eMedicine Specialties > Neurology > Headache and Pain

Migraine Variants

Rima M Dafer, MD, MPH, FAHA, Associate Professor, Department of Neurology and Neurological Surgery, Loyola University, Chicago Stritch School of Medicine

Updated: Jan 13, 2009

Introduction

Background

Migraine is a paroxysmal headache disorder affecting more than 13% of the general population in the United States. Migraine is a syndrome and not a disease; it is characterized by paroxysmal headache associated with others signs and symptoms. About 80% of migraineurs have migraine without aura, while migraine with typical aura accounts for 15-20% of cases. Isolated migraine aura without headache (acephalic migraine) may be encountered in 5% of patients.¹

Migraine variant (MV) or migraine equivalent is the term applied to migraine, which exhibits itself in a form other than head pain. MV is characterized by paroxysmal episodes of prolonged visual auras; atypical sensory, motor, or visual aura; confusion; dysarthria; focal neurologic deficits; or gastrointestinal manifestations or other constitutional symptoms with or without a headache.

The diagnosis of MV is determined by history of paroxysmal signs and symptoms with or without cephalgia, a prior history of migraine with aura, in the absence of other medical disorders that may contribute to the symptoms. Many of these patients usually have a family history of migraine.

MVs are less recognized and poorly understood. They are less common than typical migraine without and with aura, and they usually affect children and young adults.

MVs should be differentiated from trigeminal cephalic neuralgias and other primary headaches such as stabbing and thunderclap headaches, cough headaches, or hypnic headaches. MVs should also be differentiated from exertional headaches, a group of headache syndromes associated with physical activity such as running, coughing, sneezing, or sexual intercourse.

Many MVs have been defined by the International Classification of Headache Disorders (ICHD-II) 2004 classification. These include hemiplegic migraines, basilar migraine, childhood periodic syndromes, retinal migraine, complicated migraines, and ophthalmoplegic migraine. Vertiginous migraine, acute confusional migraine of childhood, and nocturnal migraine, although well recognized entities, remain unclassified by the IHCD-II.

Pathophysiology

Although activation and sensitization of the trigeminovascular in migraine is believed to generate and maintain migraine pain, cortical spreading depression (CSD) is recognized as the neuronal phenomenon underlying visual aura. CSD is believed to begin in the occipital region and to gradually spread anteriorly.² This phenomenon is accompanied by a transient oligemia, followed by hyperemia in other parts of the cortex.³ Various molecular and cellular mechanisms may lead to the increased susceptibility of CSD in migraineurs, which could potentially play an important role in the pathophysiology of MVs. Researchers have suggested that a vasogenic leakage from leptomeningeal vessels, with activation of the trigeminovascular system, probably contribute to the prolonged aura in patients with hemiplegic migraine.

Migraine with prolonged aura

The typical duration of a migraine aura, predominantly visual, is up to 30 minutes. In rare cases, the aura could be prolonged, lasting up to 60 minutes, raising concerns of possible stroke.

Migraine aura without headache or acephalic migraine

Around 3-5% of migraineurs experience an aura without headache. This presentation is more common in older patients who have had a history of migraine with aura during early age. Symptoms may include scintillating scotomata, formed stereotyped visual hallucinations in a single visual field or bilaterally, micropsia, and tunnel vision.⁴ Other auras include paroxysmal vertigo, hemisensory dysesthesias, and rarely auditory hallucinations. Acephalic migraine should be differentiated from transient ischemic attack, occipital lobe seizures, or temporal lobe seizures.

Hemiplegic migraine

Hemiplegic migraine is a very rare but well described form of MV. It was initially described in 1910 as a type of migraine consisting of recurrent headaches associated with temporary unilateral hemiparesis or hemiplegia, at times accompanied by ipsilateral numbness or tingling, with or without a speech disturbance. The focal neurologic deficit may precede or accompany the headache, which is usually less dramatic than motor deficit. Other migraine symptoms may variably be present. Patients may also experience disturbance of consciousness, and rarely coma.^5,6,7,8,9,10 The neurologic deficit is transient and usually clears in minutes to hours, or resolves with the beginning of the headache phase.^{11,12,13,14,15}

Two forms of hemiplegic migraine are known: familial and sporadic. Both familial hemiplegic migraine (FHM) and sporadic hemiplegic migraine (SHM) are phenotypically similar subtypes of migraine with aura, differentiated only by the unilateral motor symptoms.^16,17

Familial hemiplegic migraine

FHM is a genetically heterogeneous autosomal dominant disorder. FHM is a channelopathy; most of the affected families (FHM1) bear mutations in the CACNA1A gene (a defect linked to abnormal voltage-dependent P/Q-type calcium channel alpha-1A) on 19p13.^{18,19,20,21,22,23} In the familial hemiplegic migraine type 2 (FHM2), mutation in ATP1A2 (R548H) on 1q23 was identified, encoding the alpha2-subunit of sodium/potassium pumps.^24,25,26,27 A third novel mutation in sodium channel gene SCN1A has been recently identified in FHM3.²⁸

Alternating hemiplegic migraine (primarily in childhood)

Alternating hemiplegia of childhood (AHC) is a chronic progressive disorder, associated with high prevalence of neurologic deficit.²⁹ It is distinguished from familial hemiplegic migraine by its infantile onset and by its characteristic associated symptoms.³⁰ The onset of the disorder is before age 18 months.³¹ It is characterized by vomiting, headache, alternating hemiplegia, loss of consciousness, paroxysmal ocular palsies, choreoathetosis, autonomic dysfunction, and mental retardation.^32,33 Single-photon emission computed tomography (SPECT) studies have shown progressive decrease of cerebral perfusion in cases of alternating hemiplegic migraine.

Sporadic hemiplegic migraine

SHM is defined as migraine attacks associated with motor weakness in the absence of family history of similar attacks.^34,35 Cases of SHM have also been linked to the CACNA1A and ATP1A2 genes.

