Migraine

This article is about the disorder. For other uses, see Migraine (disambiguation).

Migraine (UK: /ˈmiːɡreɪn/, US: /ˈmaɪ-/)^[11][12] is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and light and sound sensitivity.^[1] Other characterizing symptoms may include nausea, vomiting, cognitive dysfunction, allodynia, and dizziness. Exacerbation of headache symptoms during physical activity is another distinguishing feature.^[13] Up to one-third of migraine sufferers experience aura, a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack.^[13] Although primarily considered to be a headache disorder, migraine is highly heterogenous in its clinical presentation and is better thought of as a spectrum disease rather than a distinct clinical entity.^[14] Disease burden can range from episodic discrete attacks, consisting of as little as several lifetime attacks, to chronic disease.^[14][15]

Migraine
Woman with migraine headache
Specialty	Neurology
Symptoms	Headaches, nausea, sensitivity to light, sound, and smell^[1]^[2]
Usual onset	Around puberty^[1]
Duration	Recurrent, long term^[1]
Causes	Environmental and genetic^[3]
Risk factors	Family history, female^[4]^[5]
Differential diagnosis	Subarachnoid hemorrhage, venous thrombosis, idiopathic intracranial hypertension, brain tumor, tension headache, sinusitis,^[6] cluster headache^[7]^[unreliable medical source?]
Prevention	Propranolol, amitriptyline, topiramate^[8]
Medication	Ibuprofen, paracetamol (acetaminophen), triptans, ergotamines^[5]^[9]
Prevalence	~15%^[10]

Migraine is believed to be caused by a mixture of environmental and genetic factors that influence the excitation and inhibition of nerve cells in the brain.^[3] An older "vascular hypothesis" postulated that the aura of migraine is produced by vasoconstriction and the headache of migraine is produced by vasodilation, but the vasoconstrictive mechanism has been disproven,^[16] and the role of vasodilation in migraine pathophysiology is uncertain.^[17][18] The accepted hypothesis suggests that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes, triggering a physiological cascade that leads to migraine symptomatology.^[19]

Initial recommended treatment for acute attacks is with over-the-counter analgesics (pain medication) such as ibuprofen and paracetamol (acetaminophen) for headache, antiemetics (anti-nausea medication) for nausea, and the avoidance of triggers.^[9] Specific medications such as triptans, ergotamines, or CGRP inhibitors may be used in those experiencing headaches that are refractory to simple pain medications.^[20] For individuals who experience four or more attacks per month, or could otherwise benefit from prevention, prophylactic medication is recommended.^[21] Commonly prescribed prophylactic medications include beta blockers like propranolol, anticonvulsants like sodium valproate, antidepressants like amitriptyline, and other off-label classes of medications.^[8] Preventive medications inhibit migraine pathophysiology through various mechanisms, such as blocking calcium and sodium channels, blocking gap junctions, and inhibiting matrix metalloproteinases, among other mechanisms.^[22][23] Nonpharmacological preventative therapies include nutritional supplementation, dietary interventions, sleep improvement, and aerobic exercise.^[24]

Globally, approximately 15% of people are affected by migraine.^[10] In the Global Burden of Disease Study, conducted in 2010, migraines ranked as the third-most prevalent disorder in the world.^[25] It most often starts at puberty and is worst during middle age.^[1] As of 2016^[update], it is one of the most common causes of disability.^[26]

Signs and symptoms

Migraine typically presents with self-limited, recurrent severe headache associated with autonomic symptoms.^[5][27] About 15–30% of people living with migraine experience episodes with aura,^[9][28] and they also frequently experience episodes without aura.^[29] The severity of the pain, duration of the headache, and frequency of attacks are variable.^[5] A migraine attack lasting longer than 72 hours is termed status migrainosus.^[30] There are four possible phases to a migraine attack, although not all the phases are necessarily experienced:^[13]

• The prodrome, which occurs hours or days before the headache
• The aura, which immediately precedes the headache
• The pain phase, also known as headache phase
• The postdrome, the effects experienced following the end of a migraine attack

Migraine is associated with major depression, bipolar disorder, anxiety disorders, and obsessive–compulsive disorder. These psychiatric disorders are approximately 2–5 times more common in people without aura, and 3–10 times more common in people with aura.^[31]

Prodrome phase

Prodromal or premonitory symptoms occur in about 60% of those with migraines,^[2][32] with an onset that can range from two hours to two days before the start of pain or the aura.^[33] These symptoms may include a wide variety of phenomena,^[34] including altered mood, irritability, depression or euphoria, fatigue, craving for certain food(s), stiff muscles (especially in the neck), constipation or diarrhea, and sensitivity to smells or noise.^[32] This may occur in those with either migraine with aura or migraine without aura.^[35] Neuroimaging indicates the limbic system and hypothalamus as the origin of prodromal symptoms in migraine.^[36]

Aura phase

Aura is a transient focal neurological phenomenon that occurs before or during the headache.^[2] Aura appears gradually over a number of minutes (usually occurring over 5–60 minutes) and generally lasts less than 60 minutes.^[37][38] Symptoms can be visual, sensory or motoric in nature, and many people experience more than one.^[39] Visual effects occur most frequently: they occur in up to 99% of cases and in more than 50% of cases are not accompanied by sensory or motor effects.^[39] If any symptom remains after 60 minutes, the state is known as persistent aura.^[40]

Visual disturbances often consist of a scintillating scotoma (an area of partial alteration in the field of vision which flickers and may interfere with a person's ability to read or drive).^[2] These typically start near the center of vision and then spread out to the sides with zigzagging lines which have been described as looking like fortifications or walls of a castle.^[39] Usually the lines are in black and white but some people also see colored lines.^[39] Some people lose part of their field of vision known as hemianopsia while others experience blurring.^[39]

Sensory aura are the second most common type; they occur in 30–40% of people with auras.^[39] Often a feeling of pins-and-needles begins on one side in the hand and arm and spreads to the nose–mouth area on the same side.^[39] Numbness usually occurs after the tingling has passed with a loss of position sense.^[39] Other symptoms of the aura phase can include speech or language disturbances, world spinning, and less commonly motor problems.^[39] Motor symptoms indicate that this is a hemiplegic migraine, and weakness often lasts longer than one hour unlike other auras.^[39] Auditory hallucinations or delusions have also been described.^[41]

Pain phase

Classically the headache is unilateral, throbbing, and moderate to severe in intensity.^[37] It usually comes on gradually^[37] and is aggravated by physical activity during a migraine attack.^[13] However, the effects of physical activity on migraine are complex, and some researchers have concluded that, while exercise can trigger migraine attacks, regular exercise may have a prophylactic effect and decrease frequency of attacks.^[42] The feeling of pulsating pain is not in phase with the pulse.^[43] In more than 40% of cases, however, the pain may be bilateral (both sides of the head), and neck pain is commonly associated with it.^[44] Bilateral pain is particularly common in those who have migraine without aura.^[2] Less commonly pain may occur primarily in the back or top of the head.^[2] The pain usually lasts 4 to 72 hours in adults;^[37] however, in young children frequently lasts less than 1 hour.^[45] The frequency of attacks is variable, from a few in a lifetime to several a week, with the average being about one a month.^[46][47]

The pain is frequently accompanied by nausea, vomiting, sensitivity to light, sensitivity to sound, sensitivity to smells, fatigue, and irritability.^[2] Many thus seek a dark and quiet room.^[48] In a basilar migraine, a migraine with neurological symptoms related to the brain stem or with neurological symptoms on both sides of the body,^[49] common effects include a sense of the world spinning, light-headedness, and confusion.^[2] Nausea occurs in almost 90% of people, and vomiting occurs in about one-third.^[48] Other symptoms may include blurred vision, nasal stuffiness, diarrhea, frequent urination, pallor, or sweating.^[50] Swelling or tenderness of the scalp may occur as can neck stiffness.^[50] Associated symptoms are less common in the elderly.^[51]

Silent migraine

Sometimes, aura occurs without a subsequent headache.^[39] This is known in modern classification as a typical aura without headache, or acephalgic migraine in previous classification, or commonly as a silent migraine.^[52][53] However, silent migraine can still produce debilitating symptoms, with visual disturbance, vision loss in half of both eyes, alterations in color perception, and other sensory problems, like sensitivity to light, sound, and odors.^[54] It can last from 15 to 30 minutes, usually no longer than 60 minutes, and it can recur or appear as an isolated event.^[53]

Postdrome

The migraine postdrome could be defined as that constellation of symptoms occurring once the acute headache has settled.^[55] Many report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed. The person may feel tired or "hung over" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness.^[56] According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."^{[57][unreliable medical source?]}

Cause

The underlying causes of migraines are unknown.^[58] However, they are believed to be related to a mix of environmental and genetic factors.^[3] They run in families in about two-thirds of cases^[5] and rarely occur due to a single gene defect.^[59] While migraines were once believed to be more common in those of high intelligence, this does not appear to be true.^[46] A number of psychological conditions are associated, including depression, anxiety, and bipolar disorder.^[60]

Success of the surgical migraine treatment by decompression of extracranial sensory nerves adjacent to vessels^[61] suggests that migraineurs may have anatomical predisposition for neurovascular compression that may be caused by both intracranial and extracranial vasodilation due to migraine triggers. This, along with the existence of numerous cranial neural interconnections,^[62] may explain the multiple cranial nerve involvement and consequent diversity of migraine symptoms.^[63]

Genetics

Main article: Genetics of migraine

Studies of twins indicate a 34% to 51% genetic influence of likelihood to develop migraine.^[3] This genetic relationship is stronger for migraine with aura than for migraines without aura.^[29] A number of specific variants of genes increase the risk by a small to moderate amount.^[59]

Single gene disorders that result in migraines are rare.^[59] One of these is known as familial hemiplegic migraine, a type of migraine with aura, which is inherited in an autosomal dominant fashion.^[64][65] Four genes have been shown to be involved in familial hemiplegic migraine.^[66] Three of these genes are involved in ion transport.^[66] The fourth is the axonal protein PRRT2, associated with the exocytosis complex.^[66] Another genetic disorder associated with migraine is CADASIL syndrome or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.^[2] One meta-analysis found a protective effect from angiotensin converting enzyme polymorphisms on migraine.^[67] The TRPM8 gene, which codes for a cation channel, has been linked to migraines.^[68]

Triggers

Migraine may be induced by triggers, with some reporting it as an influence in a minority of cases^[5] and others the majority.^[69] Many things such as fatigue, certain foods, alcohol, and weather have been labeled as triggers; however, the strength and significance of these relationships are uncertain.^[69][70] Most people with migraines report experiencing triggers.^[71] Symptoms may start up to 24 hours after a trigger.^[5]

Physiological aspects

Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches).^[69] Psychological stress has been reported as a factor by 50 to 80% of people.^[72] Migraine has also been associated with post-traumatic stress disorder and abuse.^[73] Migraine episodes are more likely to occur around menstruation.^[72] Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role.^[74] These hormonal influences seem to play a greater role in migraine without aura.^[46] Migraine episodes typically do not occur during the second and third trimesters of pregnancy, or following menopause.^[2]

Dietary aspects

Between 12% and 60% of people report foods as triggers.^[75][76]

There are many reports^{[77][78][79][80][81]} that tyramine – which is naturally present in chocolate, alcoholic beverages, most cheeses, processed meats, and other foods – can trigger migraine symptoms in some individuals. Monosodium glutamate (MSG) has been reported as a trigger for migraine,^[82] but a systematic review concluded that "a causal relationship between MSG and headache has not been proven... It would seem premature to conclude that the MSG present in food causes headache".^[83]

Environmental aspects

A 2009 review on potential triggers in the indoor and outdoor environment concluded that while there were insufficient studies to confirm environmental factors as causing migraine, "migraineurs worldwide consistently report similar environmental triggers".^[84]

Pathophysiology

 

