÃvel de dor atravÃs de escalas para quantificar a intensidade e o nÃmero de dias com dor na semana antes e apÃs a injeÃÃo de Toxina BotulÃnica em mÃsculos da face. O grupo controle recebeu SF como placebo. Os pacientes foram seguidos durante trÃs meses. Ao final concluiu-se que nÃo houve diferenÃa estatÃstica na intensidade nem na freqÃÃncia da dor de cabeÃa nos pacientes que usaram a toxina botulÃnica em relaÃÃo aos que usaram placebo (SF)
A randomized, double-blind, placebo-controlled study of the use of botulinum toxin type A in the prophylactic treatment of Migraine is presented. Migraine is a common type of primary, benign, episodic headache. It is characterized by pain usually unilateral and throbbing. Other associated symptoms are nausea, sensitivity to light and sound, or irritability. The pain is usually worsened by physical activity. There are also motor, sensitive, or visual neurological alterations, denominated aura. The physiopathology of migraine is not still perfectly understood but it could involve liberation of vasoactive neuropeptides as Substance P, Neurokinine A, and Calcitonin gene-related peptide, promoting an inflammation. Migraine, then, would be the result of a complex process that would involve the brainstem and induce local inflammation of cranial blood vessels. In spite of the therapeutic options (analgesics, steroidal and non-steroidal anti-inflammatory, triptans, neuroleptics, ergot derivatives, and opioids) only about one third of patients is satisfied with the treatment. The preventive treatment is appropriate for those that have frequent crises. It was observed that the patients using botulinum toxin for aesthetic treatment of wrinkles of the face, or dystonia presented a reduction in the amount of migraine crises. The botulinum toxin is a potent neurotoxin produced by the bacterium Clostridium botulinum. The action of the toxin is to inhibit the acetylcholin liberation from the nerve terminal. It acts also inhibiting the liberation of vasoactive neuropeptides. Therefore, Botulinum Toxin would act exactly in the core of the physiopathologic process of the disease. With the objective of testing possible analgesic effects of botulinum toxin in migraine without aura bearers, we performed a double-blind, controlled, and randomized study. The pain level was measured by scales and by the amount, and number of days of pain in a week, before and after botulinum toxinâs injection in muscles of the face. The placebo group received saline injection. The patients were followed for three months. At the end it was concluded that there was not statistic difference in intensity nor in frequency of the headache of the patients that used botulinum toxin in relation to the people that used placebo (saline)
Galdino, Gilma Serra. "MIGRÂNEAS E CEFALÉIA DO TIPO TENSIONAL CRÔNICA: ABORDAGEM DIAGNÓSTICA POR MÉDICOS NÃO-NEUROLOGISTAS." Universidade Estadual da Paraíba, 2006. http://tede.bc.uepb.edu.br/tede/jspui/handle/tede/1787.