Diagnosis of FHM is usually confirmed with repeated stereotyped reversible episodes, particularly in the presence of positive family history of similar attacks. The absence of first- and or second-degree relatives with similar disorder raises suspicion of SHM.³⁶ Differential diagnosis includes focal seizures with postictal paralysis, mitochondrial cytopathies, intracranial hemorrhage, mass, infection, or cerebral infarction.³⁷

Basilar-type migraine

Basilar migraine (BM), also known as Bickerstaff syndrome, consists of headache accompanied by dizziness, ataxia, tinnitus, decreased hearing, nausea and vomiting, dysarthria, diplopia, loss of balance, bilateral paresthesias or paresis, altered consciousness, syncope, and sometimes loss of consciousness.³⁸ BM is observed most frequently in adolescent girls and young women.³⁹ Localized vertebrobasilar vasoconstriction leading to transient posterior circulation ischemia may contribute to the symptomatology of the disorder.⁴⁰ A novel mutation in the ATP1A2 gene, similar to FHM, has been reported in members of one family with BM. Differential diagnosis includes various causes of syncopal, inner ear disease, intoxication, and posterior fossa pathologies.⁴¹

Childhood periodic syndromes that are commonly precursors of migraine

Childhood periodic syndromes are characterized by multiple cyclic attacks of pain or vomiting with our without migraine headaches. They are common in children and adolescents.

Cyclic vomiting syndrome

Cyclic vomiting of childhood is characterized by recurrent attacks of violent or prolonged vomiting without headache, which may last for hours.^42,43,44 Attacks may be precipitated by infection, menstruation, or physical or emotional stress. During the attacks, patients characteristically show other symptoms of migraine such as nausea, lethargy, yawning, and drowsiness. Cyclic vomiting is thought to result from abnormal activity in the area postrema. Additionally, gastroparesis, which occurs during migraine, has been implicated as an etiologic factor for cyclic vomiting and abdominal migraine.^45,46,47

Abdominal migraine

Abdominal migraine most typically occurs in children, although it has been reported in adults.⁴⁸ Patients usually complain of paroxysmal midabdominal pain lasting form 1-72 hours, associated with nausea and vomiting, flushing, or pallor. Like cyclic vomiting, attacks may be associated with other migraine prodromes such as fatigue and drowsiness. Aura and headaches are frequently absent or minimal. Patients may develop migraine late in their life, and family history of migraine is common. Gastroenterologic evaluation and workup is unremarkable.⁴²

Benign paroxysmal vertigo of childhood

Benign paroxysmal vertigo of childhood (BPVC) is another MV characterized by brief episodes of vertigo and disequilibrium lasting for hours, without headache, aura, hearing loss, or tinnitus. It affects children aged 1-4 years. Children usually complain of a spinning sensation during the attack. Typical migraine is common later in life, and a family history of migraine is helpful in confirming the diagnosis.

Retinal migraine

Retinal migraine (ophthalmic, ocular) is not an uncommon cause of transient monocular blindness in young adults.^49,50 It is manifested by recurrent attacks of unilateral visual disturbance or blindness lasting from minutes to 1 hour, associated with minimal or no headache. This phenomenon is frightening to patients, who usually seek medical help to exclude amaurosis fugax due to ischemia of the retinal arteries.^51,52,53 Patients describe a gradual visual disturbance in a mosaic pattern of scotomata that gradually enlarge, producing total unilateral visual loss. Postural changes, exercise, and oral contraceptive agents may precipitate attacks. The condition is thought to result from transient vasospasm of the choroidal or retinal arteries. A personal or family history of migraine confirms the diagnosis. The condition needs to be differentiated from ocular or vascular causes of transient monocular blindness, mainly carotid artery disease.^54,55

Complicated migraine

Complications of migraine include chronic migraine, status migrainosus, persistent aura without infarction, migrainous infarction, and migraine-triggered seizure.⁵⁶ Complicated migraines are rare, accounting for less than 1% of total patients with migraine. Chronic migraine and status migrainosus are not considered MVs and therefore are not included in this article.

Persistent aura

A typical migraine aura usually lasts 20-60 minutes. When the aura of migraine is prolonged, lasting for hours or days, complicated migraine including ischemic strokes need to be excluded. Prolonged aura lasting beyond 60 minutes, in the absent of radiographic evidence of cerebral infarction, is referred to as migraine with persistent aura.

Migraine infarctions

The relationship between migraine, mostly migraine with aura, and ischemic stroke has been well recognized. Migraine, generally a benign condition, has been recognized as an independent risk factor for ischemic stroke. Additionally, migraine, predominantly migraine with aura, is associated with the presence of silent infarctions or white matter changes on brain MRI.⁵⁷ When a cerebral infarction occurs during a typical migraine aura attack, the term migrainous infarction is used. The mechanism of migrainous infarction is complex. Whether the relationship between migraine and stroke is the consequence of other underlying etiologies or the presence of similar ischemic risk factors, or whether migraine is associated with conditions that could potentially cause stroke, is yet to be determined.^58,59

Migraine-triggered seizures (migralepsy)

Migraine and epilepsy are highly comorbid conditions probably sharing the same pathophysiology, but the nature of their association is unclear. Migralepsy is the term used when a seizure occurs during or within 1 hour of a typical migraine aura attack.⁶⁰ Reversible brain MRI abnormalities have been reported in a patient with migraine-triggered seizure, possibly due to supratentorial focal cerebral edema.^61,62 Electroencephalogram (EEG) findings are usually normal interictal, although various abnormalities, mainly diffuse slowing, have been reported in migraineurs.

Ophthalmoplegic migraine

This is a very rare condition in children, characterized by a migrainelike attack, followed within days by periorbital pain and diplopia secondary to cranial neuropathies.^50,63 The oculomotor nerve is most commonly involved, with pupillary abnormality and ptosis, followed by the abducens, and rarely the trochlear nerve. The attack usually lasts from days to months and resolves spontaneously.^64,65,66 A number of adult cases have been reported. Although previously considered an MV, the condition has been classified as neuralgia by the IHCD-II. The condition is thought to be due to recurrent demyelinating cranial neuropathies. Differential diagnosis includes conditions involving the parasellar, orbital, and posterior fossa leading to headache and ophthalmoplegia.⁶⁷

Acute confusional migraine (primarily in childhood)

Acute confusional migraine is a rare MV, almost exclusively seen in young children, manifested by episodes of confusion, disorientation, and vomiting, with or without headaches.^68,69,70 The attacks are usually relieved by sleep. The condition should be differentiated from seizures, and various causes of confusion, including toxic, metabolic, mitochondrial, or infectious encephalopathies.

