Journal Logo

Department: Decoding Genetics

Genetic aspects of migraine headaches

Pestka, Elizabeth L. MS, PMNCNS-BC, APNG; Nash, Virginia R. DNP, PMHCNS-BC

Author Information
doi: 10.1097/01.CCN.0000412318.51705.6f
  • Free

Suppose you develop a severe migraine headache before your scheduled night shift and end up lying in bed rather than going to work. You're aware that migraine headaches run in your family, but do you know about the genetic factors associated with this disorder? This article presents an overview of genetic aspects of migraine headaches and the clinical implications for nurses.

Genetics of migraine headaches

Up to 90% of people with migraines have a family history of this condition.1 Research suggests that genetic contributions to migraine headaches without aura and with aura are complex—that is, there's no single contributing gene—and are influenced by environmental factors (see Types of migraines with genetic causes and treatments). Although migraines aren't conclusively linked to any single genes, several susceptibility locations have been identified in genome-wide screens and candidate studies.2,3

Migraines have been investigated in family and twin studies, with results of twin studies suggesting about 50% heritability. In other words, inherited genetic factors are about 50% responsible for migraines in people identified as having the condition.2 Migraines with aura (perceptual disturbances before headache onset) have a stronger familial genetic link. The relative risk, or probability of migraines occurring in a person with a family history of the condition, is about three times greater for migraines with aura compared to migraines without aura.2

One rare serious type, familial hemiplegic migraine, is transmitted in an autosomal dominant method of inheritance (50% chance of passing to an offspring), and is linked to mutations in the calcium channel gene CACNA1A on chromosome 19 and the sodium/potassium pump gene ATP1A2 on chromosome 1.2,3 Attacks of familial hemiplegic migraine usually include an aura and are frequently characterized by motor symptoms, including unilateral weakness or paralysis and impaired consciousness, seizures, and fever.2

Who gets migraines?

Migraines affect 15% to 33% of adult women and 6% to 15% of adult men, although these percentages are likely low due to underreporting.4 About 4% of children get migraines, with the condition more common in girls than boys.4 Hormonal changes may be the reason that women are more likely to get migraines than men. Women with a history of migraines often report headaches before or during their menstrual cycle, when they have a major drop in estrogen. Other women have an increased tendency to develop migraines during pregnancy or menopause.

Does being in a stressful profession such as nursing increase your risk for migraines? Research has found that the prevalence of migraines in nurses is consistent with the reported rate of migraines among the general population.5 Nurses who reported migraines indicated that headaches affected their perceived quality of life as measured by more sick days, arriving late to work, and diminished productivity.5

Treatments for migraines

Obtaining your patient's family history may be helpful in determining the treatment plan for migraines. Treatment modalities that have been successful for biologic family members oftentimes are most effective for relatives with similar conditions. Genetic factors influence variability in drug absorption, distribution, metabolism, and excretion. For example, to provide analgesia, codeine must be biotransformed by cytochrome P450 2D6 (CYP2D6) into morphine. Between 8% and 10% of the White population and 50% of people of Asian descent have a variation of CYP2D6 that causes the enzyme to be inactive, making codeine ineffective for these patients.6 Pharmacogenetic testing, although still not routine, is readily available and can be used to help determine optimal medication choices.

Nonpharmacologic treatments include resting in a dark, quiet environment, relaxation strategies such as diaphragmatic breathing or guided imagery, cold compresses, reducing stress-producing environmental factors as much as possible, and using cognitive behavioral strategies. Growing evidence indicates that these methods can be helpful in managing migraines.7

First-line pharmacologic interventions are nonprescription medications (ibuprofen, acetaminophen, and aspirin) for acute mild-to-moderate headaches. Prescription medications for more severe headaches include triptans, ergots, antiemetics, opioids (short-term use only), and butalbital. Some medications used prophylactically to prevent headaches include tricyclic antidepressants, selective serotonin reuptake inhibitors, beta-adrenergic blockers, calcium channel blockers, antiepileptic drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), and botulinum toxin type A. The decision to initiate preventive treatment is based on frequency, duration, severity, response to acute treatments, and disability during migraines. Preventive therapy may be started for someone with two or more debilitating attacks in a month. Nonpharmacologic preventive treatments include avoiding migraine triggers (which can be foods such as alcohol, caffeine, aged cheeses, chocolate, aspartame, and monosodium glutamate; medications; or environmental stimuli), relaxation strategies, and getting regular exercise and adequate sleep.1

Table
Table:
Types of migraines with genetic causes and treatments1

Some patients develop rebound headaches from medication overuse with various agents taken more than several days per week. With these patients the medication overuse issue must be resolved; then a stronger focus on nonpharmacologic methods will likely produce better headache management.7

Clinical implications for nurses

Family history provides a considerable genetic risk for migraines, but except in rare cases, inherited risk must combine with environmental risk factors to become a problematic health condition. Some environmental headache factors can be modified, such as taking estrogen; keeping a diary of beverages, foods, or additives that may trigger headaches and altering intake accordingly; learning to cope with stress more effectively; reducing problematic stimuli that may induce headaches, such as bright lights or strong smells; and living a healthful lifestyle of adequate regular exercise and sleep. A management plan is individualized for each patient.

Provide ongoing education to help patients learn more about their migraine pattern and triggers, and to modify their lifestyle. Encourage use of nonpharmacologic management strategies and only pharmacologic interventions that are beneficial and don't lead to overuse or rebound headaches.

Feeling better

Now that you understand migraines better, you can keep a headache diary noting when headaches start, what may have precipitated them, how long they last, and what provides relief. Focus on reducing stress in your life, enhancing your coping strategies, and living a healthful lifestyle. You and your patients can't control your inherited risk for migraine headaches, but you can modify environmental risk factors contributing to the condition.

REFERENCES

1. Migraine. Mayo Clinic. 2011. http://www.mayoclinic.com/health/migraine-headache/DS00120.
2. Gardner KL. Genetics of migraine: an update. Headache. 2006;46(suppl 1):S19-S24.
3. Haan J, van den Maagdenberg A, Palotie A, Ferrari M. Migraine genetics. In: Mogil J, ed. The Genetics of Pain: Progress in Pain Research and Management. Seattle, WA: IASP Press; 2004:193–209,
4. Wieser T, Pascual J, Oterino A, Soso M, Barmada M, Gardner KL. A novel locus for familial migraine on Xp22. Headache. 2010;50(6):955–962.
5. Durham CF, Alden KR, Dalton JA, et al. Quality of life and productivity in nurses reporting migraine. Headache, 1998;38(6):427–435.
6. Miaskowski C. Understanding the genetic determinants of pain and pain management. Semin Oncol Nurs. 2009;25(2 suppl 1):S1-S7.
7. Bruce BK, Townsend CO, Hooten WM, Rome JD, Moon JS, Swanson JW. Chronic pain rehabilitation in chronic headache disorders. Curr Neurol Neurosci Rep. 2008;8(2):94–99.
© 2012 Lippincott Williams & Wilkins, Inc.