Full textDoctors belonging to a Medical Services Cooperative in Campina Grande were interviewed with the objective to determine their diagnostic accuracy when faced with clinical cases of primary headache, and also to appreciate the amplitude of their knowledge about headache classification and procedures concerning exams prescriptions and therapeutic indications. Methodology. The method of extensive direct observation through the application of a questionnaire was used. The doctors were presented with three fictitious clinical histories which represented situations of frequent primary migraines such as: migraine with aura (MA), migraine without aura (MO) and chronic tensional-type headache (CTTH) according to criteria established on International Headache Classification, second edition (IHCD-II), 2003, by the Headache Classification Subcommittee as part of the International Headache Society (IHS). 173 out of 462 doctors members of the Cooperative were contacted and 91 of these accepted to take part in the study. Results. In the group of 91 doctors interviewed, 51 (56%) were male, 35 (38,5%) were female and five (5,5%) refused to answer. Their age varied from 27 to 70 years old (44,8 + 09 years old). Their experience as doctors varied from three to 46 years (21,4 + 8,2 years). 67 (73.6%) stated to have been in a medical internship. The doctors interviewed were doctors of several areas. About the accuracy of the diagnostic test, concerning MO, 60 participants (66%) identified the case as migraine, only two (2,2%) identified the MO subtype and two (2,2%) suggested it was a case of mere headache. For the clinical case of MA, 25 doctors (27,5%) said it was a case of migraine and only one (1,1%) identified it as MA. About the diagnostic of CTTH, 12 doctors (13,2%) acknowledged it as tensional headache and there was not any reference to the CTTH subgroup. Among other possibilities of diagnostic, the most mentioned ones were migraine 36 (39,6%), secondary headache to systemic arterial hypertension 12 (13,2%) and headaches caused by brain expansive process 06 (6,6%). For the three clinical cases, most of the doctors researched 79 (86,8%) in the example of MO, 74 (81,3%) in the cases of MA and 71 (78%) in the example of CTTH wouldn´t prescribe complementary exams. Regarding treatment 77 (84,6%) in the case of MO, 80 (87,9%) in the case of MA and 67 (73,6%) in the case of CTTH decided not to treat it. Among those who forwarded the case to a neurologist, we have 67 (73,6%) for MO, 78 (85,7%) for MA and 59 (64,8%) for CTTH. 65 (71,4%) doctors who were interviewed said to be unaware of the IHS diagnostic criteria for primary headaches. Conclusion. Migraine was the most common initial diagnosis for any kind of headache without any identification of the subgroups. The CTTH was subdiagnosed being frequently misidentified as migraine cases despite it is the most prevailing kind of primary headache. Most of the doctors interviewed (p<0,05) does not prescribe complementary exams for headache patients and prefer to forward them to a specialist, choosing not to treat them. These results show the lack of information found in the doctors interviewed about the diagnostic criteria for the several kinds of primary headaches.
Foram entrevistados médicos pertencentes a uma Cooperativa de Serviços Médicos, na cidade de Campina Grande, com o objetivo de investigar a acurácia diagnóstica desses profissionais frente a casos clínicos de cefaléia primária, além de apreciar seus conhecimentos sobre a classificação das cefaléias e condutas quanto à solicitação de exames e indicações terapêuticas. Metodologia: Utilizou-se o método de observação direta extensiva através da aplicação de questionário. Foram apresentadas a todos os médicos entrevistados três histórias clínicas, fictícias, reproduzindo quadros de cefaléias primárias freqüentes, a saber: migrânea com aura (MCA), migrânea sem aura (MSA) e cefaléia do tipo tensional crônica (CTTC), seguindo os critérios da Classificação Internacional das Cefaléias, 2ª. Edição (IHCD-II), em 2003, elaborados pelo Subcomitê de Classificação das Cefaléias da Sociedade Internacional de Cefaléia (IHS). Foram contatados 173 médicos, de um total de 462 cooperados, dos quais 91 aceitaram participar do estudo. Resultados: Eles eram 51 homens (56%) e 35 mulheres (38,5%), cinco (5,5%) não identificaram o gênero. A idade variou entre 27 e 70 anos (44,8 + 09 anos). Eles tinham entre três e 46 anos de formados (21,4 + 8,2 anos). 