Shirt a Phobia

Sample Page

A migraine trigger reduces the threshold for a migraine attack in someone who is predisposed to migraine.[1][2][3] Genetic, environmental, and neurological factors affect nerve cells and chemical signals in the brain. Once stimuli exceed an individual’s sensitivity threshold, neurological changes can increase activity in pain pathways, heighten blood flow and alter pain signals.[4][5][6] In a person who experiences migraines, the brain may respond to stimuli at a lower threshold, respond more strongly to stimuli, or be less able to adjust in ways that reduce discomfort and avoid over-stimulation.[7][8]

Migraine attacks involve multiple phases: prodrome, aura, headache, and postdrome.[4][5][6] The prodrome phase begins 48 hours or more before the headache phase.[4][5][6] In about 30% of cases, an aura phase with sensory disturbances occurs just before the headache phase.[9][10] The 48 hours after the headache pain ceases is the postdrome.[11]

It can be difficult to identify the beginning of a migraine attack and to determine if something is truly a cause rather than a symptom of already-occurring changes in the brain.[2] Internal migraine triggers such as hormones, stress, disturbed sleep, and fasting affect the body’s ability to maintain a stable state. External migraine triggers such as temperature, noises, and odors can change how the body reacts to sensory information. There is strong evidence that hormonal changes, stress, quality of sleep, and fasting are causally related to migraine attacks. These “catalyst triggers” may increase activity in the hypothalamus or trigeminal system of the brain until it exceeds the migraine threshold.[2] Some sensory sensitivities, food cravings, and mood changes may be early symptoms of the prodromal phase of migraine, rather than causes of migraine.[2][12][1][3]

The most frequently reported migraine trigger for women is hormonal variation.[1][13] From puberty onwards, women experience migraine, particularly migraine without aura, more frequently and with greater severity than men.[14] Migraine without aura is strongly related to fluctuations in estrogen both monthly and across a woman’s lifespan.[15] The next most reported trigger is stress in both women and men.[1][13] Disrupted sleep, fasting, missing meals, dehydration, and sensory overstimulation are also commonly reported triggers.[16][17]

Keeping the body’s internal environment stable appears to protect the brain’s migraine sensitivity threshold, while disruption and stress may lower the sensitivity threshold.[16] Lifestyle changes that support stability, such as regular sleep, regular meals, and stress management, can help to prevent migraines.[16] Pollutants interfere with sleep[18] and increase migraine activity, so improving air quality can be helpful.[19] Whether a possible trigger is an actual cause or an early symptom, managing exposure to stimuli such as smells, lights, sound or touch may reduce discomfort.[20]

Mechanisms and timeline

Migraine attacks involve multiple phases with different neurological and physical mechanisms and symptoms.[21] Categories of possible migraine triggers include emotions, nutrition, sleep, hormones, weather, environmental factors (noise, smells, lights), and strenuous movement.[22] Relationships between mechanisms and symptoms are complex and may be bidirectional. For example, people with migraine are more likely to become anxious and depressed, but people with anxiety and depression also have a higher risk of becoming affected by migraine.[23][24]

The initial prodromal or premonitory phase of a migraine attack can start 48 hours or more before the main headache phase.[4][5][6] Studies of the brain’s structure and function indicate that brain activity in the hypothalamus, thalamus, and cortical regions changes during this time, well before the pain phase of migraine begins.[2][21]

This can cause prodromal symptoms (PSs) such as fatigue, yawning, difficulty concentrating, mood changes, dizziness, neck pain, light sensitivity, food cravings, and nausea. People experiencing these early warning symptoms can sometimes correctly predict an oncoming headache.[2] Such symptoms may persist into the pain phase and postdrome.[2] Some studies suggest that PSs may be linked to activity in particular neuroanatomical pathways and brain regions. Yawning, food cravings, homeostatic regulation, and sleep disturbance may be linked to activity in the hypothalamus. Other PSs, such as neck pain and nausea, may be related to activity in the brainstem.[2]

An aura phase involving visual or other sensory disturbances can last for 5–60 minutes, generally just prior to the onset of headache pain. Aura occurs in approximately 30% of cases.[9][10][14][25] Women are more likely than men to experience migraine without aura.[26][14][27] Women who experience migraine without aura differ from women who experience migraine with aura in onset, symptoms, and recommended treatments.[28] Migraine aura may result from a slow self-propagating spreading wave of hyper-excitation of brain cells (cortical spreading depolarization) that is followed by a lengthy recovery period with reduced blood-flow and lowered neural activity.[21][29]

The pain phase of a migraine attack can involve increased activity in the pain pathway of the brain, with heightened blood flow and transmission of pain signals.[4][5][6][21] The extent to which a possible trigger is causally linked to the onset of headache is uncertain in most cases.[30] However, there is strong evidence to show that hormonal changes, stress, quality of sleep, and fasting can be causally related to migraine. These “catalyst triggers” may act by increasing activity in the hypothalamus or trigeminal system of the brain until it exceeds the brain’s migraine threshold.[2]

