Migraine

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Migraine is a neurological disease best known for severe headaches that are its most salient symptom.^[1][2][3]. Usually migraine causes episodes of severe or moderate headache (which is often one-sided and pulsating) lasting between several hours to three days, accompanied by gastrointestinal upsets, such as nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (phonophobia). Approximately one third of people who experience migraine get a preceding aura.^[4] Migraines’ secondary characteristics are inconsistent. Triggers precipitating a particular episode of migraine vary widely. The efficacy of the simplest treatment, applying warmth or coolness to the affected area of the head, varies between persons, sometimes worsening the migraine.^[5] A particular migraine rescue drug may sometimes work and sometimes not work in the same patient. Some migraine types don’t have pain or may manifest symptoms in parts of the body other than the head. Available evidence suggests that migraine pain is one symptom of several to many disorders of the serotonergic control system, a dual hormone–neurotransmitter with numerous types of receptors. Two disorders — classic migraine with aura (MA, STG) and common migraine without aura (MO, STG) — have been shown to have a genetic factor.^[6] Studies on twins show that genes have a 60 to 65% influence on the development of migraine^[7][8]. Additional migraine types are suspected and could be proven to be genetic. Migraine understood as several or many disorders could explain the inconsistencies, especially if a single patient has more than one genetic type. However, still other migraine types might be functionally acquired due to hormone organ disease or injury. Three quarters of adult migraine patients are female, although pre-pubertal migraine affects approximately equal numbers of boys and girls. This reveals the strong correlation to hormonal cycling and hormonal-related causes or triggers. Hormonal migraine is a likely consequence of periodically falling hormone levels causing reduction in protein biosynthesis of metabolic components including intestinal tract serotonin.

The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means “half (the) head”.

Migraines can be divided in three different types: migraine without aura, typical migraine with aura and probable migraine without aura. Migraines are often underdiagnosed and misdiagnosed.^[9][10] The diagnostic criteria for migraine include recurrent headache disorder manifesting in attacks that fulfill typical characteristics in a context of normal clinical examination that rules out other diagnoses. Migraine with aura is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes.

Migraines are believed to be a neurovascular disorder^[11][12] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.^[13] Migraine begins by neuronal changes leading to the activation of the brainstem and diencephalic nuclei and subsequent dilatation of the large cranial and proximal intracranial vessels.^[11] Some researchers feel neuronal mechanisms play a greater role,^[14] while others feel blood vessels play the key role.^[15] Others feel both are likely important.^[16] High levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.^[13]

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal.In the medical literature, these factors are known as precipitants. Many people report that one or more dietary, physical, hormonal, emotional, or environmental factors precipitate their migraines. The most-often reported triggers include: pesticides (sprayed fruits/vegetables), perfumes or fragrances (30% of sufferers) stress, over-illumination or glare, alcohol, foods, too much or too little sleep, and weather. Some women experience migraines in conjunction with monthly menstrual cycles. Sometimes the migraine occurs with no apparent “cause”. The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors. Patients are urged to keep a “headache diary” in which to note what they eat and when they get a headache, to look for correlations, and to try to avoid headache by avoiding factors they identify as triggers. Typically this advice is accompanied by a list of trigger factors.

ther conditions that can cause similar symptoms to a migraine headache include temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage.^[17] Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headaches presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subaracchnoid hemorrhage with a very fast onset.^[17] Tension headaches typically occur on both sides, are not pounding, and are less disabling.^[17]

Migraine is widespread in the population. The majority of migraine (as it is referred to commonly) is actually mixed Headache. In the U.S., 18% of women and 6% of men report having had at least one migraine episode in the previous year^[18] According to reports, 10% of people have been diagnosed with migraine and 5% have migraine but have not been diagnosed, with seriousness varying from a rare annoyance to a life-threatening and/or daily experience.

Migraine with aura is associated with increased risk of subsequent stroke, a risk further amplified among females, smokers, patients on OCP and patients suffering from frequent migraine episodes. Despite the elevated risk of stroke among patients with migraine associated with aura, the incidence of stroke in this category of patients remain low particularly in young adults. Patients with migraine not associated with aura are not at an increased risk of stroke compared to the general population.^[19]

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same patient: (1) the prodrome, which occurs hours or days before the headache, (2) the aura, which immediately precedes the headache, (3) the pain phase, also known as headache phase and (4) the postdrome phase.