Animation of cortical spreading depression

Migraine is believed to be primarily a neurological disorder,^[85][86] while others believe it to be a neurovascular disorder with blood vessels playing the key role, although evidence does not support this completely.^{[87][88][89][90]} Others believe both are likely important.^{[91][92][93][94]} One theory is related to increased excitability of the cerebral cortex and abnormal control of pain neurons in the trigeminal nucleus of the brainstem.^[95]

Sensitization of trigeminal pathways is a key pathophysiological phenomenon in migraine. It is debatable whether sensitization starts in the periphery or in the brain.^[96][97]

Aura

Cortical spreading depression, or spreading depression according to Leão, is a burst of neuronal activity followed by a period of inactivity, which is seen in those with migraines with aura.^[98] There are a number of explanations for its occurrence, including activation of NMDA receptors leading to calcium entering the cell.^[98] After the burst of activity, the blood flow to the cerebral cortex in the area affected is decreased for two to six hours.^[98] It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.^[98]

Pain

The exact mechanism of the head pain which occurs during a migraine episode is unknown.^[99] Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon),^[100] while other data support the role of peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck).^[99] The potential candidate vessels include dural arteries, pial arteries and extracranial arteries such as those of the scalp.^[99] The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.^[101]

Neuromodulators

Adenosine, a neuromodulator, may be involved.^[102] Released after the progressive cleavage of adenosine triphosphate (ATP), adenosine acts on adenosine receptors to put the body and brain in a low activity state by dilating blood vessels and slowing the heart rate, such as before and during the early stages of sleep. Adenosine levels have been found to be high during migraine attacks.^[102][103] Caffeine's role as an inhibitor of adenosine may explain its effect in reducing migraine.^[104] Low levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine (5-HT), are also believed to be involved.^[105]

Calcitonin gene-related peptides (CGRPs) have been found to play a role in the pathogenesis of the pain associated with migraine, as levels of it become elevated during an attack.^[9][43]

Diagnosis

The diagnosis of a migraine is based on signs and symptoms.^[5] Neuroimaging tests are not necessary to diagnose migraine, but may be used to find other causes of headaches in those whose examination and history do not confirm a migraine diagnosis.^[106] It is believed that a substantial number of people with the condition remain undiagnosed.^[5]

The diagnosis of migraine without aura, according to the International Headache Society, can be made according the "5, 4, 3, 2, 1 criteria," which is as follows:^[13]

• Five or more attacks – for migraine with aura, two attacks are sufficient for diagnosis.
• Four hours to three days in duration
• Two or more of the following:
  • Unilateral (affecting one side of the head)
  • Pulsating
  • Moderate or severe pain intensity
  • Worsened by or causing avoidance of routine physical activity
• One or more of the following:
  • Nausea and/or vomiting
  • Sensitivity to both light (photophobia) and sound (phonophobia)

If someone experiences two of the following: photophobia, nausea, or inability to work or study for a day, the diagnosis is more likely.^[107] In those with four out of five of the following: pulsating headache, duration of 4–72 hours, pain on one side of the head, nausea, or symptoms that interfere with the person's life, the probability that this is a migraine attack is 92%.^[9] In those with fewer than three of these symptoms, the probability is 17%.^[9]

Classification

Main article: ICHD classification and diagnosis of migraine

Migraine was first comprehensively classified in 1988.^[29]

The International Headache Society updated their classification of headaches in 2004.^[13] A third version was published in 2018.^[108] According to this classification, migraine is a primary headache disorder along with tension-type headaches and cluster headaches, among others.^[109]

Migraine is divided into six subclasses (some of which include further subdivisions):^[110]

• Migraine without aura, or "common migraine", involves migraine headaches that are not accompanied by aura.
• Migraine with aura, or "classic migraine", usually involves migraine headaches accompanied by aura. Less commonly, aura can occur without a headache, or with a nonmigraine headache. Two other varieties are familial hemiplegic migraine and sporadic hemiplegic migraine, in which a person has migraine with aura and with accompanying motor weakness. If a close relative has had the same condition, it is called "familial", otherwise it is called "sporadic". Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, world spinning, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness. This type was initially believed to be due to spasms of the basilar artery, the artery that supplies the brainstem. Now that this mechanism is not believed to be primary, the symptomatic term migraine with brainstem aura (MBA) is preferred.^[49] Retinal migraine (which is distinct from visual or optical migraine) involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye.
• Childhood periodic syndromes that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo).
• Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion.
• Probable migraine describes conditions that have some characteristics of migraines, but where there is not enough evidence to diagnose it as a migraine with certainty (in the presence of concurrent medication overuse).
• Chronic migraine is a complication of migraines, and is a headache that fulfills diagnostic criteria for migraine headache and occurs for a greater time interval. Specifically, greater or equal to 15 days/month for longer than 3 months.^[111]

Abdominal migraine

The diagnosis of abdominal migraine is controversial.^[112] Some evidence indicates that recurrent episodes of abdominal pain in the absence of a headache may be a type of migraine^[112][113] or are at least a precursor to migraines.^[29] These episodes of pain may or may not follow a migraine-like prodrome and typically last minutes to hours.^[112] They often occur in those with either a personal or family history of typical migraine.^[112] Other syndromes that are believed to be precursors include cyclical vomiting syndrome and benign paroxysmal vertigo of childhood.^[29]

Differential diagnosis

Other conditions that can cause similar symptoms to a migraine headache include temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage.^[9] Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headache presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subarachnoid hemorrhage with a very fast onset.^[9] Tension headaches typically occur on both sides, are not pounding, and are less disabling.^[9]

Those with stable headaches that meet criteria for migraines should not receive neuroimaging to look for other intracranial disease.^{[114][115][116]} This requires that other concerning findings such as papilledema (swelling of the optic disc) are not present. People with migraines are not at an increased risk of having another cause for severe headaches.^{[citation needed]}

Prevention

Main article: Prevention of migraines

Preventive treatments of migraine include medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.^[9] Recommended lifestyle changes include stopping tobacco use and reducing behaviors that interfere with sleep.^[117]

The goal is to reduce the frequency, painfulness, and duration of migraine episodes, and to increase the effectiveness of abortive therapy.^[118][119] Another reason for prevention is to avoid medication overuse headache. This is a common problem and can result in chronic daily headache.^[120][121]

Medication

Preventive migraine medications are considered effective if they reduce the frequency or severity of the migraine attacks by at least 50%.^[122] Due to few medications being approved specifically for the preventative treatment of migraine headaches; many medications such as beta-blockers, anticonvulsive agents such as topiramate or sodium valproate, antidepressants such as amitriptyline and calcium channel blockers such as flunarizine are used off label for the preventative treatment of migraine headaches.^[38] Guidelines are fairly consistent in rating the anticonvulsants topiramate and divalproex/sodium valproate, and the beta blockers propranolol and metoprolol as having the highest level of evidence for first-line use for migraine prophylaxis in adults.^[123][124] Propranolol and topiramate have the best evidence in children; however, evidence only supports short-term benefit as of 2020.^[117][125]

The beta blocker timolol is also effective for migraine prevention and in reducing migraine attack frequency and severity.^[123] While beta blockers are often used for first-line treatment, other antihypertensives also have a proven efficiency in migraine prevention, namely the calcium channel blocker verapamil^[126] and the angiotensin receptor blocker candesartan.^[127][128]

Tentative evidence also supports the use of magnesium supplementation.^[129] Increasing dietary intake may be better.^[130] Recommendations regarding effectiveness varied for the anticonvulsants gabapentin and pregabalin. Frovatriptan is effective for prevention of menstrual migraine.^[123]

The antidepressants amitriptyline and venlafaxine are probably also effective.^[131] Angiotensin inhibition by either an angiotensin-converting enzyme inhibitor or angiotensin II receptor antagonist may reduce attacks.^[132]

Medications in the anti-calcitonin gene-related peptide, including eptinezumab, erenumab, fremanezumab, and galcanezumab, appear to decrease the frequency of migraines by one to two per month.^[133]

Alternative therapies

Acupuncture has a small effect in reducing migraine frequency, compared to sham acupuncture, a practice where needles are placed randomly or do not penetrate the skin.^[134] Physiotherapy, massage and relaxation, and chiropractic manipulation might be as effective as propranolol or topiramate in the prevention of migraine headaches; however, the research had some problems with methodology.^[135][136] Another review, however, found evidence to support spinal manipulation to be poor and insufficient to support its use.^[137]

Tentative evidence supports the use of stress reduction techniques such as cognitive behavioral therapy, biofeedback, and relaxation techniques.^[72] Regular physical exercise may decrease the frequency.^[42] Numerous psychological approaches have been developed that are aimed at preventing or reducing the frequency of migraine in adults including educational approaches, relaxation techniques, assistance in developing coping strategies, strategies to change the way one thinks of a migraine attack, and strategies to reduce symptoms.^[138] Other strategies include: progressive muscle relaxation, biofeedback, behavioral training, acceptance and commitment therapy, and mindfulness-based interventions.^[139] The medical evidence supporting the effectiveness of these types of psychological approaches is very limited.^[138]

Among alternative medicines, butterbur has the best evidence for its use.^[140][141] Unprocessed butterbur contains chemicals called pyrrolizidine alkaloids (PAs) which can cause liver damage, however there are versions that are PA free.^[142] In addition, butterbur may cause allergic reactions in people who are sensitive to plants such as ragweed.^[143] There is tentative evidence that coenzyme Q10 reduces migraine frequency.^[144]

Feverfew has traditionally been used as a treatment for fever, headache and migraine, women's conditions such as difficulties in labour and regulation of menstruation, relief of stomach ache, toothache and insect bites. During the last decades, it has mainly been used for headache and as a preventive treatment for migraine.^[145] The plant parts used for medicinal use are the dried leaves or the dried aerial parts. Several historical data supports feverfew's traditional medicinal uses.^[146] In addition, several clinical studies have been performed assessing the efficacy and safety of feverfew monotherapy in the prevention of migraine.^[147] The majority of the clinical trials favoured feverfew over placebo. The data also suggest that feverfew is associated with only mild and transient adverse effects. The frequency of migraine was positively affected after treatment with feverfew. Reduction of migraine severity was also reported after intake of feverfew and incidence of nausea and vomiting decreased significantly. No effect of feverfew was reported in one study.^[147]

There is tentative evidence for melatonin as an add-on therapy for prevention and treatment of migraine.^[148][149] The data on melatonin are mixed and certain studies have had negative results.^[148] The reasons for the mixed findings are unclear but may stem from differences in study design and dosage.^[148] Melatonin's possible mechanisms of action in migraine are not completely clear, but may include improved sleep, direct action on melatonin receptors in the brain, and anti-inflammatory properties.^[148][150]

Devices and surgery

Medical devices, such as biofeedback and neurostimulators, have some advantages in migraine prevention, mainly when common anti-migraine medications are contraindicated or in case of medication overuse. Biofeedback helps people be conscious of some physiological parameters so as to control them and try to relax and may be efficient for migraine treatment.^[151][152] Neurostimulation uses noninvasive or implantable neurostimulators similar to pacemakers for the treatment of intractable chronic migraine with encouraging results for severe cases.^[153][154] A transcutaneous electrical nerve stimulator and a transcranial magnetic stimulator are approved in the United States for the prevention of migraines.^[155][156] There is also tentative evidence for transcutaneous electrical nerve stimulation decreases the frequency of migraines.^[157] Migraine surgery, which involves decompression of certain nerves around the head and neck, may be an option in certain people who do not improve with medications.^[158]

Management

Main article: Migraine treatment

There are three main aspects of treatment: trigger avoidance, acute symptomatic control, and medication for prevention.^[5] Medications are more effective if used earlier in an attack.^[5] The frequent use of medications may result in medication overuse headache, in which the headaches become more severe and more frequent.^[13] This may occur with triptans, ergotamines, and analgesics, especially opioid analgesics.^[13] Due to these concerns simple analgesics are recommended to be used less than three days per week at most.^[159]

