- 6 New Migraine Treatments You Should Know About
- Migraine Overview and Summary of Current and Emerging Treatment Options
- Treatment of Acute Migraine Headache
- 25 Migraine Treatments, Preventative Meds & Abortive Drugs
- Migraine Headache Treatment & Management: Approach Considerations, Emergency Department Considerations, Reduction of Migraine Triggers
6 New Migraine Treatments You Should Know About
You probably already use one or more of the many migraine treatments out there. They can work well. But they don’t always.
If you still find it hard to stop or prevent your headaches, you’ll want to know what else you can try.
Cefaly is an electrical stimulation device. The FDA says it's effective and has few risks and side effects when used properly. It may help people who have problems with drug side effects.
You wear it a headband across your forehead.
You can use it every day, but not more than once a day:
- Apply the self-adhesive electrode to your forehead.
- Connect the headband to the electrode. This starts the flow of electricity to a nerve linked to migraines.
- You may feel a massaging or tingling sensation.
- Wear it for 20 minutes. It shuts off automatically.
It’s the first TENS (transcutaneous electrical nerve stimulation) device approved for treating migraines before they start.
Other devices may be available. Ask your doctor.
CGRP (calcitonin gene-related peptide) is a molecule involved in causing migraine pain. CGRP inhibitors are a class of drugs that block the effects of CGRP. Erenumab (Aimovig), galcanezumab (Emgality), and remanezumab (Ajovy) are approved to prevent migraine attacks.
Depending on the drug, they’re taken monthly or quarterly by self-injection with a prefilled syringe or pen. Mild pain and redness at the injection site are the most common side effects.
Less often, and in particular with galcanezumab, allergic reactions including itching, rash, hives, and trouble breathing that may require emergency care have been reported.
Your doctor might recommend this if you have chronic migraines.
About every 12 weeks, you get 31 Botox shots around your head and neck. Each session takes 10-15 minutes. After your first session, it may take 10-14 days for your symptoms to improve.
If you get migraines on fewer than 14 days a month or you get other types of headaches, Botox isn’t your answer.
SPG (sphenopalatine ganglion) nerve block. This short, simple procedure numbs the SPG, a group of nerve cells inside and behind your nose. The FDA has approved three devices for doing this.
It works because your SPG is linked to your trigeminal nerve, which is involved in these headaches.
You get the procedure in your doctor’s office. You’ll be awake for it.
Your doctor will insert a thin plastic tube, called a catheter, into your nose, one nostril at a time. Through an attached syringe, you’ll get an anesthetic to numb your SPG and the area around it. Your doctor may use an X-ray machine to be sure the tube is inserted correctly.
Once the numbness wears off, you may still feel relief for some time.
Several types of counseling can help.
In acceptance and commitment therapy (ACT), you accept that you have some migraine pain instead of trying to control it completely or avoid it.
You commit to “grow away” from a focus on migraines to discover goals and values you want more of in your life. And then you take action toward those goals.
Mindfulness-based therapy. “Mindfulness” is a practice of being aware of your mind and body right now. Distracting thoughts come up, but you let them go.
You may find that this helps you manage your migraine pain without being derailed by it. You might also feel less anxious or depressed about it.
You simply notice your thoughts, emotions, and body sensations.
You’ll still need your medicine and other treatments. Mindfulness is an additional practice you can do by yourself.
SOURCES:FDA: “Treating migraines: more ways to fight the pain.”News releases, FDA.American Headache Society: “Botox-A for suppression of chronic migraine: frequently asked questions.
”American Migraine Foundation: “Sphenopalatine ganglion blocks for headache disorders.”Medscape.com: “Image-guided lidocaine injections for headache.
”National Headache Foundation: “New procedure may bring migraine relief.”
Smitherman, T. Current Pain Headache Reports, published online March 29, 2015.
Association for Contextual Behavioral Science: “A Short Guide to Acceptance and Commitment Therapy.”American Headache Society: “Mindfulness meditation for migraine.”
Bromberg, J. Headache, 2012.
© 2020 WebMD, LLC. All rights reserved. Botox for Migraine
Migraine Overview and Summary of Current and Emerging Treatment Options
Golden L. Peters, PharmD, BCPS
Migraine is a leading cause of disability worldwide. Approximately 15% of Americans experience migraines. Most people who have migraines feel that people who do not have them often underestimate their condition. Migraines affect people’s quality of life and ability to participate in work, family, and social events. A new class of medication, calcitonin gene-related peptide (CGRP) antagonists, has been approved for migraine prevention in adults. The newly approved CGRP antagonists are erenumab, fremanezumab, and galcanezumab, while eptinezumab looks to 2020 for approval. Lasmiditan, ubrogepant, and rimegepant are currently emerging acute migraine therapies that may be added to the arsenal of current migraine management.
