Migraine Headache


Migraine is a chronic, episodic primary headache[1]. It is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).[2]

Symptoms typically last 4 to 72 hours and may be severe. Pain is often but not always unilateral, throbbing, worse with exertion, and accompanied by autonomic symptoms (eg, nausea; sensitivity to light, sound, or odors). Fortification spectra and other transient focal neurologic deficits occur in a few patients, usually just before the headache, also known as an aura.[2]  Diagnosis of migraine can usually be made by history alone.  Treatment includes lifestyle changes (diet, exercise, sleeping habits), medications including NSAIDs, analgesics, serotonin receptor agonists, beta-blockers, calcium channel blockers, and antiemetics.[2][3]


Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches at some point.[3] Epidemiological studies have documented its high prevalence and high socioeconomic and personal impacts. Lifetime prevalence is 18% for women and 6% for men in the US.   It most commonly begins during puberty or young adulthood, waxing and waning in frequency and severity over the ensuing years and usually diminishing after age 50.[2] About 45% of cases of migraine emerge during childhood or adolescence. Migraine with aura is more likely to develop at an earlier age than migraine without aura.[3] In 90% of migraines, the first attack generally develops before the age of 40 years. In women, the frequency of headaches is highest during their reproductive years, when estrogen levels are higher, and decreases to some extent after menopause.

Characteristics/Clinical Presentation

Migraine is a centrally-mediated pain disorder. This means that there is a disorder in the central nervous system (the brain and spinal cord), involving the nerves and blood vessels, which results in the pain and the neurologic symptoms associated with a migraine headache.

Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).[2]Migraine headache occurs via intracranial vasoconstriction and extracranial vasodilation. This results in cerebral hypoxia and may be responsible for the neurologic defects that characterize the aura. Acetylcholine and vasoactive intestinal polypeptide in the cranial arteries as well as dilation of the middle cerebral artery and the superficial temporal artery on the pain side during migraine cause relaxation of the vessels.[3]

The pain associated with migraine can occur from the trigeminal complex, which supplies the head and face region via cranial nerve V. Surrounding the large cerebral vessels, peal vessels, large venous sinuses, and dura mater is a plexus of largely unmyelinated fibers that arise from the ophthalmic division of the trigeminal ganglion and the upper cervical dorsal roots. The stimulation of these vessels causes the pain associated with migraines via the release of substance P and calcitonin gene-related peptide when the trigeminal ganglion is stimulated. Migraineurs may have sensitization to the mechanoreceptors in these structures enhancing the responses to mechanical stimuli and can result in allodynia (a painful response to non-noxious stimuli).[3]

There may be an aberrant mechanism in the stimulation of sensory fibers that excite GABA receptors, and the inhibition that reduces the excitability of pain neurons in the dorsal horn of the spine in order to modulate pain response to stimulation. Low levels of serotonin have been found in migraineurs. Platelets contain virtually all the serotonin present in the blood and release serotonin during aggregation. Migraineurs also tend to show hyperaggregability of platelets when free from headache.s Aggregated platelets release catecholamines and serotonin that may cause the initial stage of vasoconstriction.  Platelet aggregation is increased during the prodromal stage of migraine and a decrease of aggregation during the headache. The nuclei raphes also appear to increase blood flow in the brain and can respond to changes in serotonin transmission. The serotonin neurons located in the brainstem nuclei raphes change their firing rate during the sleep-wake cycle and may explain why sleep is often the best antidote to a migraine.[3]

Cortical spreading depression is a mechanism that starts with a small excitatory response that begins to spread through the brain and then causes a suppression of electroencephalographic (EEG) activity that moves through the cortex and can disturb the extracellular environment.  Potassium levels increase, extracellular glutamate increases, and extracellular calcium level decreases. Abnormal ion channel function is believed to be the mechanism in the rare form of familial hemiplegic migraine (FHM). Cortical spreading depression is accompanied by local vascular responsiveness.   Cortical hyperemia may be responsible for the flashing jagged light that sometimes occurs just before the pain begins.[3]   Cervical musculature can fire the neurons and cause pain and can be taut and tender during a migraine. Lastly, hormone levels, specifically estrogen can contribute ta migraine due to the falling levels of estrogen during menstruation.[3]

Migraine Classification

Migraine Without Aura

Migraine without aura is the commonest subtype of migraine. It has a higher average attack frequency and is usually more disabling than Migraine with aura.  It often has a strict menstrual relationship and is the disease most prone to accelerate with frequent use of symptomatic medication, resulting in a new headache.