For children, ibuprofen helps decrease pain and is the initially recommended treatment.^[160][161] Paracetamol does not appear to be effective in providing pain relief.^[160] Triptans are effective, though there is a risk of causing minor side effects like taste disturbance, nasal symptoms, dizziness, fatigue, low energy, nausea, or vomiting.^[160][162] Ibuprofen should be used less than half the days in a month and triptans less than a third of the days in a month to decrease the risk of medication overuse headache.^[161]

Analgesics

Recommended initial treatment for those with mild to moderate symptoms are simple analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) or the combination of paracetamol (also known as acetaminophen), aspirin, and caffeine, although caffeine overuse can be a contributor to migraine chronification as well as a migraine trigger for many patients.^[9][163] Several NSAIDs, including diclofenac and ibuprofen, have evidence to support their use.^[164][165] Aspirin (900 to 1000 mg) can relieve moderate to severe migraine pain, with an effectiveness similar to sumatriptan.^[166] Ketorolac is available in intravenous and intramuscular formulations.^[9]

Paracetamol, either alone or in combination with metoclopramide, is another effective treatment with a low risk of adverse effects.^[167] Intravenous metoclopramide is also effective by itself.^[168][169] In pregnancy, paracetamol and metoclopramide are deemed safe as are NSAIDs until the third trimester.^[9]

Naproxen by itself may not be effective as a stand-alone medicine to stop a migraine headache as it is only weakly better than a placebo medication in clinical trials.^[170]

Antiemetics

Triptans

Triptans such as sumatriptan are medications used to stop an active migraine headache (an abortive medication). Triptans are the initially recommended treatments for those with moderate to severe pain from an acute migraine headache or those with milder symptoms who do not respond to simple analgesics.^[9] Triptans have been shown to be effective for both pain and nausea in up to 75% of people.^[171][172] There are different methods or routes of administration to take sumatriptan including oral (by mouth), injectable (subcutaneous), rectal, nasal spray, and oral dissolving tablets.^{[5][173][174][175]} For people with migraine symptoms such as nausea or vomiting, taking the abortive medicine by mouth or through the nose may be difficult. All route of administration have been shown to be effective at reducing migraine symptoms, however, nasal and injectable subcutaneous administration may result in more side effects.^[175][174] The adverse effects associated with rectal administration have not been well studied.^[173] Some people may find that they respond to one type of sumatriptan better than another.^[9]

Most side effects are mild, including flushing; however, rare cases of myocardial ischemia have occurred.^[5] They are thus not recommended for people with cardiovascular disease,^[9] who have had a stroke, or have migraines that are accompanied by neurological problems.^{[176][unreliable medical source?]} In addition, triptans should be prescribed with caution for those with risk factors for vascular disease.^{[176][unreliable medical source?]} While historically not recommended in those with basilar migraines there is no specific evidence of harm from their use in this population to support this caution.^[49] Triptans are not addictive, but may cause medication-overuse headaches if used more than 10 days per month.^[177]

Sumatriptan does not prevent other migraine headaches from starting in the future.^[174] For increased effectiveness at stopping migraine symptoms, a combined therapy that includes sumatriptan and naproxen may be suggested.^[178]

CGRP receptor antagonists

Calcitonin gene-related peptide receptor antagonists (CGRP) target calcitonin gene-related peptide or its receptor to prevent migraine headaches or reduce their severity.^[38] CGRP is a signaling molecule as well as a potent vasodilator that is involved in the development of a migraine headache.^[38] There are four injectable monoclonal antibodies that target CGRP or its receptor (eptinezumab, erenumab, fremanezumab, and galcanezumab) and the medications have demonstrated efficacy in the preventative treatment of episodic and chronic migraine headaches in phase III randomized clinical trials.^[38]

Zavegepant was approved for medical use in the United States in March 2023.^{[179][180][181]}

Ergotamines

Ergotamine and dihydroergotamine are older medications still prescribed for migraines, the latter in nasal spray and injectable forms.^[5][182] They appear equally effective to the triptans^[183] and experience adverse effects that typically are benign.^[184] In the most severe cases, such as those with status migrainosus, they appear to be the most effective treatment option.^[184] They can cause vasospasm including coronary vasospasm and are contraindicated in people with coronary artery disease.^[185]

Magnesium

Magnesium is recognized as an inexpensive, over-the-counter supplement which can be part of a multimodal approach to migraine reduction. Some studies have shown to be effective in both preventing and treating migraine in intravenous form.^[186] The intravenous form reduces attacks as measured in approximately 15–45 minutes, 120 minutes, and 24-hour time periods, magnesium taken orally alleviates the frequency and intensity of migraines.^[187][188]

Other

Intravenous metoclopramide, intravenous prochlorperazine, or intranasal lidocaine are other potential options.^[9][169] Metoclopramide or prochlorperazine are the recommended treatment for those who present to the emergency department.^[9][169] Haloperidol may also be useful in this group.^[169][182] A single dose of intravenous dexamethasone, when added to standard treatment of a migraine attack, is associated with a 26% decrease in headache recurrence in the following 72 hours.^[189] Spinal manipulation for treating an ongoing migraine headache is not supported by evidence.^[137] It is recommended that opioids and barbiturates not be used due to questionable efficacy, addictive potential, and the risk of rebound headache.^[9][38] There is tentative evidence that propofol may be useful if other measures are not effective.^[190]

Occipital nerve stimulation, may be effective but has the downsides of being cost-expensive and has a significant amount of complications.^[191]

There is modest evidence for the effectiveness of non-invasive neuromodulatory devices, behavioral therapies and acupuncture in the treatment of migraine headaches.^[38] There is little to no evidence for the effectiveness of physical therapy, chiropractic manipulation and dietary approaches to the treatment of migraine headaches.^[38] Behavioral treatment of migraine headaches may be helpful for those who may not be able to take medications (for example pregnant women).^[38]

Feverfew is registered as a traditional herbal medicine in the Nordic countries under the brand name Glitinum, only powdered feverfew is approved in the Herbal community monograph issued by European Medicines Agency (EMA).

Topiramate and botulinum toxin (Botox) have evidence in treating chronic migraine.^[131][192] Botulinum toxin has been found to be useful in those with chronic migraine but not those with episodic ones.^[193][194] The anti-CGRP monoclonal antibody erenumab was found in one study to decrease chronic migraines by 2.4 days more than placebo.^[195]

Prognosis

"Migraine exists on a continuum of different attack frequencies and associated levels of disability."^[196] For those with occasional, episodic migraine, a "proper combination of drugs for prevention and treatment of migraine attacks" can limit the disease's impact on patients' personal and professional lives.^[197] But fewer than half of people with migraine seek medical care and more than half go undiagnosed and undertreated.^[198] "Responsive prevention and treatment of migraine is incredibly important" because evidence shows "an increased sensitivity after each successive attack, eventually leading to chronic daily migraine in some individuals."^[197] Repeated migraine results in "reorganization of brain circuitry," causing "profound functional as well as structural changes in the brain."^[199] "One of the most important problems in clinical migraine is the progression from an intermittent, self-limited inconvenience to a life-changing disorder of chronic pain, sensory amplification, and autonomic and affective disruption. This progression, sometimes termed chronification in the migraine literature, is common, affecting 3% of migraineurs in a given year, such that 8% of migraineurs have chronic migraine in any given year." Brain imagery reveals that the electrophysiological changes seen during an attack become permanent in people with chronic migraine; "thus, from an electrophysiological point of view, chronic migraine indeed resembles a never-ending migraine attack."^[199] Severe migraine ranks in the highest category of disability, according to the World Health Organization, which uses objective metrics to determine disability burden for the authoritative annual Global Burden of Disease report. The report classifies severe migraine alongside severe depression, active psychosis, quadriplegia, and terminal-stage cancer.^[200]

Migraine with aura appears to be a risk factor for ischemic stroke^[201] doubling the risk.^[202] Being a young adult, being female, using hormonal birth control, and smoking further increases this risk.^[201] There also appears to be an association with cervical artery dissection.^[203] Migraine without aura does not appear to be a factor.^[204] The relationship with heart problems is inconclusive with a single study supporting an association.^[201] Migraine does not appear to increase the risk of death from stroke or heart disease.^[205] Preventative therapy of migraines in those with migraine with aura may prevent associated strokes.^[206] People with migraine, particularly women, may develop higher than average numbers of white matter brain lesions of unclear significance.^[207]

Epidemiology

 

Percent of women (top) and men (bottom) who have experienced migraine in a given year

Migraine is common, with around 33% of women and 18% of men affected at some point in their lifetime.^[208] Onset can be at any age, but prevalence rises sharply around puberty, and remains high until declining after age 50.^[208] Before puberty, boys and girls are equally impacted, with around 5% of children experiencing migraines. From puberty onwards, women experience migraines at greater rates than men. From age 30 to 50, up to 4 times as many women experience migraines as men.^[208]

Worldwide, migraine affects nearly 15% or approximately one billion people.^[10] In the United States, about 6% of men and 18% of women experience a migraine attack in a given year, with a lifetime risk of about 18% and 43% respectively.^[5] In Europe, migraines affect 12–28% of people at some point in their lives with about 6–15% of adult men and 14–35% of adult women getting at least one yearly.^[209] Rates of migraine are slightly lower in Asia and Africa than in Western countries.^[46][210] Chronic migraine occurs in approximately 1.4 to 2.2% of the population.^[211]

In women, migraine without aura are more common than migraine with aura; however in men the two types occur with similar frequency.^[46]

During perimenopause symptoms often get worse before decreasing in severity.^[212] While symptoms resolve in about two-thirds of the elderly, in 3–10% they persist.^[51]

History

 

The Head Ache, George Cruikshank (1819)

An early description consistent with migraine is contained in the Ebers Papyrus, written around 1500 BCE in ancient Egypt.^[213]

The word migraine is from the Greek ἡμικρᾱνίᾱ (hēmikrāníā), 'pain in half of the head',^[214] from ἡμι- (hēmi-), 'half' and κρᾱνίον (krāníon), 'skull'.^[215]

In 200 BCE, writings from the Hippocratic school of medicine described the visual aura that can precede the headache and a partial relief occurring through vomiting.^[216]

A second-century description by Aretaeus of Cappadocia divided headaches into three types: cephalalgia, cephalea, and heterocrania.^[217] Galen of Pergamon used the term hemicrania (half-head), from which the word migraine was eventually derived.^[217] He also proposed that the pain arose from the meninges and blood vessels of the head.^[216] Migraine was first divided into the two now used types – migraine with aura (migraine ophthalmique) and migraine without aura (migraine vulgaire) in 1887 by Louis Hyacinthe Thomas, a French Librarian.^[216] The mystical visions of Hildegard von Bingen, which she described as "reflections of the living light", are consistent with the visual aura experienced during migraines.^[218]

 

A trepanated skull, from the Neolithic. The perimeter of the hole in the skull is rounded off by ingrowth of new bony tissue, indicating that the person survived the operation.

