Trigger Factors and Premonitory Features of Migraine Attacks: Summary of Studies

Pavlović, Jelena; Buse, Dawn C.; Sollars, C. Mark; Haut, Sheryl R.; Lipton, Richard B.

doi:10.1111/head.12468

Cited by 128 publications

(133 citation statements)

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“…We propose a "two-hit" hypothesis of perimenstrual migraine initiation, whereby the more rapid estrogen decline is an endogenous trait of women with migraine that confers neuroendocrine vulnerability that may facilitate initiation of migraine attack(s) by common triggers, such as stress, disrupted sleep, foods, and wine. 34 An endogenous difference in estrogen processing in women with migraine is further supported by a study of postmenopausal women in which estrogen decline following a single injection of estradiol triggered a migraine only in women with a premenopausal history of migraine associated with menstruation. 35 This neurovulnerability to rapid estrogen decline may be due to the disruption of the serotonergic mechanisms involved in inhibition of pain leading to disruption of the trigeminovascular system.…”

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confidence: 95%

Sex hormones in women with and without migraine

et al. 2016

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Objective: To compare daily sex hormone levels and rates of change between women with history of migraine and controls.Methods: History of migraine, daily headache diaries, and daily hormone data were collected in ovulatory cycles of pre-and early perimenopausal women in the Study of Women's Health Across the Nation. Peak hormone levels, average daily levels, and within-woman day-to-day rates of decline over the 5 days following each hormone peak were calculated in ovulatory cycles for conjugated urinary estrogens (E1c), pregnanediol-3-glucuronide, luteinizing hormone, and follicle-stimulating hormone. Comparisons were made between migraineurs and controls using 2-sample t tests on the log scale with results reported as geometric means.Results: The sample included 114 women with history of migraine and 223 controls. Analyses of within-woman rates of decline showed that E1c decline over the 2 days following the luteal peak was greater in migraineurs for both absolute rate of decline (33.8 [95% confidence interval 28.0-40.8] pg/mgCr vs 23.1 [95% confidence interval 20.1-26.6] pg/mgCr, p 5 0.002) and percent change (40% vs 30%, p , 0.001). There was no significant difference between migraineurs and controls in absolute peak or daily E1c, pregnanediol-3-glucuronide, luteinizing hormone, and follicle-stimulating hormone levels. Secondary analyses demonstrated that, among migraineurs, the rate of E1c decline did not differ according to whether a headache occurred during the cycle studied.Conclusions: Migraineurs are characterized by faster late luteal phase E1c decline compared to controls. The timing and rate of estrogen withdrawal before menses may be a marker of neuroendocrine vulnerability in women with migraine. Neurology ® 2016;87:49-56 GLOSSARY BMI 5 body mass index; DHS 5 Daily Hormone Study; E1c 5 conjugated urinary estrogens; ELA 5 evidence of luteal activity; FSH 5 follicle-stimulating hormone; ICHD 5 International Classification of Headache Disorders; LH 5 luteinizing hormone; MHx 5 women with history of migraine; Pdg 5 pregnanediol-3-glucuronide; SWAN 5 Study of Women's Health Across the Nation.

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Sex hormones in women with and without migraine

et al. 2016

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“…Understanding the interactions that occur when processing multiple external stimuli and activation of the trigeminal system may help to explain migraine symptoms and mechanisms by which exposure to visual, auditory, and olfactory stimuli can trigger migraine attacks. However, identifying trigger factors or premonitory features that reliably predict headache onset in migraine remains an ongoing clinical challenge (Lipton et al, 2014; Pavlovic et al, 2014). …”

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confidence: 99%

Cortico–Cortical Connections of Primary Sensory Areas and Associated Symptoms in Migraine

