No description available.

Migraine, comprised of migraine with aura (MA) and migraine without aura (MO), is a painful neurovascular disease, affecting approximately 16% of the general population. It is characterised by a wide variety of symptoms including headache, nausea and vomiting, and photo- and phonophobia. The disorder is complex involving not only multiple genes, but also specific environmental factors, which can induce attacks in genetically predisposed individuals. Hyperhomocysteinaemia is a known risk factor for cerebrovascular, peripheral vascular and coronary heart disease. The Methylenetetrahydrofolate Reductase (MTHFR) enzyme is involved in homocysteine metabolism. Furthermore, it has been reported that a homozygous mutation (677C to T; Ala to Val) in the 5,10-MTHFR gene is associated with an elevation in plasma homocysteine levels (Frosst et al., 1995). This common mutation in the MTHFR gene has recently been associated with migraine with aura in a Japanese cohort (Kowa et al., 2000). The present study was designed to determine the prevalence of the MTHFR C677T mutation in Australian patients with migraine and to determine whether this mutation is associated with the disease in Caucasians. A large case-control study, consisting of 270 patients with migraine (167 with aura and 103 without aura), and 270 normal matched controls was investigated. Genotypic results indicated that the prevalence of the homozygous (T/T) genotype in migraine sufferers (15%) was higher than that of controls (9%) (P = 0.084). Furthermore, the frequency of the mutant (T/T) genotype in individuals with MA (19%) was significantly higher than in controls (9%) (P = 0.006). Interestingly, the risk of MA was ~2.5-fold higher in suffers possessing the homozygous variant (OR = 2.52, CI: 1.42 - 4.47, P = 0.0012). To confirm the MTHFR allelic association with MA, family-based tests were performed in an independent pedigrees group, where only those with MA were considered affected. Results from both the Pedigree Disequilibrium Test (PDT) and Family-Based Association Test (FBAT) analysis revealed slight, although not significant (PDT test, P = 132; and FBAT test, P = 0.390), over-transmission of the mutant allele (T) from parents to affected offspring. However, despite the MTHFR variant having a high heterozygosity (0.48), there were a limited number of informative transmissions for the MTHFR variant in the pedigree group resulting in reduced power for these tests. In conclusion, our results support the trends reported in the Japanese migraine study and suggest that the homozygous 677T gene variant causing mild hyperhomocysteinaemia, is a genetic risk factor for migraine, and indicate that further studies investigating the role of this gene are warranted. Mutations in various ion channel genes are responsible for neurovascular and other neurological disorders. Inherited ion channel mutations or "channelopathies" are increasingly found to be the cause of various neurological disorders in humans. Wittekindt and colleagues (1998) reported that the calcium-activated potassium channel (hKCa3) gene is a good candidate for schizophrenia and bipolar disorder (BD), as well as for other neurological disorders such as migraine. The hKCa3 gene is a neuronal small conductance calcium-activated potassium channel, which contains a polyglutamine tract, encoded by a polymorphic CAG repeat in the gene. The hKCa3 gene encodes a protein of 731 amino acids containing two adjacent polyglutamine sequences in its N-terminal domain separated by 25 amino acids. The C-terminal polyglutamine sequence is highly polymorphic in length (Austin et al., 1999). hKCa3 plays a critical role in determining the firing pattern of neurons via the generation of slow after-polarization pulses and the regulation of intracellular calcium channels (Kohler et al., 1996). Three distinct mutations in the a1 calcium channel gene have been shown to cause SCA-6, episodic ataxia-2 and familial hemiplegic migraine (FHM) (Ophoff et al., 1996). The hKCa3 gene contains a highly polymorphic CAG repeat that was initially mapped (Chandy et al., 1997) to a schizophrenia locus on chromosome 22 (Pulver et al., 1994). Recently Austin et al (1999) re-mapped hKCa3 and found it to reside on chromosome 1q21, a region that has been linked to FHM (Austin et al., 1999), a rare subtype of MA (Ducros et al., 1997; Gardner et al., 1998), and a region recently showing genetic linkage to typical migraine (Lea et al., 2002). The hKCa3 polymorphism results in small variations in polyglutamine number, similar to those that occur in the calcium channel a1a subunit gene (CACNA1A), which is encoded by CAG expansions and thought to cause Spinocerebellar Ataxia Type 6 via loss of channel function (Austin et al., 1999). Given the recent linkage of FHM to the region of chromosome 1q21, to which hKCa3 resides, and also linkage of typical migraine to this region, a large case-control study investigating this hKCa3 CAG marker and consisting of 270 migraine and 270 stringently matched healthy controls was undertaken. Our results indicated that there was no statistically significant difference in allele distributions for this marker between migraine and non-migraine patients (P >0.05). No significant difference in the allelic distribution was observed in the MA or MO groups when compared to controls (P >0.05) and there was no significant difference in CAG repeat length distribution between the migraine group and controls (P = 0.92), or between the MA and MO groups (P = 0.72) collectively. Hence, the CAG repeat in this gene does not show expansion in migraine. Overall, our results provide no genetic evidence to suggest that the hKCa3 CAG repeat polymorphism is involved in migraine aetiology in Australian Caucasians. Thus the involvement of the hKCa3 gene in migraine is not likely, although the hKCa3 gene remains an important candidate for other neurological disorders that may be linked to the 1q21.3 chromosomal region.