Vertiginous migraine

Growing evidence suggests that recurrent episodes of vertigo are related to migraine.^42,71 Vertigo, a common complaint among migraineurs, has been reported in one third of cases. Recurrent episodes of vertigo lasting between 5 minutes and 1 hour, with or without nausea, vomiting, photophobia, or headache, in the setting of a previous personal history or a positive family history of migraine supports the diagnosis of vestibular or vertiginous migraine. The pathophysiology of migraine-related vertigo is not fully understood.⁷² Differential diagnosis includes vertebrobasilar insufficiency and paroxysmal vestibular syndromes.

Nocturnal migraine

Frequency

United States

Migraine affects nearly 13% of the adult US population, with a postpubertal female-to-male ratio of 4:1. The frequency of the less common MVs varies with type and age. The prevalence of hemiplegic migraine is 0.03%; both familial and sporadic forms are equally frequent. The prevalence of the distinct alternating hemiplegic migraine of infancy is unknown. Similarly, the frequency of ophthalmoplegic, retinal, and confusional migraine is unknown.

Sex

Sex prevalence may be observed in some types of MVs. Basilar migraine and migraine aura without headaches are more common in women than in men. Similarly, hemiplegic migraine is more common in women, with a sex ratio (male-to-female) of 1:3.

• Basilar migraine in adults is more common in women than in men.
• Benign coital headache has a male-to-female ratio of 4:1.

Age

Specific MVs are observed at a higher incidence in different age groups. Ophthalmoplegic migraine, childhood periodic vomiting, and abdominal migraine are almost exclusively of childhood onset, affecting children younger than 10 years. In contrary, basilar and retinal migraines are more frequent in adolescents and young adults, while migraine aura without headache is mainly encountered in adults with long-standing history of migraine aura in early life. Hemiplegic migraine in its familial and sporadic forms has been reported in all age groups, while alternating hemiplegia of childhood is exclusive to children younger than 18 months.

Clinical

History

A detailed headache history is necessary to establish the diagnosis of MVs. As many as 20% of patients with MV may experience prodromal symptoms without subsequent headaches. Such paroxysmal symptoms, with the recurrent attacks of transient neurologic symptoms, whether a headache is absent or present, with a positive family history of migraine, and with a normal neurologic examination interictally are confirmatory.

• History of recurrent transient hemiplegia or hemiparesis that occurs during an attack of migraine headache suggests hemiplegic migraine. The hemiparesis may resolve prior to the headache or may persist for days to week.
  • Migraine aura without headaches is suspected in patients with history of recurrent attacks of unilateral transient monocular blindness in patients with otherwise absent risk factors for other causes of carotid disease and a personal or family history of migraine.
  • Patients with basilar migraine usually present with symptoms of vertebrobasilar insufficiency, which may precede a headache. The most common symptoms are dizziness and vertigo. Other symptoms, including visual disturbance (usually bilateral), dysarthria, acroparesthesias, tinnitus, confusion, or diplopia, may occur.
• Ophthalmoplegic migraine present with diplopia and periorbital pain with or without headache. Other symptoms include alteration of consciousness, acute confusion, recurrent vomiting, or seizures.
• Retinal migraine: A history of recurrent attacks of transient monocular visual disturbance or blindness with or without a headache, in the absence of other neurological symptoms is suggestive of retinal migraine.
• Cyclic vomiting should be suspected in children presenting with recurrent attacks of vomiting without headache, especially when a family history of migraine is present.
• A history of recurrent episodes of vertigo accompanied by other migrainous symptoms such as photophobia, headache, nausea, or vomiting is suggestive of vestibular migraine, predominantly in patients with a personal or family history of migraine.

Physical

The neurologic examination in between attack is nonfocal. Ictally, hemiparesis, ophthalmoplegia, or altered consciousness may be observed. Abnormalities of oculomotor nerve with pupillary involvement are seen in ophthalmoplegic migraine, followed by the abducens, and less commonly trochlear nerve palsy. Children with abdominal migraine or cyclic vomiting may show subtle clumsiness, attention deficit, or development delay. In migrainous infarction, some form of neurologic deficit with abnormal neuroimaging is present. Rarely, when patients with retinal migraine are evaluated and examined during an attack of visual loss, optic pallor or narrowing of the retinal vessels can be seen.

Differential Diagnoses

Other Problems to Be Considered

Cerebral autosomal dominant arteriopathy and subcortical infarcts and leukoencephalopathy (CADASIL)
Episodic ataxia
Gastrointestinal motility disorders
Miller-Fisher syndrome
Volvulus

Workup

Imaging Studies

• Patients with MV usually undergo unnecessary extensive and invasive diagnostic and laboratory evaluations before the diagnosis is made. A careful history of multiple attacks with complete recovery, with a symptom-free period in between attacks, and a family history of migraine or similar disorder is usually helpful in confirming the diagnosis.
• Neuroimaging (CT, MRI) is indicated when the patient presents with a first attack of focal neurologic deficits or altered mental status, or when focal findings persist between attacks. Neuroimaging studies are frequently obtained to exclude other acute causes of the symptoms and to exclude migrainous infarction in patients with persistent aura.
  • Imaging with MRI of the brain and MRA of the circle of Willis is indicated in ophthalmoplegic migraine to exclude posterior fossa or orbital pathologies associated with ophthalmoplegia. Abnormal enhancement on MRI and enlargement of the cisternal portion of the oculomotor nerve, have been reported. Further assessment may include a CT angiogram or lumbar puncture.
  • The yield for diagnostic testing in basilar migraine is low. Transient abnormalities on CT scan and MRI have been reported during or immediately following attacks. SPECT studies suggest decreased regional cerebral blood flow in the posterior circulation in basilar migraine during attacks, but transcranial Doppler studies have not revealed changes in blood flow velocities.
  • Invasive testing in children with periodic syndromes with a strong family history of migraine is unnecessary. A high-resolution MRI and magnetic resonance angiography (MRA) are indicated in suspicious cases in the absence of supportive family history.
• In retinal migraine, ruling out eye disease or vascular causes, especially when risk factors for arteriosclerosis exist, is important. Carotids Duplex sonography, transcranial Doppler study, MRA, or CT angiography examinations of the brain are helpful. Fluorescein or cerebral angiographies are rarely necessary. Hypercoagulability workup and sedimentation rate may be useful in excluding other coagulation disorders associated with retinal vasculopathy.