Am J Manag Care. 2019;25:-S0Introduction to Migraine
The reach of migraine headaches spans the globe.1 Migraine is sometimes confused with other types of headache, such as tension headache. Those with migraines may not receive the correct diagnosis, adequate treatment, or proper support from family, friends, or coworkers.
Migraine treatment usually consists of acute or abortive medications, whereas preventive medications are used by a minority of individuals with migraine. The triptans, or selective serotonin 5-HT1B/1D receptor agonists, were approved for acute migraine therapy in the 1990s.
2 The calcitonin gene-related peptide (CGRP) antagonists approved in 2018 are the first class of medications specifically approved for migraine prevention, contrary to all the other migraine agents that are also used for other conditions.
There are 3 newly approved CGRP monoclonal antibodies (mAbs) and a fourth mAb, a ditan, and 2 CGRP receptor antagonists (gepants) in development for migraine treatments. Erenumab, fremanezumab, and galcanezumab are newly approved CGRP mAbs for the prevention of migraines in adults. The emerging migraine treatments include the mAb eptinezumab, the ditan lasmiditan, and gepants ubrogepant and rimegepant.
Migraines are a leading cause of disability and suffering worldwide. 3 Migraine was ranked as the sixth cause of years lost due to disability globally in 2013.3 Head pain or headache accounted for 3% of emergency department (ED) visits annually and was the fourth or fifth leading reason for patients to visit the ED.
1 In a review by Burch et al, various US government health surveys were analyzed to examine the prevalence and impact of migraines. According to the review, 1 in 6 individuals in the United States are affected by migraines. Contrary to most chronic conditions, people who are usually healthy and young or middle-aged are largely affected.
In Americans aged 15 to 64 years, approximately 1 in 6 people and 1 in 5 women have reported either severe headaches or migraines in the past 3 months. The review also reported the highest migraine prevalence in people aged 18 to 44 years. Of this group, 17.9% experienced a migraine within the previous 3 months. The prevalence of migraines decreases as people age.
For those aged 45 to 64 years, the prevalence was 15.9%, followed by 7.3% for those aged 65 to 74 years and 5.1% in individuals 75 years and older.1
When examining other factors, Burch et al discovered differences regarding gender, ethnicity, work status, income, and insurance type.1 Women were more prone than men to experience migraines. In 1 of the government surveys examined, the 2015 National Health Interview Study reported the overall prevalence of migraines or severe headache to be 15.3%, with 20.
7% prevalence in women and 9.7% prevalence in men. This has remained stable when compared with data from 2006 to 2015. In contrast to previous reports, 18.4% of native Americans (Alaskan natives or American Indians) were the most affected ethnicity compared with white, black, or Hispanic individuals.
4,5 People who worked full-time reported the least number of severe headaches or migraines (13.2%) compared with people working part-time (15.6%), those who were unemployed or had never worked (16.6%), and those who were unemployed but had previously worked (21.4%). Migraine prevalence was highest in those living below the poverty level (21.
7%) and with an annual household income of less than $35,000 (19.9%). This may be explained by increased exposure to migraine triggers and decreased access to treatment and healthcare resources. Burch et al divided the findings relative to insurance by age in 2 groups, younger than 65 years and 65 years and older.
In people younger than 65 years, those with Medicaid had the highest migraine prevalence (26.0%) as compared with those with no insurance (17.1%) and private insurance (15.1%). In those 65 years and older, participants with both Medicare and Medicaid coverage had the highest prevalence at 16.4% compared with those with Medicare Advantage (6.7%), Medicare only (5.
8%), private insurance (4.4%), and other coverage (5.9%). The estimate for the uninsured patients in this age range was considered unreliable due to a relative standard error over 50% and therefore not reported.3
There are several headache classifications outlined by the International Headache Society Headache Classification Committee.6 The more common headaches are outlined in Table 1.6 Migraines are classified as with or without aura.
Migraines with aura have fully reversible sensory, visual, or other symptoms related to the central nervous system. The aura usually begins before migraine onset but may occur with headache onset or after the headache has stopped.
The most common type of aura in patients with migraine is visual aura, followed by sensory disturbances, and, less frequently, speech disturbances. Sensory disturbances may include a pins-and-needles sensation that slowly travels from a point of origin and affects 1 side of the tongue, body, and/or face.
It may also be accompanied by numbness; however, numbness may also occur independently as the only symptom. Speech disturbances are usually aphasic and more difficult to categorize. The prodromal phase occurs hours to days before a headache and/or as a postdromal phase after the headache has resolved.
Pro- and postdromal symptoms may include pain, fatigue, neck stiffness, hypo- or hyperactivity, food cravings, repetitive yawning, and/or depression. Prodromal symptoms may also include various combinations of pallor, blurred vision, fatigue, yawning, difficulty concentrating, nausea, and sensitivity to sound and/or light.6
Episodic migraines are defined as headaches occurring less than 15 days per month.7 Chronic migraines are defined as headache occurring on 15 or more days per month for more than 3 months with at least 8 days having migraine features.
