Medical Oophorectomy With and Without Estrogen Add‐Back Therapy in the Prevention of Migraine Headache

Martin, Vincent T.; Wernke, Suzanne; Mandell, Karen; Zoma, Willie D.; Bean, Judy A.; Pinney, Susan M.; Liu, James H.; Ramadan, Nabih M.; Rebar, Robert W.

doi:10.1046/j.1526-4610.2003.03065.x

Cited by 82 publications

(74 citation statements)

References 29 publications

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“…The other group received a placebo patch. At 2 months into therapy, the group that had received the 17 beta estradiol patch reported improvement in pain intensity, disability, and severity but not in episode frequency [29].…”

Section: Migraine and Surgical Menopausementioning

confidence: 93%

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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Section: Migraine and Surgical Menopausementioning

confidence: 93%

Migraine in perimenopausal women

et al. 2015

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“…Patient sex appears to be a risk factor for several trigeminal pain disorders, including temporomandibular disorders (Warren and Fried, 2001), trigeminal neuralgia (Katusic et al, 1990), pain after oral surgery (Gear et al, 1996), and migraine (Martin et al, 2003). Moreover, several of these conditions are exacerbated during the menstrual cycle or during episodes of altered circulating levels of estrogens or other steroids (Somerville, 1975;LeResche, 1997;Isselee et al, 2001Isselee et al, , 2002.…”

Section: Introductionmentioning

confidence: 99%

Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons

et al. 2006

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Sex dependency in pain perception is well documented and is thought to be attributable to the effect of reproductive hormones on nociceptive processing. In the present study, we evaluated whether estradiol alters gene transcription in the trigeminal ganglia (TG) of ovariectomized rats (OVX). These experiments demonstrated a dramatic (40-fold) upregulation of prolactin (PRL) expression in TG by 17-␤-estradiol (E2). PRL expression was restricted to TG neurons and was highly overlapped with transient potential receptor vanilloid type 1 (TRPV1) (ϳ90%) in TG. Additionally, PRL is released from neurons during stimulation. Both forms of PRL receptors (PRLRs), short and long, were also present in TG neurons. Moreover, expression of the long PRLRs was under control of estradiol. We next evaluated the novel hypothesis that PRL acts as a neuromodulator of sensory neurons. PRL pretreatment significantly enhanced capsaicin-evoked inward currents, calcium influx, and immunoreactive calcitonin gene-related peptide release from cultured TG neurons. This PRL modulation of capsaicin responses was abolished by withdrawal of E2 from TG cultures. Biochemical analysis demonstrated that PRL increased (Ͼ50%) phosphorylation levels of TRPV1 in TG. In a behavioral test, PRL pretreatment significantly potentiated capsaicin-evoked nocifensive behavior in female rats at proestrous and in OVX rats after E2 treatment. The in vivo potentiating effect of PRL on capsaicin responses was also dependent on E2. Collectively, these data demonstrate that PRL is a novel modulator of sensory neurons tightly regulated by E2. These findings are consistent with the hypothesis that PRL could contribute to the development of certain pain disorders, possibly including those modulated by estrogen.

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“…'Add-back' continuous combined oestrogen and progestogen can be given to counter these concerns. 55,56 Given these limitations, in addition to increased cost, such treatment should be instigated only in specialist departments.…”

Section: Nsaidsmentioning

confidence: 99%

Diagnosis and management of menstrual migraine

MacGregor¹

2011

Prog Neurol Psychiatry

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Despite affecting one in seven of the UK population, migraine is underdiagnosed and undertreated. 1 Prevalence is highest during the peak reproductive years with a female predilection, affecting one in five women compared with one in 13 men. 1 The diagnosis of migraine is based on recurrent episodic headaches lasting between four and 72 hours associated with photophobia, nausea and limitation of normal function in an otherwise healthy person. 2 Prevalence of menstrual migraineMenstruation is a significant risk factor for attacks of migraine without aura, with 50-60 per cent of women reporting a link between their menstrual periods and migraine. [3][4][5] Most women with menstrual exacerbation of migraine also experience attacks at other times of the month ('menstrually-related' migraine). 6,7 Fewer than 10 per cent of women report migraine exclusively with menstruation ('pure' menstrual migraine). [5][6][7][8][9] Characteristics of menstrual migraine Timing of attacks Compared with all other phases of the menstrual cycle, attacks of migraine without aura are most likely to occur during a five-day window that starts two days before the onset of menses and continues through the first three days of menstruation. 8,10-12 Studies suggest that women are over 70 per cent more likely to have migraine in the two days before menstruation and more than 2.5 times more likely to have attacks during the first three days of bleeding. 12 How attacks differ from non-menstrual attacks Menstrual attacks last longer, are more severe, are more likely to relapse, are less responsive to treatment, and are associated with greater disability when compared with attacks at other times of the cycle. 5,[11][12][13][14][15][16][17][18][19] DiagnosisThe International Headache Society (IHS) recognises two types of menstrual migraine: menstrually-related migraine, which is migraine without aura that regularly occurs on or between two days before menstruation and third day of bleeding (days -2 to +3), with additional attacks of migraine with or without aura at other times of the cycle; and pure menstrual migraine, which is migraine without aura that occurs only on or between days -2 to +3, ie with no attacks at any other time during the cycle. 6,20 To confirm the diagnosis, migraine attacks during the day -2 to +3 window must occur in at least two of three menstrual cycles to establish a relationship that is greater than chance alone. Relying on the history to confirm the diagnosis can be misleading. 21 Use of a three-month diar y to record migraine patterns can reveal the predictable patterns associated with menstrual migraine, aiding diagnosis. PathophysiologyResearch has found an increased risk of migraine associated with oestrogen 'withdrawal'. This occurs during the late luteal phase of the natural menstrual cycle and also during the hormone-free interval of combined hormonal contraceptives. 17,22 Prostaglandins have also been implicated in menstrual migraine. There is a three-fold increase in prostaglandin levels in the uterine endometriu...

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Medical Oophorectomy With and Without Estrogen Add‐Back Therapy in the Prevention of Migraine Headache

Cited by 82 publications

References 29 publications

Migraine in perimenopausal women

Migraine in perimenopausal women

Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons

Diagnosis and management of menstrual migraine

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