Other Tests

• EEG is unnecessary in MVs, except in conditions where seizure disorders need to be excluded, such as migraine-triggered seizure, and in patients with recurrent episodes of confusion. EEG generally does not offer additional information in migraineurs. In general, nonspecific interictal EEG abnormalities, including epileptiform activity, are reported in higher frequencies in migraineurs during or immediately after an episode, with slowing in focal or generalized patterns, and occipital spike-wave complexes.
• Continuous ambulatory or video EEG may be useful in patients with episodic confusion or recurrent focal neurologic deficits to exclude partial seizures or nonconvulsive status epilepticus.
• Genetic testing is now available for familial hemiplegic migraine using polymerase chain reaction to detect point mutations in the CACNA1A and ATP1A2 genes using and DNA sequencing is now available. Genetic testing may also be performed for other conditions associated with migraine such as CADASIL, an autosomal dominant disorder in which patients may present with migraine, multiple subcortical strokes, and dementia in early adulthood.
• In children with cyclic vomiting, a serum lactate level is helpful in excluding mitochondrial disorders. Other tests including, upper and lower gastrointestinal series and vagal autonomic function testing, are rarely indicated.
• More recently, functional neuroimaging studies during and immediately after an attack of migraine have demonstrated abnormalities of perfusion and have helped in understanding the pathophysiology of auras. Similarly, SPECT might show hypoperfusion during the aura phase.

Treatment

Medical Care

The first step in treatment is to establish the diagnosis. Once the syndromes are recognized, MVs respond to typical migraine preventive medications.

Treatment is divided into eliminating particular triggers, acute management of the specific attack, and long-term preventive approach. Patients should follow risk factor modifications including smoking cessation, and they should avoid the use of hormonal replacement therapy and birth control pills, all of which could potentially increase the risk of hypercoagulability migraineurs

• In hemiplegic migraine, acute treatment options include antiemetics, nonsteroidal anti-inflammatory drugs, and nonnarcotic pain relievers. Triptans and ergotamine preparations are contraindicated because of their potential vasoconstrictive effects.⁷³ Prophylactic treatment is generally warranted because of the severity of the attacks. No data are available to support the use of any particular antimigraine agent. Beta-blockers, low-dose tricyclics, anticonvulsants, and calcium channel blockers can be administered. Acetazolamide has been frequently prescribed to patients with hemiplegic migraine, but its benefit in decreasing the frequency or severity of the attacks is questionable.⁷⁴ No data support the use of antiplatelet therapy to decrease the risk of stroke.
• In ophthalmoplegic migraine, prednisone has been used with mixed results. The data on the benefit of prophylactic therapy with beta-blockers, such as propranolol, are anecdotal.
• In retinal migraine, vasoconstrictive agents such as triptans and ergots should be avoided. The use of prophylactic therapy is also anecdotal; when considered, calcium channel blockers are preferred.^49,55
• In migraine-triggered seizures, antiepileptic agents are drugs of choice because of their dual benefit in migraine prevention and seizure control
• In childhood periodic vomiting syndrome, early use of intravenous fluids containing adequate glucose (to prevent a catabolic state) and analgesics may abort the attack. Some patients respond to the triptans or ergotamine classes of medication. Antiemetic drugs are usually not effective, but ondansetron may be more efficacious given its central mechanism of action. Preventive medications such as cyproheptadine and tricyclic antidepressants are preferred in children.
• Abdominal migraine symptoms are usually relieved with sleep. Antiemetics may help aborting an acute attack. For chronic prevention, low doses of tricyclic antidepressants and flunarizine, a calcium channel blocker, are effective.⁷⁵ Other migraine prevention medications are occasionally of some benefit.
• Triptans, ergots, and dihydroergotamine are contraindicated in patients with migrainous infarction. These patients may respond to nonsteroidal anti-inflammatory drugs (NSAIDs), antiemetics, and non-narcotic pain relievers. Prophylactic therapy is recommended, with tricyclics, beta-blockers, calcium channel blockers, or antiepileptic drugs. Long-term antiplatelet therapy is indicated in patients with migrainous infarction.
• Patients with vertiginous migraine rarely respond to migraine prophylactic therapy. Anecdotal data are available on the benefit of verapamil, a calcium channel blocker, and amitriptyline, a tricyclic antidepressant, because of their anticholinergic properties, which may help control the vertigo.

Consultations

Consultation with a neuro-ophthalmologist is warranted in patients who present with persistent visual aura, retinal migraine, or recurrent ophthalmoplegia. Children with cyclic vomiting syndrome rarely require an evaluation by a gastroenterologist to exclude other gastrointestinal disorders. An evaluation by an audiologist may be necessary to exclude other vestibulopathies in patients with vertiginous migraine.

Diet

Certain food products and food additives may trigger migraine attacks in some patients. Such triggers include monosodium glutamate, nitrates-containing processed meat, aged or smoked cheese, onion, pickled products, avocados, dairy products, nuts, chocolate, caffeine, and alcoholic beverages, in particular red wine. Identifying and avoiding individual food triggers is key in preventing migraine attacks.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Carbonic anhydrase inhibitors (diuretic)

Carbonic anhydrase (CA) is an enzyme found in many tissues. It catalyzes a reversible reaction whereby carbon dioxide becomes hydrated and carbonic acid dehydrated. These changes may result in a decrease in cerebrospinal fluid by the choroid plexus.