6 Transformed migraines is an additional term used to describe chronic migraines because they evolve from episodic migraines.7 Medication-overuse headaches are the most common cause of symptoms suggestive of chronic migraine.
6 It is defined as taking opioids, triptans, ergotamine, or combination analgesics for more than 9 days monthly, and aspirin, acetaminophen, or nonsteroidal anti-inflammatory drugs (NSAIDs) for more than 14 days monthly.
6 Since the use of combination butalbital products or opioids for fewer than 9 days monthly may increase migraine frequency, these medications should generally be avoided.7,8 Once the medication is withdrawn, approximately 50% of patients return to episodic migraines, suggesting the patient was misdiagnosed with chronic migraines.6
Fewer than 10% of women experience migraines associated with their menstrual cycles. Most women with migraines do not have an aura with menstrual migraines. These attacks are usually coupled with more severe nausea and last longer than nonmenstrual cycle attacks.6
There are several risk factors associated with migraine occurrence. Nonmodifiable factors include genetics, gender, and age. The probability of migraines is 40% in a person with 1 parent with migraines and 75% if both parents experience migraines.
Adult women are 3 times more ly than men to have migraines. However, in preadolescents, migraines are more common in boys.
Migraines usually have an onset in late childhood/early adolescence, and the prevalence peaks in individuals in their 50s, with notable decreases as people enter their 60s and 70s and rare occurrences in people 80 years and older.9
Ineffective acute treatment,10 acute migraine medication overuse,5,7,11-16 obesity,17,18 and stressful life events5,19 are modifiable risk factors that may increase the risk of progression from episodic to chronic migraines.
19 It is also important to note that patients who did not believe they could influence their headache or felt that their headache was due to fate or chance are more ly to insufficiently manage their headaches, resulting in poorer overall disability.20,21 These factors highlight the need for education on methods to best manage and cope with migraines.
Healthcare professionals should educate patients on protective factors that may increase the migraine threshold, including the use of migraine-preventive medication,22 physical exercise, and stress management.19
Migraine triggers are patient specific. Examples include food additives, caffeine, artificial sweeteners, and delayed or missed meals. To determine the probability of an item being a trigger, patients should avoid the item for at least 4 weeks and then slowly reintroduce it, keeping in mind that migraines may start 24 to 48 hours before headache onset.9
Stigma and Impact on the Individual
In 2017, Neilsen conducted a survey sponsored by Eli Lilly, resulting in the Migraine Impact Report.23,24 The report examined the economic, physical, and social impact of migraines. Of the 1018 US adult respondents, 518 were medically diagnosed with migraine, 200 respondents knew a person who experienced migraines, and 300 members of the community did not know anyone with migraines.
Respondents who had given birth ranked the pain of their worst migraine higher than childbirth pain (8.6 vs 7.3 a scale of 1 to 10). Additionally, respondents with medically diagnosed migraines ranked their worst migraine pain (8.6) higher than pain associated with broken bones (7.0) and kidney stones (8.3).
According to the report, people without migraines regularly underestimated the average migraine length (20.7 hours vs 31 hours) and pain. The average pain rating for a typical migraine determined by those without migraines was 6.2 compared with 7.1 by those with migraines. Among people with migraines, 91% indicated that people without migraines are not fully aware of the disease severity.
Sixty-two percent also reported masking the full impact of their migraines when at school or work.
The reporting for those with migraine demonstrated their concerns with the effect of the condition on their lives. Some examples of this include the following24:
- 54%: “I worry that people think I’m lazy because of the impact migraines have on my life and ability to perform tasks.”
- 40%: “I have been told to ‘get over it’ when I am experiencing a migraine attack.”
- 29%: “I sometimes feel my job is in jeopardy because of migraines.”
- 28%: “I have been made fun of for having migraines.”
Most people with migraines also indicated that their migraine attacks frequently interfere with work productivity and advancement, attending important events, and spending time with family and friends, resulting in the addition of more stress, which is a migraine trigger. These statistics highlight the stigma connected to and lack of awareness about migraines.
Migraine Pain Theories (vs Vascular Theory)
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Treatment of Acute Migraine Headache
1. Lipton RB, Stewart WF, Diamond S, Diamond ML, Reed M. Prevalence and burden of migraine in the United States: data from the American Migraine Study II. Headache. 2001;41(7):646–657….
2. International Headache Society. IHS Classification ICHD-II. 1. Migraine. http://ihs-classification.org/en/02_klassifikation/02_teil1/01.01.00_migraine.html. Accessed November 3, 2010.