The migraine postdrome, or “migraine hangover”, includes the 48 hours after the pain ceases. Symptoms during this period can include tiredness, difficulty concentrating, mood changes, thirst,[31] dizziness and euphoria.[11]

Hormonal changes

Hormonal variation is the most frequently reported migraine trigger for women.[1][13] From puberty onwards, women experience migraine attacks more frequently and with greater severity than men.[14] A population-based study in Denmark suggests the sex difference in attack frequency is largely due to higher rates of migraine without aura (11% in females and 3.59% in males). In comparison, sex differences were not significant in migraine with aura (1.72% in females and 1.58% in males).[32]

This divergence in patterns of migraine attacks in men and women is a result of changes in sex hormones.[14] The incidence of attacks of migraine without aura is strongly related to hormonal fluctuations in estrogen, which varies monthly and across a woman’s lifespan.[15] Migraine episodes are more likely to occur immediately before and during menstruation, possibly due to the drop in estrogen levels before the menstrual period.[33][34]

The occurrence of migraine without aura displays an age-related pattern.[14][26] First onset of migraine is often reported around the first menstrual cycle, and the likelihood of occurrence increases from early adulthood throughout the childbearing years.[32] Incidence and severity of migraine without aura peaks between ages 35 and 50.[26][28] Attacks may worsen during perimenopause due to irregular periods and fluctuating estrogen levels. In some cases, the first onset of migraine may occur during perimenopause.[35][28] Following menopause, estrogen levels tend to stabilize at a lower rate, and migraine frequency and severity are likely to decrease.[14][28]

Migraine episodes tend to diminish during the 2nd and 3rd trimesters of pregnancy, when elevated estrogen levels are stable. They are likely to return following the abrupt drop in estrogen levels after childbirth.[14]

Relationships between oral contraceptive use and migraine are less clear, and may differ depending on migraine type, age, and characteristics of the menstrual cycle. In some cases, use of combined hormonal contraception or hormone replacement therapy can help to stabilize estrogen levels and prevent migraines.[33][34] However, suddenly stopping hormonal contraceptives may be associated with increased attacks.[14][34] Transgender women receiving hormone therapy may experience an increased incidence of migraine. and care should be taken to maintain steady levels of estrogen and monitor carefully for increased risk of ischemic stroke in cases of migraine with aura.[21]

Women who experience migraine with aura differ from women who experience migraine without aura in onset, symptoms, and recommended treatments. Women who perceive aura are more likely to have experienced the first onset of migraine before menarche (the first occurrence of a menstrual cycle).[28] For women who experience migraine with aura, migraines are less likely to improve during pregnancy, and use of oral contraceptives may worsen attacks or increase other health risks.[14] Migraine with aura is associated with higher risks for ischemic stroke and heart disease.[36][34]

Underlying mechanisms are complex and inter-related. Estrogens affect multiple neurotransmitter systems involved in migraine development and pain perception. They activate several types of estrogen receptors in the central nervous system (CNS), influencing neurotransmission and cell function, and setting off intracellular signaling cascades that can modify those neurotransmitter systems. Estrogens can enhance activity in the serotonergic system, helping to protect against migraine attacks. However, estrogens can also reduce activation of the opioid system, increasing susceptibility to pain. By increasing the excitatory neurotransmission of glutamate, estrogens may increase the likelihood of migraine aura.[34]

Stress

The headache trigger that people are most aware of is stress, ranking second to hormonal factors for women and first in reports for men.[1][13][17] Psychological best practices for addressing stress as a possible migraine trigger include relaxation therapy, biofeedback, and cognitive behavioral therapy (CBT).[37] Activities such as relaxation therapy are more likely to be effective when used as a routine part of daily life or to address incidents of stress, rather than during the pain phase of a migraine attack.[38]

Sleep

Migraineurs report a variety of sleep-related issues as possible triggers. These include undersleeping, irregular sleep, frequent night-time waking, and oversleeping. Those who experience chronic migraine may be less likely to maintain consistent sleep habits than those who experience episodic migraines.[17] Jet-lag, shift work, and other disruptions of circadian rhythms may increase migraines.[39][40][41] Changes in migraine frequency have been reported in relation to changes between daylight saving time and standard time.[42]

Sleep habits are negatively affected by factors such as air quality and exposure to ambient and indoor pollutants.[18] A nationwide study of household fuel use in China found that those using solid fuel rather than cleaner fuel were more likely to develop migraines; those who switched from solid fuels to cleaner fuels showed a lower risk of migraines. However, those who used solid fuel but reported good sleep duration were not at a significantly higher risk for migraines, suggesting that sleep played a protective role.[43] Sleep hygiene improvements and maintaining a consistent sleep schedule are among the most frequently recommended migraine management techniques.[44][45][46][47]