The majority of patients with headaches complaints have a normal physical and neurological examination. Signs suggestive of a serious cause of headache, such as systemic symptoms, focal neurological signs, seizures or impairment of the level of consciousness should be ruled out.

Migraine is a clinical diagnosis that does not require any laboratory tests. Laboratory tests can be ordered to rule out any suspected coexistent metabolic problems or to determine the baseline status of the patient before initiation of migraine therapy. When the headache is suggestive of meningitis, lumbar puncture should be done and an appropriate management of meningitis should be initiated.

Neuroimaging is not necessary in patients with a clinical diagnosis of migraine. Head images such CT and MRI might be needed to rule out other suspected possible causes of headache. It is suggested to order a CT scan without contrast among patients with an unusual headache.

MRI is indicated when there is suspicion of posterior fossa lesions and cerebrospinal fluid (CSF) leak. Magnetic resonance angiography (MRA) and magnetic resonance venography (MRV) are indicated in arterial or venous lesions.

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and preventive drugs. Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine attack. Medical therapy can be divided into two treatment regimens: non-specific treatment such as non-steroidal anti-inflammatory drug and analgesics and specific treatment such as triptans and ergot derivatives.^[20] Patients who experience migraines often find that the recommended treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all.

Following treatment of an acute migraine, it is important to consider preventive measures. Preventive measures include medications such as NSAIDs, amitryptilline, devalproex, valproic acid, propranolol, timolol and topiramate among others. If the preventive measure is not effective after two to three months, the dose of the medication should be adjusted. If no improvement is noted, another first line therapy or a combination of two first line therapies should be initiated.^[21][22]

Treatments are typically expensive. Periodic or unpredictable disability can cause impoverishment due to patients’ inability to work enough or to hold a job at all.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means “half (the) head.”

An early description consistent with migraines is contained in the Ebers papyrus, written around 1500 BCE in ancient Egypt.^[1] 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.^[2] A second-century description by Aretaeus of Cappadocia divided headaches into three types: cephalalgia, cephalea, and heterocrania.^[3] Galen of Pergamon used the term hemicrania (half-head), from which the word migraine was eventually derived.^[3] He also proposed that the pain arose from the meninges and blood vessels of the head.^[2] Migraines were 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.^[2]

Trepanation, the deliberate drilling of holes into a skull, was practiced as early as 7,000 BCE.^[1] While sometimes people survived, many would have died from the procedure due to infection.^[4] It was believed to work via “letting evil spirits escape”.^[5] William Harvey recommended trepanation as a treatment for migraines in the 17th century.^[6]

While many treatments for migraines have been attempted, it was not until 1868 that use of a substance which eventually turned out to be effective began.^[2] This substance was the fungus ergot from which ergotamine was isolated in 1918.^[7] Methysergide was developed in 1959 and the first triptan, sumatriptan, was developed in 1988.^[7] During the 20th century with better study design effective preventative measures were found and confirmed.^[2]

Shown below is an image depicting ‘The Head Ache’ by George Cruikshank.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Migraines can be divided in three different types: migraine without aura, typical migraine with aura and probable migraine without aura. Migraines are often underdiagnosed and misdiagnosed.^[1][2] The diagnostic criteria for migraine include recurrent headache disorder manifesting in attacks that fulfill typical characteristics in a context of normal clinical examination that rules out other diagnoses. Migraine with aura is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes.

The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria:^[3]

• A – ≥ 5 attacks characterized by the symptoms presented in the criteria B through D
• B – Headaches can last form 4 to 72 hours.
• C – Headaches must contain at least one of the following:
  • Unilateral location
  • Pulsating quality
  • Moderate to severe pain
  • Aggravation or causing of the pain from normal physical activity
• D – Presence of one of the following:
  • Nausea and/or vomit
  • Photophobia and/or phonophobia
• E – The symptoms can not be better accounted for by any other diagnosis.

The mnemonic POUNDing (Pulsating, duration of 4-72 hOurs, Unilateral, Nausea, Disabling) can help diagnose migraine. If 4 of the 5 criteria are met, then the positive likelihood ratio for diagnosing migraine is 24.^[4]. The presence of either disability, nausea or sensitivity, can diagnose migraine with^[5] sensitivity of 81% and specificity of 75%. Patients that meet the criterai for Migraine without aura, but have fewer than 5 attacks, are classified as Probable Migraine without aura.