Acetazolamide (Diamox)

For familial hemiplegic migraine. This recommended medication not typically used in migraine, but in hemiplegic MV. Available in 125 mg and 250 mg tab.

Dosing

Adult

8-30 mg/kg IV/IM divided qid; optimal adult dose 250-1000 mg/dose

Pediatric

5-25 mg/kg IV/IM divided qid

Interactions

Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Contraindications

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction; coadministration with aspirin

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients

Antiemetics

These agents typically are used in migraine and MVs, especially when nausea and vomiting are prominent.

Ondansetron (Zofran)

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally.

Dosing

Adult

8 mg PO bid

Pediatric

<4 years: Not established
4-12 years: 4 mg PO tid
>12 years: Administer as in adults

Interactions

Although potential for cytochrome P-450 inducers (eg, barbiturates, rifampin, carbamazepine, phenytoin) to change half-life and clearance, dosage adjustment not usually required

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

To be administered for prevention of nausea and vomiting, not for rescue of nausea and vomiting

Promethazine (Phenergan)

Used to control symptoms of nausea and vomiting.

Dosing

Adult

12.5-25 mg PO/IV/IM/PR q6h

Pediatric

<2 years: Contraindicated
>2 years: 12.5-25 mg PO/PR q6h prn

Interactions

May have additive effects when used concurrently with other CNS depressants or anticonvulsants; coadministration with epinephrine may cause hypotension

Contraindications

Documented hypersensitivity; asthma; children younger than 2 y (incidences of death due to respiratory depression)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, asthma, bone marrow depression, compromised respiratory function, stenosing peptic ulcer, seizure disorders, pediatric patients > 2 y

Calcium channel blockers

These agents inhibit calcium ions from entering slow channels, select voltage-sensitive areas, or vascular smooth muscle.

Verapamil (Calan, Calan SR, Covera-HS, Verelan)

Relaxes smooth muscles and increases oxygen delivery during vasospasms. Used for migraine prophylaxis.

Dosing

Adult

80 mg PO 3-4 times/d

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Contraindications

Documented hypersensitivity; severe CHF; sick sinus syndrome or second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Depresses impulse formation, AV block, negative inotropism, and vasodilation, which can result in hypotension, shock, pulmonary edema, and death; hepatocellular injury may occur; transient elevations of transaminases levels with or without concomitant elevations in alkaline phosphatase and bilirubin levels have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver function periodically

Flunarizine

Not available in the US.

Dosing

Adult

10 mg PO qhs

Pediatric

Not established; suggested dosing includes
<40 kg: 5 mg PO qd
>40 kg: 10 mg PO qd

Interactions

Avoid with beta-blockers

Contraindications

Documented hypersensitivity; depression; extrapyramidal symptoms

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause drowsiness

Antihistamines

These agents prevent histamine response in sensory nerve endings and blood vessels. They are more effective in preventing histamine response than in reversing it.

Cyproheptadine (Periactin)

Occasionally useful for migraine prophylaxis. An antihistamine that has been used for migraine prevention in children more than in adults. Usually well tolerated. Mechanism of action not clarified and hypotheses include antihistaminic and anti-5-HT 2 effects.

Dosing

Adult

4 mg PO bid/tid; not to exceed 20 mg/d

Pediatric

<2 years: Not established
2-6 years: 2 mg PO bid/tid; maximum dose 12 mg/d
6-14 years: 4 mg PO bid/tid; maximum dose 16 mg/d
>14 years: Administer as in adults

Interactions

Potentiates effects of CNS depressants; MAOIs may prolong and intensify anticholinergic and sedative effects of antihistamines

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; stenosing peptic ulcer; symptomatic prostatic hypertrophy; bladder neck obstruction; pyloroduodenal obstruction; lower respiratory tract symptoms

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with a predisposition to urinary retention, history of bronchial asthma, increased intraocular pressure, hyperthyroidism, cardiovascular disease, or hypertension; may thicken bronchial secretions caused by anticholinergic properties and may inhibit expectoration and sinus drainage

Tricyclic antidepressants

These agents are used for migraine prophylaxis that is effective independent of antidepressant effect. Mechanism of action is unknown. These agents inhibit activity of such diverse agents as histamine, 5-HT, and acetylcholine.

Amitriptyline (Elavil)

Tricyclic antidepressant used traditionally for migraine prophylaxis. Antimigraine effect is independent from antidepressant effects. Mechanism of action is not clear, but possibly is due to enhanced central serotoninergic and noradrenergic. Cannot be formally recommended for individuals <12 y. Amitriptyline also has been used for long-term prophylactic treatment of chronic tension-type headache. Mechanism of action is possibly central serotonin enhancement but has never been proven.

Dosing

Adult

10-175 mg PO qd; effective dosage varies; start at 25 mg qhs, increase by 10 mg qwk; highest dosages used for patients with comorbid depression

Pediatric

<12 years: 1-10 mg PO hs
>12 years: 10-25 mg PO; titrate up slowly

Interactions

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase amitriptyline levels; amitriptyline inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Contraindications

Documented hypersensitivity; use of MAOIs within 14 d of initiating therapy; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances and history of hyperthyroidism, renal or hepatic impairment; avoid using in elderly persons

Anticonvulsants

Anticonvulsants, particularly those that interact with the GABAergic system, seem to have a positive effect in reducing migraine attacks. Valproate and gabapentin are most commonly used in this manner.

Topiramate (Topamax)

Indicated for migraine headache prophylaxis. Precise mechanism unknown, but the following properties may contribute to its efficacy: (1) electrophysiological and biochemical evidence showing blockage of voltage-dependent sodium channels, (2) augments the activity of the neurotransmitter GABA at some GABA-A receptor subtypes, (3) antagonizes AMPA/kainate subtype of the glutamate receptor, and (4) inhibits the carbonic anhydrase enzyme, particularly isozymes II and IV.