Migraine headaches may be dull or throbbing, may last for 4 to 72 hours and may/may not present with photophobia (sensitivity to light), phonophobia (sensitivity to sound), and maybe aggravated by physical activity.  This type of migraine is most commonly seen in clinical practice and is usually bilateral and periorbital.[4] Vomiting may occasionally terminate the headache.[4] There are often various combinations of fatigue, difficulty in concentrating, neck stiffness, blurred vision, yawning, and pallor. When the headache resolves, there is commonly a feeling of heaviness and aching in the head, the scalp may be tender, and there may be considerable fatigue. The trigeminal brainstem nuclear complex has a somatotopic representation of the trigeminal dermatome that is continuous with the representation of the posterior head and neck region in the upper cervical dorsal horn. Pain patterns representing increased neuronal activity in the trigeminal nucleus caudalis and dorsal horn include upper cervical pain, usually on one side only.[3]


Recurrent headache disorder manifesting in attacks lasting 4–72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea and/or photophobia and phonophobia.

Diagnostic Criteria

  1. At least five attacks fulfilling criteria 2-5
  2. Headache attacks lasting 4-72 hours [when untreated]
  3. Headache has at least two of the following characteristics
    • unilateral location
    • pulsating quality
    • moderate or severe pain intensity
    • aggravation by or causing avoidance of routine physical activity
  4. During the headache at least one of the following
    • Nausea and/or vomiting
    • Photophobia and phonophobia
  5. Not attributed to another disorder

Migraine With Aura

This type of headache is typically preceded by depression, irritability, loss of appetite, which can be a result of the spreading cortical depression. Paresthesias can also be present and are second in frequency to visual symptoms. Paresthesias of the hand and face are the most common, specifically the tongue, which can help differentiate from a transient ischemic attack (TIA).  Speech difficulty during an aura reflects the involvement of the dominant hemisphere. Vertigo and dizziness may be related to brainstem activity or changes in blood flow around the vestibular mechanism.[3]

The aura consists of fully reversible symptoms that precede or accompany the headache (HA). The aura is commonly described as changes in the visual field. Visual images change, and there can be a loss of focus, spots of darkness, and zigzag flashing lights.  It often begins with a hazy spot close to the center of vision and can form into a star shape that further develops into a shape known as fortification (semicircular with angles). This scintillating vision consists of luminous, bright, flickering colors of the spectrum, like a prism catching the light. It can be combined with a scotoma (an area of vision that appears to be obstructed, or missing).  The visual image fades as the headache begins. The headache is intense, throbbing, and usually contralateral to the visual field changes.[3]


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. Headache with the features of migraine without aura usually follows the aura symptoms. Less commonly, headache lacks migrainous features or is completely absent.

Diagnostic Criteria

  1. At least 2 attacks fulfilling criterion 2
  2. Migraine aura fulfilling criteria 2 and 3 for one of the following:
    • Typical aura with migraine headache
    • Typical aura with non-migraine headache
    • Typical aura without headache
    • Familial hemiplegic migraine (FHM)
    • Sporadic hemiplegic migraine
    • Basilar-type migraine
  3. Not attributed to another disorder

Typical Aura Without Headache

In some cases, the aura symptoms are not followed by headache. This becomes very important in the differential diagnosis if these symptoms begin after the age of 40. Aura without headache is seen primarily in men and in advancing age. [3]

Sporadic and Familial Hemiplegic Migraine

The presentation is migraine with aura, including motor weakness and impaired coordination. Prodromal symptoms include numbness of the face and arm that may spread to involve one side of the body. Basilar symptoms may present with dysphasia or aphasia causing difficulty with speech. Pain may be ipsilateral or contralateral to symptoms and on rare occasions, there is a loss of consciousness. Although the symptoms appear to resemble a TIA, migrainous infarction is rare. The age of onset is 10-15 years usually accompanied by a family history via chromosome 19 or 1. This type of migraine is considered sporadic if there is no 1st or 2nd degree relative with hemiplegic migraine.[3]

Basilar-Type Migraine

Basilar migraine has a symptom profile that suggests posterior fossa involvement localizing to the vascular territory of the basilar artery- the brainstem, cerebellum, and occipital lobes.  The prodromal symptoms reflect brainstem dysfunction: altered level of consciousness, dysarthria, tinnitus, ataxia, diplopia, symptoms in both the temporal and nasal fields of both eyes, and peripheral dysesthesias, followed byan occipital headache. These symptoms complicate differential diagnosis and can be confused with hydrops or vertebrobasilar TIA. [3]

Vestibular Migraine

When dizziness is the primary complaint or is the predominant component of the aura, then it may be considered as vestibular migraine. Vertigo occurring as an aura may arise from the same transient inhibition of neuronal function responsible for the visual aura. Episodic vertigo from vestibular migraine can be thought of as a subset of basilar migraine. Spells usually last approximately an hour but can last up to several hours or days.  Nausea, vomiting, hypersensitivity to motion and postural instability are cardinal signs. The dizziness can also be associated with benign paroxysmal positional vertigo.[3]

Retinal Migraine

Retinal migraine is repeated attacks of monocular visual disturbance, including scintillations, scotomata, or blindness, associated with migraine headache. Visual changes are strictly unilateral. There may be neuronal spreading depression or involvement of the posterior ciliary vasculature. TIA must be ruled out, as emboli from the carotid artery can cause similar symptoms.[3]

Results in pain around the eye and paralysis in the distribution of the third, fourth, and sixth cranial nerve and can produce diplopia (double vision). The headache always precedes the oculomotor deficit by several days. The paralysis can progress from being transient to last several days, and in some persons it becomes permanent. People with ophthalmoplegic migraine typically have a long history of migraine prior to oculomotor involvement.[3]


Repeated attacks of monocular visual disturbance, including scintillations, scotomata, or blindness, associated with migraine headache.  Some patients who complain of monocular visual disturbance in fact have hemianopia. Some cases without headache have been reported, but their migrainous nature cannot be ascertained. Other causes of transient monocular blindness (amaurosis fugax), such as optic neuropathy or carotid dissection, must be excluded.