Diet

Fasting or missing meals are commonly perceived triggers for migraines, and dietary modifications are a frequent management technique.[17] Missing meals like breakfast can reduce brain glucose levels, leading to hypoglycemia and triggering the release of stress hormones like cortisol and adrenaline, which can affect migraines. Irregular meals are particularly strong predictors of attacks for those experiencing chronic migraines. Eating balanced meals at consistent times and hydrating well can help prevent migraines and lessen migraine symptoms.[48][49]

A wide variety of specific foods and drinks have been reported as possible triggers, including alcohol, coffee, chocolate, cheese, processed meats, monosodium glutamate (MSG), fatty foods,[50] nuts, citrus fruits, and aspartame.[48] Mechanisms of action have been proposed for some of the commonly reported foods and drinks, such as red and white wine, hot dogs, and chocolate.[1] Tyramine, which is naturally present in some alcoholic beverages, most cheeses, processed meats, and other foods. may trigger migraine symptoms in some individuals.[51][52][50] Tyramine is present at low levels in chocolate,[53] but the chemistry of chocolate and the effects of its components on migraine are complex. In some cases, chocolate may be beneficial by helping to prevent inflammatory responses.[50] MSG has been reported as a trigger for migraine in some individuals, but whether or not there is a causative relationship continues to be debated.[54][50]

People may experience food cravings as a result of changes in brain activity during the prodromal phase of migraine. Reports that foods such as chocolate are triggers may actually reflect an increased desire for such foods as an early symptom of migraine attacks.[55][2]

Sensory sensitivity

Sensitivity to light (photophobia), sensitivity to sound (phonophobia), and sensitivity to smells (osmophobia) are often reported as migraine triggers. Some migraineurs may also report sensitivity to touch (allodynia).[56][57] Neuroimaging and neurophysiological studies show changes in sensory thresholds related to sensitivity to light, sound and smell and to pain perception.[2][58] Patient reports of sensitivity triggers may be early symptoms in the prodrome phase of a migraine attack.[59] People often deal with migraine attacks by seeking a dark and quiet space, and limiting further sensory stimulation, including movement, light, sounds, touch, or smells.[57]

Light

Sensitivity to light is a common symptom in migraine. Discomfort is associated with four categories of stimulation: bright light, flickering light, pattern, and color. While the retina of the eye also may be involved, processes in the cerebral cortex of the brain are increasingly seen as explaining discomfort from visual stimulation.[8]

People have been shown to have different thresholds for discomfort from stimuli. During migraine, stimulation can provoke a hyperexcitable cortical response involving specific subsets of neurons. Both the thresholds at which a response occurs and the size of the response may be involved. For example, those with a more sensitive discomfort glare threshold have been shown to display greater activity in the cuneus, lingual gyri, and superior parietal lobules in response to peripheral lights. Photophobia may reflect individual differences in homeostatic response to stimuli, in which cortical hyper-excitability is further aggravated by visual stimulation.[8] Those who are less sensitive to light may better reduce discomfort and avoid over-stimulation.[7][8] It has been suggested that migraineurs may experience dysfunction in inhibitory mechanisms, have difficulty habituating to ongoing stimuli, and even become sensitized to such stimuli.[60]

Strategies for reducing discomfort may include staying in a darkened room, wearing sunglasses or hats to avoid direct sunlight and minimize glare, using fluorescent light filters to soften and diffuse light and reduce flicker,[61] using green lights in preference to other colors,[62] and using anti-glare filters with computers. Evaluating workspace ergonomics and using suitable chairs and proper posture while working may also be helpful.[61]

Sound

Migraineurs frequently report hypersensitivity to sound. Research indicates that they generally may have lower hearing thresholds[63] and lower discomfort thresholds for sounds than non-migraineurs, not just during migraine attacks.[64] Migraineurs also experience lower hearing thresholds than usual during headaches. Lower hearing threshold correlates with headache frequency, and with frequency of auditory, visual, and tactile triggers. Phonophobia in migraineurs correlates with higher brainstem neuronal excitability.[63][65] There is some evidence suggesting that migraineurs may react equally or more strongly to repeated stimuli (potentiation), rather than becoming accustomed to it (habituation).[57]

Smell

Migraineurs may report symptoms related to sense of smell, such as increased aversion to normally unoffensive smells or a heightened awareness of smell.[66][20] This is a possible diagnostic marker of migraine, distinguishing it from other types of headaches.[67] It is more often observed in people with a longer history of migraines and greater migraine-related impairment. This may suggest that sensitivity to stimuli increases over time.[68] Migraineurs who experience scent-related symptoms are more likely to experience insomnia, depression, fatigue, and neuropathic pain, and to report lower quality of life than those without osmophobia.[69]

The brain processes smells through the olfactory, trigeminal, and pheromone systems. There is evidence that different odors may activate different brain regions. Reported trigger smells have been grouped into six general product categories: oil derivatives and others; fetid odors; cooking smells; shampoos and conditioners; cleaning products; and perfumes, insecticides, and rose scent.[59] Perfumes were the smells most frequently reported in connection with migraine attacks.[59][70][71] Those with chronic migraines appear more likely than those with episodic migraines to be sensitive to floral scents. Strategies for reducing scent exposure include using fragrance-free products, improving ventilation and air quality, wearing masks, and using air cleaners.[59][20]