3. Wilson JF. In the clinic. Migraine [published correction appears in Ann Intern Med 2008;148(5):408]. Ann Intern Med. . 2007;147(9):ITC11-1–ITC11-16.
4. Ebell MH. Diagnosis of migraine headache. Am Fam Physician. 2006;74(12):2087–2088.
5. Morey SS. Headache Consortium releases guidelines for use of CT or MRI in migraine work-up. Am Fam Physician. 2000;62(7):1699–1701. https://www.aafp.org/afp/20001001/practice.html. Accessed August 20, 2010.
6. Locker TE, Thompson C, Rylance J, Mason SM. The utility of clinical features in patients presenting with nontraumatic headache: an investigation of adult patients attending an emergency department. Headache. 2006;46(6):954–961.
7. Goldstein J, Silberstein SD, Saper JR, Ryan RE Jr, Lipton RB. Acetaminophen, aspirin, and caffeine in combination versus ibuprofen for acute migraine: results from a multicenter, double-blind, randomized, parallel-group, single-dose, placebo-controlled study. Headache. 2006;46(3):444–453.
8. Ferrari MD, Roon KI, Lipton RB, Goadsby PJ. Oral triptans (serotonin 5-HT(1B/1D) agonists) in acute migraine treatment: a meta-analysis of 53 trials. Lancet. 2001;358(9294):1668–1675.
9. Goldstein J, Silberstein SD, Saper JR, et al. Acetaminophen, aspirin, and caffeine versus sumatriptan succinate in the early treatment of migraine: results from the ASSET trial. Headache. 2005;45(8):973–982.
10. Brandes JL, Kudrow D, Stark SR, et al. Sumatriptan-naproxen for acute treatment of migraine: a randomized trial. JAMA. 2007;297(13):1443–1454.
11. Colman I, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral metoclopramide for acute migraine: meta-analysis of randomised controlled trials. BMJ. 2004;329(7479):1369–1373.
12. Singh A, Alter HJ, Zaia B. Does the addition of dexamethasone to standard therapy for acute migraine headache decrease the incidence of recurrent headache for patients treated in the emergency department? A meta-analysis and systematic review of the literature [published correction appears in Acad Emerg Med. 2009;16(5):435]. Acad Emerg Med. 2008;15(12):1223–1233.
13. Maizels M, Scott B, Cohen W, Chen W. Intranasal lidocaine for treatment of migraine: a randomized, double-blind, controlled trial. JAMA. 1996;276(4):319–321.
14. Morey SS. Guidelines on migraine: part 2. General principles of drug therapy. Am Fam Physician. 2000;62(8):1915–1917. https://www.aafp.org/afp/20001015/practice.html. Accessed August 21, 2010.
15. Mathew NT, Landy S, Stark S, et al. Fixed-dose sumatriptan and naproxen in poor responders to triptans with a short half-life. Headache. 2009;49(7):971–982.
16. Colman I, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral dihydroergotamine for acute migraine headache: a systematic review of the literature. Ann Emerg Med. 2005;45(4):393–401.
17. Freitag FG, Cady R, DiSerio F, et al. Comparative study of a combination of isometheptene mucate, dichloralphenazone with acetaminophen and sumatriptan succinate in the treatment of migraine. Headache. 2001;41(4):391–398.
18. Colman I, Friedman BW, Brown MD, et al. Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence. BMJ. 2008;336(7657):1359–1361.
19. Goadsby PJ, Zanchin G, Geraud G, et al. Early vs. non-early intervention in acute migraine-‘Act when Mild (AwM)’. A double-blind, placebo-controlled trial of almotriptan [published correction appears in Cephalalgia. 2008;28(6):679]. Cephalalgia. 2008;28(4):383–391.
20. Migraine headache. AAN summary of evidence-based guideline for clinicians. St Paul, Minn.: American Academy of Neurology; 2009. http://www.aan.com/practice/guideline/uploads/120.pdf. Accessed December 14, 2010.
21. Suthisisang C, Poolsup N, Kittikulsuth W, Pudchakan P, Wiwatpanich P. Efficacy of low-dose ibuprofen in acute migraine treatment: systematic review and meta-analysis. Ann Pharmacother. 2007;41(11):1782–1791.
22. Dib M, Massiou H, Weber M, Henry P, Garcia-Acosta S, Bousser MG; Bi-Profenid Migraine Study Group. Efficacy of oral ketoprofen in acute migraine: a double-blind randomized clinical trial. Neurology. 2002;58(11):1660–1665.
23. Meredith JT, Wait S, Brewer KL. A prospective double-blind study of nasal sumatriptan versus IV ketorolac in migraine. Am J Emerg Med. 2003;21(3):173–175.