Diagnostic Criteria

  1. At least 2 attacks fulfilling criteria 2 and 3
  2. Fully reversible monocular positive and/or negative visual phenomena (eg, scintillations, scotomata, or blindness) confirmed by examination during an attack or (after proper instruction) by the patient's drawing of a monocular field defect during an attack
  3. Headache fulfilling criteria 2-4 for Migraine without aura begins during the visual symptoms or follows them within 60 minutes
  4. Normal ophthalmological examination between attacks
  5. Not attributed to another disorder

Childhood Periodic Syndromes That Are Commonly Precursors of Migraine

Cyclical Vomiting

Cyclical vomiting is a self-limiting episodic condition of childhood, with periods of complete normality between episodes. Recurrent episodic attacks, usually stereotypical in the individual patient, of vomiting and intense nausea which are associated with pallor and lethargy. The clinical features of this syndrome resemble those found in association with migraine headaches, and multiple threads of research over the last years have suggested that cyclical vomiting is a condition related to migraine.

Abdominal Migraine

An idiopathic recurrent disorder is seen mainly in children and characterized by episodic midline abdominal pain manifesting in attacks lasting 1-72 hours with normality between episodes. The pain is of moderate-to-severe intensity and associated with vasomotor symptoms, nausea, and vomiting.  Pain is severe enough to interfere with normal daily activities.  Most children with abdominal migraine will develop migraine headaches later in life.

Benign Paroxysmal Vertigo of Childhood

This probably a heterogeneous disorder which is characterized by recurrent brief episodic attacks of vertigo occurring without warning and resolving spontaneously in otherwise healthy children.

Associated Co-morbidities


It was found that ther were differences in the number of positives for IgG food allergens between patients with migraine and a controlled group, elimination diets successfully control the migraine without the need of medications.

Ménière's disease|Meniere's disease

Migraine occurs more often in patients diagnosed with Meniere disease.

Systemic Lupus Erythematosus


Although studies vary, individuals with either migraine or epilepsy are more than twice as likely to have the other disorder. 5 Possible causes for comorbid:

  1. Migraine could cause epilepsy by inducing brain ischemia and injury.
  2. Epilepsy could cause migraine by activating the trigeminovascular system, in which we would expect an excess risk of migraine after, but not before, the onset of epilepsy.
  3. Shared environmental risk factors because the risk of migraine is significantly increased in people with idiopathic or cryptogenic epilepsy, known environmental risk factors cannot account for all of the comorbidity.
  4. Shared genetic risk factors might account for comorbidity.
  5. Ottman and Lipton proposed that an altered brain state (increased excitability) might increase the risk of both migraine and epilepsy and account for comorbidity, a hypothesis that draws support from therapeutic similarities.[5]


  • The migraine-stroke association is most apparent for young women with migraine with aura. Although there are several hypotheses about the biologic link between migraine with aura and ischemic stroke, the precise mechanisms remain unclear. However, because the absolute risk of stroke is low in patients with migraine with aura, and migraine without aura is likely not associated with ischemic stroke, most migraine patients will not experience a stroke event.[6]
  • According to large series, migrainous infarct accounts for 0.5-1.5% of all ischaemic strokes and 10-14% in young patients. Migraine itself might cause spasm or even hyperplasia. It is unlikely to be the cause of embolism or among other disorders. dissection. Migrainous infarct due to severe hypoperfusion during an attack is rare and mostly involves the posterior-cerebral-artery territory and is more common during attacks of migraine with aura than without aura. The precise mechanism of this severe hypoperfusion is unknown. Increased risk due to treatments used in migraine, particularly vasoconstrictors, is supported by the increase in white-matter abnormalities and in mortality found in patients taking ergotamine, but two recent studies found no increase in severe vascular events with triptans. Drugs widely used in migraine, such as aspirin and non-steroidal anti-inflammatory drugs, decrease the risk of cerebral ischaemic events.[7]
  • Migraine headache can occur as a comorbidity of ischaemic stroke, carotid or vertebral artery dissection, arteriovenous malformations, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL syndrome), or platelet disorders (eg, thrombocytosis).[8]

Complications of Migraine

Chronic Migraine

Migraine headache occurring on 15 or more days per month for more than 3 months in the absence of medication overuse.

