Migraine Headache

“Migraine” is a complex, chronic neurologic disorder characterized by recurrent moderate to severe headaches.  The diagnosis of migraine headaches is subdivided into “migraine without aura” (formerly common migraine) and “migraine with aura” (formerly classic migraine).  (1) “Aura” is the collection of autonomic nervous system symptoms that occur immediately prior to the headache. (2) Aura symptoms may include visual disturbances, extremity paresthesias, nausea, vomiting, and hypersensitivity to light or sound.

Explanations

Early explanations for the genesis of migraine headaches focused on cerebrovascular vasoconstriction with subsequent vasodilation. (3)  Migraine is now recognized as a more complex series of neurologic and vascular events wherein vasodilation may or may not be present. (4-8) Evidence suggests that a migraineur’s brain is hyperexcitable and uniquely predisposed migraine headaches in much the same way that an epileptic is susceptible to seizures.  (8,9) 

Worldwide, the lifetime prevalence of migraine is 14%.  (10)  The one-year prevalence of migraine is 10% and shows little variance worldwide.  (11)  Over 30 million Americans suffer at least one migraine headache each year.  (12)  The condition affects 18% of females and 6% of males and is the leading cause of “severe” headaches.  (12) One in six American women suffer from migraine headaches.  (13) Over 80% of migraineurs miss work as a result of their headaches, with an average of 4-6 absences per year.  (14)       The economic cost of migraine headaches due to lost workdays is estimated at over 13 billion dollars per year in the United States. 

Migraine Prevalence

The incidence of migraine without aura peaks in boys at age 10 and in girls age 17.  (13) Interestingly, the incidence of migraine with aura peaks almost 5 years earlier for both sexes.  (13) Before puberty, migraine is more common in boys.  (15)  At puberty, this ratio flips, and adult females are three times more likely than their male counterparts to experience migraines.  (15)  Migraine prevalence peaks in the third decade and attacks generally decrease in severity and frequency after age 40.  (15,81) The onset of a new migraine headache after age 50 is rare.  (15) 

Risk Factors

Various risk factors have been identified for the development of this disorder. Migraine headaches demonstrate a strong genetic component.  Having a first-degree relative with migraine increases one’s risk fourfold. (16) If one parent has migraines, the child has a 50% risk of developing the disorder.  If both parents are affected, the risk climbs to 75%. (17) Overweight patients are more susceptible to migraines.  (18) Vascular risk factors include hypertension, hypercholesterolemia, impaired insulin sensitivity, coronary artery disease, and a history of stroke.  (18) Medication overuse is one of the more important risk factors for migraine progression.  (19) Migraines tend to become “chronic” following overuse of acetaminophen, naproxen, aspirin, opiates, barbiturates, and triptans. (19)  One study demonstrated that NSAIDs were beneficial when used less than 10 days a month but induced migraine progression to a chronic state when used at a higher frequency.  (19) 

The (hyperexcitable) migraineur brain is susceptible to various “triggers.” Migraines develop when the number of triggers exceeds a critical threshold for a given patient.  Known triggers include: stress, smoking, strong odors (i.e. perfumes), bright or flickering lights, fluorescent lighting, excessive or insufficient sleep, head trauma, weather changes, motion sickness, cold stimulus (i.e. ice cream headaches), lack of activity/exercise, dehydration, hunger or fasting, and hormonal changes, including menstruation, and ovulation.  (20) Upper cervical tension or the presence of a cervicogenic headache may be a trigger for a migraine. (59,65)

Medications

Certain medications, including estrogen, oral contraceptives, vasodilators such as nitroglycerin, histamines, reserpine, hydralazine, and ranitidine, are known triggers.  (21) Food triggers are inconsistent among migraineurs, but the following foods are regularly implicated: alcohol (especially beer or red wine with tannins), excessive caffeine, artificial sweeteners, MSG, soy sauce, citrus foods, papayas, avocados, red plums, overripe bananas, dried fruits with sulfites (figs, raisins, etc), sour cream, buttermilk, nuts, peanut butter, sourdough bread, aged meats and cheeses, processed meats, and anything fermented, pickled or marinated.  (22,23) It is unclear whether chocolate is a trigger to migraine, or a craving brought on at the onset of an attack.  (22) 

Stages

Migraine progresses through various symptomatic stages, including prodrome, aura, attack, and postdrome. The features of migraine headaches, including prodrome, vary widely but tend to be consistent for any given individual.  (8)

Prodrome

Approximately 60% of sufferers report prodromal symptoms in the hours to days before headache onset.  (8) These symptoms include lethargy, yawning, food cravings, mood changes, excessive thirst, fluid retention, constipation, diarrhea, and hypersensitivity to light, sound, or odors.  (8) 