24. McCrory DC, Gray RN. Oral sumatriptan for acute migraine. Cochrane Database Syst Rev. 2003;(3):CD002915.
25. Färkkilä M, Olesen J, Dahlöf C, et al. Eletriptan for the treatment of migraine in patients with previous poor response or tolerance to oral sumatriptan. Cephalalgia. 2003;23(6):463–471.
26. Tfelt-Hansen P, De Vries P, Saxena PR. Triptans in migraine: a comparative review of pharmacology, pharmacokinetics and efficacy. Drugs. 2000;60(6):1259–1287.
27. O'Quinn S, Davis RL, Gutterman DL, Pait GD, Fox AW. Prospective large-scale study of the tolerability of subcutaneous sumatriptan injection for acute treatment of migraine. Cephalalgia. 1999;19(4):223–231.
28. Jamieson DG. The safety of triptans in the treatment of patients with migraine. Am J Med. 2002;112(2):135–140.
29. Sclar DA, Robison LM, Skaer TL. Concomitant triptan and SSRI or SNRI use: a risk for serotonin syndrome. Headache. 2008;48(1):126–129.
30. Matchar DB, Young WB, Rosenberg JH, et al.; U.S. Headache Consortium. Evidence-based guidelines for migraine headache in the primary care setting: pharmacological management of acute attacks. http://www.aan.com/professionals/practice/pdfs/gl0087.pdf. Accessed December 16, 2010.
31. Touchon J, Bertin L, Pilgrim AJ, Ashford E, Bès A. A comparison of subcutaneous sumatriptan and dihydroergotamine nasal spray in the acute treatment of migraine. Neurology. 1996;47(2):361–365.
32. Winner P, Ricalde O, Le Force B, Saper J, Margul B. A double-blind study of subcutaneous dihydroergotamine vs subcutaneous sumatriptan in the treatment of acute migraine. Arch Neurol. 1996;53(2):180–184.
33. Maizels M, Geiger AM. Intranasal lidocaine for migraine: a randomized trial and open-label follow-up [published correction appears in Headache. 1999;39(10):764]. Headache. 1999;39(8):543–551.
34. Bigal ME, Serrano D, Buse D, Scher A, Stewart WF, Lipton RB. Acute migraine medications and evolution from episodic to chronic migraine: a longitudinal population-based study. Headache. 2008;48(8):1157–1168.
35. Olesen J, Diener HC, Husstedt IW, et al.; BIBN 4096 BS Clinical Proof of Concept Study Group. Calcitonin gene-related peptide receptor antagonist BIBN 4096 BS for the acute treatment of migraine. N Engl J Med. 2004;350(11):1104–1110.
36. Lipton RB, Dodick DW, Silberstein SD, et al. Single-pulse transcranial magnetic stimulation for acute treatment of migraine with aura: a randomised, double-blind, parallel-group, sham-controlled trial. Lancet Neurol. 2010;9(4):373–380.
37. CARE Study Group. Maternal caffeine intake during pregnancy and risk of fetal growth restriction: a large prospective observational study [published correction appears in BMJ. 2010;340:c2331]. BMJ. 2008;337:a2332.
38. Olsen J, Bech BH. Caffeine intake during pregnancy. BMJ. 2008;337:a2316.
39. Pringsheim T, Davenport WJ, Dodick D. Acute treatment and prevention of menstrually related migraine headache: evidence-based review. Neurology. 2008;70(17):1555–1563.
40. Lewis D, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S. Practice parameter: pharmacological treatment of migraine headache in children and adolescents: report of the American Academy of Neurology Quality Standards Subcommittee and the Practice Committee of the Child Neurology Society. Neurology. 2004;63(12):2215–2224.
41. Lewis DW, Winner P, Hershey AD, Wasiewski WW; Adolescent Migraine Steering Committee. Efficacy of zolmitriptan nasal spray in adolescent migraine. Pediatrics. 2007;120(2):390–396.
25 Migraine Treatments, Preventative Meds & Abortive Drugs
Drugs for migraine headaches can relieve the pain and symptoms of a migraine attack and help prevent further migraine attacks.
Migraines can be treated with two types of drugs: abortive and preventive.
Abortive: The goal of abortive treatment is to stop a migraine once it starts. Abortive medications stop a migraine when you feel one coming or once it has begun. Abortive medications can be taken by self-injection, mouth, skin patch, or nasal spray. These forms of medication are especially useful for people who have nausea or vomiting related to their migraine, and they work quickly.
Abortive treatments include the triptans and ditans, which specifically target serotonin. They are all very similar in their action and chemical structure. The triptans are used only to treat headache and do not relieve pain from back problems, arthritis, menstruation, or other conditions. People with certain medical conditions should not take these medications.