Most cases start without aura. The criterion for chronic migraine is headache for 15 or more days a month for more than 3 months. Medication overuse is the most common cause of chronic migraine, and they report a change in symptoms over time, with decreasing photophobia, and nausea, and a headache that resembles a mixture of tension-type headache and migraine.[3]

Status Migrainosus

This type of headache lasts more than 72 hours and a usual trigger will set it off. This resembles a person's typical migraine, but the pain may spread as well as the allodynia. The premenstrual part of the female cycle is a time of particular risk for SM, and changes in hormone status, pregnancy, miscarriage, or change in birth control pills can be factors. Upper respiratory or urinary tract infections can also be the trigger for SM. Overuse of analgesics and rebound withdrawal-type headache, the headache that comes when not taking medication, can trigger SM. Prolonged vomiting to the point of dehydration is common. Severe pain and fatigue limit activity, and hospital admission may be appropriate. Comorbid depression is frequently seen.[3]

Migraine Aura Status

Aura symptoms persist for more than 1 week without radiographic evidence of infarction.

This is a rare subtype with persistent aura without infarction. One or more symptoms that the individual usually experiences as part of his/her typical migraine aura persist for more than 1 week. Visual symptoms are most common, but it can be any symptoms. Most of typical treatment is ineffective, and the problem often must run its course.[3]

Migrainous Infarction

One or more migrainous aura symptoms associated with an ischaemic brain lesion inappropriate territory demonstrated by neuroimaging

Migraine-Triggered Seizure

A seizure triggered by a migraine aura.


Common causes include: 

  • Vasodilators (eg, Nitroglycerin)[4]
  • Skipping meals[2]
  • Weather changes[2]
  • Sleep deprivation[2]
  • Stress[2][4]
  • Excessive afferent stimuli (eg, flashing lights, strong odors)[2]
  • Head trauma, neck pain, or temporomandibular joint dysfunction can trigger or exacerbate a migraine[2]
  • Hormonal factors: fluctuating estrogen levels are a potent migraine trigger. Many women have the onset of migraine at menarche, severe attacks during menstruation (menstrual migraine: appear to be more frequently in migraine with aura[3]) and, worsening migraine during menopause.[2] Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura.[2] Pregnancy can either exacerbate or relieve migraine attacks.
  • Certain foods can precipitate a migraine attack (including, but not limited to):
    • Tyramine-containing chesses[4]
    • Meat, such as hot dogs or bacon, with nitrate preservatives[4]
    • Chocolate containing phenylethylamine but not chocolate alone[4]
    • Food additives such as monosodium glutamate, a commonly used flavor enhancer[4]
    • Coffee and alcohol (especially red wine)[3][2]
    • Sugar (in vulnerable individuals)[3]
  • Genetics: There is a positive family history of migraine in about 60% of cases, which suggests a hereditary factor.[3] All twin studies done so far (comparison of concordance rates between monozygotic and dizygotic twins) show that migraine has a genetic component in addition to environmental factors.[9] Familial hemiplegic migraine (FHM), a rare type of migraine with aura, is the only form in which a monogenic mendelian mode of inheritance has been clearly established.[9]

Trigger Factors

Trigger factors increase the probability of a migraine attack in the short term (usually <48 hours) in a person with migraine. Though some trigger factors have been reasonably well studied epidemiologically (eg, menstruation) or in clinical trials (eg, chocolate, aspartame), causal attribution in individual patients may be difficult.

Aggravating Factors

Migraine may be aggravated by a number of factors. That is, in a person who already meets the criteria for migraine, particular factors may be associated with a relatively long-term (usually weeks to months) increase in the severity or frequency of attacks. Examples of commonly-reported aggravating factors include psychosocial stress, frequent intake of alcoholic beverages, other environmental factors.

Systemic Involvement

Migraines can affect various other systems of the body aside from the headache itself.  As mentioned previously, migraines produce extracranial vasodilation and intracranial vasoconstriction. This vasoconstriction along with the cortical spreading depression can have various effects on vision, and hearing. The most common effect of migraine with aura is the scintillating scotoma and many migraineurs with or without aura have a hypersensitivity to light and sound. This is why they generally seek a quiet, dark environment to lie down. The extracranial vasodilation can affect functions within the migraine, specifically the locus ceruleus and nucleus raphe. The locus ceruleus is responsible for attention and the nucleus raphe produces serotonin. Also mentioned in the clinical presentation, serotonin production can affect the aggregability of platelets. However, serotonin levels also affect mood. The medullary raphe nuclei send axons into the spinal cord to modulate sensory, autonomic, and motor activity. The medullary raphe has an effect on the effect on pain by releasing serotonin onto interneurons in the dorsal horn that inhibits the transmission of pain information. Raphe spinal endings in the lateral horn influence the cardiovascular system. This vasodilation and imbalance of serotonin during the migraine can have profound effects on mood, sensory, autonomic, and motor activity as well as pain. Familial hemiplegic migraine has an effect on sensory and motor activity on one side of the body. ☃☃There is also a small percentage of patients that may experience cardiovascular events during a migraine including myocardial infarction or an obstruction of blood flow to the brain causing a transient ischemic attack or cerebrovascular accident. This is why differential diagnosis is critical and referral back to the physician or emergency room is pertinent if the therapist suspects the patient is experiencing a stroke or a cardiovascular event.