Trepanation, the deliberate drilling of holes into a skull, was practiced as early as 7,000 BCE.^[213] While sometimes people survived, many would have died from the procedure due to infection.^[219] It was believed to work via "letting evil spirits escape".^[220] William Harvey recommended trepanation as a treatment for migraines in the 17th century.^[221] The association between trepanation and headaches in ancient history may simply be a myth or unfounded speculation that originated several centuries later. In 1913, the world-famous American physician William Osler misinterpreted the French anthropologist and physician Paul Broca's words about a set of children's skulls from the Neolithic age that he found during the 1870s. These skulls presented no evident signs of fractures that could justify this complex surgery for mere medical reasons. Trepanation was probably born of superstitions, to remove "confined demons" inside the head, or to create healing or fortune talismans with the bone fragments removed from the skulls of the patients. However, Osler wanted to make Broca's theory more palatable to his modern audiences, and explained that trepanation procedures were used for mild conditions such as "infantile convulsions headache and various cerebral diseases believed to be caused by confined demons."^[222]

While many treatments for migraine have been attempted, it was not until 1868 that use of a substance which eventually turned out to be effective began.^[216] This substance was the fungus ergot from which ergotamine was isolated in 1918.^[223] Methysergide was developed in 1959 and the first triptan, sumatriptan, was developed in 1988.^[223] During the 20th century with better study-design, effective preventive measures were found and confirmed.^[216]

Society and culture

Migraine is a significant source of both medical costs and lost productivity. It has been estimated that migraine is the most costly neurological disorder in the European Community, costing more than €27 billion per year.^[224] In the United States, direct costs have been estimated at $17 billion, while indirect costs – such as missed or decreased ability to work – is estimated at $15 billion.^[225] Nearly a tenth of the direct cost is due to the cost of triptans.^[225] In those who do attend work during a migraine attack, effectiveness is decreased by around a third.^[224] Negative impacts also frequently occur for a person's family.^[224]

Research

Potential prevention mechanisms

Transcranial magnetic stimulation shows promise,^[9][226] as does transcutaneous supraorbital nerve stimulation.^[227] There is preliminary evidence that a ketogenic diet may help prevent episodic and long-term migraine.^[228][229]

Potential sex dependency

While no definitive proof has been found linking migraine to sex, statistical data indicates that women may be more prone to having migraine, showing migraine incidence three times higher among women than men.^[230][231] The Society for Women's Health Research has also mentioned hormonal influences, mainly estrogen, as having a considerable role in provoking migraine pain. Studies and research related to the sex dependencies of migraine are still ongoing, and conclusions have yet to be achieved.^{[232][233][234]}