Weather and air quality

Migraines have been reported to be triggered by changes in weather conditions such as temperature, ambient pressure, and humidity, but studies have shown mixed results.[72][73][74][1] Air quality may be a related environmental factor, as is season. A study of adult patients in Be’er Sheva, Israel examined interactions between ambient air pollution, climatic factors, and migraines. Pollutants analyzed included NO2, SO2, PM2.5, and PM10 among others. Meteorologic parameters included solar radiation, relative humidity, and temperature.[19]

Short-term exposures to NO2 and solar radiation were associated with an increase in migraine-related emergency treatment. Cumulative exposures to NO2 and to PM2.5 were associated with greater use of migraine-related medication. Temperature and humidity were secondary factors modulating the short-term effects of pollutants: high temperatures and low humidity in the summer increased NO2 risk, while cold and humid winter conditions increased effects of PM2.5.[19]

References

  1. ^ a b c d e f g h Kesserwani H (1 April 2021). “Migraine Triggers: An Overview of the Pharmacology, Biochemistry, Atmospherics, and Their Effects on Neural Networks”. Cureus. 13 (4) e14243. doi:10.7759/cureus.14243. PMC 8088284. PMID 33954064.
  2. ^ a b c d e f g h i j k Sebastianelli G, Atalar AÇ, Cetta I, Farham F, Fitzek M, Karatas-Kursun H, et al. (October 2024). “Insights from triggers and prodromal symptoms on how migraine attacks start: The threshold hypothesis”. Cephalalgia. 44 (10) 3331024241287224. doi:10.1177/03331024241287224. hdl:11573/1724075. PMID 39380339.
  3. ^ a b Karsan N, Bose P, Newman J, Goadsby PJ (May 2021). “Are some patient-perceived migraine triggers simply early manifestations of the attack?”. Journal of Neurology. 268 (5): 1885–1893. doi:10.1007/s00415-020-10344-1. PMC 8068686. PMID 33399964.
  4. ^ a b c d e Ashina S, Bentivegna E, Martelletti P, Eikermann-Haerter K (June 2021). “Structural and Functional Brain Changes in Migraine”. Pain and Therapy. 10 (1): 211–223. doi:10.1007/s40122-021-00240-5. PMC 8119592. PMID 33594593.
  5. ^ a b c d e Levy D, Moskowitz MA (10 July 2023). “Meningeal Mechanisms and the Migraine Connection”. Annual Review of Neuroscience. 46: 39–58. doi:10.1146/annurev-neuro-080422-105509. ISSN 0147-006X. PMC 11412714. PMID 36913712.
  6. ^ a b c d e Burstein R, Noseda R, Borsook D (April 2015). “Migraine: multiple processes, complex pathophysiology”. The Journal of Neuroscience. 35 (17): 6619–6629. doi:10.1523/JNEUROSCI.0373-15.2015. PMC 4412887. PMID 25926442.
  7. ^ a b Salvati V, Otani S, Tartaglia EM (2025). “Neural signatures of extreme sensitivities to light: cortical markers in hypersensitive and hyposensitive individuals via EEG”. Frontiers in Neuroscience. 19 1542154. doi:10.3389/fnins.2025.1542154. PMC 11931066. PMID 40129722.
  8. ^ a b c d Wilkins AJ, Haigh SM, Mahroo OA, Plant GT (October 2021). “Photophobia in migraine: A symptom cluster?”. Cephalalgia. 41 (11–12): 1240–1248. doi:10.1177/03331024211014633. PMC 8497413. PMID 33990148.
  9. ^ a b Raggi A, Leonardi M, Arruda M, Caponnetto V, Castaldo M, Coppola G, et al. (31 October 2024). “Hallmarks of primary headache: part 1 – migraine”. The Journal of Headache and Pain. 25 (1): 189. doi:10.1186/s10194-024-01889-x. PMC 11529271. PMID 39482575.
  10. ^ a b Dodick DW (May 2018). “A Phase-by-Phase Review of Migraine Pathophysiology”. Headache. 58 Suppl 1: 4–16. doi:10.1111/head.13300. PMID 29697154.
  11. ^ a b Pescador Ruschel MA, De Jesus O (2024). “Migraine Headache”. StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809622. Retrieved 13 September 2024.
  12. ^ Zobdeh F, Ben Kraiem A, Attwood MM, Chubarev VN, Tarasov VV, Schiöth HB, et al. (December 2021). “Pharmacological treatment of migraine: Drug classes, mechanisms of action, clinical trials and new treatments”. British Journal of Pharmacology. 178 (23): 4588–4607. doi:10.1111/bph.15657. PMID 34379793.