The ascending reticular activating system (ARAS) is located in the brainstem and is responsible for regulating consciousness and is located in the reticular formation of the brainstem. Generally, the migraineur will lie down and rest and sleep can resolve the symptoms of the migraine.  The vestibular nuclei are located in the brainstem at the cerebellopontine angle. Migraineurs that have vestibular effects may have problems with balance, coordination, head movements, postural control, motor planning, and eye movements.[10]  Migraineurs may also have difficulty concentrating. 

The musculoskeletal system can also be affected specifically in the cervical spine.  It is common for migraine headache sufferers to have increased muscular tone in the suboccipital and paraspinal musculature as well as an underlying cervical dysfunction that may occur at the same time as the migraine and must be addressed. With familial hemiplegic migraine, they may have weakness in their extremities and also can be addressed with physical therapy. Many migraineurs have an intolerance to a certain amount of physical activity. Again, this can also be addressed with physical therapy.  

Other systems may be affected via the medication that is prescribed depending on dosage, how long the patient has been taking the medication, and any interactions from taking multiple medications for various other conditions the patient may also have in addition to migraine.  The systems that may be affected by medications could include pulmonary, gastrointestinal, endocrine, hepatic, hematologic, genitourinary, and neurological systems.  It is recommended that these patients are monitored by their physician and/or pharmacist to monitor adverse side effects and potentially serious drug interaction effects. 

Diagnostic Tests/Lab Tests/Lab Values

Diagnosis is based on characteristic symptoms and a normal physical (including neurologic) examination. Typical cases without worrisome findings do not require CNS imaging. Patients requiring very urgent CT or MRI to look for hemorrhage, increased intracranial pressure, and other structural causes of headache include those with[2]:

  • Sudden-onset thunderclap headache: an abrupt severe headache that may be a sign of bleeding in the brain and requires immediate medical attention.
  • Altered mental status, including seizure
  • Focal neurologic deficits
  • Papilledema: an optic disc swelling that is secondary to elevated intracranial pressure.[11]
  • Severe hypertension

Medical Management


According to Clinical Neurology (6th ed)[4], the following medications are generally used:

Acute Treatment Medication Comments
Simple Analgaesics
  • Aspirin[12]
  • Naproxen Sodium
  • Ibuprofen
  • Acetaminophen
May cause gastric pain or bleeding and rebound headache if used frequently. 
Ergot Preparations
  • Ergotamine,caffeine
  • Dihydroergotamine
May cause nausea and vomiting; contraindicated by pregnancy or peripheral vascular disease; use with metoclopramide (antiemetic)
Narcotic Analgesics
  • Codeine/asprin
  • Codeine/asprin/acetaminophen
  • Meperidine
  • Butorphanol
5-HT Antagonists (Serotonin Receptor Agonists)
  • Sumatriptan (Imitrex)
  • Rizatriptan (Amaxalt)
  • Zomitriptan (Zomig)
  • Naratriptan (Amerge)
  • Almotriptan (Axert)
  • Frovatriptan (Frova)
  • Eletriptan (Relpax)
10% incidence nausea and vomiting; contraindicated by pregnancy or coronary or peripheral vascular disease, and with monoamine oxidase inhibitors
Other Agents
  • Caffiene/butalbital/asprin (Fiorinal)
  • Prochlorperazine
Can cause hypotension and drug-induced dystonia
Prophylactic Treatment Medication Comments
Anti-inflammatory Agents
  • Asprin[12]
  • Naproxen Sodium
May cause gastric pain or bleeding and rebound headache if used frequently

Beta Blockers

  • Amitriptylline
  • Nortriptylline
  • Protriptylline
  • Doxepin
  • Propranolol
May cause dry mouth, urinary retention, and sedation; contraindicated in glaucoma or protatism
Ergot Alkaloids
  • Methergine
Occurrence of retroperitoneal fibrosis with urethral obstruction and mediastinal fibrosis, although uncommon, should be monitored with creatinine, ultrasonography, or intravenous urograms, and chest x-rays every 6 months; a drug holiday every 6 months is prudent
  • Phenytoin
  • Valproic Acid
  • Topiramate[13]
  • Gabapentin
Calcium Channel Antagonists
  • Verapamil
  • Nicardipine
  • Flunarizine
Contraindicated by severe left ventricular dysfunction, hypotension, sick sinus syndrome without artificial pacemaker, or second or third degree AV node block; constipation is the most common side effect; not for use with beta blockers.
Other Treatment Medication Comments

Other Agents

  • Prochlorperazine
  • Hydroxyzine
  • Metoclopramide
Adjunct to treatment; improves enteric drug absorption and reduces nausea; dystonia and akathisia may occur and respond to IV benedryl