67 (73,6%) afirmaram ter feito residência médica. Os médicos entrevistados atuavam nas mais diversas especialidades. Em relação ao índice de acerto diagnóstico, no exemplo de MSA, 60 participantes (66,2%) identificaram o quadro como migrânea, enquanto apenas dois (2,2%) identificaram o subtipo MSA e dois (2,2 %) sugeriram tratar-se apenas de cefaléia. No caso clínico de MCA, 25 (27,5%) disseram tratar-se de quadro de migrânea e apenas um (1,1%) respondeu ser MCA. Quanto ao diagnóstico de CTTC, 12 (13,2%) reconheceram tratar-se de cefaléia tensional, não houve acerto diagnóstico no subgrupo CTTC, e dentre outras possibilidades diagnósticas as mais citadas foram: migrânea 36 (39.6%), cefaléia secundária a hipertensão arterial sistêmica 12 (13,2%) e cefaléias ocasionadas por processo expansivo cerebral seis (6,6%). Nos três casos clínicos, a maior parte dos profissionais pesquisados 79 (86,8%) no exemplo de MSA, 74 (81,3%) nos casos de MCA e 71 (78%) no exemplo de CTTC - não solicitaria exames complementares. Quanto ao tratamento: 77 médicos (84,6%) no caso de MSA, 80 (87,9%) no caso de MCA e 67 (73,6%) no caso de CTTC, optaram por não tratar. Preferiram encaminhar ao neurologista: 67 médicos (73,6%) para MSA, 78 (85,7%) para MCA e 59 (64,8%) para CTTC. 65 (71,4%) dos entrevistados afirmaram desconhecer os critérios diagnósticos da IHS para cefaléias primárias. Conclusão: O diagnóstico inicial mais freqüente foi migrânea, comumente usado para identificar qualquer tipo de cefaléia, sem, contudo identificar seus subgrupos. A cefaléia do tipo tensional foi subdiagnosticada, freqüentemente sendo confundida com quadros de migrânea, a despeito de ser o tipo mais prevalente de cefaléia primária. A maioria (p<0,05) dos médicos não solicita exames complementares para portadores de cefaléia e prefere encaminhá-los ao especialista, optando por não tratar. Esses resultados demonstram a falta de informações por parte dos médicos entrevistados sobre os critérios diagnósticos para os diversos tipos de cefaléias primárias.
Mansur, Thiago de Oliveira Santos 1981. "Estudo da associação de polimorfismos genéticos da sintase induzida do óxido nítrico (inos) com migrânea : Inducible nitric oxide synthase haplotype associated with migraine and aura." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313604.
Full textTexto em Português e Inglês
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-21T01:17:42Z (GMT). No. of bitstreams: 1 Mansur_ThiagodeOliveiraSantos_M.pdf: 2436576 bytes, checksum: 758101c18ea505521a064b2102236380 (MD5) Previous issue date: 2012
Resumo: A migrânea é uma cefaléia primária episódica com incidência mundial de 10% e alto impacto socioeconômico, afetando predominantemente as mulheres. Em 30% dos casos, as crises de migrânea são acompanhadas por sintomas neurológicos focais que caracterizam o fenômeno da aura. A fisiopatologia da migrânea continua sob investigação. Todavia, acredita-se tratar de um distúrbio neurovascular no qual a ativação de fibras aferentes do sistema trigeminovascular (TGVS) e a consequente liberação de óxido nítrico (NO) levariam à vasodilatação e neurotransmissão da dor durante a crise de migrânea. A formação de NO é atribuída à atividade de três isoformas de NO sintases (NOS): endotelial, neuronal e induzível, respectivamente eNOS, nNOS e iNOS e os genes que codificam tais enzimas exibem polimorfismos. Dessa forma, acredita-se que tais polimorfismos poderiam estar envolvidos na susceptibilidade à migrânea. No presente trabalho foi testada a hipótese de que dois polimorfismos clinicamente importantes no gene da iNOS: C-1026A (rs2779249) e G2087A (rs2297518) bem como a combinação de seus alelos em haplótipos estariam associados com a susceptibilidade à migrânea com e sem aura. Para tanto, foram estudadas 142 mulheres saudáveis (grupo controle) e 200 mulheres com migrânea, subdivididas em dois grupos: 148 pacientes com migrânea sem aura e 52 pacientes com migrânea com aura. Os genótipos e alelos foram determinados por PCR em tempo real utilizando o ensaio Taqman®. Os haplótipos foram inferidos através do programa PHASE versão 2.1. Os principais resultados do presente estudo indicam que o haplótipo H4, que combina o alelo A para os polimorfismos mencionados, pode estar associado à migrânea com aura enquanto o polimorfismo G2087A e o haplótipo H4 podem afetar a suscetibilidade à aura em pacientes com migrânea. Tais achados podem ter implicações terapêuticas ao se analisar os efeitos de possíveis inibidores seletivos da iNOS na população com esse perfil genotípico
