Migraine and the Menopause

Fettes, Ivy

doi:10.1016/s0849-5831(16)31116-8

Cited by 22 publications

(30 citation statements)

References 15 publications

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“…Ovarian hormones, rather than sex chromosome-related developmental differences in synaptic organization and structure, were implicated in aged female mice and after ovariectomy. These findings may be clinically relevant, since migraine improves at menopause in two-thirds of patients (40). The frequency of migraine attacks decreases after age 50, both in patients with FHM and those with more typical migraine subtypes (9).…”

Section: Discussionmentioning

confidence: 84%

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Eikermann-Haerter¹,

Dileköz²,

Kudo³

et al. 2008

J. Clin. Invest.

186

290

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Familial hemiplegic migraine type 1 (FHM1) is an autosomal dominant subtype of migraine with aura that is associated with hemiparesis. As with other types of migraine, it affects women more frequently than men. FHM1 is caused by mutations in the CACNA1A gene, which encodes the α 1A subunit of Ca v 2.1 channels; the R192Q mutation in CACNA1A causes a mild form of FHM1, whereas the S218L mutation causes a severe, often lethal phenotype. Spreading depression (SD), a slowly propagating neuronal and glial cell depolarization that leads to depression of neuronal activity, is the most likely cause of migraine aura. Here, we have shown that transgenic mice expressing R192Q or S218L FHM1 mutations have increased SD frequency and propagation speed; enhanced corticostriatal propagation; and, similar to the human FHM1 phenotype, more severe and prolonged post-SD neurological deficits. The susceptibility to SD and neurological deficits is affected by allele dosage and is higher in S218L than R192Q mutants. Further, female S218L and R192Q mutant mice were more susceptible to SD and neurological deficits than males. This sex difference was abrogated by ovariectomy and senescence and was partially restored by estrogen replacement, implicating ovarian hormones in the observed sex differences in humans with FHM1. These findings demonstrate that genetic and hormonal factors modulate susceptibility to SD and neurological deficits in FHM1 mutant mice, providing a potential mechanism for the phenotypic diversity of human migraine and aura.

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Section: Discussionmentioning

confidence: 84%

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Eikermann-Haerter¹,

Dileköz²,

Kudo³

et al. 2008

J. Clin. Invest.

186

290

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“…A history of PMS is considered a predictor for the development of migraine during the menopausal transition as it may indicate a higher sensitivity to hormonal fluctuations and greater predisposition to developing moderate-to-severe climacteric symptoms [2]. Furthermore, the intensity and duration of climacteric symptoms (hot flashes, palpitations, night sweats, and mood swings) can contribute to exacerbation of migraine attacks [9]. Worsening of migraine may also be secondary to concomitant conditions such as depression, which raises the risk of the development of chronic pain and insomnia that could increase migraine frequency [10,11].…”

Section: Menopausal Stages and Clinical Evolution Of Migrainementioning

confidence: 99%

Migraine in perimenopausal women

et al. 2015

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Hormonal changes during the reproductive cycle are thought to account for the variation in migraine occurrence and intensity. Although the majority of women and the specialists treating them do not consider migraine as a component of the climacteric syndrome, many women, in fact, do experience migraine during perimenopause. If a woman already suffers from migraine, the attacks often worsen during menopausal transition. Initial onset of the condition during this period is relatively rare. Women with the premenstrual syndrome (PMS) prior to entering menopause are more likely to experience, during late menopausal transition, an increased prevalence of migraine attacks. Hormone replacement therapy (HRT) can be initiated during the late premenopausal phase and the first years of postmenopause to relieve climacteric symptoms. The effect of HRT on migraine, either as a secondary effect of the therapy or as a preventive measure against perimenopausal migraine, has been variously investigated. HRT preparations should be administered continuously, without intervals, to prevent sudden estrogen deprivation and the migraine attacks that will ensue. Wide varieties of formulations, both systemic and topical, are available. Treatment with transdermal patches and estradiol-based gels is preferable to oral formulations as they maintain constant blood hormone levels. Natural menopause is associated with a lower incidence of migraine as compared with surgical menopause; data on the role of hysterectomy alone or associated with ovariectomy in changing the occurrence of migraine are till now unclear.

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“…70 In addition, many women with migraine, especially those with a history of menstrual migraine, experience an exacerbation as they approach menopause. 71 Therefore, even though no statistically significant correlation was found between rCBF and mean hormonal level, rCBF changes can be related to abnormalities in the cyclic fluctuation of estrogen levels. Moreover, although no linear correlation was found between rCBFs and clinical and laboratory variables (age, menopause status, KKSI, SDS, and serum levels of estradiol, FSH, and LH) in the areas of rCBF reductions, this may also be due in part to the small number of women and to variability in the phase of menopause status.…”

Section: Discussionmentioning

confidence: 93%

Medial frontal cortex perfusion abnormalities as evaluated by positron emission tomography in women with climacteric symptoms

Abe¹,

Bereczki²,

Takahashi³

et al. 2006

Menopause

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The present study revealed reductions in relative rCBF of the prefrontal cortex of Japanese women with moderate to severe climacteric symptoms. This area is close to that previously addressed in studies of familial bipolar depression and familial unipolar depression, although our participants did not satisfy criteria for depression. This reduction of rCBF may be related to the three climacteric symptom clusters, but further studies are needed for evaluation of its significance. Our results should stimulate investigations into the positron emission tomography rCBF change of these women as to the integration of multiple entities in climacteric symptoms.

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Migraine and the Menopause

Cited by 22 publications

References 15 publications

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Migraine in perimenopausal women

Medial frontal cortex perfusion abnormalities as evaluated by positron emission tomography in women with climacteric symptoms

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