Proper use of medications is an important part of successfully managing migraine headache, yet migraineurs frequently switch, discontinue, or delay taking effective prescription therapies such as triptans. Adherence is complicated by the recurrent yet unpredictable nature of the disease and variations in individual medication utilization patterns. Furthermore, the progression of migraine may accelerate or remit over time for any given individual, prompting adjustments in medication type or dose. While efficacy, cost, drug tolerability, and side effects impact whether a patient takes migraine medication, low perceived disease importance, and factors related to the patient's internal decision-making process play a strong role in the sustained use of acute medication for a migraine attack. Bozena et al[14] propose a model that combines the patient's perceived severity of migraine, their beliefs regarding the safety of acute medications, and factors related to the physician–patient relationship to identify migraineurs at high risk for medication adherence problems.

Current Approaches to the Management of Pediatric Migraine

The differential diagnosis for children is crucial for proper treatment[15].   Determining the cause of headaches in children can help decide what form of treatment is appropriate. Children can present with any of the following conditions that may mask the true migraine with other symptoms that occur simultaneously or that can exacerbate migraine headache symptoms.

  • Allergies and sinus disease
  • Head Injury
  • Obesity
  • Sleep
  • Psychological Factors

Treatment in the younger population should center around a treatment that will minimize the side effects with a rapid return to normal function. Drugs that have been used for the prevention of pediatric migraine include antidepressants (eg, amitriptylline), antihypertensives (eg, propranolol), antihistamines ,or antiserotonergics (eg, cyproheptadine), and antiepileptic medications (eg, valproic acid and topiramate).[15] According to this article, only almotriptan has been approved by the FDA for use in the pediatric population, while nasal sumatriptan and zolmitriptan have been approved in Europe by the European Medicines Agency (EMEA) for the acute treatment of adolescent migraine.[15] Additional studies have indicated that NSAIDs (particularly ibuprofen) are effective when used early in the attacks at an adequate dose and that triptans are effective when NSAIDs do not completely relieve symptoms, particularly during the more severe attacks.[15] On the basis of controlled studies of acute treatment to date, the general conclusions that can be drawn are that NSAIDs (particularly ibuprofen) are used fewer than 2-3 times per week to minimize the risk of medication overuse.[15]

Physical Therapy Management

Research regarding physical therapy for the treatment of migraine headache is limited. However, migraineurs can still benefit from physical therapy intervention. As mentioned in the clinical presentation, pericranial muscles can be the cause of migraine and will be tender during a migraine.  There may also be changes in suboccipital and paraspinal muscle tone and underlying cervical dysfuntcion between migraine episodes.   This can be addressed through physical therapy using manual therapy, specific exercise training (including, stretching, strengthening, and self-distraction), education, and modalities to decrease the frequency/onset of the attack and duration/intensity of the attack.

A key systematic review in 2011 showed that massage therapy, physiotherapy, relaxation, and chiropractic spinal manipulative therapy might be equally efficient as propranolol and topiramate in the prophylactic management of migraine[16] (many other studies can be accessed from the reference list of this open access article).   Some studies have demonstrated that physiotherapy is most effective for the treatment of migraine when combined with other treatments such as thermal biofeedback, relaxation training, and exercise[17]

Migraineurs can also benefit from physical therapy for vestibular related dysfunction as seen in vestibular migraine[18][19]. If the migraine is accompanied or caused by benign paroxysmal positional vertigo (BPPV), PT can assist in reducing the frequency of attacks.

Value has been placed on the therapeutic relationship that physiotherapists have with individuals with migraine with indications that physiotherapy could be a compliment or an alternative to medication to ease the consequences of migraine[20].

More research needs to be done on physical therapy treatment for migraine headaches.  A multidisciplinary approach should be considered to coordinate care to improve the probability of long term success for the migraineur. 

Spinal Manipulation

Manual therapy techniques have been shown to be effective as some drugs in the prophylactic management of migraine[16][17] It has also shown to  decrease pain intensity and reduce the number of days with migraine as well as working disability, and partly on the improvement of HRQoL[21] Cervical manipulation has been found to be successful for short term treatment of migraine headache, but caution should be taken for the possible risk for vertebral artery dissection, stroke, or transient ischemic attack[17]


Cold therapy in the form of a frozen neck wrap at applied onset of migraine headache targeting the carotid arteries at the neck significantly reduced recorded pain in participants with migraine headaches[22]

Exercise Therapy

Exercise has been suggested as a means of migraine management[23][24].  Exercise has also been found to be effective in reducing the intensity of migraine headache, but it does not provide a significant reduction in the frequency or duration of migraine attacks.[25]  More research is needed regarding the value of exercise for the treatment of migraine headaches.