The diagnosis of migraine with aura, according to the International Headache Society, can be made according to the following criteria:^[3]

• A – ≥ 2 attacks characterized by the symptoms presented in the criteria B through D
• B – At least 1 of the following reversible symptoms:
  • Visual
  • Motor skill
  • Sensory
  • Speech/language
  • Retinal
• C – At least two of the following:
  • At least one aura symptom spreading gradually over >5 minutes and/or two or more aura symptoms occur in succession over >5 minutes
  • Each individual symptom lasting between 5 to 60 minutes
  • The aura is accompanied or followed by 60 minutes of headache.
• D – The symptoms can not be better accounted for by any other diagnosis.

Where these criteria are not fully met, a diagnosis of “probable migraine with aura” may be considered, although other neurological causes must also be excluded.

If the picture complies with the criteria but includes one-sided muscular weakness or paralysis, a diagnosis of “sporadic hemiplegic migraine” or “familial hemiplegic migraine” should be considered.

Are recurrent episodic attacks that last from 1 hour to 5 days of nausea and vomiting at least 4 times per hour, free of symptoms between attacks and it is not attributed to another disorder.

Is a recurrent disorder of unknown origin which occurs mainly in children. It is characterised by episodes of moderate to severe central abdominal pain lasting 1-72 hours. There is usually associated nausea and vomiting but the child is entirely well between attacks. In order to diagnose abdominal migraine, there must be at least five attacks, not attributable to another cause, fulfilling the following criteria

1. Attacks lasting 1-72 hours when untreated

2. Pain must have ALL of the following characteristics

• Location in the midline, around the umbilicus or poorly localised

• Dull or ‘just sore’ quality

• Moderate or severe intensity

3. During an attack there must be at least two of the following

• Loss of appetite

• Nausea

• Vomiting

• Pallor

Most children with abdominal migraine will develop migraine headache later in life and the two may co-exist during adolescence.

Are recurrent brief episodic attacks of vertigo. In order to diagnose benign paroxysmal vertigo of childhood there must have been at least 5 attacks of multiple episodes with severe vertigo, starting without warning and resolving spontaneously. The patient must have a normal neurological, audiometric and vestibular functions between attacks and a normal electroencephalogram.

Also called ocular migraine is a rare condition described as multiples attacks of monocular scotoma or blindness. In order to diagnose retinal migraine there must have been at least 2 attacks with reversible monocular (positive and/or negative) visual phenomena (eg, scotoma or blindness) and a headache fulfilling criteria for Migraine without aura begins during the visual symptoms or follows them within 60 minutes. The patient should have normal ophthalmological examination between attacks and is not attributed to another disorder.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Migraines are believed to be a neurovascular disorder^[1][2] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.^[3] Migraine begins by neuronal changes leading to the activation of the brainstem and diencephalic nuclei and subsequent dilatation of the large cranial and proximal intracranial vessels.^[1] Some researchers feel neuronal mechanisms play a greater role,^[4] while others feel blood vessels play the key role.^[5] Others feel both are likely important.^[6] High levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.^[3]

Cortical spreading depression or spreading depression of Leão is bursts of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura.^[7] There are a number of explanations for its occurrence including activation of NMDA receptors leading to calcium entering the cell.^[7] After the burst of activity the blood flow to the cerebral cortex in the area affected is decreased for two to six hours.^[7] It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.^[7]

Shown below is an image depicting cortical spreading depression which is the underlying pathophysiology of aura.

The exact mechanism of the head pain which occurs during a migraine is unknown.^[8] Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon)^[9] while other data support the role peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck).^[8] The potential candidate vessels include dural arteries, pial arteries and extracranial arteries such as those of the scalp.^[8] The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.^[10]

Studies of twins indicate a 34% to 51% genetic influence of likelihood to develop migraine headaches.^[11] This genetic relationship is stronger for migraines with aura than for migraines without aura. A number of specific variants of genes increase the risk by a small to moderate amount.^[12]

Single gene disorders that result in migraines are rare.^[12] One of these is known as familial hemiplegic migraine, a type of migraine with aura, which is inherited in anautosomal dominant fashion.^[13][14] Four genes have been shown to be involved in familial hemiplegic migraine.^[15] Three of these genes are involved in ion transport.^[15] The fourth is an axonal protein associated with the exocytosis complex.^[15] Another genetic disorder associated with migraine is CADASIL syndrome or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.^[16]