See also

• Headache
• Cluster headache
• Tension headache
• Trigeminal neuralgia

References

1. "Headache disorders Fact sheet N°277". October 2012. from the original on 16 February 2016. Retrieved 15 February 2016.
2. Simon RP, Aminoff MJ, Greenberg DA (2009). Clinical neurology (7 ed.). New York, N.Y: Lange Medical Books/McGraw-Hill. pp. 85–88. ISBN 9780071664332.
3. Piane M, Lulli P, Farinelli I, Simeoni S, De Filippis S, Patacchioli FR, et al. (December 2007). "Genetics of migraine and pharmacogenomics: some considerations". The Journal of Headache and Pain. 8 (6): 334–9. doi:10.1007/s10194-007-0427-2. PMC 2779399. PMID 18058067.
4. Lay CL, Broner SW (May 2009). "Migraine in women". Neurologic Clinics. 27 (2): 503–11. doi:10.1016/j.ncl.2009.01.002. PMID 19289228.
5. Bartleson JD, Cutrer FM (May 2010). "Migraine update. Diagnosis and treatment". Minnesota Medicine. 93 (5): 36–41. PMID 20572569.
6. Swanson JW, Sakai F (2006). "Diagnosis and Differential Diagnosis of Migraines". In Olesen J (ed.). The Headaches. Lippincott Williams & Wilkins. p. 424. ISBN 978-0-7817-5400-2. from the original on 8 September 2017.
7. . American Migraine Foundation. 15 February 2017. Archived from the original on 9 May 2018. Retrieved 23 October 2017.
8. Kumar A, Kadian R (September 2022). "Migraine Prophylaxis". StatPearls Publishing. PMID 29939650. Bookshelf ID: NBK507873. from the original on 8 March 2023. Retrieved 22 August 2023.
9. Gilmore B, Michael M (February 2011). "Treatment of acute migraine headache". American Family Physician. 83 (3): 271–280. PMID 21302868.
10. Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMC 6350784. PMID 23245607.
11. Wells JC (2008). Longman Pronunciation Dictionary (3rd ed.). Longman. ISBN 978-1-4058-8118-0.
12. Jones D (2011). Roach P, Setter J, Esling J (eds.). Cambridge English Pronouncing Dictionary (18th ed.). Cambridge University Press. ISBN 978-0-521-15255-6.
13. Headache Classification Subcommittee of the International Headache Society (2004). "The International Classification of Headache Disorders: 2nd edition". Cephalalgia. 24 (Suppl 1): 9–160. doi:10.1111/j.1468-2982.2004.00653.x. PMID 14979299.
14. Katsarava Z, Buse DC, Manack AN, Lipton RB (February 2012). "Defining the differences between episodic migraine and chronic migraine". Current Pain and Headache Reports. 16 (1): 86–92. doi:10.1007/s11916-011-0233-z. PMC 3258393. PMID 22083262.
15. Shankar Kikkeri N, Nagalli S (December 2022). "Migraine With Aura". StatPearls Publishing. PMID 32119498. Bookshelf ID: NBK554611. from the original on 8 June 2023. Retrieved 23 August 2023.
16. Amin FM, Asghar MS, Hougaard A, Hansen AE, Larsen VA, de Koning PJ, et al. (May 2013). "Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study". The Lancet. Neurology. 12 (5): 454–461. doi:10.1016/S1474-4422(13)70067-X. PMID 23578775. S2CID 25553357. from the original on 28 July 2023. Retrieved 28 July 2023.
17. Mason BN, Russo AF (2018). "Vascular Contributions to Migraine: Time to Revisit?". Frontiers in Cellular Neuroscience. 12: 233. doi:10.3389/fncel.2018.00233. ISSN 1662-5102. PMC 6088188. PMID 30127722.
18. Jacobs B, Dussor G (3 December 2016). "Neurovascular contributions to migraine: moving beyond vasodilation". Neuroscience. 338: 130–144. doi:10.1016/j.neuroscience.2016.06.012. ISSN 0306-4522. PMC 5083225. PMID 27312704.
19. 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.
20. Tzankova V, Becker WJ, Chan TL (January 2023). "Diagnosis and acute management of migraine". CMAJ. 195 (4): E153–E158. doi:10.1503/cmaj.211969. PMC 9888545. PMID 36717129. from the original on 4 July 2023. Retrieved 22 August 2023.
21. Silberstein SD (August 2015). "Preventive Migraine Treatment". Continuum. 21 (4 Headache): 973–989. doi:10.1212/CON.0000000000000199. PMC 4640499. PMID 26252585. from the original on 25 August 2023. Retrieved 22 August 2023.
22. Noseda R, Burstein R (December 2013). "Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain". Pain. 154 (Suppl 1): S44–S53. doi:10.1016/j.pain.2013.07.021. PMC 3858400. PMID 24347803.
23. Spierings EL (July 2001). "Mechanism of migraine and action of antimigraine medications". The Medical Clinics of North America. 85 (4): 943–958, vi–vii. doi:10.1016/s0025-7125(05)70352-7. PMID 11480266. from the original on 1 March 2023. Retrieved 22 August 2023.
24. Haghdoost F, Togha M (1 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.
25. Gobel H. "1. Migraine". ICHD-3 The International Classification of Headache Disorders 3rd edition. from the original on 24 October 2020. Retrieved 22 October 2020.
26. Vos T, Abajobir AA, Abate KH, Abbafati C, Abbas KM, Abd-Allah F, et al. (GBD 2016 Disease and Injury Incidence and Prevalence Collaborators) (September 2017). "Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016". Lancet. 390 (10100): 1211–1259. doi:10.1016/S0140-6736(17)32154-2. PMC 5605509. PMID 28919117.
27. Bigal ME, Lipton RB (June 2008). "The prognosis of migraine". Current Opinion in Neurology. 21 (3): 301–8. doi:10.1097/WCO.0b013e328300c6f5. PMID 18451714. S2CID 34805084.
28. Gutman SA (2008). Quick reference neuroscience for rehabilitation professionals: the essential neurologic principles underlying rehabilitation practice (2nd ed.). Thorofare, NJ: SLACK. p. 231. ISBN 9781556428005. from the original on 12 March 2017.
29. Olesen J, Goadsby PJ (2006). "The Migraines: Introduction". In Olesen J (ed.). The Headaches (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 232–233. ISBN 978-0-7817-5400-2. from the original on 13 March 2017.
30. Tfelt-Hansen P, Young WB, Silberstein (2006). "Antiemetic, Prokinetic, Neuroleptic and Miscellaneous Drugs in the Acute Treatment of Migraine". In Olesen J (ed.). The Headaches (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. p. 512. ISBN 978-0-7817-5400-2. from the original on 22 December 2016.
31. Baskin SM, Lipchik GL, Smitherman TA (October 2006). "Mood and anxiety disorders in chronic headache". Headache. 46 (Suppl 3): S76-87. doi:10.1111/j.1526-4610.2006.00559.x. PMID 17034402. S2CID 35451906.
32. Lynn DJ, Newton HB, Rae-Grant A (2004). The 5-minute neurology consult. Philadelphia: Lippincott Williams & Wilkins. p. 26. ISBN 9780683307238. from the original on 13 March 2017.
33. Buzzi MG, Cologno D, Formisano R, Rossi P (October–December 2005). "Prodromes and the early phase of the migraine attack: therapeutic relevance". Functional Neurology. 20 (4): 179–83. PMID 16483458.
34. Rossi P, Ambrosini A, Buzzi MG (October–December 2005). "Prodromes and predictors of migraine attack". Functional Neurology. 20 (4): 185–91. PMID 16483459.
35. Ropper AH, Adams RD, Victor M, Samuels MA (2009). Adams and Victor's principles of neurology (9 ed.). New York: McGraw-Hill Medical. pp. Chapter 10. ISBN 9780071499927.
36. May A, Burstein R (November 2019). "Hypothalamic regulation of headache and migraine". Cephalalgia. 39 (13): 1710–1719. doi:10.1177/0333102419867280. PMC 7164212. PMID 31466456.
37. Tintinalli JE (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 1116–1117. ISBN 978-0-07-148480-0.
38. Ashina M (November 2020). "Migraine". The New England Journal of Medicine. 383 (19): 1866–1876. doi:10.1056/NEJMra1915327. PMID 33211930. S2CID 227078662.
39. Cutrer FM, Olesen J (2006). "Migraines with Aura and Their Subforms". In Olesen J (ed.). The Headaches (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 238–240. ISBN 978-0-7817-5400-2. from the original on 13 March 2017.
40. Viana M, Sances G, Linde M, Nappi G, Khaliq F, Goadsby PJ, et al. (August 2018). "Prolonged migraine aura: new insights from a prospective diary-aided study". The Journal of Headache and Pain. 19 (1): 77. doi:10.1186/s10194-018-0910-y. PMC 6119171. PMID 30171359.
41. Slap, GB (2008). Adolescent medicine. Philadelphia, PA: Mosby/Elsevier. p. 105. ISBN 9780323040730. from the original on 13 March 2017.
42. Amin FM, Aristeidou S, Baraldi C, Czapinska-Ciepiela EK, Ariadni DD, Di Lenola D, et al. (September 2018). "The association between migraine and physical exercise". The Journal of Headache and Pain. 19 (1): 83. doi:10.1186/s10194-018-0902-y. PMC 6134860. PMID 30203180.
43. Qubty W, Patniyot I (June 2020). "Migraine Pathophysiology". Pediatric Neurology. 107: 1–6. doi:10.1016/j.pediatrneurol.2019.12.014. PMID 32192818. S2CID 213191464.
44. Tepper SJ, Tepper DE (1 January 2011). The Cleveland Clinic manual of headache therapy. New York: Springer. p. 6. ISBN 9781461401780. from the original on 22 December 2016.
45. Bigal ME, Arruda MA (July 2010). "Migraine in the pediatric population--evolving concepts". Headache. 50 (7): 1130–43. doi:10.1111/j.1526-4610.2010.01717.x. PMID 20572878. S2CID 23256755.
46. Rasmussen BK (2006). "Epidemiology of Migraine". In Olesen J (ed.). The Headaches (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 238–240. ISBN 978-0-7817-5400-2. from the original on 13 March 2017.
47. Dalessio DJ (2001). Silberstein SD, Lipton RB, Dalessio DJ (eds.). Wolff's headache and other head pain (7 ed.). Oxford: Oxford University Press. p. 122. ISBN 9780195135183.
48. Lisak RP, Truong DD, Carroll W, Bhidayasiri R (2009). International neurology: a clinical approach. Chichester, UK: Wiley-Blackwell. p. 670. ISBN 9781405157384.
49. Kaniecki RG (June 2009). "Basilar-type migraine". Current Pain and Headache Reports. 13 (3): 217–20. doi:10.1007/s11916-009-0036-7. PMID 19457282. S2CID 22242504.
50. Glaser JS (1999). Neuro-ophthalmology (3rd ed.). Philadelphia: Lippincott Williams & Wilkins. p. 555. ISBN 9780781717298. from the original on 13 March 2017.
51. Dodick DW, Capobianco DJ (2008). "Chapter 14: Headaches". In Sirven JI, Malamut BL (eds.). Clinical neurology of the older adult (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 197. ISBN 9780781769471. from the original on 12 March 2017.
52. Robblee J (21 August 2019). "Silent Migraine: A Guide". American Migraine Foundation. from the original on 28 January 2021. Retrieved 22 January 2021.
53. He Y, Li Y, Nie Z (February 2015). "Typical aura without headache: a case report and review of the literature". Journal of Medical Case Reports. 9 (1): 40. doi:10.1186/s13256-014-0510-7. PMC 4344793. PMID 25884682.
54. Leonard J (7 September 2018). Han S (ed.). "Silent migraine: Symptoms, causes, treatment, prevention". Medical News Today. from the original on 19 January 2021. Retrieved 22 January 2021.
55. Bose P, Goadsby PJ (June 2016). "The migraine postdrome". Current Opinion in Neurology. 29 (3): 299–301. doi:10.1097/WCO.0000000000000310. PMID 26886356. S2CID 22445093.
56. Kelman L (February 2006). "The postdrome of the acute migraine attack". Cephalalgia. 26 (2): 214–20. doi:10.1111/j.1468-2982.2005.01026.x. PMID 16426278. S2CID 21519111.
57. Halpern AL, Silberstein SD (2005). . In Kaplan PW, Fisher RS (eds.). Imitators of Epilepsy (2 ed.). New York: Demos Medical. ISBN 978-1-888799-83-5. NBK7326. Archived from the original on 27 August 2011. Retrieved 5 September 2017.
58. Robbins MS, Lipton RB (April 2010). "The epidemiology of primary headache disorders". Seminars in Neurology. 30 (2): 107–19. doi:10.1055/s-0030-1249220. PMID 20352581. S2CID 260317083.
59. Schürks M (January 2012). "Genetics of migraine in the age of genome-wide association studies". The Journal of Headache and Pain. 13 (1): 1–9. doi:10.1007/s10194-011-0399-0. PMC 3253157. PMID 22072275.
60. The Headaches, pp. 246–247
61. Bink T, Duraku LS, Ter Louw RP, Zuidam JM, Mathijssen IM, Driessen C (December 2019). "The Cutting Edge of Headache Surgery: A Systematic Review on the Value of Extracranial Surgery in the Treatment of Chronic Headache". Plastic and Reconstructive Surgery. 144 (6): 1431–1448. doi:10.1097/PRS.0000000000006270. PMID 31764666. S2CID 208273535.
62. Adair D, Truong D, Esmaeilpour Z, Gebodh N, Borges H, Ho L, et al. (May 2020). "Electrical stimulation of cranial nerves in cognition and disease". Brain Stimulation. 13 (3): 717–750. doi:10.1016/j.brs.2020.02.019. PMC 7196013. PMID 32289703.
63. 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.
64. de Vries B, Frants RR, Ferrari MD, van den Maagdenberg AM (July 2009). "Molecular genetics of migraine". Human Genetics. 126 (1): 115–32. doi:10.1007/s00439-009-0684-z. PMID 19455354. S2CID 20119237.
65. Montagna P (September 2008). "Migraine genetics". Expert Review of Neurotherapeutics. 8 (9): 1321–30. doi:10.1586/14737175.8.9.1321. PMID 18759544. S2CID 207195127.
66. Ducros A (May 2013). "[Genetics of migraine]". Revue Neurologique. 169 (5): 360–71. doi:10.1016/j.neurol.2012.11.010. PMID 23618705.