Dosing

Adult

100 mg/d PO divided bid

Pediatric

<2 years: Not established
>2 years: 50 mg/d PO divided bid

Interactions

Phenytoin, carbamazepine, and valproic acid can significantly decrease topiramate levels; reduces digoxin and norethindrone levels, when administered concomitantly; concomitant use with carbonic anhydrase inhibitors may increase risk of renal stone formation and should be avoided; extreme caution when administering concurrently with CNS depressants since may have an additive effect in CNS depression as well as other cognitive or neuropsychiatric adverse events

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Risk of developing a kidney stone formation is increased 2-4 times that of untreated population; risk may be reduced by increasing fluid intake; caution in renal or hepatic impairment; patients taking topiramate should seek immediate medical attention if they experience blurred vision or periorbital pain; continued usage after symptoms develop can lead to glaucoma; primary treatment is discontinuation of topiramate; if left untreated, serious sequelae, including permanent vision loss, may occur
Oligohidrosis and hyperthermia have been reported predominantly in children during vigorous exercise or exposure to warm environmental temperatures (ensure proper hydration prior and during activity and warm temperatures); may cause hyperchloremic, nonanion gap metabolic acidosis or acute or chronic metabolic acidosis resulting in hyperventilation and nonspecific symptoms, such as fatigue and anorexia, or more severe adverse effects including cardiac arrhythmias or stupor; chronic, untreated metabolic acidosis may increase nephrolithiasis or nephrocalcinosis risk, osteomalacia (ie, rickets in pediatric patients), or osteoporosis with an increased risk for bone fractures; chronic metabolic acidosis in pediatric patients may also reduce growth rates; measure baseline and periodic serum bicarbonate

Valproic acid (Depakote, Depakene)

Delayed-release or extended-release dosage forms are used for prophylaxis of migraine headaches. Although mechanism of action is not established, activity may be related to increased brain levels of GABA, or enhanced GABA action.

Dosing

Adult

Delayed-release: 250 mg PO bid initially; may titrate upward, not to exceed 1000 mg/d divided bid
Extended-release: 500 mg PO qd initially; may increase dose, not to exceed 1000 mg/d

Pediatric

<10 years: Not established
>10 years: 250 mg PO bid; 1000 mg/d maximum

Interactions

Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce valproate levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); valproate may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in HIV-seropositive patients

Contraindications

Documented hypersensitivity; hepatic disease/dysfunction; hyperammonemic encephalopathy and urea cycle disorders

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and >135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis/coagulation disorder occur; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness

Follow-up

Inpatient & Outpatient Medications

• Acetazolamide
• Ondansetron

Patient Education

Benign coital headache: If coital headaches have been a problem for a significant period of time, the patient or couple may need psychological counseling.

References

1. Lipton RB, Bigal ME. Migraine: epidemiology, impact, and risk factors for progression. Headache. Apr 2005;45 Suppl 1:S3-S13. [Medline].

2. Cutrer FM, O'Donnell A, Sanchez del Rio M. Functional neuroimaging: enhanced understanding of migraine pathophysiology. Neurology. 2000;55(9 Suppl 2):S36-45. [Medline].

3. Goadsby PJ. Migraine pathophysiology. Headache. Apr 2005;45 Suppl 1:S14-24. [Medline].

4. Tomsak RL, Jergens PB. Benign recurrent transient monocular blindness: a possible variant of acephalgic migraine. Headache. Feb 1987;27(2):66-9. [Medline].

5. Evers S, Bahra A, Goadsby PJ. Coincidence of familial hemiplegic migraine and hemicrania continua? A case report. Cephalalgia. Jun 1999;19(5):533-5. [Medline].

6. Feely MP, O'Hare J, Veale D, Callaghan N. Episodes of acute confusion or psychosis in familial hemiplegic migraine. Acta Neurol Scand. Apr 1982;65(4):369-75. [Medline].

7. Hayashi R, Tachikawa H, Watanabe R, Honda M, Katsumata Y. Familial hemiplegic migraine with irreversible brain damage. Intern Med. Feb 1998;37(2):166-8. [Medline].

8. Kors EE, Melberg A, Vanmolkot KR, Kumlien E, Haan J, Raininko R. Childhood epilepsy, familial hemiplegic migraine, cerebellar ataxia, and a new CACNA1A mutation. Neurology. Sep 28 2004;63(6):1136-7. [Medline].

9. Spacey SD, Vanmolkot KR, Murphy C, van den Maagdenberg AM, Hsiung RG. Familial hemiplegic migraine presenting as recurrent encephalopathy in a Native Indian family. Headache. Oct 2005;45(9):1244-9. [Medline].

10. Spranger M, Spranger S, Schwab S, Benninger C, Dichgans M. Familial hemiplegic migraine with cerebellar ataxia and paroxysmal psychosis. Eur Neurol. 1999;41(3):150-2. [Medline].

11. Barbour PJ, Castaldo JE, Shoemaker EI. Hemiplegic migraine during pregnancy: unusual magnetic resonance appearance with SPECT scan correlation. Headache. Mar 2001;41(3):310-6. [Medline].

12. Benatar M, Ford CC, Ford CM. Familial hemiplegic migraine: more than just a headache. Neurology. Feb 22 2005;64(4):592-3. [Medline].

13. Butteriss DJ, Ramesh V, Birchall D. Serial MRI in a case of familial hemiplegic migraine. Neuroradiology. May 2003;45(5):300-3. [Medline].

14. Crawford JS, Konkol RJ. Familial hemiplegic migraine with crossed cerebellar diaschisis and unilateral meningeal enhancement. Headache. Oct 1997;37(9):590-3. [Medline].

15. Koenderink JB, Zifarelli G, Qiu LY, et al. Na,K-ATPase mutations in familial hemiplegic migraine lead to functional inactivation. Biochim Biophys Acta. May 15 2005;1669(1):61-8. [Medline].

16. Wieser T, Mueller C, Evers S, Zierz S, Deufel T. Absence of known familial hemiplegic migraine (FHM) mutations in the CACNA1A gene in patients with common migraine: implications for genetic testing. Clin Chem Lab Med. Mar 2003;41(3):272-5. [Medline].

17. May A, Ophoff RA, Terwindt GM, Urban C, van Eijk R, Haan J. Familial hemiplegic migraine locus on 19p13 is involved in the common forms of migraine with and without aura. Hum Genet. Nov 1995;96(5):604-8. [Medline].