  13. ^ a b c d Stubberud A, Buse DC, Kristoffersen ES, Linde M, Tronvik E (20 December 2021). “Is there a causal relationship between stress and migraine? Current evidence and implications for management”. The Journal of Headache and Pain. 22 (1): 155. doi:10.1186/s10194-021-01369-6. PMC 8685490. PMID 34930118.
  14. ^ a b c d e f g h i j Kuruvilla DE, Hutchinson S, Moriarty M, Abbott C, Brown A, Leroue C, et al. (January 2025). “Understanding migraine throughout a woman’s life and the role of calcitonin gene-related peptide: A narrative review”. Women’s Health (London, England). 21 17455057251376878. doi:10.1177/17455057251376878. PMC 12547133. PMID 41109841.
  15. ^ a b Pavlović JM (2020). “The impact of midlife on migraine in women: summary of current views”. Women’s Midlife Health. 6 11. doi:10.1186/s40695-020-00059-8. PMC 7542111. PMID 33042563.
  16. ^ a b c Jenkins B (1 October 2020). “Migraine management”. Aust Prescr. 43 (5): 148–151. doi:10.18773/austprescr.2020.047. PMC 7572189. PMID 33093740.
  17. ^ a b c d Elmazny A, Magdy R, Hussein M, Ismaeel AY, Essmat A, Elbeltagy KE, et al. (1 September 2025). “Migraine triggers and lifestyle modifications: an assessment of patients’ awareness and the role of healthcare providers in patient education”. The Journal of Headache and Pain. 26 (1): 189. doi:10.1186/s10194-025-02107-y. PMC 12400567. PMID 40890611.
  18. ^ a b Liu J, Wu T, Liu Q, Wu S, Chen JC (July 2020). “Air pollution exposure and adverse sleep health across the life course: A systematic review”. Environmental Pollution. 262 114263. Bibcode:2020EPoll.26214263L. doi:10.1016/j.envpol.2020.114263. PMC 7877449. PMID 32443219.
  19. ^ a b c Peles I, Novack L, Gordon M, Sarov B, Novack V, Ifergane G (12 May 2026). “Acute Environmental Triggers and Intermediate-Term Modulators of Emergency Migraine-Related Health Care Encounters”. Neurology. 106 (9) e214936. doi:10.1212/WNL.0000000000214936. PMC 13089202. PMID 41985109.
  20. ^ a b c Smith L (6 February 2025). “Osmophobia and Migraine”. Association of Migraine Disorders. Retrieved 17 November 2025.
  21. ^ a b c d e Ahmad SR, Rosendale N (July 2022). “Sex and Gender Considerations in Episodic Migraine”. Current Pain and Headache Reports. 26 (7): 505–516. doi:10.1007/s11916-022-01052-8. PMC 9325838. PMID 35679008.
  22. ^ “Migraine Triggers: Avoid or Cope?”. Migraine Canada. 2024-06-28. Retrieved 2025-11-11.
  23. ^ Duan S, Ren Z, Xia H, Wang Z, Zheng T, Li G, et al. (2023). “Associations between anxiety, depression with migraine, and migraine-related burdens”. Frontiers in Neurology. 14 1090878. doi:10.3389/fneur.2023.1090878. PMC 10166814. PMID 37181566.
  24. ^ Giri S, Tronvik EA, Hagen K (21 January 2022). “The bidirectional temporal relationship between headache and affective disorders: longitudinal data from the HUNT studies”. The Journal of Headache and Pain. 23 (1): 14. doi:10.1186/s10194-022-01388-x. PMC 8903630. PMID 35062883.
  25. ^ Ashina M (November 2020). “Migraine”. The New England Journal of Medicine. 383 (19): 1866–1876. doi:10.1056/NEJMra1915327. PMID 33211930. S2CID 227078662.
  26. ^ a b c Allais G, Chiarle G, Sinigaglia S, Airola G, Schiapparelli P, Benedetto C (December 2020). “Gender-related differences in migraine”. Neurological Sciences. 41 (Suppl 2): 429–436. doi:10.1007/s10072-020-04643-8. PMC 7704513. PMID 32845494.
  27. ^ Denney DE, Hendry M, Pahlevan N, Ayaz A, Denney DA (16 May 2024). “Migraine Throughout a Woman’s Life: A Guide to Management”. Journal of the Mississippi State Medical Association. 65 (5/6).
  28. ^ a b c d e Bugge NS, Vetvik KG, Alstadhaug KB, Braaten T (20 June 2025). “Migraine through puberty and menopausal transition-data from the population-based Norwegian Women and Health study (NOWAC)”. The Journal of Headache and Pain. 26 (1): 145. doi:10.1186/s10194-025-02083-3. PMC 12180204. PMID 40542382.