The tendency to develop head pain when faced with a stressor or strong sensory stimuli can be explained in two ways. First, it may be a side effect of other CNS processes that provide important evolutionary advantages. One example is counteracting the dilation of cranial arteries to counteract dangerous vasoconstriction in the brain.^[17] Second, migraine may be an example of how pain has evolved to encourage organisms to avoid potentially harmful situations. Olfactory-induced migraines (migraines stimulated by strong smells) have been explained as an attempt to interrupt the entry of toxins into the brain via the olfactory nerve.^[18] Similarly, the low threshold for nausea and vomiting may be a mechanism to enhance elimination of ingested toxins in food. Migraineurs have a lower prevalence of malignant neoplasms in the brain than controls, suggesting that migraines are protective against tumors. However, the mechanism responsible for this difference is unknown.^[19]

A headache-prone CNS may have resulted from interactions with other organisms in two ways. The first possibility is that migraine offers an advantage to the organism in fighting infection by increasing blood flow to the brain. The second possibility is that certain pathogens evolved to cause headache as a way of speeding their transmission to other organisms.^[20] Finally, migraine may benefit neither the host nor the pathogen, but may simply be the result of certain infections.^[21] This last explanation is concordant with the apparent negative impact of migraine on human fitness.

Modern environmental factors, with an increased sensory overload, may be especially permissive of the expression of genes that predispose for the disorder. If so, natural selection may not have had a chance to eliminate these genes yet. The increasing prevalence of migraine is easily a result of increased known triggers, such as bright light, loud noise, altered sleep/wake patterns, and emotional stress. This is an example of mismatch theory, which states that the current environment differs from the evolutionary environment of a particular trait.^[20]

Migraine is influenced on a polygenetic level (controlled by multiple genes). Therefore, researchers have theorized that migraine is a tradeoff and that it exists as a spectrum of susceptibility, with the majority of the population falling in the “heterozygous” zone between the two extremes of experiencing no headache and experiencing frequent, incapacitating headache. While it is not known for certain how or whether mild forms of the disorder would enhance survival, there is evidence of enhanced visual sensitivity in family members of migraineurs.^[22] Additionally, this compromise theory may explain the higher prevalence among women, especially pregnant women and women of reproductive age (25-40). The avoidance of threatening environments is historically more important to the reproductive success of women.^[23] The compromise between genetic harms and benefits is commonly seen in other disorders, such as cystic fibrosis and sickle cell anemia.

Finally, migraine may be a component of imperfect central nervous system design. Evidence has suggested a dysfunction of pain-inhibitory pathways in migraine and discordant interaction between the ancient brain stem design and the more evolved neocortex.^[24] The brain stem may be unable to suppress excessive input from higher brain centers.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal.In the medical literature, these factors are known as precipitants. Many people report that one or more dietary, physical, hormonal, emotional, or environmental factors precipitate their migraines. The most-often reported triggers include: pesticides (sprayed fruits/vegetables), perfumes or fragrances (30% of sufferers) stress, over-illumination or glare, alcohol, foods, too much or too little sleep, and weather. Some women experience migraines in conjunction with monthly menstrual cycles. Sometimes the migraine occurs with no apparent “cause”. The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors. Patients are urged to keep a “headache diary” in which to note what they eat and when they get a headache, to look for correlations, and to try to avoid headache by avoiding factors they identify as triggers. Typically this advice is accompanied by a list of trigger factors.

Shown below is a list of migraine attacks triggers according to the National Library of Medicine’s Medical Encyclopedia:

• Allergic reactions
• Bright lights, loud noises, and certain odors or perfumes
• Physical or emotional stress
• Changes in sleep patterns
• Smoking or exposure to smoke
• Skipping meals
• Alcohol or caffeine
• Menstrual cycle fluctuations, birth control pills
• Exposure to pesticides (sprayed fruits/vegetables)
• Tension headaches Headache
• Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate (MSG), or nitrates (like bacon, hot dogs, and salami)
• Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.^[1]
• Drugs like Apremilast, conjugated estrogens, Cidofovir

It is very common for patients with migraine to have an associated musculoskeletal component. This portion of the migraine may be perceived as due to tension (which may in fact be a trigger in and of itself), an old neck injury that the afflicted does not realize can cause migraine like headache or degenerative changes in the neck. Less obvious sources of cervicogenic Headache may be postural related. For example in the presence of an old ankle injury center of gravity can be shifted forward. As a result, the neck must be held in extension in order to stand up right. In this instance every step taken aggravates the condition ^[2].