18. Barrett CF, Cao YQ, Tsien RW. Gating deficiency in a familial hemiplegic migraine type 1 mutant P/Q-type calcium channel. J Biol Chem. Jun 24 2005;280(25):24064-71. [Medline].

19. Beauvais K, Cave-Riant F, De Barace C, et al. New CACNA1A gene mutation in a case of familial hemiplegic migraine with status epilepticus. Eur Neurol. 2004;52(1):58-61. [Medline].

20. Brugnoni R, Leone M, Rigamonti A, Moranduzzo E, Cornelio F, Mantegazza R. Is the CACNA1A gene involved in familial migraine with aura?. Neurol Sci. Apr 2002;23(1):1-5. [Medline].

21. Kraus RL, Sinnegger MJ, Koschak A, Glossmann H, Stenirri S, Carrera P. Three new familial hemiplegic migraine mutants affect P/Q-type Ca(2+) channel kinetics. J Biol Chem. Mar 31 2000;275(13):9239-43. [Medline].

22. Melliti K, Grabner M, Seabrook GR. The familial hemiplegic migraine mutation R192Q reduces G-protein-mediated inhibition of P/Q-type (Ca(V)2.1) calcium channels expressed in human embryonic kidney cells. J Physiol. Jan 15 2003;546(Pt 2):337-47. [Medline].

23. Ophoff RA, Terwindt GM, Vergouwe MN, Frants RR, Ferrari MD. Familial hemiplegic migraine: involvement of a calcium neuronal channel. Neurologia. Dec 1997;12 Suppl 5:31-7. [Medline].

24. Ambrosini A, D'Onofrio M, Grieco GS, Di Mambro A, Montagna G, Fortini D. Familial basilar migraine associated with a new mutation in the ATP1A2 gene. Neurology. Dec 13 2005;65(11):1826-8. [Medline].

25. Gardner K. The genetic basis of migraine: how much do we know?. Can J Neurol Sci. Nov 1999;26 Suppl 3:S37-43. [Medline].

26. Jurkat-Rott K, Freilinger T, Dreier JP, Herzog J, Gobel H, Petzold GC. Variability of familial hemiplegic migraine with novel A1A2 Na+/K+-ATPase variants. Neurology. May 25 2004;62(10):1857-61. [Medline].

27. Marconi R, De Fusco M, Aridon P, et al. Familial hemiplegic migraine type 2 is linked to 0.9Mb region on chromosome 1q23. Ann Neurol. Mar 2003;53(3):376-81. [Medline].

28. Vanmolkot KR, Babini E, de Vries B, Stam AH, Freilinger T, Terwindt GM, et al. The novel p.L1649Q mutation in the SCN1A epilepsy gene is associated with familial hemiplegic migraine: genetic and functional studies. Mutation in brief #957. Online. Hum Mutat. May 2007;28(5):522. [Medline].

29. Haan J, Kors EE, Terwindt GM, et al. Alternating hemiplegia of childhood: no mutations in the familial hemiplegic migraine CACNA1A gene. Cephalalgia. Oct 2000;20(8):696-700. [Medline].

30. Swoboda KJ, Kanavakis E, Xaidara A, et al. Alternating hemiplegia of childhood or familial hemiplegic migraine? A novel ATP1A2 mutation. Ann Neurol. Jun 2004;55(6):884-7. [Medline].

31. Lance JW. Is alternating hemiplegia of childhood (AHC) a variant of migraine?. Cephalalgia. Oct 2000;20(8):685. [Medline].

32. Alsup S, Fogelson MH. Alternating hemiplegic migraine in childhood. J Neurosci Nurs. Dec 1991;23(6):381-5. [Medline].

33. Kors EE, Vanmolkot KR, Haan J, et al. Alternating hemiplegia of childhood: no mutations in the second familial hemiplegic migraine gene ATP1A2. Neuropediatrics. Oct 2004;35(5):293-6. [Medline].

34. Black DF. Sporadic and familial hemiplegic migraine: diagnosis and treatment. Semin Neurol. Apr 2006;26(2):208-16. [Medline].

35. Black DF. Sporadic hemiplegic migraine. Curr Pain Headache Rep. Jun 2004;8(3):223-8. [Medline].

36. Thomsen LL, Olesen J. Sporadic hemiplegic migraine. Cephalalgia. Dec 2004;24(12):1016-23. [Medline].

37. Dora B, Balkan S. Sporadic hemiplegic migraine and Sturge-Weber syndrome. Headache. Feb 2001;41(2):209-10. [Medline].

38. Kuhn WF, Kuhn SC, Daylida L. Basilar migraine. Eur J Emerg Med. Mar 1997;4(1):33-8. [Medline].

39. Lapkin ML, Golden GS. Basilar artery migraine. A review of 30 cases. Am J Dis Child. Mar 1978;132(3):278-81. [Medline].

40. La Spina I. Basilar artery migraine: transcranial Doppler EEG and SPECT from the aura phase to the end. Headache. 1997;37(1):43-7.

41. Evans RW, Linder SL. Management of basilar migraine. Headache. May 2002;42(5):383-4. [Medline].

42. Catto-Smith AG, Ranuh R. Abdominal migraine and cyclical vomiting. Semin Pediatr Surg. Nov 2003;12(4):254-8. [Medline].

43. Crevits L, Bosman T. Migraine-related vertigo: towards a distinctive entity. Clin Neurol Neurosurg. Feb 2005;107(2):82-7. [Medline].

44. Cupini LM, Santorelli FM, Iani C, et al. Cyclic vomiting syndrome, migraine, and epilepsy: a common underlying disorder?. Headache. Apr 2003;43(4):407-9. [Medline].

45. Gupta VK. Cyclic vomiting syndrome: anticipatory stress response in migraine?. Headache. Jan 2004;44(1):106-7. [Medline].

46. Li BU. Cyclic vomiting syndrome: age-old syndrome and new insights. Semin Pediatr Neurol. Mar 2001;8(1):13-21. [Medline].