  29. ^ O’Hare L, Asher JM, Hibbard PB (10 June 2021). “Migraine Visual Aura and Cortical Spreading Depression—Linking Mathematical Models to Empirical Evidence”. Vision. 5 (2): 30. doi:10.3390/vision5020030. PMC 8293461. PMID 34200625.
  30. ^ Grangeon L, Lange KS, Waliszewska-Prosół M, Onan D, Marschollek K, Wiels W, et al. (20 February 2023). “Genetics of migraine: where are we now?”. The Journal of Headache and Pain. 24 (1): 12. doi:10.1186/s10194-023-01547-8. PMC 9940421. PMID 36800925.
  31. ^ Thuraiaiyah J, Ashina H, Christensen RH, Al-Khazali HM, Ashina M (21 February 2024). “Postdromal symptoms in migraine: a REFORM study”. The Journal of Headache and Pain. 25 (1): 25. doi:10.1186/s10194-024-01716-3. PMC 10880332. PMID 38383318.
  32. ^ a b Chalmer MA, Kogelman LJ, Callesen I, Christensen CG, Techlo TR, Møller PL, et al. (June 2023). “Sex differences in clinical characteristics of migraine and its burden: a population-based study”. European Journal of Neurology. 30 (6): 1774–1784. doi:10.1111/ene.15778. PMID 36905094.
  33. ^ a b Reddy N, Desai MN, Schoenbrunner A, Schneeberger S, Janis JE (10 March 2021). “The complex relationship between estrogen and migraines: a scoping review”. Systematic Reviews. 10 (1): 72. doi:10.1186/s13643-021-01618-4. PMC 7948327. PMID 33691790.
  34. ^ a b c d e Nappi RE, Tiranini L, Sacco S, De Matteis E, De Icco R, Tassorelli C (15 April 2022). “Role of Estrogens in Menstrual Migraine”. Cells. 11 (8): 1355. doi:10.3390/cells11081355. PMC 9025552. PMID 35456034.
  35. ^ Ferrari MD, Goadsby PJ, Burstein R, Kurth T, Ayata C, Charles A, et al. (January 2022). “Migraine”. Nature Reviews. Disease Primers. 8 (1) 2. doi:10.1038/s41572-021-00328-4. PMID 35027572. S2CID 245883895.
  36. ^ Tana C, Onan D, Messina R, Waliszewska-Prosół M, Garcia-Azorin D, Leal-Vega L, et al. (August 2025). “From Headache to Heart Health: Investigating the Migraine-Cardiovascular Disease Connection”. Neurology and Therapy. 14 (4): 1229–1268. doi:10.1007/s40120-025-00785-z. PMC 12255647. PMID 40540097.
  37. ^ Penzien DB, Irby MB (1 January 2024). “Biobehavioral treatments of migraine”. In Swanson JW, Matharu M (eds.). Handbook of Clinical Neurology, Vol. 199 (3rd series) Migraine Management. Vol. 199. Elsevier. pp. 155–169. doi:10.1016/B978-0-12-823357-3.00031-8. ISBN 978-0-12-823357-3. PMID 38307643.
  38. ^ Sturgeon JA, Ehde DM, Darnall BD, Barad MJ, Clauw DJ, Jensen MP (June 2023). “Psychological Approaches for Migraine Management”. Anesthesiology Clinics. 41 (2): 341–355. doi:10.1016/j.anclin.2023.02.002. PMC 10513739. PMID 37245946.
  39. ^ Woldeamanuel YW, Rahman A, Hyimanot ET, Chirravuri R, Fani M, Javaheri ED, et al. (2025). “Disrupting the clock: Meta-analysis of irregular night shifts and migraine, proposing shift work migraine disorder with chronobiology strategies”. Frontiers in Neurology. 16 1684169. doi:10.3389/fneur.2025.1684169. medRxiv 10.1101/2025.07.31.25332540. PMC 12728237. PMID 41451422.
  40. ^ Stanyer EC, Brookes J, Pang JR, Urani A, Holland PR, Hoffmann J (8 September 2023). “Investigating the relationship between sleep and migraine in a global sample: a Bayesian cross-sectional approach”. The Journal of Headache and Pain. 24 (1): 123. doi:10.1186/s10194-023-01638-6. PMC 10486047. PMID 37679693.
  41. ^ Leso V, Gervetti P, Mauro S, Macrini MC, Ercolano ML, Iavicoli I (January 2020). “Shift work and migraine: A systematic review”. Journal of Occupational Health. 62 (1) e12116. doi:10.1002/1348-9585.12116. PMC 7154593. PMID 32515906.
  42. ^ Göbel CH, Heinze-Kuhn K, Heinze A, Cirkel A, Göbel H (5 March 2025). “The Impact of Biseasonal Time Changes on Migraine”. Neurology International. 17 (3): 40. doi:10.3390/neurolint17030040. PMC 11944957. PMID 40137461.
  43. ^ Yan J, Wang X, Ding B, Zhang M, He Q, Zeng Y, et al. (2025). “Household fuel use and migraine among Chinese adults aged 45 years and older: The modifying effects of sleep”. PLOS ONE. 20 (12) e0335407. Bibcode:2025PLoSO..2035407Y. doi:10.1371/journal.pone.0335407. PMC 12668480. PMID 41325283.