Th.--Méd.--Nancy 1, 1983. N°: 137.

This study was completed to better understand and treat couples wherein one partner suffers from chronic migraines. I interviewed eight couples about their experiences in dealing with migraines as a patient, as a partner, and together. The interviews were transcribed and analyzed by a team of seven researchers. We developed a theory that can be used to understand how patients and their partners adapt to chronic migraines. The theory was grounded in the experiences of the patients and partners who were interviewed. We found that patients and partners alike dealt with burdens and costs associated with chronic migraines. Coping, healthcare, couple experience, and identity were found to be the means through which patients and partners adapted to their burdens. These concepts are broken down and discussed in greater detail. A model is provided that can be used to create a visual representation of how well a couple deals with migraines. Suggestions for couples who are dealing with chronic migraines, and for medical providers and therapists who work with couples affected by chronic migraines, are provided.

No description available.

Ginger (Zingiber Officinale) has been used in Asia for centuries to treat various ailments. Ginger has been reported to alleviate migraine pain via four bioactive compounds that can reduce nitric oxide synthase (NOS) resulting in the inhibition of nitric oxide (NO). The inhibition of nitric oxide results in the vasoconstriction of the intracranial blood vessels alleviating migraine pain. It is hypothesized that ginger has structural similarities to vasoconstrictor drugs causing similar receptor interactions. A review of the bioactive compounds in ginger and popular vasoconstrictor drugs was done to determine structural similarities. The results of this study show that the compounds in ginger share no structural similarities with vasoconstrictor drugs used in the treatment of migraine headaches.

Personer som lider av migrän har i de flesta fall någon gång funderat över vad som är den utlösande faktorn. Ibland vet de svaret, ibland är svaret inte lika tydligt. Att ha kunskap och förståelse över sin migrän kan öka chanserna till självhjälp och ökad empowerment. Patienterna har tillräcklig kunskap för att kunna ta beslut som bidra till en bättre hälsa för individen. Patienten hjälper således sig själv till ett bättre välmående utifrån den kunskap som patienten har om sig själv och sin sjukdom. För att skapa en förståelse och större kunskap för sin sjukdom kan det underlätta att dokumentera sina migränanfall. Dokumentationen kan sedan användas för att hitta en gemensam nämnare till anfallen. Att dokumentera migränanfall kan också kallas för att föra en migrändagbok. Migrändagböcker kan ordineras ut av hälso- och sjukvård i form av enklare dokumentation på pappersark. Det finns också digitala lösningar där personer som lider av migrän kan dokumentera in mer utförliga uppgifter om sin migränattack via olika migränappar som finns att ladda ner. En digital lösning ger större möjlighet till en rikare information om personens sjukdom, men saknar ofta anpassning för migränpatienters särskilda behov och upplevda problematik. Personer som lider av migrän kan uppleva problematik med att interagera med digitala skärmar. Att interagera med skärmar kan vara en bidragande orsak till ett sämre mående, vilket framkom i denna undersökning. Syftet med denna studie var att undersöka hur ett gränssnitt för en mobil hälsoapplikation för migränpatienter kunde utformas med fokus på empowerment och god användarupplevelse. För att ta reda på detta, genomfördes 7 stycken semistrukturerade intervjuer. Informanterna fick berätta om sina upplevelse av migrän, deras egen kunskap om sin sjukdom, samt tekniska aspekter om hur de vill interagera med mobilappar under tiden som de har migrän. Den data som uppkom utifrån intervjuerna analyserades sedan med hjälp av kvalitativ kodning som resulterade i fyra olika teman. Behovet visar att dokumentation av migränanfall genom mobilapplikationer ska ske med så lite interaktionstid med skärmen som möjligt. Dokumentation av migränanfall kan med fördel ske med hjälp av tal och ljud. Själva gränssnittet ska vara enkelt och simpelt med avskalade ikoner som tydligt ska gå att identifiera. Det ska finnas möjlighet att manuellt eller med automatiska inställningar dämpa ljuset på skärmen. Resultatet av undersökningen mynnade sedan ut i lämpliga gränssnittsförslag i form av mockuper. För framtida forskning rekommenderas att utföra användartester med utökade prototyper, för att undersöka huruvida de designförslag som tagits fram i denna studie upplevs som en god användarupplevelse och bidrar till empowerment. / People who suffer from migraines have probably at some point thought about what the triggering factor is. Sometimes the answer is clear, and sometimes it’s not that obvious. To have understanding and knowledge of their migraine can increase the chances of self-help and also higher levels of empowerment. With self-help, the patient can make better decisions based on the knowledge of the disease, which can lead to a better well-being. In order to establish an understanding and more knowledge about their illness, it can be helpful to document the migraine attacks. The documentation can then be used to find a possible cause of the attacks. This is also called a migraine journal. Migraine journals can be prescribed by the health services, where you get a template with less words and with simple instructions of the tasks on them. There are also digital solutions, like mobile applications, that supports more detailed documentation. A digital solution provides more opportunities for more detailed information about the person's illness, but mobile apps often lacks adaption for the patient's specific needs and problems. Persons who suffers from a migraine attack, can experience difficulties when documenting a large amount of information on applications. The interaction with digital screens may worsen the symptom. This is one of the findings of this study. The purpose of this study was to examine how a user interface for a mobile health application, could be designed with focus of empowerment and a good user experience. To find out, 7 semi structured interviews were conducted. The informants were asked to tell about their experiences, their knowledge about their illness and some technical aspects of how they want to interact with mobile applications while they are suffering from an attack. The data that was obtained from the interviews were then analyzed using qualitative coding that resulted in four different themes. The study showed that the potential users wish to interact as little as possible with the screen. Documentation of migraine attacks can be done with the help of speech and sound. The interface itself should be easy with simple icons which are easy to identify. It should be possible to manually or automatically adjust the light on the screen. The result of the study contributed to suggestions for how to design a suitable interface for migraine patients. The interface is visualised in this report in the form of mockups. For future research , it is recommended to perform user tests with extended prototypes to investigate whether the design principles and design suggestions developed in this study are perceived as a good user experience and contribute to empowerment.