Thermal Biofeedback and Neurofeedback

Neurofeedback and biofeedback literature is increasing with positive outcomes for the treatment of migraine headache.  Neurotherapy is a broad term referring to the many types of biofeedback used to deliver information about the central nervous system which involves blood flow, thermal output from the brain, or electrical activity. Neurofeedback (also called neuro biofeedback or EEG biofeedback) usually refers to frequency-based biofeedback that uses an EEG to give clients information about their brainwaves and gradually and subtly teaches people how to alter their brainwave activity.[26] These techniques have enabled patients to automatically learn to abort their headaches without having to use neurofeedback devices. These patients described the biofeedback as helping them to acquire the ability to better self-regulate by learning to control their EEG and reducing muscle tension, slowing the rate of their breathing, and warming their hands and forehead, all of which were necessary for the types of biofeedback they had undergone.[26] Home training has also been shown to be an essential component of the efficacy and maintenance of treatment benefits. Treatment manuals incorporating home training led to nearly 20% higher treatment effects for headache reduction.[27]


Lifestyle Modification

One aspect of physical therapy that could be beneficial to the migraine patient could be education on general health, exercise, sleep, diet (a more in depth look at diet needs to be addressed by a registered dietitian), and relaxation techniques.  

Relaxation Techniques

There is controversial evidence on the effectiveness on migraine and relaxation techniques.  However, a considerable amount of the literature supports RT as an adjunct treatment to the patient's current medical management for their headaches.


Acupuncture has been shown to have similar efficacy compared with continuous treatment with standard drug therapy[29] and also effective for long lasting effects and decreased intake of medication.[30]


Massage therapy can have beneficial effects on migraine experience, stress arousal, and sleep for individuals with migraine. Most notably, massage therapy has been shown to significantly reduce migraine frequency both during the 6 weeks of massage therapy as well as during the 3 weeks following the end of therapy[31] This is the first evidence that massage therapy may reduce migraine frequency beyond the end of treatment, and research is now needed to further evaluate the durability of these effects.

Migraine Art

Numerous artists are expressing the pain of migraine through their artwork. The following is some examples of art-work done by different artists with links to follow to view more artwork.

Origin b.jpg Laceration b.jpg
Origin Laceration
Blast of light b.jpg Migraine.png
Blast of Light Slideshow from the NY Times

Differential Diagnosis

Due to the complexity of the pathophysiology and signs and symptoms attributed to migraine headaches, differential diagnosis from other types of Headache is crucial for determining whether the headache is a medical emergency or a non-life threatening headache from other causes.  The International Headache Society classifies each type of headache into either primary, secondary, or other causes of headache with subclasses for each category for specific diagnosis[32] (See more about the classification on the Headache page). 

Pathologic Conditions Causing Headache

Pathologic conditions[3] must also be ruled out.

Subdural Haematoma Mild to severe, intermittent headache; neurologic symptoms including fluctuating consciousness
Subarachnoid Haemorrhage Sudden onset, sever and constant headache; elevated BP; can change in consciousness
Increased Intracranial Pressure Mild to severe headache; neurologic symptoms including hemiparesis, visual changes, and brainstem symptoms such as vomiting and altered consciousness
Meningitis, viral and bacterial infections Severe headache with radiation down neck; acute illness and fever; positive Kernig's sign
Brain abscess Mild to severe headache; local or distant infection; fever may not be present; neurologic signs consistent with local site of infection
Central Nervous System Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
Central nervous system neoplasm Localized headache and often focal neurologic symptoms; cranial nerve symptoms often seen
Toxicity Generalized headache, pulsating; other signs of toxicity may be present
Sinusitis Frontal or dull headache, usually worse in the morning; increased pain in cold damp air; nasal discharge
Otitis media, mastoiditis Feeling of fullness in the ear, stabbing pains in the head, vertigo, and tinnitus

Case Reports

Chronic migraine and chiropractic rehabilitation

Migraine Headache Case Study


Multidisciplinary Management Of Migraine: Contemporary Issues in Physical Therapy and Rehabilitation Medicine by César Fernández-de-las-Peñas, Leon Chaitow and Jean Schoenen [Book: ISBN 978-1449600501]