  44. ^ Robblee J, Starling AJ (November 2019). “SEEDS for success: Lifestyle management in migraine”. Cleveland Clinic Journal of Medicine. 86 (11): 741–749. doi:10.3949/ccjm.86a.19009. PMID 31710587.
  45. ^ Daou M, Vgontzas A (August 2024). “Sleep Symptoms in Migraine”. Current Neurology and Neuroscience Reports. 24 (8): 245–254. doi:10.1007/s11910-024-01346-x. PMID 38864968.
  46. ^ Waliszewska-Prosół M, Nowakowska-Kotas M, Chojdak-Łukasiewicz J, Budrewicz S (24 May 2021). “Migraine and Sleep-An Unexplained Association?”. International Journal of Molecular Sciences. 22 (11): 5539. doi:10.3390/ijms22115539. PMC 8197397. PMID 34073933.
  47. ^ Duan S, Ren Z, Xia H, Wang Z, Zheng T, Liu Z (2022). “Association between sleep quality, migraine and migraine burden”. Frontiers in Neurology. 13 955298. doi:10.3389/fneur.2022.955298. PMC 9459411. PMID 36090858.
  48. ^ a b Legesse SM, Addila AE, Jena BH, Jikamo B, Abdissa ZD, Hailemarim T (26 March 2025). “Irregular meal and migraine headache: a scoping review”. BMC Nutrition. 11 (1): 60. doi:10.1186/s40795-025-01048-8. PMC 11938733. PMID 40140884.
  49. ^ Arca KN, Halker Singh RB (15 July 2021). “Dehydration and Headache”. Current Pain and Headache Reports. 25 (8): 56. doi:10.1007/s11916-021-00966-z. PMC 8280611. PMID 34268642.
  50. ^ a b c d Tu YH, Chang CM, Yang CC, Tsai IJ, Chou YC, Yang CP (13 February 2025). “Dietary Patterns and Migraine: Insights and Impact”. Nutrients. 17 (4): 669. doi:10.3390/nu17040669. PMC 11858445. PMID 40004997.
  51. ^ Özturan A, Şanlıer N, Coşkun Ö (2016). “The Relationship Between Migraine and Nutrition”. Turk J Neurol. 22 (2): 44–50. doi:10.4274/tnd.37132.
  52. ^ Fayed AI, Emam H, Abdel-Fattah AN, Shamloul RM, Elkholy TA, Yassen EM, et al. (20 February 2024). “The correlation between the frequent intake of dietary migraine triggers and increased clinical features of migraine (analytical cross-sectional study from Egypt)”. Scientific Reports. 14 (1): 4150. Bibcode:2024NatSR..14.4150F. doi:10.1038/s41598-024-54339-8. PMC 10879089. PMID 38378909.
  53. ^ Deus VL, Bispo E, Franca AS, Gloria M (1 December 2020). “Influence of cocoa clones on the quality and functional properties of chocolate – Nitrogenous compounds”. LWT. 134 110202. doi:10.1016/j.lwt.2020.110202. hdl:1843/41303. ISSN 0023-6438.
  54. ^ Ahdoot E, Cohen F (March 2024). “Unraveling the MSG-Headache Controversy: an Updated Literature Review”. Current Pain and Headache Reports. 28 (3): 119–124. doi:10.1007/s11916-023-01198-z. PMID 38079074.
  55. ^ Lisicki M, Schoenen J (2021). “Old Habits Die Hard: Dietary Habits of Migraine Patients Challenge our Understanding of Dietary Triggers”. Frontiers in Neurology. 12 748419. doi:10.3389/fneur.2021.748419. PMC 8636453. PMID 34867734.
  56. ^ Aguilar-Shea AL, Membrilla Md JA, Diaz-de-Teran J (February 2022). “Migraine review for general practice”. Atencion Primaria. 54 (2) 102208. doi:10.1016/j.aprim.2021.102208. PMC 8605054. PMID 34798397.
  57. ^ a b c Villar-Martinez MD, Goadsby PJ (September 2022). “Pathophysiology and Therapy of Associated Features of Migraine”. Cells. 11 (17): 2767. doi:10.3390/cells11172767. PMC 9455236. PMID 36078174.
  58. ^ Russo A, Coppola G, Pierelli F, Parisi V, Silvestro M, Tessitore A, et al. (2018). “Pain Perception and Migraine”. Frontiers in Neurology. 9 576. doi:10.3389/fneur.2018.00576. PMC 6082953. PMID 30116215.
  59. ^ a b c d Imai N, Osanai A, Moriya A, Katsuki M, Kitamura E (25 May 2023). “Classification of odors associated with migraine attacks: a cross-sectional study”. Scientific Reports. 13 (1): 8469. Bibcode:2023NatSR..13.8469I. doi:10.1038/s41598-023-35211-7. PMC 10213061. PMID 37230996.