Les canaux de potassium voltage-dépendant (Kv) sont des tétramères séparés en 12 familles. Chaque sous-unité est composée de six segments transmembranaires (S1-S6). Les quatre premiers (S1-S4) forment le senseur de voltage dont le rôle est de détecter des variations en potentiel membranaire grâce à des acides aminés chargés. Ces acides aminés vont bouger et ce mouvement va être transmis au second domaine, celui du pore (S5-S6). Les domaines du pore des quatre sous-unités vont se combiner pour créer le pore. Ces sous-unités peuvent former des canaux homomériques où chaque sous-unité est identique ou des canaux hétéromériques avec des membres de la même famille. Kv6.4 (KCNG4) est un membre de la famille de sous-unité silencieuse Kv6. Les familles de sous-unités silencieuses incluent également Kv5, Kv8 et Kv9. Ils ne peuvent pas former d’homomères. À la place, il doit former des hétéromères avec Kv2. Les canaux Kv2.1/Kv6.4 ont des propriétés différentes, lorsque comparées aux homomères de Kv2.1, particulièrement avec un décalage de l’inactivation vers les négatifs. Avec la technique du « cut-open voltage clamp fluorometry » (COVCF), nous avons pu déterminer que l’absence d’une charge positive à la position Kv6.4-Y345 est responsable pour une partie du décalage tout en étant capable de réduire ce décalage avec la mutation Kv6.4-Y345R. Nous avons également pu produire l’effet inverse dans Kv2.1 avec Kv2.1-R306Y. Également, nous avons déterminé que la mutation Kv6.4-L360P trouvée chez des patients souffrant de migraines mène à cette pathologie à cause d’un problème de trafic où les sous-unités mutées ne peuvent pas atteindre la surface et produire des canaux fonctionnels. Ce problème est causé par un bris dans l’hélice alpha du segment S4-S5. Uniquement des homomères de Kv2.1 se rendent à la surface ce qui réduit l’excitabilité membranaire. Nous proposons que lorsqu’exprimée dans le ganglion trigéminal, cette mutation mène à des migraines. / Voltage-gated potassium channels (Kv) are tetramers split into 12 families. Each subunit is composed of six transmembrane helices (S1-S6). The first four of those (S1-S4) form the voltage sensor domain whose role it is to detect variations in the membrane potential through charged amino acids. The movement of those amino acids will be transmitted to the second domain, the pore domain (S5-S6). The pore domain of all four subunits will combine to form the ion conducting pore. These subunits can form homomers where all four subunits are identical or heteromers with members of the same family. Kv6.4 (KCNG4) is a member of the silent subunit family Kv6, which also includes Kv5, Kv8 and Kv9. They cannot form functioning homomers. Instead, they form heteromers with Kv2. Kv2.1/Kv6.4 channels have different properties when compared to Kv2.1 homomers, particularly a negative shift of the voltage dependence of inactivation. With the cut-open voltage clamp fluorometry (COVC) technique, we were able to determine that the absence of a gating charge at position Kv6.4-Y345 is responsible for part of this shift. We were able to recover part of this shift with the mutation Kv6.4-Y345R. We were also able to produce the inverse effect in Kv2.1 with the mutation Kv2.1-R306Y. Also, we determined that the mutation Kv6.4-L360P. which is found in patients suffering from migraines, leads to this condition because of a trafficking defect caused by the mutation stopping the subunits from reaching the membrane and making functional channels. The defect is caused by a kink in the alpha helix of the S4-S5 linker. Only Kv2.1 homomers reach the membrane which reduces membrane excitability. We propose that when expressed in the trigeminal ganglion, this mutation leads to migraines because of this trafficking defect.