  1. International Headache Society. Classification of Headaches (ICHD-II). Available from: http://ihs-classification.org/en/02_klassifikation/ (accessed 26 November 2013)
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M. The Merck Manual of Diagnosis and Therapy 18th ed. Whitehouse Station:Merck Research Laboratories, 2006. p847-1849
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist 3rd ed. St. Louis: Saunders Elsevier, 2009. p1551-1559.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 Aminoff MJ, Greenberg DA, Simon RP. Clinical Neurology 6th ed. New York: Lange Medical Books/McGraw-Hill, 2005. p85-90.
  5. Haut SR, Bigal ME, Lipton RB. Chronic disorders with episodic manifestations: focus on epilepsy and migraine. Lancet Neurol. 2006; 5: 148-157.
  6. Kurth T, Diener HC. Current views of the risk of stroke for migraine with and migraine without aura. Current pain and headache reports. 2006 Jun 1;10(3):214-20.
  7. Bousser MG, Welch KM. Relation between migraine and stroke. The Lancet Neurology. 2005 Sep 1;4(9):533-42.
  8. Dalkara T, Nozari A, Moskowitz MA. Migraine aura pathophysiology: the role of blood vessels and microembolisation. The Lancet Neurology. 2010 Mar 1;9(3):309-17.
  9. 9.0 9.1 Ducros A, Tournier-Lasserve E, Bousser MG. The Genetics of Migraine. Lancet Neurology. 2002; 1: 285-293.
  10. Lundy-Eckman L. Neuroscience: Fundamentals for Rehabilitation 3rd Ed. St. Louis: Elsevier, 2007: p379-381, 386.
  11. Gossman MV, Giovannini J, Grant D. Papilledema. Available from: http://emedicine.medscape.com/article/1217204-overview. (accessed on 24 March 2010).
  12. 12.0 12.1 Kirthi V, Derry S, Moore RA, McQuay HJ. Aspirin with or without an antiemetic for acute migraine headaches in adults. Cochrane Database Syst Rev 2010;(4):CD008041
  13. Diener HC, Agosti R, Allais G, Bergmans P, Bussone G, Davies B, et al. Cessation versus continuation of 6-month migraine preventive therapy with topiramate (PROMPT): a randomised, double-blind, placebo-controlled trial. Lancet Neurol 2007; 6(12): 1054-1062.
  14. Katić BJ, Krause SJ, Tepper SJ, Hu HX, Bigal ME. Adherence to Acute Migraine Medication: What Does It Mean, Why Does It Matter? Headache. 2010;50(1):117
  15. 15.0 15.1 15.2 15.3 15.4 Hershey AD. Current approaches to the diagnosis and management of pediatric migraine. Lancet Neurol. 2010; 9: 190-204.
  16. 16.0 16.1 Chaibi A, Tuchin PJ, Russell MB. Manual therapies for migraine: a systematic review. The journal of headache and pain. 2011 Apr 1;12(2):127-33.
  17. 17.0 17.1 17.2 Biondi DM. Physical treatments for headache: a structured review. Headache: The Journal of Head and Face Pain. 2005 Jun;45(6):738-46.
  18. Vitkovic J, Winoto A, Rance G, Dowell R, Paine M. Vestibular rehabilitation outcomes in patients with and without vestibular migraine. Journal of neurology. 2013 Dec 1;260(12):3039-48.
  19. Hansson EE, Troein M. Vestibular rehabilitation for vestibular migraine. Advances in Physiotherapy. 2011 Mar 1;13(1):34-7.
  20. Rutberg S, Kostenius C, Öhrling K. Professional tools and a personal touch–experiences of physical therapy of persons with migraine. Disability and rehabilitation. 2013 Sep 1;35(19):1614-21.
  21. Voigt K, Liebnitzky J, Burmeister U, Sihvonen-Riemenschneider H, Beck M, Voigt R, Bergmann A. Efficacy of osteopathic manipulative treatment of female patients with migraine: results of a randomized controlled trial. The Journal of alternative and complementary medicine. 2011 Mar 1;17(3):225-30.
  22. Sprouse-Blum AS, Gabriel AK, Brown JP, Yee MH. Randomized controlled trial: targeted neck cooling in the treatment of the migraine patient. Hawai'i Journal of Medicine & Public Health. 2013 Jul;72(7): 237–241.
  23. Varkey E. On the prevention of migraine-focus on exercise and the patient's perspective. 2012 Feb 3.
  24. Darabaneanu S, Overath CH, Rubin D, Lüthje S, Sye W, Niederberger U, Gerber WD, Weisser B. Aerobic exercise as a therapy option for migraine: a pilot study. International journal of sports medicine. 2011 Jun;32(06):455-60.
  25. Busch V, Gaul C. Exercise in Migraine Therapy—Is There Any Evidence for Efficacy? A Critical Review. Headache 2008;48:890-899.
  26. 26.0 26.1 Stokes and Lappin: Neurofeedback and Biofeedback with 37 migraineurs: a clinical outcome study. Behavioral and Brain Functions 2010; 6:9.
  27. Nestoriuc Y, Martin A, Rief W, Andrasik F. Biofeedback Treatment for Headache Disorders: A Comprehensive Efficacy Review. Appl Psychophysiol Biofeedback (2008) 33:125–140.
  28. ufovnis Neurofeedback for migraine headache treatment available from https://www.youtube.com/watch?v=SKY-TlAt4co
  29. Diener HC, et al. Efficacy of acupuncture for the prophylaxis of migraine: a multicentre randomised controlled clinical trial. Lancet Neurol 2006; 5: 310-316.
  30. Facco E, et al. Traditional Acupuncture in Migraine: A Controlled, Randomized Study. Headache 2008;48:398-407.
  31. Lawler SP, Cameron LD. A randomized, controlled trial of massage therapy as a treatment for migraine. Annals of Behavioral Medicine. 2006 Aug 1;32(1):50-9.
  32. IHS Classification of Headaches. Available at: http://ihs-classification.org/en/02_klassifikation/. Accessed on (5 March 2010).