  60. ^ Fong CY, Law W, Fahrenfort JJ, Braithwaite JJ, Mazaheri A (5 April 2022). “Attenuated alpha oscillation and hyperresponsiveness reveals impaired perceptual learning in migraineurs”. The Journal of Headache and Pain. 23 (1): 44. doi:10.1186/s10194-022-01410-2. PMC 8981672. PMID 35382735.
  61. ^ a b Haghdoost F, Togha M (January 2022). “Migraine management: Non-pharmacological points for patients and health care professionals”. Open Medicine. 17 (1): 1869–1882. doi:10.1515/med-2022-0598. PMC 9691984. PMID 36475060.
  62. ^ Martin LF, Patwardhan AM, Jain SV, Salloum MM, Freeman J, Khanna R, et al. (February 2021). “Evaluation of green light exposure on headache frequency and quality of life in migraine patients: A preliminary one-way cross-over clinical trial”. Cephalalgia. 41 (2): 135–147. doi:10.1177/0333102420956711. PMC 8034831. PMID 32903062.
  63. ^ a b Kalita J, Misra UK, Bansal R (March 2021). “Phonophobia and brainstem excitability in migraine”. The European Journal of Neuroscience. 53 (6): 1988–1997. doi:10.1111/ejn.15078. PMID 33305448.
  64. ^ Mourgela A, Vikelis M, Reiss JD (1 September 2023). “Investigation of Frequency-Specific Loudness Discomfort Levels in Listeners With Migraine: A Case-Control Study”. Ear and Hearing. 44 (5): 1007–1013. doi:10.1097/AUD.0000000000001339. PMC 10426780. PMID 36790444.
  65. ^ Kalita J, Bansal R, Mahajan R, Jha V (November 2025). “Effect of High-Rate Repetitive Transcranial Magnetic Stimulation on Phonophobia and Brainstem Auditory Evoked Potential in Migraine”. Molecular Neurobiology. 62 (11): 14079–14088. doi:10.1007/s12035-025-05190-z. PMID 40660010.
  66. ^ Fornazieri MA, Neto AR, de Rezende Pinna F, Gobbi Porto FH, de Lima Navarro P, Voegels RL, et al. (November 2016). “Olfactory symptoms reported by migraineurs with and without auras”. Headache. 56 (10): 1608–1616. doi:10.1111/head.12973. PMID 27779326.
  67. ^ Delussi M, Laporta A, Fraccalvieri I, de Tommaso M (18 September 2021). “Osmophobia in primary headache patients: associated symptoms and response to preventive treatments”. The Journal of Headache and Pain. 22 (1): 109. doi:10.1186/s10194-021-01327-2. PMC 8449918. PMID 34537019.
  68. ^ Gossrau G, Frost M, Klimova A, Koch T, Sabatowski R, Mignot C, et al. (15 July 2022). “Interictal osmophobia is associated with longer migraine disease duration”. The Journal of Headache and Pain. 23 (1): 81. doi:10.1186/s10194-022-01451-7. PMC 9284850. PMID 35840888.
  69. ^ Meşe Pekdemir E, Tanik N (October 2023). “Clinical significance of osmophobia and its effect on quality of life in people with migraine”. Acta Neurologica Belgica. 123 (5): 1747–1755. doi:10.1007/s13760-022-02030-y. PMID 35864435.
  70. ^ Kazemi Z, Aboutaleb E, Shahsavani A, Kermani M, Kazemi Z (June 2022). “Evaluation of pollutants in perfumes, colognes and health effects on the consumer: a systematic review”. Journal of Environmental Health Science & Engineering. 20 (1): 589–598. Bibcode:2022JEHSE..20..589K. doi:10.1007/s40201-021-00783-x. PMC 9163252. PMID 35669814.
  71. ^ Rádis-Baptista G (1 March 2023). “Do Synthetic Fragrances in Personal Care and Household Products Impact Indoor Air Quality and Pose Health Risks?”. Journal of Xenobiotics. 13 (1): 121–131. doi:10.3390/jox13010010. PMC 10051690. PMID 36976159.
  72. ^ Li S, Liu Q, Ma M, Fang J, He L (17 April 2025). “Association between weather conditions and migraine: a systematic review and meta-analysis”. Journal of Neurology. 272 (5): 346. doi:10.1007/s00415-025-13078-0. PMID 40246758.
  73. ^ Denney DE, Lee J, Joshi S (April 2024). “Whether Weather Matters with Migraine”. Current Pain and Headache Reports. 28 (4): 181–187. doi:10.1007/s11916-024-01216-8. PMC 10940451. PMID 38358443.
  74. ^ Cioffi I, Farella M, Chiodini P, Ammendola L, Capuozzo R, Klain C, et al. (May 2017). “Effect of weather on temporal pain patterns in patients with temporomandibular disorders and migraine”. Journal of Oral Rehabilitation. 44 (5): 333–339. doi:10.1111/joor.12498. PMID 28244179.