Causes and Risk Factors of Migraine

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The causes of migraines are primarily neurologic, but also involve genetic factors. Symptoms, including premonitory symptoms, aura, headache, and postdrome phase, involve dysfunction in several parts of the brain, pain pathways, and brain chemicals. There are also many exacerbating factors that are associated with the triggering of migraines.

Migraine risk factors
Verywell / Brianna Gilmartin  

Common Causes

Migraines are thought to have a variety of possibly causes, including:


It is very difficult to pinpoint the genetic basis of migraines because it is likely a complex interaction of many factors. However, migraines are probably inherited. In fact, there's a higher rate of both twins having migraine headaches in identical twins, with the same genetic makeup, versus fraternal twins, with different genetic makeup.

The risk of a person having a migraine is three times greater if they have relatives who also experience migraines.

There are a few abnormalities in the neural pathways of the brain that have been identified in certain groups and individuals who get migraines that are linked to genetics. However, genes do not act alone—additional environmental factors make individuals more prone to migraines. Researchers are still looking for the exact genetic causes so effective treatments can be created.

Brain Structure

Some studies have shown that some people with migraines have altered blood flow to areas of the brain that involve migraine symptoms. Structural changes in the brain have also been identified.


Women may be prone to migraines since estrogen has several important actions in the central nervous system. Usually, menstrual migraines occur within a window of two days before the onset of period bleeding to three days after the onset of bleeding. Estrogen may affect some chemical mediators, such as magnesium, which may alter the excitatory and inhibitory neural pathways in the brain.

When estrogen concentrations decline in the brain during your period, serotonin concentrations decline too. This causes a release of substances that cause vasodilation (widening) of cranial blood vessels and sensitization of specific nerves in the brain that may lead to the symptoms of a migraine.

Cortical spreading depression

It is believed the pain that follows a migraine with aura is due to something called cortical spreading depression. This is when parts of the brain become depressed, causing inflammatory changes in the pain-sensitive parts of the brain that generate the headache of migraine.


Sensitization is the process by which neurons, the cells in the brain, become increasingly responsive to stimulation. This is likely the cause for many of the clinical symptoms of a migraine, which includes worsening of pain with certain motion, sensitivity to painful stimuli, throbbing sensation, and even increased sensitivity to painful things that may not normally cause pain.


The evidence is currently conflicting, but associations have been made between migraines and a congenital heart defect called a patent foramen ovale. A patent foramen ovale, also known as a right-to-left cardiac shunt, is when the hole between the right and left atrium doesn't close at birth. Other congenital heart defects, such as an atrial septal defect, have been linked to migraines. The mechanism as to why this might occur is not completely understood. It's possible that an underlying genetic basis ties the two conditions together. Other theories involve the change in direction of blood flow with these heart defects.

Migraine Triggers

In a study published in 2007, 1,200 patients were evaluated to determine the relationship between triggers and migraines; 75.9 percent of them reported triggers. Forty percent infrequently had triggers, 26.7 percent frequently had triggers, and 8.8 percent very frequently had triggers. The leading triggers were:

  • Stress, reported by 80% of participants
  • Hormone changes in women, reported by 65%
  • Not eating, reported by 57%
  • Weather, reported by 53%
  • Sleep disturbance, reported by 50%
  • Odors, such as perfume, reported by 44%
  • Neck pain, reported by 38%
  • Lights, reported by 38%
  • Alcohol, reported by 38%
  • Smoke, reported by 36%
  • Sleeping late, reported by 32%
  • Heat, reported by 30%
  • Food, reported by 27%
  • Exercise, reported by 22%
  • Sexual activity, reported by 5%

Poor sleep quality and obesity have both been associated with increased migraine frequency and severity. Sleep apnea, jaw clenching, or teeth grinding may also trigger migraines. These things may exist together, as those who are obese may have sleeping disorders, such as sleep apnea.

Migraine headaches can sometimes get worse by constant movement, physical exertion, and rapid head motion. Certain psychiatric conditions may also impact migraine frequency. Caffeine can be a trigger as well.

Frequently Asked Questions

  • What causes an ocular migraine?

    An ocular migraine has two types: a migraine with an aura or a retinal migraine. A migraine with an aura, or flashes of light, is thought to be caused by abnormal electrical activity in the brain's cortex. A retinal migraine, with short periods of vision loss in one eye, is caused by similar disturbances in the back of the eye's retina or decreased blood flow to the retina. Triggers may include harsh lights and electronic screens.

  • What causes migraines in children?

    Children can have some of the same causes of migraines as adults. Some common triggers for children and adolescents include:

    • Stress, especially related to school, friends, and family
    • Lack of sleep
    • Skipping meals
    • Caffeine
    • Weather changes
    • Menstruation
    • Changes in routine with travel or illness
    • Certain foods or food additives
    • Some medications, such as asthma treatments or those for ADHD
5 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
  1. Dalkara T, Nozari A, Moskowitz MA. Migraine aura pathophysiology: the role of blood vessels and microembolisation. Lancet Neurol. 2010;9(3):309-17.

  2. Chai NC, Peterlin BL, Calhoun AH. Migraine and estrogen. Curr Opin Neurol. 2014;27(3):315-24. doi:10.1097/WCO.0000000000000091

  3. Cui Y, Kataoka Y, Watanabe Y. Role of cortical spreading depression in the pathophysiology of migraine. Neurosci Bull. 2014;30(5):812-22. doi:10.1007/s12264-014-1471-y

  4. American Migraine Foundation. Understanding ocular migraine.

  5. Cleveland Clinic. Migraines in children and adolescents.

Additional Reading
  • Granziera C, DaSilva AF, Snyder J, Tuch DS, Hadjikhani N. Anatomical alterations of the visual motion processing network in migraine with and without aura. PLoS Med. 2006 Oct;3(10):e402. DOI: 10.1371/journal.pmed.0030402

  • Kelman L. The triggers or precipitants of the acute migraine attack. Cephalalgia. 2007;27(5):394. DOI: 10.1111/j.1468-2982.2007.01303.x

  • Martin VT, Behbehani M. Ovarian hormones and migraine headache: understanding mechanisms and pathogenesis--part I. Headache. 2006;46(1):3. DOI: 10.1111/j.1526-4610.2006.00309.x

  • Merikangas KR, Risch NJ, Merikangas JR, Weissman MM, Kidd KK, Migraine and depression: association and familial transmission. J Psychiatr Res. 1988;22(2):119

  • Walters AB, Hamer JD, Smitherman TA. Sleep disturbance and affective comorbidity among episodic migraineurs. Headache. 2014 Jan;54(1):116-24

By Lyndsey Garbi, MD
Lyndsey Garbi, MD, is double board-certified in pediatrics and neonatology. She is an assistant professor at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell and chief pediatrician at Blueberry Pediatrics.