In 2005, authors who reviewed the medical literature^[3] found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients. Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants. The authors say dehydration deserves more attention, and that some patients report sensitivity to red wine. The authors found little or no demonstrated evidence that notorious suspected triggers chocolate, cheese, or that histamine, tyramine, nitrates, or nitrites normally present in foods trigger headaches. The artificial sweetener aspartame (NutraSweet®) has not been shown to trigger headache, but in a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo. The review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine.On the other hand, several headache clinics have had good results with individually tailored dietary restriction as a therapy. Dr. Ian Livingstone, director of the Princeton Headache Clinic, recommends eliminating the following common headache triggers from the diet: aged cheese, monosodium glutamate, processed fish and meats containing nitrates (such as hot dogs), dark chocolate, aspartame, certain alcoholic beverages (including red wine), citrus fruits, and caffeine. After a period of one to two months, these foods can be reintroduced one at a time to determine their trigger potential for that individual. Adding large amounts of the suspected trigger in a short time may generate a response that is easy to observe.Dr. David Buchholz, a neurologist who treats headaches at Johns Hopkins Hospital, has a longer list of suspected migraine triggers. He also recommends eliminating the triggers from the diet altogether, and then reintroducing them slowly after many weeks to measure the effects. His list includes: coffee (including decaf), chocolate, monosodium glutamate, processed meats and fish (aged, canned, preserved, processed with nitrates, and some meats that contain tyramine), cheese and dairy products (the more aged, the worse), nuts, citrus and some other fruits, certain vegetables (especially onions), fresh risen yeast baked goods, dietary sources of tyramine (including the foods listed above), and whatever gives you a headache. The National Headache Foundation has a more specific list of triggers based on the tyramine theory, which differs slightly from David Buchholz’s list. For example, it says that decaffeinated coffee is allowed. The list details “Allowed”, “Use with caution”, and “Avoid” triggers.^[4]

Several studies have found some migraines are triggered by changes in weather. One study^[5] noted that 62% of the subjects in the study thought that weather was a factor, in fact 51% were actually sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.
2. Significant changes in weather
3. Changes in barometric pressure (See Abortive Treatment)

Another study^[6]‘ researched whether chinook winds (warm westerly winds occurring along the Front Ranges of the Rocky Mountains) are a migraine trigger. Many patients had increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause is “through increased air positive ion concentrations.” In the 40’s the Lancet published the first article on “Barre lieou“. This is a weather sensitive headache syndrome associated with blurred vision, ringing in the ears, dizziness and nausea. It is also referred to as The Posterior Cervical Sympathetic Syndrome of Barre-Lieou [2]. Sympathetic galvonic skin response studies utilizing infrared imaging have been reported to be helpful in the diagnosis of this syndrome.

Another trigger for migraine has been proposed by Dr.K.Ravishankar, a neurologist and headache specialist from India. He reported an unusual trigger for migraine seen among Indian women, Hair Wash Headache. It is described as a migraine headache that originates with a head bath. Most Indian women have long hair and so they wash their hair two or three times a week. Very often they do not use a hair dryer and often plait their hair when wet. This results in a gradual build up of pain which ultimately results in migraine.^[7]

• Desogestrel and Ethinyl Estradiol
• Histrelin
• Niacin
• Polidocanol
• Valdecoxib

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Other conditions that can cause similar symptoms to a migraine headache include temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage.^[1] Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headaches presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subaracchnoid hemorrhage with a very fast onset.^[1] Tension headaches typically occur on both sides, are not pounding, and are less disabling.^[1]

Migraine should be differentiated from other diseases causing severe headache for example: ^{[2][3][4][5][6][7][8][9][10][11]}

Migraine must be differentiated from other causes of headache,seizures and loss of consciousness.

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• Acute glaucoma
• Hysteria
• Temporal arteritis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Migraine is widespread in the population. The majority of migraine (as it is referred to commonly) is actually mixed Headache. In the U.S., 18% of women and 6% of men report having had at least one migraine episode in the previous year^[1] According to reports, 10% of people have been diagnosed with migraine and 5% have migraine but have not been diagnosed, with seriousness varying from a rare annoyance to a life-threatening and/or daily experience.

