The Effect of Oral Contraceptives on Migraine

Whitty, C. W. M.; Hockaday, Judith M.; Whitty, M.M.

doi:10.1016/s0140-6736(66)90189-9

Cited by 109 publications

(59 citation statements)

References 5 publications

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“…B. ), in contrast in some respects to that of Whitty et al (1966), that many patients subject to migraine have had their symptoms markedly increased by the use of oral contraceptives, and in some of them migraine has started for the first time. One of our colleagues, Dr. Michael Small, has allowed us to refer to a nurse who, while subject to migrainous headaches in the past.…”

Section: Discussionmentioning

confidence: 85%

Cerebral arterial insufficiency and oral contraceptives.

Bickerstaff¹,

Holmes²

1967

BMJ

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The question of whether there is an association between the use of oral contraceptives and cerebrovascular accidents has been bedevilled by the lack of accurate knowledge of the frequency (or rarity) of Because of the fallacy of trying to make a diagnosis of a cerebral thrombosis from the clinical picture alone, the criteria must be stated on which it was assumed that the patient had had an episode of cerebral arterial insufficiency. These criteria have been applied to all cases in the present study.

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Section: Discussionmentioning

confidence: 85%

Cerebral arterial insufficiency and oral contraceptives.

Bickerstaff¹,

Holmes²

1967

BMJ

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“…Further support for a relationship between hormonal variations and migraine includes reports of the oral contraceptive pill precipitating a first attack of migraine, or worsening or improving the frequency and severity of existing attacks [Dalton, 1976;Kudrow, 1975;Larson-Cohn and Lundberg, 1970;Mears and Grant, 1962;Phillips, 1968;Ryan, 1978;Whitty et al, 1966]. 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].…”

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

115

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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“…Progesterones were initially implicated as a causative factor in MM due to the peak and decline of progesterone during the late luteal phase when MM occurs. In 1966, Whitty [9] was the fi rst to suggest that the withdrawal of synthetic progesterone precipitated migraine. In 1971, Somerville [10] examined 10 women with recurrent "severe throbbing headaches" who experienced at least one severe headache episode each month immediately before menses for 6 months.…”

Section: Ovarian Hormones and MMmentioning

confidence: 99%

Perimenstrual headache: Treatment options

Henry

Cohen

2009

Current Science Inc

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At least half of women migraineurs experience menstrual migraine (MM), suggesting a hormonal explanation for the incidence of these headaches. Basic science efforts suggest a relationship between estrogen and the neurotransmitters and neuronal structures critical in the pathophysiology of migraine. The notion that MM is more severe, longer in duration, and more resistant to treatment than headaches occurring at other times during the menstrual cycle may apply more to women seeking treatment for their headaches than to migraineurs in the general population. Triptans have been shown to be effective as both an abortive and short-term preventive treatment, and estradiol has been shown to be an effective short-term preventive treatment. Ergotamines, combinations of drugs such as sumatriptan-naproxen sodium, and rizatriptan with dexamethasone show promise in the treatment of MM.

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The Effect of Oral Contraceptives on Migraine

Cited by 109 publications

References 5 publications

Cerebral arterial insufficiency and oral contraceptives.

Cerebral arterial insufficiency and oral contraceptives.

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

Perimenstrual headache: Treatment options

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