Hodkinson

Veggeberg

Kucyi

et al. 2016

eNeuro

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Migraine is a recurring, episodic neurological disorder characterized by headache, nausea, vomiting, and sensory disturbances. These events are thought to arise from the activation and sensitization of neurons along the trigemino–vascular pathway. From animal studies, it is known that thalamocortical projections play an important role in the transmission of nociceptive signals from the meninges to the cortex. However, little is currently known about the potential involvement of cortico–cortical feedback projections from higher-order multisensory areas and/or feedforward projections from principle primary sensory areas or subcortical structures. In a large cohort of human migraine patients (N = 40) and matched healthy control subjects (N = 40), we used resting-state intrinsic functional connectivity to examine the cortical networks associated with the three main sensory perceptual modalities of vision, audition, and somatosensation. Specifically, we sought to explore the complexity of the sensory networks as they converge and become functionally coupled in multimodal systems. We also compared self-reported retrospective migraine symptoms in the same patients, examining the prevalence of sensory symptoms across the different phases of the migraine cycle. Our results show widespread and persistent disturbances in the perceptions of multiple sensory modalities. Consistent with this observation, we discovered that primary sensory areas maintain local functional connectivity but express impaired long-range connections to higher-order association areas (including regions of the default mode and salience network). We speculate that cortico–cortical interactions are necessary for the integration of information within and across the sensory modalities and, thus, could play an important role in the initiation of migraine and/or the development of its associated symptoms.

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“…6,7 Therefore, there is an increasing need to understand the mediation of such symptoms, and their differentiation from migraine triggers, to allow patients to understand their condition better and effectively manage their lifestyles accordingly.…”

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confidence: 99%

“…6 Increasingly, the evidence suggests that many of the triggers reported by patients are not reproducible in experimental research, and may actually represent the manifestation of premonitory-like symptomatology. 6,7 Therefore, there is an increasing need to understand the mediation of such symptoms, and their differentiation from migraine triggers, to allow patients to understand their condition better and effectively manage their lifestyles accordingly.…”

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Premonitory-like Symptomatology in Migraine

Karsan

Goadsby²

2017

European Neurological Review

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It has been historically accepted that migraine involves symptomatology outside of head pain. These symptoms can be as equally disabling as the pain, and can include tiredness, concentration impairment, memory impairment and mood change. The symptoms may start before the onset of pain and can persist throughout the headache phase, and even after effective headache treatment into the postdrome. Despite knowledge of these symptoms, their neurobiologic basis and relationship to migraine pain is poorly understood. The fact that these symptoms start early, up to hours to days before the onset of headache, and are so symptomatically heterogeneous, suggests that the neurobiology of migraine extends beyond conventionally accepted anatomical pain areas within the brain -what has been known as the pain matrix or network. In a research area where no effective acute abortive drugs have gained a license for migraine since the triptans (serotonin 5-HT 1B/1D receptor agonists), in the 1990s, further understanding of such symptomatology will allow therapeutic advances for treatments that may work before the onset of migraine pain and thus prevent it. This review will outline our current understanding about the phenotype and neurobiology of the premonitory (prodromal) symptoms, which for the purpose of this review will be called 'premonitorylike', given they can start before or during pain. Symptoms starting after pain resolution (postdromal symptoms) will not be covered here. KeywordsMigraine, premonitory, prodrome, functional imaging Disclosure: Nazia Karsan is an Association of British Neurologists/Guarantors of Brain Clinical Research Training Fellow. Peter J Goadsby reports personal fees from Allergan, Amgen, and Eli-Lilly and Company; and personal fees from Akita Biomedical, Alder Biopharmaceuticals, Autonomic Technologies Inc., Avanir Pharma, Cipla Ltd, CoLucid Pharmaceuticals Inc., Dr Reddy's Laboratories, eNeura, ElectroCore LLC, Novartis, Pfizer Inc., Promius Pharma, Quest Diagnostics, Scion, Teva Pharmaceuticals, Trigemina Inc., Scion; and personal fees from MedicoLegal work, Journal Watch, Up-to-Date, Oxford University Press; in addition, Peter J Goadsby has a magnetic stimulation for headache patent pending assigned to eNeura. No funding was received for the publication of this article. Peter J Goadsby is a member of the European Neurological Review Editorial Board. Compliance with Ethics:This study involves a review of the literature and did not involve any studies with human or animal subjects performed by any of the authors.Authorship: All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this manuscript, take responsibility for the integrity of the work as a whole and have given final approval for the version to be published.Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation, and reproduction provided the original author(s) and source are giv...

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Trigger Factors and Premonitory Features of Migraine Attacks: Summary of Studies

Cited by 128 publications

References 61 publications

Sex hormones in women with and without migraine

Sex hormones in women with and without migraine

Cortico–Cortical Connections of Primary Sensory Areas and Associated Symptoms in Migraine

Premonitory-like Symptomatology in Migraine

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