Aura

About 20-33 percent of migraine sufferers experience auras during or before the headache attack. (17,26) Aura symptoms develop slowly, over 5-20 minutes and can last up to an hour.  Symptoms are most commonly visual but may also include a combination of sensory and motor components.  The most common visual symptom is a band of absent vision with an irregular shimmering border (scintillating scotoma). (8)  Various other visual field defects, including tunnel vision, have been reported.  Paresthesias are the next most common aura, occurring in 40% of cases.  (28) Paresthesias may be followed by a numbness that often begins in the hand and progresses up the arm, to the face, lips, and tongue. Less than one in five migraine sufferers experience motor symptoms, including a sense of heaviness in their limbs or speech and language disturbances.  (28) Motor and sensory complaints, including paresthesia and numbness rarely occur in isolation.  (28) Visual disturbances that occur in isolation are called “ophthalmic” migraine, aka “retinal,” or “ocular.” Ophthalmic migraines generally produce a lateral field deficit and are more common in children.  (8) The slow development of auras (5-20 minutes) is a helpful characteristic in distinguishing migraine from other cerebrovascular pathology.  (Stroke, TIA)  (28) 

Attack Phase

During the attack phase, patients will typically complain of a unilateral, moderate to severe, throbbing or pulsating headache.  The pain may be felt anywhere in the head and neck but is most common in the frontal, temporal and ocular areas.  Headache pain develops over a period of one to two hours and can last between 4 and 72 hours.  Patients often report hypersensitivity to sound or light and retreat to quiet, dark places.  Eighty percent of migraine sufferers experience nausea. (30-32) Vomiting occurs in 1/3-1/2 of patients.  (30-32) Seventy-five percent of migraine sufferers report some type of associated neck discomfort.  (32)

Postdrome

Postdromal symptoms occur in the hours following a migraine and generally include fatigue, irritability, euphoria, myalgia, food insensitivity, or cravings.  (22)

Diagnosis

According to the International Headaches Society, the diagnosis of migraine requires at least five episodic headaches, each lasting four to 72 hours associated with nausea/ vomiting or photophobia/ phonophobia and at least of two of the following characteristics:  moderate to severe intensity, unilateral presence, pulsating quality, and aggravated by physical activity.  (34) Although the aforementioned criteria “define” migraine, it is important to note that not all patients meet these criteria.  Forty-one percent of migraine patients report bilateral pain and 50% report “non-pulsating” pain.  (30-32)

Predictors

Researchers have identified the presence of nausea, disability, and photophobia as the most significant predictors for migraines. (36) A self-administered screening tool called ID migraine ® poses the following questions: 

1. Are you nauseated or sick to your stomach when you have a headache?
2. Has the headache limited your activities for a day or more in the last three months?
3. Does light bother you a lot more when you have a headache?

An affirmative response on 2 of 3 questions yields high sensitivity (81%) and specificity (75%). (36)

Red Flags

Clinicians should be alert to “red flags” that suggest a more threatening diagnosis, including: headaches that are becoming progressively worse over time, sudden onset, severe headaches, new or unfamiliar headache, headache following a recent head injury, unexplained weight loss, impaired consciousness, presence of fever, significant neck stiffness, rash, nuchal rigidity, vertigo, diplopia, drop attacks, difficulty speaking, difficulty swallowing, difficulty walking, and nystagmus. 

The American Headache Society endorses the acronym “SNOOP” to identify worrisome headache red flags. (37-38)

Systemic symptoms: fever, weight loss, or the presence of systemic risk factors (i.e. cancer, HIV). 

Neurologic signs: confusion, impaired alertness, or consciousness.

Onset: sudden or abrupt headaches that develop and peak very quickly.

Older: new headaches in patients over 50 (Giant cell arteritis, aka temporal arteritis)

Previous headache history:  any new headache that deviates significantly from a prior pattern of frequency, severity, and clinical features.

Patient History

The diagnosis of migraine is based on the patient’s history.  (39)  A thorough physical and neurologic assessment is required to exclude a more threatening diagnosis; however, the results are normal in most migraine patients. Measurement of vital signs may demonstrate transient irregularities during a migraine attack, including tachycardia, bradycardia, hypertension, or hypotension.  A physical exam may demonstrate a mild Horner’s syndrome (potosis, miosis) on the same side as the headache. (8) The presence of papilledema warrants consultation. Clinicians should palpate the temporal artery in those over age 50 to exclude Giant cell arteritis.