Abstract: Migraine is an episodic primary headache with worldwide incidence of 10% and high socioeconomic impact affecting mainly women. In 30% of cases, migraine attacks are followed by focal neurological symptoms that characterize the aura phenomenon. The migraine pathophysiology continues under investigation, although it is believed to consist of a neurovascular disorder in which the activation of afferent fibers of the trigeminovascular system (TGVS), leads to an nitric oxide (NO) release which, would be responsible for vasodilation and pain during migraine attacks. The formation of NO is attributed to the activity of three isoforms of NO synthases (NOS): endothelial (eNOS), neuronal (nNOS) and inducible (iNOS), and the genes that codify these enzymes exhibit polymorphisms. Thus, it is believed that these polymorphisms could be involved in the susceptibility to migraine. In this study, we tested the hypothesis that two clinically important iNOS gene polymorphisms: C-1026A (rs2779249) and G2087A (rs2297518), as well as the combination of their alleles in haplotypes, would be associated with migraine with or without aura. Therefore, we studied 142 healthy women (control group) and 200 women with migraine, who were subdivided into two groups: 148 with migraine without aura and 52 with migraine with aura. Genotypes and alleles were determined by real-time PCR, using the Taqman® assay. Haplotypes were inferred by the PHASE program (version 2.1). The main results of the present study indicate that H4 haplotype, which combines the A allele for both polymorphisms may be associated with migraine with aura, while G2087A polymorphism and H4 haplotype may affect the susceptibility to aura in patients with migraine. These findings may have therapeutic implications when analyzing the possible selective inhibitor effects of iNOS on the population with this genotype profile
Mestrado
Farmacologia
Mestre em Farmacologia
Velupandian, Uma Maheshwari. "The diagnosis of Patent Foramen Ovale, its importance in migraine, and an insight into its genetic basis." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/the-diagnosis-of-patent-foramen-ovale-its-importance-in-migraine-andan-insight-into-its-genetic-basis(d13d4a0b-b1f3-437a-899a-960015f9b33f).html.
Full textLouwrens, Bernadette. "Relationship between migraine triggers, auras and treatment." Thesis, Nelson Mandela Metropolitan University, 2017. http://hdl.handle.net/10948/18266.
Full textPaquette, Megan. "Migraine auras and hypergraphia and their connection to Hildegard Von Bingen." Honors in the Major Thesis, University of Central Florida, 2001. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/244.
Full textBachelors
Arts and Sciences
Art History
Weichselbaum, Annette. "Die Rolle von Varianten des Kalzium-aktivierten Kaliumkanals KCNN3 bei sporadischer Migräne mit und ohne Aura." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976099039.
Full textGonzales, Coty James. "Understanding the migraine aura : combining visual discomfort with stress." Thesis, 2008. http://hdl.handle.net/10125/20859.
Full textGovender, Catherine Olly. "Biopsychosocial correlates of health-related quality of life in migraine without aura." Thesis, 2016. http://hdl.handle.net/10500/22683.
Full textPsychology
D.Litt. et Phil. (Psychology)
Harvey, Jaqueline Ceridwyn. "The relationship between temperament and serum serotonin concentration in migraine without aura." Diss., 2016. http://hdl.handle.net/10500/21681.
Full textPsychology
M.A. (Psychology (Research Consultation))
Trexler, Gitta Gertrud. "The analgesic effectiveness of hypnosis in the treatment of migraine and aura." Thesis, 1997. https://vuir.vu.edu.au/15320/.
Full textMilovan, Denise L. "Neuropsychological functioning of migraine patients with- and without aura, and cerebral hemisphere laterality." Thesis, 2005. http://spectrum.library.concordia.ca/8816/1/NR16276.pdf.
Full textDreier, J. P., J. Kleeberg, Majid A. Alam, S. Major, M. Kohl-Bareis, C. P. Gabor, I. Victorov, I. U. Dirnagl, Tihomir P. Obrenovitch, and J. Priller. "Endothelin-1-induced spreading depression in rats is associated with a microarea of selective neuronal necrosis." 2007. http://hdl.handle.net/10454/3761.