67. Wan D, Wang C, Zhang X, Tang W, Chen M, Dong Z, et al. (1 January 2016). "Association between angiotensin-converting enzyme insertion/deletion polymorphism and migraine: a meta-analysis". The International Journal of Neuroscience. 126 (5): 393–9. doi:10.3109/00207454.2015.1025395. PMID 26000817. S2CID 34902092.
68. Dussor G, Cao YQ (October 2016). "TRPM8 and Migraine". Headache. 56 (9): 1406–1417. doi:10.1111/head.12948. PMC 5335856. PMID 27634619.
69. Levy D, Strassman AM, Burstein R (June 2009). "A critical view on the role of migraine triggers in the genesis of migraine pain". Headache. 49 (6): 953–7. doi:10.1111/j.1526-4610.2009.01444.x. PMID 19545256. S2CID 31707887.
70. Martin PR (June 2010). "Behavioral management of migraine headache triggers: learning to cope with triggers". Current Pain and Headache Reports. 14 (3): 221–7. doi:10.1007/s11916-010-0112-z. PMID 20425190. S2CID 5511782.
71. Pavlovic JM, Buse DC, Sollars CM, Haut S, Lipton RB (2014). "Trigger factors and premonitory features of migraine attacks: summary of studies". Headache. 54 (10): 1670–9. doi:10.1111/head.12468. PMID 25399858. S2CID 25016889.
72. Radat F (May 2013). "[Stress and migraine]". Revue Neurologique. 169 (5): 406–12. doi:10.1016/j.neurol.2012.11.008. PMID 23608071.
73. Peterlin BL, Katsnelson MJ, Calhoun AH (October 2009). "The associations between migraine, unipolar psychiatric comorbidities, and stress-related disorders and the role of estrogen". Current Pain and Headache Reports. 13 (5): 404–12. doi:10.1007/s11916-009-0066-1. PMC 3972495. PMID 19728969.
74. Chai NC, Peterlin BL, Calhoun AH (June 2014). "Migraine and estrogen". Current Opinion in Neurology. 27 (3): 315–24. doi:10.1097/WCO.0000000000000091. PMC 4102139. PMID 24792340.
75. Finocchi C, Sivori G (May 2012). "Food as trigger and aggravating factor of migraine". Neurological Sciences. 33 (Suppl 1): S77-80. doi:10.1007/s10072-012-1046-5. PMID 22644176. S2CID 19582697.
76. Rockett FC, de Oliveira VR, Castro K, Chaves ML, Perla A, Perry ID (June 2012). "Dietary aspects of migraine trigger factors". Nutrition Reviews. 70 (6): 337–56. doi:10.1111/j.1753-4887.2012.00468.x. PMID 22646127.
77. Ghose K, Carroll JD (1984). "Mechanism of tyramine-induced migraine: similarity with dopamine and interactions with disulfiram and propranolol in migraine patients". Neuropsychobiology. 12 (2–3): 122–126. doi:10.1159/000118123. PMID 6527752.
78. Moffett A, Swash M, Scott DF (August 1972). "Effect of tyramine in migraine: a double-blind study". Journal of Neurology, Neurosurgery, and Psychiatry. 35 (4): 496–499. doi:10.1136/jnnp.35.4.496. PMC 494110. PMID 4559027.
79. "Tyramine and Migraines: What You Need to Know". excedrin.com. Retrieved 4 March 2022.
80. Encyclopedia of Food Sciences and Nutrition (Second ed.). Academic Press. 2003. ISBN 978-0-12-227055-0.
81. Özturan A, Şanlıer N, Coşkun Ö (2016). "The Relationship Between Migraine and Nutrition" (PDF). Turk J Neurol. 22 (2): 44–50. doi:10.4274/tnd.37132. (PDF) from the original on 23 August 2023. Retrieved 4 March 2022.
82. Sun-Edelstein C, Mauskop A (June 2009). (PDF). The Clinical Journal of Pain. 25 (5): 446–452. CiteSeerX 10.1.1.530.1223. doi:10.1097/AJP.0b013e31819a6f65. PMID 19454881. S2CID 3042635. Archived from the original (PDF) on 13 August 2017.
83. Obayashi Y, Nagamura Y (17 May 2016). "Does monosodium glutamate really cause headache? : a systematic review of human studies". The Journal of Headache and Pain. 17 (1): 54. doi:10.1186/s10194-016-0639-4. PMC 4870486. PMID 27189588.
84. Friedman DI, De ver Dye T (June 2009). "Migraine and the environment". Headache. 49 (6): 941–52. doi:10.1111/j.1526-4610.2009.01443.x. PMID 19545255. S2CID 29764274.
85. Andreou AP, Edvinsson L (December 2019). "Mechanisms of migraine as a chronic evolutive condition". The Journal of Headache and Pain. 20 (1): 117. doi:10.1186/s10194-019-1066-0. PMC 6929435. PMID 31870279.
86. "Migraine". National Institute of Neurological Disorders and Stroke. 11 July 2023. Retrieved 25 August 2023.
87. Hoffmann J, Baca SM, Akerman S (April 2019). "Neurovascular mechanisms of migraine and cluster headache". Journal of Cerebral Blood Flow and Metabolism. 39 (4): 573–594. doi:10.1177/0271678x17733655. PMC 6446418. PMID 28948863.
88. Brennan KC, Charles A (June 2010). "An update on the blood vessel in migraine". Current Opinion in Neurology. 23 (3): 266–74. doi:10.1097/WCO.0b013e32833821c1. PMC 5500293. PMID 20216215.
89. Spiri D, Titomanlio L, Pogliani L, Zuccotti G (January 2012). "Pathophysiology of migraine: The neurovascular theory". Headaches: Causes, Treatment and Prevention: 51–64.
90. Goadsby PJ (January 2009). "The vascular theory of migraine--a great story wrecked by the facts". Brain. 132 (Pt 1): 6–7. doi:10.1093/brain/awn321. PMID 19098031.
91. Dodick DW (April 2008). "Examining the essence of migraine--is it the blood vessel or the brain? A debate". Headache. 48 (4): 661–7. doi:10.1111/j.1526-4610.2008.01079.x. PMID 18377395. S2CID 6272233.
92. Chen D, Willis-Parker M, Lundberg GP (October 2020). "Migraine headache: Is it only a neurological disorder? Links between migraine and cardiovascular disorders". Trends in Cardiovascular Medicine. 30 (7): 424–430. doi:10.1016/j.tcm.2019.10.005. PMID 31679956.
93. Jacobs B, Dussor G (December 2016). "Neurovascular contributions to migraine: Moving beyond vasodilation". Neuroscience. 338: 130–144. doi:10.1016/j.neuroscience.2016.06.012. PMC 5083225. PMID 27312704.
94. Mason BN, Russo AF (2018). "Vascular Contributions to Migraine: Time to Revisit?". Frontiers in Cellular Neuroscience. 12: 233. doi:10.3389/fncel.2018.00233. PMC 6088188. PMID 30127722.
95. Dodick DW, Gargus JJ (August 2008). "Why migraines strike". Scientific American. 299 (2): 56–63. Bibcode:2008SciAm.299b..56D. doi:10.1038/scientificamerican0808-56. PMID 18666680.
96. Edvinsson L, Haanes KA (May 2020). "Views on migraine pathophysiology: Where does it start?". Neurology and Clinical Neuroscience. 8 (3): 120–127. doi:10.1111/ncn3.12356. ISSN 2049-4173. S2CID 214320892.
97. Do TP, Hougaard A, Dussor G, Brennan KC, Amin FM (January 2023). "Migraine attacks are of peripheral origin: the debate goes on". The Journal of Headache and Pain. 24 (1): 3. doi:10.1186/s10194-022-01538-1. PMC 9830833. PMID 36627561.
98. The Headaches, Chp. 28, pp. 269–72
99. Olesen J, Burstein R, Ashina M, Tfelt-Hansen P (July 2009). "Origin of pain in migraine: evidence for peripheral sensitisation". The Lancet. Neurology. 8 (7): 679–90. doi:10.1016/S1474-4422(09)70090-0. PMID 19539239. S2CID 20452008.
100. Akerman S, Holland PR, Goadsby PJ (September 2011). "Diencephalic and brainstem mechanisms in migraine". Nature Reviews. Neuroscience. 12 (10): 570–84. doi:10.1038/nrn3057. PMID 21931334. S2CID 8472711.
101. Shevel E (March 2011). "The extracranial vascular theory of migraine--a great story confirmed by the facts". Headache. 51 (3): 409–417. doi:10.1111/j.1526-4610.2011.01844.x. PMID 21352215. S2CID 6939786.
102. Burnstock G (January 2016). "Purinergic Mechanisms and Pain". In Barrett JE (ed.). Pharmacological Mechanisms and the Modulation of Pain. Advances in Pharmacology. Vol. 75. pp. 91–137. doi:10.1016/bs.apha.2015.09.001. ISBN 9780128038833. PMID 26920010.
103. Davidoff R (14 February 2002). Migraine: Manifestations, Pathogenesis, and Management. Oxford University Press. ISBN 978-0-19-803135-2. from the original on 23 August 2023. Retrieved 12 November 2020.
104. Lipton RB, Diener HC, Robbins MS, Garas SY, Patel K (October 2017). "Caffeine in the management of patients with headache". The Journal of Headache and Pain. 18 (1): 107. doi:10.1186/s10194-017-0806-2. PMC 5655397. PMID 29067618.
105. Hamel E (November 2007). "Serotonin and migraine: biology and clinical implications". Cephalalgia. 27 (11): 1293–300. doi:10.1111/j.1468-2982.2007.01476.x. PMID 17970989. S2CID 26543041.
106. • Lewis DW, Dorbad D (September 2000). "The utility of neuroimaging in the evaluation of children with migraine or chronic daily headache who have normal neurological examinations". Headache. 40 (8): 629–32. doi:10.1046/j.1526-4610.2000.040008629.x. PMID 10971658. S2CID 14443890.
     • Silberstein SD (September 2000). "Practice parameter: evidence-based guidelines for migraine headache (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 55 (6): 754–62. doi:10.1212/WNL.55.6.754. PMID 10993991.
     • Medical Advisory Secretariat (2010). "Neuroimaging for the evaluation of chronic headaches: an evidence-based analysis". Ontario Health Technology Assessment Series. 10 (26): 1–57. PMC 3377587. PMID 23074404.
107. Cousins G, Hijazze S, Van de Laar FA, Fahey T (July–August 2011). "Diagnostic accuracy of the ID Migraine: a systematic review and meta-analysis". Headache. 51 (7): 1140–8. doi:10.1111/j.1526-4610.2011.01916.x. PMID 21649653. S2CID 205684294.
108. "Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition". Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. PMID 29368949.
109. Nappi G (September 2005). "Introduction to the new International Classification of Headache Disorders". The Journal of Headache and Pain. 6 (4): 203–4. doi:10.1007/s10194-005-0185-y. PMC 3452009. PMID 16362664.
110. "Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition". Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. ISSN 0333-1024. PMID 29368949.
111. Negro A, Rocchietti-March M, Fiorillo M, Martelletti P (December 2011). "Chronic migraine: current concepts and ongoing treatments". European Review for Medical and Pharmacological Sciences. 15 (12): 1401–20. PMID 22288302.
112. Davidoff RA (2002). Migraine : manifestations, pathogenesis, and management (2 ed.). Oxford [u.a.]: Oxford Univ. Press. p. 81. ISBN 9780195137057. from the original on 22 December 2016.
113. Russell G, Abu-Arafeh I, Symon DN (2002). "Abdominal migraine: evidence for existence and treatment options". Paediatric Drugs. 4 (1): 1–8. doi:10.2165/00128072-200204010-00001. PMID 11817981. S2CID 12289726.
114. Lewis DW, Dorbad D (September 2000). "The utility of neuroimaging in the evaluation of children with migraine or chronic daily headache who have normal neurological examinations". Headache. 40 (8): 629–32. doi:10.1046/j.1526-4610.2000.040008629.x. PMID 10971658. S2CID 14443890.
115. Silberstein SD (September 2000). "Practice parameter: evidence-based guidelines for migraine headache (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 55 (6): 754–62. doi:10.1212/WNL.55.6.754. PMID 10993991.
116. Medical Advisory Secretariat (2010). "Neuroimaging for the evaluation of chronic headaches: an evidence-based analysis". Ontario Health Technology Assessment Series. 10 (26): 1–57. PMC 3377587. PMID 23074404.
117. Oskoui M, Pringsheim T, Billinghurst L, Potrebic S, Gersz EM, Gloss D, et al. (September 2019). "Practice guideline update summary: Pharmacologic treatment for pediatric migraine prevention: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 93 (11): 500–509. doi:10.1212/WNL.0000000000008105. PMC 6746206. PMID 31413170.
118. Modi S, Lowder DM (January 2006). "Medications for migraine prophylaxis". American Family Physician. 73 (1): 72–78. PMID 16417067. from the original on 2 March 2020. Retrieved 19 February 2010.
119. Ha H, Gonzalez A (January 2019). "Migraine Headache Prophylaxis". American Family Physician. 99 (1): 17–24. PMID 30600979. from the original on 5 April 2023. Retrieved 25 August 2023.
120. Diener HC, Limmroth V (August 2004). "Medication-overuse headache: a worldwide problem". The Lancet. Neurology. 3 (8): 475–483. doi:10.1016/S1474-4422(04)00824-5. PMID 15261608. S2CID 43840120.
121. Fritsche G, Diener HC (November 2002). "Medication overuse headaches -- what is new?". Expert Opinion on Drug Safety. 1 (4): 331–338. doi:10.1517/14740338.1.4.331. PMID 12904133. S2CID 23422679.
122. Kaniecki R, Lucas S (2004). "Treatment of primary headache: preventive treatment of migraine". Standards of care for headache diagnosis and treatment. Chicago: National Headache Foundation. pp. 40–52.
123. Loder E, Burch R, Rizzoli P (June 2012). "The 2012 AHS/AAN guidelines for prevention of episodic migraine: a summary and comparison with other recent clinical practice guidelines". Headache. 52 (6): 930–45. doi:10.1111/j.1526-4610.2012.02185.x. PMID 22671714. S2CID 540800.
124. Linde M, Mulleners WM, Chronicle EP, McCrory DC (June 2013). "Antiepileptics other than gabapentin, pregabalin, topiramate, and valproate for the prophylaxis of episodic migraine in adults". The Cochrane Database of Systematic Reviews. 2021 (6): CD010608. doi:10.1002/14651858.CD010608. PMC 8221229. PMID 23797674.
125. Locher C, Kossowsky J, Koechlin H, Lam TL, Barthel J, Berde CB, et al. (April 2020). "Efficacy, Safety, and Acceptability of Pharmacologic Treatments for Pediatric Migraine Prophylaxis: A Systematic Review and Network Meta-analysis". JAMA Pediatrics. 174 (4): 341–349. doi:10.1001/jamapediatrics.2019.5856. PMC 7042942. PMID 32040139.