- Almotriptan (Axert)
- Eletriptan (Relpax)
- Frovatriptan (Frova)
- Naratriptan (Amerge)
- Rizatriptan (Maxalt)
- Sumatriptan ( Alsuma, Imitrex, Onzetra, Sumavel, Zembrace)
- Zolmitriptan (Zomig)
The following drugs are also used for treatment:
- OTC pain meds and combination pain meds including: Advil Migraine (containing ibuprofen), Excedrin Migraine (containing aspirin, acetaminophen,caffeine), isometheptene-dichloralphenazone-acetaminophen (Midrin),and Motrin Migraine Pain (containing ibuprofen)
- Ergots including: Dihydroergotamine (D.H.E. 45 Injection, Migranal Nasal Spray), Ergotamine tartrate (Cafergot)
- CGRP antagonists – rimegepant (Nurtec ODT) and ubrogepant (Ubrelvy)
The following drugs are sometimes used for nausea related to migraine headaches, in addition to migraine treatment:
Some drugs are used for headache pain, but are not specific for migraines. These include analgesics, narcotics, and barbiturates. Since some of these can be habit forming, they are less desirable than specific headache drugs listed above. These drugs should be used primarily as a “backup” for the occasions when a specific drug does not work.
Preventive: This type of treatment is considered if migraines occur frequently, typically more than one migraine per week, or if migraine symptoms are severe. The goal is to lessen the frequency and severity of the migraine attacks. Medication to prevent a migraine can be taken daily. Preventive treatment medications include the following:
Some nontraditional supplement treatments for migraine prevention includecertified PA-free butterbur, coenzyme Q10, and feverfew. Whether they really help isn't known, because studies have shown mixed results.Check with your doctor before using any supplements as they are not regulated prescription medicines and they may contain substances that are not safe.
If you can't take medication or wish not to, a device might be worth considering. These include:
- Cefaly, a small headband device that sends electrical pulses through the forehead to stimulate a nerve linked with migraines
- Spring TMS or eNeura sTM, a device for people who have an aura before migraine headaches. You hold it at the back of your head at the first sign of a headache, and it gives off a magnetic pulse that stimulates part of the brain.
- Noninvasive vagus nerve stimulator (nVS) gammaCore is a hand-held portable device placed over the vagus nerve in the neck. It releases a mild electrical stimulation to the nerve's fibers to relieve pain.
- Nerivio, a wireless remote electrical neuromodulation device that is self-applied to the upper-arm and should be used in the home environment at the onset of migraine headache..
National Headache Foundation: “Migraine.”
Journal of the American Medical Association, June 24, 2009.
National Institute of Neurological Disorders and Stroke: “Migraine Information Page.”
News release, NuPathe Inc.
Migraine Treatments from eMedicineHealth.
News release, FDA.
© 2020 WebMD, LLC. All rights reserved.
Migraine Headache Treatment & Management: Approach Considerations, Emergency Department Considerations, Reduction of Migraine Triggers
Headache Classification Committee of the International Headache Society. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018 Jan. 38 (1):1-211. [Medline].
Hughes S. Choosing Wisely: 5 Headache Interventions Discouraged. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/814816. Accessed: November 25, 2013.
Loder E, Weizenbaum E, Frishberg B, Silberstein S; the American Headache Society Choosing Wisely Task Force. Choosing Wisely in Headache Medicine: The American Headache Society's List of Five Things Physicians and Patients Should Question. Headache. Available at http://onlinelibrary.wiley.com/doi/10.1111/head.12233/abstract. Accessed: November 25, 2013.
[Guideline] Matchar DB, Young WB, Rosenberg JA, et al. Evidence-based guidelines for migraine headache in the primary care setting: Pharmacological management of acute attacks. American Academy of Neurology. Accessed February 10, 2011. [Full Text].
Silberstein SD, Freitag FG. Preventative treatment of migraine. Neurology. 2003. 60(7):S38-44.
Anderson P. New Screening Tool for Chronic Migraine. Medscape Medical News. Available at http://www.medscape.com/viewarticle/831261. Accessed: September 8, 2014.
Anderson P. New Headache Classification System Published. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/807334. Accessed: July 15, 2013.
[Guideline] Solomon GD, Cady RK, Klapper JA, Ryan RE Jr. Standards of care for treating headache in primary care practice. National Headache Foundation. Cleve Clin J Med. 1997 Jul-Aug. 64(7):373-83. [Medline].
[Guideline] Ducharme J. Canadian Association of Emergency Physicians Guidelines for the acute management of migraine headache. J Emerg Med. 1999 Jan-Feb. 17(1):137-44. [Medline].
Perciaccante A. Migraine is characterized by a cardiac autonomic dysfunction. Headache. 2008 Jun. 48(6):973. [Medline].
May A, Goadsby PJ. The trigeminovascular system in humans: pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. J Cereb Blood Flow Metab. 1999 Feb. 19(2):115-27. [Medline].