Full textTwo different theories of migraine aura exist: In the vascular theory of Wolff, intracerebral vasoconstriction causes migraine aura via energy deficiency, whereas in the neuronal theory of Leão and Morison, spreading depression (SD) initiates the aura. Recently, it has been shown that the cerebrovascular constrictor endothelin-1 (ET-1) elicits SD when applied to the cortical surface, a finding that could provide a bridge between the vascular and the neuronal theories of migraine aura. Several arguments support the notion that ET-1¿induced SD results from local vasoconstriction, but definite proof is missing. If ET-1 induces SD via vasoconstriction/ischemia, then neuronal damage is likely to occur, contrasting with the fact that SD in the otherwise normal cortex is not associated with any lesion. To test this hypothesis, we have performed a comprehensive histologic study of the effects of ET-1 when applied topically to the cerebral cortex of halothane-anesthetized rats. Our assessment included histologic stainings and immunohistochemistry for glial fibrillary acidic protein, heat shock protein 70, and transferase dUTP nick-end labeling assay. During ET-1 application, we recorded (i) subarachnoid direct current (DC) electroencephalogram, (ii) local cerebral blood flow by laser-Doppler flowmetry, and (iii) changes of oxyhemoglobin and deoxyhemoglobin by spectroscopy. At an ET-1 concentration of 1 µM, at which only 6 of 12 animals generated SD, a microarea with selective neuronal death was found only in those animals demonstrating SD. In another five selected animals, which had not shown SD in response to ET-1, SD was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment also resulted in a microarea of neuronal damage. In contrast, SD invading from outside did not induce neuronal damage in the absence of ET-1 (n = 4) or in the presence of ET-1 if ET-1 was coapplied with BQ-123, an ETA receptor antagonist (n = 4). In conclusion, SD in presence of ET-1 induced a microarea of selective neuronal necrosis no matter where the SD originated. This effect of ET-1 appears to be mediated by the ETA receptor.
Liang, Yu-Syuan, and 梁宇萱. "The alterations of pain-related brain regions in migraine without aura: Diffusion kurtosis imaging and voxel-based morphometry analysis." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/cnd4uv.
Full text高雄醫學大學
醫學影像暨放射科學系碩士班
106
Purpose: Specific white matter alterations in migraine have been shown in many studies. Because the sensations of pain are performed by pain matrix, the integrity of white matter near these regions might be altered in migraine patients. Diffusion tensor imaging (DTI) has been used in a lot of studies to detect white matter alterations. However, because the Gaussian assumption in DTI is not a suitable model in the intracellular microenvironment, diffusion kurtosis imaging (DKI) which considers not only the Gaussian distribution but also the non-Gaussian distribution were demonstrated to better characterize white matter microstructural alterations. In addition, voxel-based morphometry (VBM) has been used in many studies to estimate the volume or density changes of gray matter in the cerebral cortex. Therefore, the aim of our study was to use DKI and VBM to comprehensively observe white matter and gray matter alterations near the regions of pain matrix in migraine. Materials and Method: Our study acquired whole brain T1 and DKI datasets from 19 Migraine without aura (MWoA) subjects (M/F=5/14, age=42±10 y/o) and13 healthy controls (M/F=5/8, age=32±9 y/o) on a Siemens 3.0T Skyra System. The DKI dataset were acquired using three b values(0, 1000 and 2000) in 20 non-collinear diffusion directions and repeated three times to improve data quality. For white matter analysis, all DKI images were post-processed with DKE tool (Diffusion Kurtosis Estimator) to obtain axial diffusivity (AD), radial diffusivity (RD), mean diffusivity (MD), Fractional Anisotropy (FA), axial kurtosis (AK), radial kurtosis (RK), and mean kurtosis (MK). For gray matter analysis, we used DARTEL VBM analysis for a series of automatic image processing, such as segmentation, modulation, and normalization. After spatial normalization, SPM8 (Statistical Parametric Mapping version 8) was performed for statistical analysis. Results: The results showed that there were more white matter alterations found by DKI than DTI. We found significantly increased diffusivity and decreased diffusion anisotropy in multiple white matter regions, especially at left side of brain near the pain matrix in migraine subjects, and also found there were more alterations in the parameters of radial direction (RD and RK). Moreover, the gray matter density were significantly decreased at the left side of brain near pain matrix in migraine subjects, but were significantly increased in cerebellum. Conclusion: The mechanism of migraine is still to be investigated. Our results demonstrated that DKI technique is helpful and more sensitive for detection of subtle white matter microstructural alterations in migraine subjects and can provide more in-depth insight into the distribution of water diffusion related to tissue microstructural alterations. Besides, DARTEL VMB is also helpful for detection of gray matter alterations in migraine subjects. Although the significance of these changes in migraine is still to be elucidated, our study preliminarily evaluated the alterations of both white matter and gray matter structures in migraine and the results may provide the direction for future research and clinical diagnosis.