Migraine is an extremely common condition which will affect 12-28% of people at some point in their lives.^[2] However this figure — the lifetime prevalence — does not provide a very clear picture of how many patients there are with active migraine at any one time. Typically, therefore, the burden of migraine in a population is assessed by looking at the one-year prevalence — a figure that defines the number of patients who have had one or more attacks in the previous year. The third figure, which helps to clarify the picture, is the incidence — this relates to the number of first attacks occurring at any given age and helps understanding of how the disease grows and shrinks over time. Based on the results of a number of studies, one year prevalence of migraine ranges from 6-15% in adult men and from 14-35% in adult women.^[3] These figures vary substantially with age: approximately 4-5% of children aged under 12 suffer from migraine, with little apparent difference between boys and girls.^[4] There is then a rapid growth in incidence amongst girls occurring after puberty,^[5][6][7] which continues throughout early adult life.^[8] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.^[9][10] After menopause, attacks in women tend to decline dramatically, so that in the over 70s there are approximately equal numbers of male and female sufferers, with prevalence returning to around 5%.^[2] At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1.^[11][12] Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.^[13] Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15-50 year olds^[14][15]Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low,^[16][17] but they do not fall outside the range of values seen in European and North American studies.^[18][19]The incidence of migraine is related to the incidence of epilepsy in families, with migraine twice as prevalent in family members of epilepsy sufferers, and more common in epilepsy sufferers themselves.^[20]

Shown below is the age-standardised disability-adjusted life year (DALY) rates from Migraine by country (per 100,000 inhabitants).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The cause of migraine remains unknown. It seems that both genetics and environmental contribute to the cause. Risk factors for migraine include a young age, a female sex and a positive family history.

• Family history of migraines
• Age less than 40 years
• Female

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Migraine with aura is associated with increased risk of subsequent stroke, a risk further amplified among females, smokers, patients on OCP and patients suffering from frequent migraine episodes. Despite the elevated risk of stroke among patients with migraine associated with aura, the incidence of stroke in this category of patients remain low particularly in young adults. Patients with migraine not associated with aura are not at an increased risk of stroke compared to the general population.^[1]

• Status migrainosus: The migraine episode lasts more than 72 hours.
• Persistent aura without infarction: The symptoms of aura last for more than a week in the absence of any neuroimaging findings suggestive of infarction.
• Migrainous infarction: The symptoms of aura last for more than a week in the context of any neuroimaging findings suggestive of infarction in the corresponding brain territory.
• Seizure triggered by a migrainous aura^[2]

The association between migraine and increased risk of subsequent stroke has long been suspected.^[3] In fact, migraine with aura is associated with two times increase of ischemic stroke, while migraine without aura was not demonstrated to be linked to an increased risk of subsequent stoke. Although patients suffering from migraine with aura are at a double risk of ischemic stroke, the incidence of stroke remains a rare event particularly among young adults. The risk of subsequent stroke is higher among females and among patients suffering from a high frequency of migraine with aura episodes.^[4] Some risk factors that predispose to stroke among migraine patients are smoking, OCP use and genetic mutations.^[3][5][6] In addition, patients with patent foramen ovale and migraine are at increased risk of stroke. Closure of patent foramen ovale has been reported to improve migraine and therefore decrease the risk of subsequent stroke episodes; however, randomized clinical trials failed to demonstrate these benefits.^[1]

The link between stroke and migraine is far more complicated than a simple risk or predisposition relationship. Migraine, as well as of stroke, involves changes in the vascular and neuronal structure of the brain. Therefore, it is difficult to differentiate whether stroke is a result of the aura of the primary migraine, or if it results from vascular abnormalities predisposing to both migraines and strokes. Some of the vascular abnormalities that are associated with migraines are AV malformations, moyamoya syndrome, hereditary telengectasia, lupus, antiphospholipid syndrome, cardiac myxoma among other vascular medical conditions. It is worth mentioning that migraine was not only associated with ischemic strokes, but also hemorrhagic strokes and lacunar infarcts.^[1]

In addition, the underlying pathophysiology of aura is explained by a synchronized depression of the activity of neurons throughout the cortex of the brain causing not only electrolyte changes but also decrease in the cerebral blood flow. This decrease in the cerebral flow lowers the threshold for ischemic stroke. And vice versa, a decrease in the cerebral blood flow as in the case of hypoperfusion, ischemia or embolism leads to cellular changes predisposing to aura. This adds to the complexity of the association between stroke and migraine, which remains unclear.^[1]

Many patients with migraine can relieve pain and reduce frenquency with treatments.

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