Cutrer FM, Charles A. The neurogenic basis of migraine. Headache. 2008 Oct. 48(9):1411-4. [Medline].
Waeber C, Moskowitz MA. Therapeutic implications of central and peripheral neurologic mechanisms in migraine. Neurology. 2003 Oct 28. 61(8 Suppl 4):S9-20. [Medline].
Welch KM. Contemporary concepts of migraine pathogenesis. Neurology. 2003 Oct 28. 61(8 Suppl 4):S2-8. [Medline].
Hauge AW, Asghar MS, Schytz HW, Christensen K, Olesen J. Effects of tonabersat on migraine with aura: a randomised, double-blind, placebo-controlled crossover study. Lancet Neurol. 2009 Aug. 8(8):718-23. [Medline].
Moulton EA, Burstein R, Tully S, Hargreaves R, Becerra L, Borsook D. Interictal dysfunction of a brainstem descending modulatory center in migraine patients. PLoS One. 2008. 3(11):e3799. [Medline]. [Full Text].
Richter F, Lehmenkühler A. [Cortical spreading depression (CSD): a neurophysiological correlate of migraine aura]. Schmerz. 2008 Oct. 22(5):544-6, 548-50. [Medline].
Martins-Oliveira A, Speciali JG, Dach F, Marcaccini AM, Gonçalves FM, Gerlach RF, et al. Different circulating metalloproteinases profiles in women with migraine with and without aura. Clin Chim Acta. 2009 Oct. 408(1-2):60-4. [Medline].
Imamura K, Takeshima T, Fusayasu E, Nakashima K. Increased plasma matrix metalloproteinase-9 levels in migraineurs. Headache. 2008 Jan. 48(1):135-9. [Medline].
Piilgaard H, Lauritzen M. Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex. J Cereb Blood Flow Metab. 2009 Sep. 29(9):1517-27. [Medline].
Burstein R, Yarnitsky D, Goor-Aryeh I, Ransil BJ, Bajwa ZH. An association between migraine and cutaneous allodynia. Ann Neurol. 2000 May. 47(5):614-24. [Medline].
Peroutka SJ. Dopamine and migraine. Neurology. 1997 Sep. 49(3):650-6. [Medline].
Sun-Edelstein C, Mauskop A. Role of magnesium in the pathogenesis and treatment of migraine. Expert Rev Neurother. 2009 Mar. 9(3):369-79. [Medline].
Napoli R, Guardasole V, Zarra E, Matarazzo M, D'Anna C, Saccà F, et al. Vascular smooth muscle cell dysfunction in patients with migraine. Neurology. 2009 Jun 16. 72(24):2111-4. [Medline].
Gruber HJ, Bernecker C, Lechner A, Weiss S, Wallner-Blazek M, Meinitzer A, et al. Increased nitric oxide stress is associated with migraine. Cephalalgia. 2010 Apr. 30(4):486-92. [Medline].
Tietjen GE, Herial NA, White L, Utley C, Kosmyna JM, Khuder SA. Migraine and biomarkers of endothelial activation in young women. Stroke. 2009 Sep. 40(9):2977-82. [Medline].
Hamed SA. The vascular risk associations with migraine: relation to migraine susceptibility and progression. Atherosclerosis. 2009 Jul. 205(1):15-22. [Medline].
Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology. 2008 Nov 25. 71(22):1821-8. [Medline].
Kors EE, Haan J, Ferrari MD. Genetics of primary headaches. Curr Opin Neurol. 1999 Jun. 12(3):249-54. [Medline].
Barbas NR, Schuyler EA. Heredity, genes, and headache. Semin Neurol. 2006 Nov. 26(5):507-14. [Medline].
Chasman DI, Schürks M, Anttila V, de Vries B, Schminke U, Launer LJ, et al. Genome-wide association study reveals three susceptibility loci for common migraine in the general population. Nat Genet. 2011 Jun 12. 43(7):695-8. [Medline]. [Full Text].
Anttila V, Stefansson H, Kallela M, Todt U, Terwindt GM, Calafato MS, et al. Genome-wide association study of migraine implicates a common susceptibility variant on 8q22.1. Nat Genet. 2010 Oct. 42(10):869-73. [Medline]. [Full Text].
Ligthart L, de Vries B, Smith AV, Ikram MA, Amin N, Hottenga JJ, et al. Meta-analysis of genome-wide association for migraine in six population-based European cohorts. Eur J Hum Genet. 2011 Aug. 19(8):901-7. [Medline]. [Full Text].
Ophoff RA, Terwindt GM, Vergouwe MN, van Eijk R, Oefner PJ, Hoffman SM, et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNL1A4. Cell. 1996 Nov 1. 87(3):543-52. [Medline].