Kittel, Heiner Peter. "A study to determine the efficiency of upper cervical vertebral manipulation as opposed to a combination of upper cervical and upper thoracic vertebral manipulation in the treatment of migraine without aura." Thesis, 2014. http://hdl.handle.net/10210/11759.
Full textThe object of this study was to compare two chiropractic treatment approaches to each other in the management of migraine without aura. It was hypothesised that a combination of upper cervical and upper thoracic chiropractic manipulative therapy would be more effective than upper cervical chiropractic manipulative therapy alone. Migraine without aura was diagnosed according to the criteria of the International Headache Society (1988) and based on a structured case history, physical examination as well as regional orthopaedic and neurological examinations. Forty-one (41) subjects were randomly allocated to one of the two treatment groups in this single blind, randomised trial. Thirty-three patients completed the trial. Both groups received their respective chiropractic manipulative treatments twice a week for a total period of four weeks. During this time and a period of eight weeks thereafter, each patient kept a daily headache diary, noting migraine frequency, duration, headache intensity and associated analgesic pill consumption. Statistical analysis of the collected data involved inter-group comparisons of the above mentioned variables using Mann-Whitney Rank Sum tests, and intra-group comparisons of the above. mentioned variables using Wilcoxon Signed Rank tests at a 95% level of confidence. Intra-group analysis of the data revealed statistically significant (P < 0.05) decreases in migraine frequency and headache intensity for both groups. Migraine duration followed a similar pattern but for a sudden increase in duration in the third month for the group receiving a combination of upper cervical and upper thoracic chiropractic manipulative therapy. Inter-group analysis of the data established no statistically significant differences (P > 0.05) between the two treatment groups before or during the study. Throughout the study, there was a notable difference in average analgesic pill consumption between the two groups. The results indicate that both chiropractic manipulative therapy approaches had positive effects on the frequency, duration and headache intensity of migraines without aura. The effect of chiropractic manipulative therapy on the associated analgesic pill consumption is speculative, since there was no pre-treatment assessment of analgesic pill consumption. The sudden increase in migraine duration during the third month for the group that received both upper cervical and upper thoracic manipulation may be due to this treatment being less effective than upper cervical manipulation alone. The significance of this sudden increase will need to be established by future studies. Neither one of the two chiropractic treatment protocols applied in this study fared significantly better than the other. It is suggested that future studies consider any disability associated with migraines without aura. A pre-treatment trial period would provide reliable pre-treatment statistics for the variables investigated during such a trial and larger samples would represent the overall migraineur population better. It is suggested that a third group, receiving only chiropractic manipulative therapy to the upper thoracic spine, also be included.
Hamzeh, Minhal. "Randomisierte, kontrollierte Parallelgruppenstudie zur Untersuchung der Wirksamkeit der manuellen Lymphdrainage und klassischen Massage zur Prophylaxe der Migräne mit und ohne Aura." Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-0006-B2B8-9.
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