47. Olson AD, Li BU. The diagnostic evaluation of children with cyclic vomiting: a cost-effectiveness assessment. J Pediatr. Nov 2002;141(5):724-8. [Medline].

48. d'Onofrio F, Cologno D, Buzzi MG, Petretta V, Caltagirone C, Casucci G. Adult abdominal migraine: a new syndrome or sporadic feature of migraine headache? A case report. Eur J Neurol. Jan 2006;13(1):85-8. [Medline].

49. Blau JN, MacGregor EA. Retinal migraine. Lancet. Nov 6 1993;342(8880):1185. [Medline].

50. Pradhan S, Chung SM. Retinal, ophthalmic, or ocular migraine. Curr Neurol Neurosci Rep. Sep 2004;4(5):391-7. [Medline].

51. Doyle E, Vote BJ, Casswell AG. Retinal migraine: caught in the act. Br J Ophthalmol. Feb 2004;88(2):301-2. [Medline].

52. Evans RW, Daroff RB. Expert opinion: monocular visual aura with headache: retinal migraine?. Headache. Jul-Aug 2000;40(7):603-4. [Medline].

53. Grosberg BM, Solomon S, Lipton RB. Retinal migraine. Curr Pain Headache Rep. Aug 2005;9(4):268-71. [Medline].

54. Appleton R, Farrell K, Buncic JR. Amaurosis fugax in teenagers. A migraine variant. Am J Dis Child. Mar 1988;142(3):331-3. [Medline].

55. Killer HE, Forrer A, Flammer J. Retinal vasospasm during an attack of migraine. Retina. Apr 2003;23(2):253-4. [Medline].

56. Tourbah A, Mas JL, Baron JC, Bousser MG. Complicated migraine, migrainous infarction ... or what?. Headache. Nov 1988;28(10):689. [Medline].

57. Gladstone JP, Dodick DW. Migraine and cerebral white matter lesions: when to suspect cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Neurologist. Jan 2005;11(1):19-29. [Medline].

58. Agostoni E, Aliprandi A. The complications of migraine with aura. Neurol Sci. May 2006;27 Suppl 2:S91-5. [Medline].

59. Glenn AM, Shaw PJ, Howe JW, Bates D. Complicated migraine resulting in blindness due to bilateral retinal infarction. Br J Ophthalmol. Mar 1992;76(3):189-90. [Medline].

60. Milligan TA, Bromfield E. A case of "migralepsy". Epilepsia. 2005;46 Suppl 10:2-6. [Medline].

61. Friedenberg S, Dodick DW. Migraine-associated seizure: a case of reversible MRI abnormalities and persistent nondominant hemisphere syndrome. Headache. Jun 2000;40(6):487-90. [Medline].

62. Mateo I, Foncea N, Vicente I, et al. Migraine-associated seizures with recurrent and reversible magnetic resonance imaging abnormalities. Headache. Mar 2004;44(3):265-70. [Medline].

63. Weiss AH, Phillips JO. Ophthalmoplegic migraine. Pediatr Neurol 2004. 2006;30(1):64-6.

64. Ferrante E. Ophthalmoplegic migraine. Cephalalgia. Mar 2006;26(3):357; author reply 357-8. [Medline].

65. Lee TG, Choi WS, Chung KC. Ophthalmoplegic migraine with reversible enhancement of intraparenchymal abducens nerve on MRI. Headache. Feb 2002;42(2):140-1. [Medline].

66. Levin M, Ward TN. Ophthalmoplegic migraine. Curr Pain Headache Rep. Aug 2004;8(4):306-9. [Medline].

67. Doran M, Larner AJ. MRI findings in ophthalmoplegic migraine: nosological implications. J Neurol. Jan 2004;251(1):100-1. [Medline].

68. Nezu A, Kimura S, Ohtsuki N, Tanaka M, Takebayashi S. Acute confusional migraine and migrainous infarction in childhood. Brain Dev. Mar 1997;19(2):148-51. [Medline].

69. Ossipova VV, Kolosova OA, Vein AM. Migraine associated with panic attacks. Cephalalgia. Oct 1999;19(8):728-31. [Medline].

70. Sheth RD, Riggs JE, Bodensteiner JB. Acute confusional migraine: variant of transient global amnesia. Pediatr Neurol. Feb 1995;12(2):129-31. [Medline].

71. Kitamura K, Kudo Y. Benign recurrent vertigo in Japanese. Auris Nasus Larynx. 1990;17(4):211-6. [Medline].

72. Thakar A, Anjaneyulu C, Deka RC. Vertigo syndromes and mechanisms in migraine. J Laryngol Otol. Oct 2001;115(10):782-7. [Medline].

73. Fournier JA, Fernandez-Cortacero JA, Granado C, Gascón D. Familial migraine and coronary artery spasm in two siblings. Clin Cardiol. Mar 1986;9(3):121-5. [Medline].

74. Athwal BS, Lennox GG. Acetazolamide responsiveness in familial hemiplegic migraine. Ann Neurol. Nov 1996;40(5):820-1. [Medline].

75. Kothare SV. Efficacy of flunarizine in the prophylaxis of cyclical vomiting syndrome and abdominal migraine. Eur J Paediatr Neurol. 2005;9(1):23-6. [Medline].

Keywords

migraine equivalents, migraine aura without headache, familial hemiplegic migraine, sporadic hemiplegic migraine, alternating hemiplegic migraine, basilar type migraine, childhood periodic syndromes, cyclic vomiting, abdominal migraine, benign paroxysmal vertigo of childhood, retinal migraine, ocular migraine, vertiginous migraine, vestibular migraine, migrainous infarction, migraine triggered seizure

Contributor Information and Disclosures

Author

Rima M Dafer, MD, MPH, FAHA, Associate Professor, Department of Neurology and Neurological Surgery, Loyola University, Chicago Stritch School of Medicine
Rima M Dafer, MD, MPH, FAHA is a member of the following medical societies: American Academy of Neurology, American Headache Society, and American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Joseph Carcione Jr, DO, MBA, Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans
Joseph Carcione Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Robert A Egan, MD, Director of Neuro-Ophthalmology, St Helena Hospital
Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

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