Thomsen LL, Kirchmann M, Bjornsson A, Stefansson H, Jensen RM, Fasquel AC, et al. The genetic spectrum of a population-based sample of familial hemiplegic migraine. Brain. 2007 Feb. 130:346-56. [Medline].
Ferrari MD. Heritability of migraine. Neurology. 2003. 60(7):S15-20.
De Fusco M, Marconi R, Silvestri L, Atorino L, Rampoldi L, Morgante L, et al. Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump alpha2 subunit associated with familial hemiplegic migraine type 2. Nat Genet. 2003 Feb. 33(2):192-6. [Medline].
Kahlig KM, Rhodes TH, Pusch M, Freilinger T, Pereira-Monteiro JM, Ferrari MD, et al. Divergent sodium channel defects in familial hemiplegic migraine. Proc Natl Acad Sci U S A. 2008 Jul 15. 105(28):9799-804. [Medline]. [Full Text].
Dichgans M, Freilinger T, Eckstein G, Babini E, Lorenz-Depiereux B, Biskup S, et al. Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine. Lancet. 2005 Jul 30-Aug 5. 366(9483):371-7. [Medline].
Opherk C, Peters N, Herzog J, Luedtke R, Dichgans M. Long-term prognosis and causes of death in CADASIL: a retrospective study in 411 patients. Brain. 2004 Nov. 127:2533-9. [Medline].
Richards A, van den Maagdenberg AM, Jen JC, Kavanagh D, Bertram P, Spitzer D, et al. C-terminal truncations in human 3'-5' DNA exonuclease TREX1 cause autosomal dominant retinal vasculopathy with cerebral leukodystrophy. Nat Genet. 2007 Sep. 39(9):1068-70. [Medline].
Gould DB, Phalan FC, van Mil SE, Sundberg JP, Vahedi K, Massin P, et al. Role of COL4A1 in small-vessel disease and hemorrhagic stroke. N Engl J Med. 2006 Apr 6. 354(14):1489-96. [Medline].
Stam AH, Haan J, van den Maagdenberg AM, Ferrari MD, Terwindt GM. Migraine and genetic and acquired vasculopathies. Cephalalgia. 2009 Sep. 29(9):1006-17. [Medline].
MacGregor EA. Menstrual migraine. Curr Opin Neurol. 2008 Jun. 21(3):309-15. [Medline].
Allais G, Gabellari IC, De Lorenzo C, Mana O, Benedetto C. Oral contraceptives in migraine. Expert Rev Neurother. 2009 Mar. 9(3):381-93. [Medline].
Wöber C, Brannath W, Schmidt K, Kapitan M, Rudel E, Wessely P, et al. Prospective analysis of factors related to migraine attacks: the PAMINA study. Cephalalgia. 2007 Apr. 27(4):304-14. [Medline].
Klein E, Spencer D. Migraine frequency and risk of cardiovascular disease in women. Neurology. 2009 Aug 25. 73(8):e42-3. [Medline].
Woodward M. Migraine and the risk of coronary heart disease and ischemic stroke in women. Womens Health (Lond Engl). 2009 Jan. 5(1):69-77. [Medline].
Bushnell CD, Jamison M, James AH. Migraines during pregnancy linked to stroke and vascular diseases: US population based case-control study. BMJ. 2009 Mar 10. 338:b664. [Medline]. [Full Text].
Anderson, P. Migraine Tied to Hypertension Risk in Women. Medscape Medical News. Available at http://www.medscape.com/viewarticle/879249. April 28, 2017; Accessed: May 9, 2017.
Scher AI, Gudmundsson LS, Sigurdsson S, Ghambaryan A, Aspelund T, Eiriksdottir G, et al. Migraine headache in middle age and late-life brain infarcts. JAMA. 2009 Jun 24. 301(24):2563-70. [Medline].
Kurth T, Winter AC, Eliassen AH, Dushkes R, Mukamal KJ, Rimm EB, et al. Migraine and risk of cardiovascular disease in women: prospective cohort study. BMJ. 2016 May 31. 353:i2610. [Medline].
Kruit MC, Launer LJ, Overbosch J, van Buchem MA, Ferrari MD. Iron accumulation in deep brain nuclei in migraine: a population-based magnetic resonance imaging study. Cephalalgia. 2009 Mar. 29(3):351-9. [Medline].
Welch KM. Iron in the migraine brain; a resilient hypothesis. Cephalalgia. 2009 Mar. 29(3):283-5. [Medline].
Nguyen RH, Ford S, Calhoun AH, Holden JK, Gracely RH, Tommerdahl M. Neurosensory assessments of migraine. Brain Res. 2013 Jan 5. [Medline].
Lipton RB, Scher AI, Kolodner K, Liberman J, Steiner TJ, Stewart WF. Migraine in the United States: epidemiology and patterns of health care use. Neurology. 2002 Mar 26. 58(6):885-94. [Medline].