Graded sequential therapy in the menopause: A double-blind study

Martin, Purvis L.; Burnier, Andre; Segre, Eugene J.; Huix, F. Avier

doi:10.1016/0002-9378(71)90887-8

Cited by 28 publications

(7 citation statements)

References 13 publications

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“…In addition, many women with migraine have fewer attacks during pregnancy [Callaghan, 1968; Nattero, 1982; Somerville, 1972], although the condition may be exacerbated in the post-partum period [Stein, 1981]. Also, some women have fewer attacks or cease to have attacks after menopause [Martin et al, 1971]. …”

Section: Discussionmentioning

confidence: 99%

Common genetic influences underlie comorbidity of migraine and endometriosis

Nyholt

Gillespie²,

Merikangas

et al. 2008

Genetic Epidemiology

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We examined the co-occurrence of migraine and endometriosis within the largest known collection of families containing multiple women with surgically confirmed endometriosis and in an independent sample of 815 monozygotic and 457 dizygotic female twin pairs. Within the endometriosis families, a significantly increased risk of migrainous headache was observed in women with endometriosis compared to women without endometriosis (odds ratio [OR] 1.57, 95% confidence interval [CI]: 1.12–2.21, P = 0.009). Bivariate heritability analyses indicated no evidence for common environmental factors influencing either migraine or endometriosis but significant genetic components for both traits, with heritability estimates of 69 and 49%, respectively. Importantly, a significant additive genetic correlation (rG = 0.27, 95% CI: 0.06–0.47) and bivariate heritability (h2 = 0.17, 95% CI: 0.08–0.27) was observed between migraine and endometriosis. Controlling for the personality trait neuroticism made little impact on this association. These results confirm the previously reported comorbidity between migraine and endometriosis and indicate common genetic influences completely explain their co-occurrence within individuals. Given pharmacological treatments for endometriosis typically target hormonal pathways and a number of findings provide support for a relationship between hormonal variations and migraine, hormone-related genes and pathways are highly plausible candidates for both migraine and endometriosis. Therefore, taking into account the status of both migraine and endometriosis may provide a novel opportunity to identify the genes underlying them. Finally, we propose that the analysis of such genetically correlated comorbid traits can increase power to detect genetic risk loci through the use of more specific, homogenous and heritable phenotypes.

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Section: Discussionmentioning

confidence: 99%

Common genetic influences underlie comorbidity of migraine and endometriosis

Nyholt

Gillespie²,

Merikangas

et al. 2008

Genetic Epidemiology

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“…In addition, many women with migraine have fewer attacks during pregnancy [Callaghann, 1968;Nattero, 1982;Somerville, 1972], although the condition may be exacerbated in the postpartum period [Stein, 1981]. Also, some women have fewer attacks or cease to have attacks after menopause [Martin et al, 1971].…”

Section: Genetic Influence and Sex-limitationmentioning

confidence: 99%

Latent class and genetic analysis does not support migraine with aura and migraine without aura as separate entities

Nyholt

Gillespie

Heath

et al. 2004

Genetic Epidemiology

112

121

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Latent class and genetic analyses were used to identify subgroups of migraine sufferers in a community sample of 6,265 Australian twins (55% female) aged 25-36 who had completed an interview based on International Headache Society (IHS) criteria. Consistent with prevalence rates from other population-based studies, 703 (20%) female and 250 (9%) male twins satisfied the IHS criteria for migraine without aura (MO), and of these, 432 (13%) female and 166 (6%) male twins satisfied the criteria for migraine with aura (MA) as indicated by visual symptoms. Latent class analysis (LCA) of IHS symptoms identified three major symptomatic classes, representing 1) a mild form of recurrent nonmigrainous headache, 2) a moderately severe form of migraine, typically without visual aura symptoms (although 40% of individuals in this class were positive for aura), and 3) a severe form of migraine typically with visual aura symptoms (although 24% of individuals were negative for aura). Using the LCA classification, many more individuals were considered affected to some degree than when using IHS criteria (35% vs. 13%). Furthermore, genetic model fitting indicated a greater genetic contribution to migraine using the LCA classification (heritability, h(2)=0.40; 95% CI, 0.29-0.46) compared with the IHS classification (h(2)=0.36; 95% CI, 0.22-0.42). Exploratory latent class modeling, fitting up to 10 classes, did not identify classes corresponding to either the IHS MO or MA classification. Our data indicate the existence of a continuum of severity, with MA more severe but not etiologically distinct from MO. In searching for predisposing genes, we should therefore expect to find some genes that may underlie all major recurrent headache subtypes, with modifying genetic or environmental factors that may lead to differential expression of the liability for migraine.

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“…In women who are postmenopausal, hormone replacement therapy has been reported to improve and worsen headache. [12][13][14][15] These conflicting past studies led us to study the role of estrogen and medical oophorectomy in the prevention of headache. We postulated that changes in serum estrogen or other sex hormones, which occur as part of a normal menstrual cycle, could trigger headache in female migraineurs.…”

Section: April 2003mentioning

confidence: 99%

“…Most headaches occurred during the placebo week, which represented a period of a rapid fall of serum estrogen levels. In women who are postmenopausal, hormone replacement therapy has been reported to improve and worsen headache 12–15 …”

mentioning

confidence: 99%