Concurrent Issues

Clinicians should be cognizant of potential concurrent cardiovascular and cerebrovascular issues when assessing migraine patients.  The presence of migraine increases one’s risk of cardiovascular disease (stroke and myocardial infarction) by approximately 25%.  Those experiencing migraine with aura have an almost twofold increased risk of cardiovascular disease.  (41,42)

Radiology

Patients whose symptoms fit the broad definition of migraine rarely require imaging. (43) Plain film radiographs have little value in the diagnosis of migraine headache.  When alternate pathology is suspected, MRI is the preferred neuroimaging choice over CT.  (43)  Suspicion of cerebral vascular pathology (aneurysm, vasculitis, arterial dissection) is better screened through magnetic resonance angiography (MRA).  (44) The use of EEG lacks sensitivity and specificity for the diagnosis of migraine.  (45)

Primary Conditions

The primary conditions to consider in the differential diagnosis of migraine headaches are a tension-type headache, TIA and stroke.  Tension-type headaches are typically bilateral, non-pulsatile, and not aggravated by physical activity.  Patients report that their symptoms are less intense and are generally not associated with nausea or vomiting.  The symptoms of stroke or TIA generally develop more quickly, last longer (days to indefinitely), and do not occur in isolation.  Other conditions to consider in the differential diagnosis of migraine headaches include giant cell arteritis, cluster headaches, acute glaucoma, meningitis, neoplasm, and cerebrovascular bleed.  (46) 

Treatment

Migraine treatment is subdivided into “abortive” therapies that seek to stop or reverse the progression of an existing headache and “prophylactic” treatments, which seek to prevent or reduce the frequency of future attacks.  Abortive treatments are most effective when given within the first minutes of an attack.  (47) Abortive medications include analgesics, NSAIDs, selective serotonin receptor agonists, and ergot alkaloids.  (48) Narcotics are commonly used for the emergency treatment of migraine, although evidence suggests they are ineffective and may lead to prolonged hospital stays.  (82) Overuse of abortive medical therapy may generate a self-perpetuating, chronic “rebound” cycle of migraines. (50,51) For recurrent headaches, the American Headache Society discourages the use of over-the-counter pain medications or the prescription of opioids or butalbital medications.  (43)

Prophylactic Treatment

Prophylactic treatment is aimed at controlling migraine triggers.  Several clinical trials and research studies suggest that spinal manipulation is an appropriate treatment for migraine headaches.  (49,52-62) One study demonstrated that a “significant reduction” of migraine intensity in almost half of those patients receiving spinal manipulation.  Nearly ¼ of migraine patients reported greater than 90% fewer attacks.  (55) Spinal manipulation has demonstrated similar effectiveness but longer lasting benefit with fewer side effects when compared to a well-known and efficacious medical treatment (amitriptyline).  (55,57,58,61) Spinal manipulation is thought to inhibit pain through various mechanisms, including CNS activation, the elevation of endorphin levels, disruption of pain-spasm-pain cycles, and reduction of mechanical triggers.  (63-65)

Soft tissue manipulation and massage therapy have demonstrated success in the treatment of migraine headaches.  (66,67) Upper cervical hypertonicity or joint dysfunction is thought to be a trigger for headaches, including migraines.  (65) Clinicians should pay particular attention to the suboccipital muscles because of the rectus capitus posterior minor shares a dense connective tissue bridge with the pain-sensitive spinal dura at the level of the atlantooccipital junction. Soft tissue manipulation and myofascial release techniques are appropriate for the treatment of related cervical, interscapular, and shoulder girdle musculature. Clinicians should assess for and treat posture abnormalities, including weakness of the deep neck flexors and upper crossed syndrome. Acupuncture and biofeedback may be useful in the treatment of migraine.  (51,68,69,79,83) The FDA recently approved a transcranial magnetic stimulator (TMS) for the treatment of migraine headaches.  Early studies have demonstrated improved outcomes from TMS over no treatment.  (70,71)

The patient’s self-management should focus on trigger avoidance and stress management.  (72) A headache diary is essential to help identify and eliminate triggers. (73) No specific diet has been shown to help migraine, but patients should be coached to identify and eliminate their unique food triggers.  (22) Patients with medication triggers, including oral contraceptives and hormones should consult with their medical provider about changing or discontinuing those drugs.  (47) Exercising for 40 minutes, three times per week has shown similar benefits to a proven prophylactic medication. (84) Overweight migraineurs should be given dietary advice. Migraineurs with aura should be counseled on the increased risk of stroke associated with smoking and oral contraceptive use. (8) Limited data support the use of Feverfew (125mg/ day), riboflavin (400mg/ day), and Magnesium (400-600mg/ day) for the prevention of migraine in non-pregnant patients. (50,75-78,85)

Conclusion

Medications used for the prophylaxis of migraine include β-blockers, tricyclic antidepressants, and divalproex sodium or valproic acid. (50) Recently, Botox injections have been used with varying levels of success for the treatment of migraine. Surgical deactivation of migraine trigger points is discouraged by the American Headache Society.  (43) 

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