126. Merison K, Jacobs H (November 2016). "Diagnosis and Treatment of Childhood Migraine". Current Treatment Options in Neurology. 18 (11): 48. doi:10.1007/s11940-016-0431-4. PMID 27704257. S2CID 28302667.
127. Dorosch T, Ganzer CA, Lin M, Seifan A (September 2019). "Efficacy of Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in the Preventative Treatment of Episodic Migraine in Adults". Current Pain and Headache Reports. 23 (11): 85. doi:10.1007/s11916-019-0823-8. PMID 31515634. S2CID 202557362.
128. Cernes R, Mashavi M, Zimlichman R (2011). "Differential clinical profile of candesartan compared to other angiotensin receptor blockers". Vascular Health and Risk Management. 7: 749–59. doi:10.2147/VHRM.S22591. PMC 3253768. PMID 22241949.
129. Rajapakse T, Pringsheim T (April 2016). "Nutraceuticals in Migraine: A Summary of Existing Guidelines for Use". Headache. 56 (4): 808–16. doi:10.1111/head.12789. PMID 26954394. S2CID 31097792.
130. Teigen L, Boes CJ (September 2015). "An evidence-based review of oral magnesium supplementation in the preventive treatment of migraine". Cephalalgia. 35 (10): 912–22. doi:10.1177/0333102414564891. PMID 25533715. S2CID 25398410.
131. Silberstein SD, Holland S, Freitag F, Dodick DW, Argoff C, Ashman E (April 2012). "Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 78 (17): 1337–45. doi:10.1212/WNL.0b013e3182535d20. PMC 3335452. PMID 22529202.
132. Shamliyan TA, Choi JY, Ramakrishnan R, Miller JB, Wang SY, Taylor FR, et al. (September 2013). "Preventive pharmacologic treatments for episodic migraine in adults". Journal of General Internal Medicine. 28 (9): 1225–37. doi:10.1007/s11606-013-2433-1. PMC 3744311. PMID 23592242.
133. Ibekwe A, Perras C, Mierzwinski-Urban M (February 2018). "Monoclonal Antibodies to Prevent Migraine Headaches". CADTH Issues in Emerging Health Technologies. Ottawa (ON): Canadian Agency for Drugs and Technologies in Health. PMID 30855775. Bookshelf ID: NBK538376. from the original on 23 August 2023. Retrieved 28 July 2023.
134. Linde K, Allais G, Brinkhaus B, Fei Y, Mehring M, Vertosick EA, et al. (June 2016). "Acupuncture for the prevention of episodic migraine". The Cochrane Database of Systematic Reviews. 2018 (6): CD001218. doi:10.1002/14651858.CD001218.pub3. PMC 4977344. PMID 27351677.
135. Chaibi A, Tuchin PJ, Russell MB (April 2011). "Manual therapies for migraine: a systematic review". The Journal of Headache and Pain. 12 (2): 127–33. doi:10.1007/s10194-011-0296-6. PMC 3072494. PMID 21298314.
136. Millstine D, Chen CY, Bauer B (May 2017). "Complementary and integrative medicine in the management of headache". BMJ. 357: j1805. doi:10.1136/bmj.j1805. PMID 28512119. S2CID 19155758.
137. Posadzki P, Ernst E (June 2011). "Spinal manipulations for the treatment of migraine: a systematic review of randomized clinical trials". Cephalalgia. 31 (8): 964–70. doi:10.1177/0333102411405226. PMID 21511952. S2CID 31205541.
138. Sharpe L, Dudeney J, Williams AC, Nicholas M, McPhee I, Baillie A, et al. (July 2019). "Psychological therapies for the prevention of migraine in adults". The Cochrane Database of Systematic Reviews. 7 (7): CD012295. doi:10.1002/14651858.CD012295.pub2. PMC 6603250. PMID 31264211.
139. "Behavioral Interventions for Migraine Prevention (A Systematic Review)". Patient-Centered Outcomes Research Institute. 14 July 2022. from the original on 23 August 2023. Retrieved 14 April 2023.
140. Holland S, Silberstein SD, Freitag F, Dodick DW, Argoff C, Ashman E (April 2012). "Evidence-based guideline update: NSAIDs and other complementary treatments for episodic migraine prevention in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 78 (17): 1346–53. doi:10.1212/WNL.0b013e3182535d0c. PMC 3335449. PMID 22529203.
141. Pringsheim T, Davenport W, Mackie G, Worthington I, Aubé M, Christie SN, et al. (March 2012). "Canadian Headache Society guideline for migraine prophylaxis". The Canadian Journal of Neurological Sciences. 39 (2 Suppl 2): S1-59. PMID 22683887.
142. "Butterbur: Uses, Side Effects, Interactions, Dosage, and Warning". webmd.com. from the original on 7 December 2019. Retrieved 7 December 2019.
143. "Butterbur". National Center for Complementary and Integrative Health (NCCIH). 8 February 2012. from the original on 7 December 2019. Retrieved 7 December 2019.
144. Littarru GP, Tiano L (November 2005). "Clinical aspects of coenzyme Q10: an update". Current Opinion in Clinical Nutrition and Metabolic Care. 8 (6): 641–6. doi:10.1097/01.mco.0000171123.60665.16. PMID 16205466. S2CID 25010508.
145. Groenewegen WA, Knight DW, Heptinstall S (1992). "Progress in the medicinal chemistry of the herb feverfew". Progress in Medicinal Chemistry. 29: 217–38. doi:10.1016/s0079-6468(08)70009-2. ISBN 9780444894724. PMID 1475370.
146. Barnes J, Anderson LA, Philipson JD (2007). Herbal Medicines (3rd ed.). London: Pharmaceutical Press.
147. EMA. "Assessment report on Tanacetum parthenium (L.) Schultz Bip., herba" (PDF). Europa (web portal). (PDF) from the original on 2 November 2020. Retrieved 8 July 2020.
148. Gelfand AA, Goadsby PJ (September 2016). "The Role of Melatonin in the Treatment of Primary Headache Disorders". Headache (Review). 56 (8): 1257–66. doi:10.1111/head.12862. PMC 5012937. PMID 27316772.
149. Long R, Zhu Y, Zhou S (January 2019). "Therapeutic role of melatonin in migraine prophylaxis: A systematic review". Medicine. 98 (3): e14099. doi:10.1097/MD.0000000000014099. PMC 6370052. PMID 30653130.
150. Nesbitt AD, Leschziner GD, Peatfield RC (September 2014). "Headache, drugs and sleep". Cephalalgia (Review). 34 (10): 756–66. doi:10.1177/0333102414542662. PMID 25053748. S2CID 33548757.
151. Nestoriuc Y, Martin A (March 2007). "Efficacy of biofeedback for migraine: a meta-analysis". Pain. 128 (1–2): 111–27. doi:10.1016/j.pain.2006.09.007. PMID 17084028. S2CID 23351902.
152. Nestoriuc Y, Martin A, Rief W, Andrasik F (September 2008). "Biofeedback treatment for headache disorders: a comprehensive efficacy review". Applied Psychophysiology and Biofeedback. 33 (3): 125–40. doi:10.1007/s10484-008-9060-3. PMID 18726688. S2CID 29122354.
153. Schoenen J, Allena M, Magis D (2010). "Neurostimulation therapy in intractable headaches". In Vinken PJ, Bruyn GW (eds.). Headache. Handbook of Clinical Neurology. Vol. 97. pp. 443–50. doi:10.1016/S0072-9752(10)97037-1. ISBN 9780444521392. PMID 20816443.
154. Reed KL, Black SB, Banta CJ, Will KR (March 2010). "Combined occipital and supraorbital neurostimulation for the treatment of chronic migraine headaches: initial experience". Cephalalgia. 30 (3): 260–71. doi:10.1111/j.1468-2982.2009.01996.x. PMID 19732075. S2CID 18639211.
155. . Food and Drug Administration (Press release). 11 March 2014. Archived from the original on 25 July 2014. Retrieved 25 July 2014.
156. "FDA approves transcranial magnetic stimulator" (PDF). (PDF) from the original on 21 February 2014.
157. Tao H, Wang T, Dong X, Guo Q, Xu H, Wan Q (May 2018). "Effectiveness of transcutaneous electrical nerve stimulation for the treatment of migraine: a meta-analysis of randomized controlled trials". The Journal of Headache and Pain. 19 (1): 42. doi:10.1186/s10194-018-0868-9. PMC 5975046. PMID 29845369. We found significant reduction of monthly headache days
158. Kung TA, Guyuron B, Cederna PS (January 2011). "Migraine surgery: a plastic surgery solution for refractory migraine headache". Plastic and Reconstructive Surgery. 127 (1): 181–189. doi:10.1097/PRS.0b013e3181f95a01. PMID 20871488. S2CID 18817383.
159. . Choosing Wisely. Archived from the original on 3 December 2013. Retrieved 24 November 2013.
160. Richer L, Billinghurst L, Linsdell MA, Russell K, Vandermeer B, Crumley ET, et al. (April 2016). "Drugs for the acute treatment of migraine in children and adolescents". The Cochrane Database of Systematic Reviews. 4 (4): CD005220. doi:10.1002/14651858.CD005220.pub2. PMC 6516975. PMID 27091010.
161. Oskoui M, Pringsheim T, Holler-Managan Y, Potrebic S, Billinghurst L, Gloss D, et al. (September 2019). "Practice guideline update summary: Acute treatment of migraine in children and adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 93 (11): 487–499. doi:10.1212/WNL.0000000000008095. PMID 31413171.
162. Wang G, Tan T, Liu Y, Hong P (August 2020). "Drugs for Acute Attack of Pediatric Migraine: A Network Meta-analysis of Randomized Controlled Trials". Clinical Neurology and Neurosurgery. 195: 105853. doi:10.1016/j.clineuro.2020.105853. PMID 32464520. S2CID 215814011.
163. Nowaczewska M, Wiciński M, Kaźmierczak W (July 2020). "The Ambiguous Role of Caffeine in Migraine Headache: From Trigger to Treatment". Nutrients. 12 (8): 2259. doi:10.3390/nu12082259. PMC 7468766. PMID 32731623.
164. Rabbie R, Derry S, Moore RA (April 2013). "Ibuprofen with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews. 2019 (4): CD008039. doi:10.1002/14651858.CD008039.pub3. PMC 4161114. PMID 23633348.
165. Derry S, Rabbie R, Moore RA (April 2013). "Diclofenac with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews. 2019 (4): CD008783. doi:10.1002/14651858.CD008783.pub3. PMC 4164457. PMID 23633360.
166. Kirthi V, Derry S, Moore RA (April 2013). "Aspirin with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews. 2019 (4): CD008041. doi:10.1002/14651858.CD008041.pub3. PMC 4163048. PMID 23633350.
167. Derry S, Moore RA (April 2013). "Paracetamol (acetaminophen) with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews. 2019 (4): CD008040. doi:10.1002/14651858.CD008040.pub3. PMC 4161111. PMID 23633349.
168. Eken C (March 2015). "Critical reappraisal of intravenous metoclopramide in migraine attack: a systematic review and meta-analysis". The American Journal of Emergency Medicine. 33 (3): 331–7. doi:10.1016/j.ajem.2014.11.013. PMID 25579820.
169. Orr SL, Friedman BW, Christie S, Minen MT, Bamford C, Kelley NE, et al. (June 2016). "Management of Adults With Acute Migraine in the Emergency Department: The American Headache Society Evidence Assessment of Parenteral Pharmacotherapies". Headache. 56 (6): 911–40. doi:10.1111/head.12835. PMID 27300483.
170. Law S, Derry S, Moore RA (October 2013). "Naproxen with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews. 2013 (10): CD009455. doi:10.1002/14651858.CD009455.pub2. PMC 6540401. PMID 24142263.
171. Singh RB, VanderPluym JH, Morrow AS, Urtecho M, Nayfeh T, Roldan VD, et al. (December 2020). Acute Treatments for Episodic Migraine. AHRQ Comparative Effectiveness Reviews. Rockville (MD): Agency for Healthcare Research and Quality (US). PMID 33411427. Bookshelf ID: NBK566246. from the original on 15 January 2021. Retrieved 28 June 2021.
172. Johnston MM, Rapoport AM (August 2010). "Triptans for the management of migraine". Drugs. 70 (12): 1505–1518. doi:10.2165/11537990-000000000-00000. PMID 20687618. S2CID 41613179.
173. Derry CJ, Derry S, Moore RA (February 2012). "Sumatriptan (rectal route of administration) for acute migraine attacks in adults". The Cochrane Database of Systematic Reviews. 2012 (2): CD009664. doi:10.1002/14651858.CD009664. PMC 4170908. PMID 22336868.
174. Derry CJ, Derry S, Moore RA (February 2012). "Sumatriptan (intranasal route of administration) for acute migraine attacks in adults". The Cochrane Database of Systematic Reviews. 2012 (2): CD009663. doi:10.1002/14651858.CD009663. PMC 4164476. PMID 22336867.
175. Derry CJ, Derry S, Moore RA (February 2012). "Sumatriptan (subcutaneous route of administration) for acute migraine attacks in adults". The Cochrane Database of Systematic Reviews. 2012 (2): CD009665. doi:10.1002/14651858.CD009665. PMC 4164380. PMID 22336869.
176. "Generic migraine drug could relieve your pain and save you money". Best Buy Drugs. Consumer Reports. from the original on 4 August 2013.
177. Tepper SJ, Tepper DE (April 2010). "Breaking the cycle of medication overuse headache". Cleveland Clinic Journal of Medicine. 77 (4): 236–42. doi:10.3949/ccjm.77a.09147. PMID 20360117. S2CID 36333666.
178. Law S, Derry S, Moore RA (April 2016). "Sumatriptan plus naproxen for the treatment of acute migraine attacks in adults". The Cochrane Database of Systematic Reviews. 4 (4): CD008541. doi:10.1002/14651858.CD008541.pub3. PMC 6485397. PMID 27096438.
179. "Zavzpret- zavegepant spray". DailyMed. 9 March 2023. from the original on 25 August 2023. Retrieved 25 August 2023.
180. "Drug Approval Package: Zavzpret". U.S. Food and Drug Administration (FDA). 3 April 2023. from the original on 25 August 2023. Retrieved 25 August 2023.
181. "Pfizer's Zavzpret (zavegepant) Migraine Nasal Spray Receives FDA Approval" (Press release). Pfizer. 10 March 2023. from the original on 8 April 2023. Retrieved 10 March 2023 – via businesswire.com.
182. Sumamo Schellenberg E, Dryden DM, Pasichnyk D, Ha C, Vandermeer B, Friedman BW, et al. (November 2012). "Acute Migraine Treatment in Emergency Settings". AHRQ Comparative Effectiveness Reviews. Rockville (MD): Agency for Healthcare Research and Quality (US). PMID 23304741. Report No.: 12(13)-EHC142-EF. from the original on 23 August 2023. Retrieved 28 July 2023.
183. Kelley NE, Tepper DE (January 2012). "Rescue therapy for acute migraine, part 1: triptans, dihydroergotamine, and magnesium". Headache. 52 (1): 114–28. doi:10.1111/j.1526-4610.2011.02062.x. PMID 22211870. S2CID 45767513.
184. Morren JA, Galvez-Jimenez N (December 2010). "Where is dihydroergotamine mesylate in the changing landscape of migraine therapy?". Expert Opinion on Pharmacotherapy. 11 (18): 3085–93. doi:10.1517/14656566.2010.533839. PMID 21080856. S2CID 44639896.
185. Tfelt-Hansen P, Saxena PR, Dahlöf C, Pascual J, Láinez M, Henry P, et al. (January 2000). "Ergotamine in the acute treatment of migraine: a review and European consensus". Brain. 123 (Pt 1): 9–18. doi:10.1093/brain/123.1.9. PMID 10611116.
186. Yablon LA, Mauskop A (2011). "Magnesium in headache". In Vink R, Nechifor M (eds.). Magnesium in the Central Nervous System. Adelaide (AU): University of Adelaide Press. ISBN 978-0-9870730-5-1. PMID 29920023. Bookshelf ID: NBK507271. from the original on 14 August 2020. Retrieved 19 August 2020.
187. Chiu HY, Yeh TH, Huang YC, Chen PY (January 2016). "Effects of Intravenous and Oral Magnesium on Reducing Migraine: A Meta-analysis of Randomized Controlled Trials". Pain Physician. 19 (1): E97-112. PMID 26752497.
188. Veronese N, Demurtas J, Pesolillo G, Celotto S, Barnini T, Calusi G, et al. (February 2020). "Magnesium and health outcomes: an umbrella review of systematic reviews and meta-analyses of observational and intervention studies". European Journal of Nutrition. 59 (1): 263–272. doi:10.1007/s00394-019-01905-w. hdl:10447/360041. PMID 30684032. S2CID 59275463. from the original on 3 February 2023. Retrieved 22 December 2022.
189. Colman I, Friedman BW, Brown MD, Innes GD, Grafstein E, Roberts TE, et al. (June 2008). "Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence". BMJ. 336 (7657): 1359–1361. doi:10.1136/bmj.39566.806725.BE. PMC 2427093. PMID 18541610.
190. Piatka C, Beckett RD (February 2020). "Propofol for Treatment of Acute Migraine in the Emergency Department: A Systematic Review". Academic Emergency Medicine. 27 (2): 148–160. doi:10.1111/acem.13870. PMID 31621134.
191. Vukovic Cvetkovic V, Jensen RH (January 2019). "Neurostimulation for the treatment of chronic migraine and cluster headache". Acta Neurologica Scandinavica. 139 (1): 4–17. doi:10.1111/ane.13034. PMID 30291633. S2CID 52923061.
192. Herd CP, Tomlinson CL, Rick C, Scotton WJ, Edwards J, Ives N, et al. (June 2018). "Botulinum toxins for the prevention of migraine in adults". The Cochrane Database of Systematic Reviews. 2018 (6): CD011616. doi:10.1002/14651858.CD011616.pub2. PMC 6513576. PMID 29939406.
193. Jackson JL, Kuriyama A, Hayashino Y (April 2012). "Botulinum toxin A for prophylactic treatment of migraine and tension headaches in adults: a meta-analysis". JAMA. 307 (16): 1736–45. doi:10.1001/jama.2012.505. PMID 22535858.
194. Simpson DM, Hallett M, Ashman EJ, Comella CL, Green MW, Gronseth GS, et al. (May 2016). "Practice guideline update summary: Botulinum neurotoxin for the treatment of blepharospasm, cervical dystonia, adult spasticity, and headache: Report of the Guideline Development Subcommittee of the American Academy of Neurology". Neurology. 86 (19): 1818–26. doi:10.1212/WNL.0000000000002560. PMC 4862245. PMID 27164716.
195. Markham A (July 2018). "Erenumab: First Global Approval". Drugs. 78 (11): 1157–1161. doi:10.1007/s40265-018-0944-0. PMID 29968151. S2CID 49559342.
196. Silberstein SD, Lee L, Gandhi K, Fitzgerald T, Bell J, Cohen JM (November 2018). "Health care Resource Utilization and Migraine Disability Along the Migraine Continuum Among Patients Treated for Migraine". Headache. 58 (10): 1579–1592. doi:10.1111/head.13421. PMID 30375650. S2CID 53114546.
197. "Migraine Information Page: Prognosis" 10 June 2020 at the Wayback Machine, National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (US).
198. "Key facts and figures about migraine". The Migraine Trust. 2017. from the original on 12 March 2017. Retrieved 13 June 2021.
199. Brennan KC, Pietrobon D (March 2018). "A Systems Neuroscience Approach to Migraine". Neuron. 97 (5): 1004–1021. doi:10.1016/j.neuron.2018.01.029. PMC 6402597. PMID 29518355.
200. World Health Organization (2008). "Disability classes for the Global Burden of Disease study" (table 8), The Global Burden of Disease: 2004 Update 13 June 2021 at the Wayback Machine, p 33.
201. Schürks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T (October 2009). "Migraine and cardiovascular disease: systematic review and meta-analysis". BMJ. 339: b3914. doi:10.1136/bmj.b3914. PMC 2768778. PMID 19861375.
202. Kurth T, Chabriat H, Bousser MG (January 2012). "Migraine and stroke: a complex association with clinical implications". The Lancet. Neurology. 11 (1): 92–100. doi:10.1016/S1474-4422(11)70266-6. PMID 22172624. S2CID 31939284.
203. Rist PM, Diener HC, Kurth T, Schürks M (June 2011). "Migraine, migraine aura, and cervical artery dissection: a systematic review and meta-analysis". Cephalalgia. 31 (8): 886–96. doi:10.1177/0333102411401634. PMC 3303220. PMID 21511950.
204. Kurth T (March 2010). "The association of migraine with ischemic stroke". Current Neurology and Neuroscience Reports. 10 (2): 133–9. doi:10.1007/s11910-010-0098-2. PMID 20425238. S2CID 27227332.
205. Schürks M, Rist PM, Shapiro RE, Kurth T (September 2011). "Migraine and mortality: a systematic review and meta-analysis". Cephalalgia. 31 (12): 1301–14. doi:10.1177/0333102411415879. PMC 3175288. PMID 21803936.
206. Weinberger J (March 2007). "Stroke and migraine". Current Cardiology Reports. 9 (1): 13–9. doi:10.1007/s11886-007-0004-y. PMID 17362679. S2CID 46681674.
207. Hougaard A, Amin FM, Ashina M (June 2014). "Migraine and structural abnormalities in the brain". Current Opinion in Neurology. 27 (3): 309–14. doi:10.1097/wco.0000000000000086. PMID 24751961.
208. Ferrari MD, Goadsby PJ, Burstein R, Kurth T, Ayata C, Charles A, et al. (January 2022). "Migraine". Nat Rev Dis Primers. 8 (1): 2. doi:10.1038/s41572-021-00328-4. PMID 35027572. S2CID 245883895.
209. Stovner LJ, Zwart JA, Hagen K, Terwindt GM, Pascual J (April 2006). "Epidemiology of headache in Europe". European Journal of Neurology. 13 (4): 333–45. doi:10.1111/j.1468-1331.2006.01184.x. PMID 16643310. S2CID 7490176.
210. Wang SJ (March 2003). "Epidemiology of migraine and other types of headache in Asia". Current Neurology and Neuroscience Reports. 3 (2): 104–8. doi:10.1007/s11910-003-0060-7. PMID 12583837. S2CID 24939546.
211. Natoli JL, Manack A, Dean B, Butler Q, Turkel CC, Stovner L, et al. (May 2010). "Global prevalence of chronic migraine: a systematic review". Cephalalgia. 30 (5): 599–609. doi:10.1111/j.1468-2982.2009.01941.x. PMID 19614702. S2CID 5328642.
212. Nappi RE, Sances G, Detaddei S, Ornati A, Chiovato L, Polatti F (June 2009). "Hormonal management of migraine at menopause". Menopause International. 15 (2): 82–6. doi:10.1258/mi.2009.009022. PMID 19465675. S2CID 23204921.
213. Miller N (2005). Walsh and Hoyt's clinical neuro-ophthalmology (6 ed.). Philadelphia, Pa.: Lippincott Williams & Wilkins. p. 1275. ISBN 9780781748117. from the original on 12 March 2017.
214. Liddell HG, Scott R. "ἡμικρανία". A Greek-English Lexicon. from the original on 8 November 2013. on Perseus
215. Anderson K, Anderson LE, Glanze WD (1994). Mosby's Medical, Nursing & Allied Health Dictionary (4 ed.). Mosby. p. 998. ISBN 978-0-8151-6111-0.
216. Borsook D (2012). The migraine brain : imaging, structure, and function. New York: Oxford University Press. pp. 3–11. ISBN 9780199754564. from the original on 13 March 2017.
217. Waldman SD (2011). Pain management (2 ed.). Philadelphia, PA: Elsevier/Saunders. pp. 2122–2124. ISBN 9781437736038. from the original on 23 August 2023. Retrieved 24 September 2016.
218. "Sex(ism), Drugs, and Migraines". Distillations. Science History Institute. 15 January 2019. from the original on 14 March 2021. Retrieved 6 February 2020.
219. Margaret C, Simon M (2002). Human osteology : in archaeology and forensic science (Repr. ed.). Cambridge [etc.]: Cambridge University Press. p. 345. ISBN 9780521691468. from the original on 17 June 2013.
220. Colen C (2008). Neurosurgery. Colen Publishing. p. 1. ISBN 9781935345039.
221. Daniel BT (2010). Migraine. Bloomington, IN: AuthorHouse. p. 101. ISBN 9781449069629. from the original on 13 March 2017.
222. Butticè C (April 2022). What you need to know about headaches. Santa Barbara, California: Greenwood Publishing Group. pp. 29–30. ISBN 978-1-4408-7531-1. OCLC 1259297708. from the original on 28 November 2022. Retrieved 2 November 2022.
223. Tfelt-Hansen PC, Koehler PJ (May 2011). "One hundred years of migraine research: major clinical and scientific observations from 1910 to 2010". Headache. 51 (5): 752–78. doi:10.1111/j.1526-4610.2011.01892.x. PMID 21521208. S2CID 31940152.
224. Stovner LJ, Andrée C (June 2008). "Impact of headache in Europe: a review for the Eurolight project". The Journal of Headache and Pain. 9 (3): 139–46. doi:10.1007/s10194-008-0038-6. PMC 2386850. PMID 18418547.
225. Mennini FS, Gitto L, Martelletti P (August 2008). "Improving care through health economics analyses: cost of illness and headache". The Journal of Headache and Pain. 9 (4): 199–206. doi:10.1007/s10194-008-0051-9. PMC 3451939. PMID 18604472.
226. Magis D, Jensen R, Schoenen J (June 2012). "Neurostimulation therapies for primary headache disorders: present and future". Current Opinion in Neurology. 25 (3): 269–76. doi:10.1097/WCO.0b013e3283532023. PMID 22543428.
227. Jürgens TP, Leone M (June 2013). "Pearls and pitfalls: neurostimulation in headache". Cephalalgia. 33 (8): 512–25. doi:10.1177/0333102413483933. PMID 23671249. S2CID 42537455.
228. Barbanti P, Fofi L, Aurilia C, Egeo G, Caprio M (May 2017). "Ketogenic diet in migraine: rationale, findings and perspectives". Neurological Sciences (Review). 38 (Suppl 1): 111–115. doi:10.1007/s10072-017-2889-6. PMID 28527061. S2CID 3805337.
229. Gross EC, Klement RJ, Schoenen J, D'Agostino DP, Fischer D (April 2019). "Potential Protective Mechanisms of Ketone Bodies in Migraine Prevention". Nutrients. 11 (4): 811. doi:10.3390/nu11040811. PMC 6520671. PMID 30974836.
230. Artero-Morales M, González-Rodríguez S, Ferrer-Montiel A (2018). "TRP Channels as Potential Targets for Sex-Related Differences in Migraine Pain". Frontiers in Molecular Biosciences. 5: 73. doi:10.3389/fmolb.2018.00073. PMC 6102492. PMID 30155469.
231. Stewart WF, Lipton RB, Celentano DD, Reed ML (January 1992). "Prevalence of migraine headache in the United States. Relation to age, income, race, and other sociodemographic factors". JAMA. 267 (1): 64–69. doi:10.1001/jama.1992.03480010072027. PMID 1727198.
232. "Speeding Progress in Migraine Requires Unraveling Sex Differences". SWHR. 28 August 2018. from the original on 18 June 2020. Retrieved 17 March 2021.
233. Smith L (11 March 2021). Hamilton K (ed.). "Migraine in Women Needs More Sex-Specific Research". Migraine Again. from the original on 12 March 2021. Retrieved 17 March 2021.
234. Schroeder RA, Brandes J, Buse DC, Calhoun A, Eikermann-Haerter K, Golden K, et al. (August 2018). "Sex and Gender Differences in Migraine-Evaluating Knowledge Gaps". Journal of Women's Health. 27 (8): 965–973. doi:10.1089/jwh.2018.7274. PMID 30129895. S2CID 52048078.

Further reading

• Ashina M (November 2020). Ropper AH (ed.). "Migraine". The New England Journal of Medicine. 383 (19): 1866–1876. doi:10.1056/nejmra1915327. PMID 33211930. S2CID 227078662.
• Oskoui M, Pringsheim T, Billinghurst L, Potrebic S, Gersz EM, Gloss D, et al. (September 2019). "Practice guideline update summary: Pharmacologic treatment for pediatric migraine prevention: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 93 (11): 500–509. doi:10.1212/WNL.0000000000008105. PMC 6746206. PMID 31413170.
• Oskoui M, Pringsheim T, Holler-Managan Y, Potrebic S, Billinghurst L, Gloss D, et al. (September 2019). "Practice guideline update summary: Acute treatment of migraine in children and adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society". Neurology. 93 (11): 487–499. doi:10.1212/WNL.0000000000008095. PMID 31413171. S2CID 199662718.

January 01, 1970