eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Vertigo & Dizziness

Migraine-Associated Vertigo: Treatment & Medication

Author: Aaron G Benson, MD, Clinical Adjunct Professor, Division of Neurotology, Department of Otolaryngology Head and Neck Surgery, University of Michigan; Consulting Staff, Toledo Ear, Nose and Throat, Inc
Coauthor(s): Davin W Chark, MD, Staff Physician, Department of Otolaryngology, University of California Irvine Medical Center; Hamid R Djalilian, MD, Associate Professor of Otolaryngology, Director of Neurotology and Skull Base Surgery, University of California Irvine Medical Center; Wayne K Robbins, DO, FAOCO, Program Director, Department of Otolaryngology-Facial Plastic Surgery, Genesys Regional Medical Center, Michigan State University; Robert A Battista, MD, FACS, Assistant Professor of Otolaryngology, Northwestern University Medical School; Physician, Ear Institute of Chicago, LLC
Contributor Information and Disclosures

Updated: Nov 20, 2008

Treatment

Medical Care

Because most patients equate migraine with headache exclusively, convincing them that symptoms other than headache are due to migraine may be difficult. Dizziness secondary to migraine usually responds to the same treatment used for migraine headaches. The 3 broad classes of migraine headache treatment include a reduction of risk factors, abortive medications, and prophylactic medical therapy.

In general, drugs used to abort migraine headaches have not been found effective in treating dizziness secondary to migraine. Reduction of risk factors includes an attempt to avoid certain conditions (eg, stress, anxiety, hypoglycemia, fluctuating estrogen, certain foods, smoking) that can trigger migraine. Elimination of birth control pills or estrogen replacement products may be helpful. Specific foods to avoid are discussed in the Diet section. Prophylactic medications are described in the Medication section.

Consultations

Consultation with a neurologist is warranted if the patient has or develops focal neurologic deficits, if the patient develops migrainous infarction (see International Headache Society classification of migraine in the Background section), or if the examining physician is uncomfortable using prophylactic medications that may be appropriate in the treatment of migraine-associated vertigo.

Diet

Avoiding certain foods helps fewer than 25-30% of all people who experience migraines. In general, the following foods should be avoided: monosodium glutamate (MSG), certain alcoholic beverages (eg, red wine, port, sherry, scotch, bourbon), aged cheese (eg, Colby, Roquefort, Brie, Gruyere, cheddar, bleu, mozzarella, Parmesan, Boursault, Romano), chocolate (including carob), and aspartame. MSG is often found in certain soups, Chinese food and fast food, soy sauce, yeast, yeast extract, meat tenderizers, seasoned salt, and several salad dressings.

Because dietary restrictions are helpful in fewer than 25-30% of migraine cases, an elimination diet for 1 month may be prescribed. If, after 1 month, symptoms are not better, diet modification is not helpful. If foods are a trigger for symptoms, the offending food(s) can be identified by adding back one food at a time until symptoms return. A food diary is an alternative option to an elimination diet. A food diary may be helpful because certain foods cause migraine symptoms almost immediately (eg, red wine, MSG), whereas other foods (eg, chocolate, cheese) may cause symptoms the next day. The diary should include all foods consumed for 24 hours prior to the onset of a dizzy spell.

Medication

Prophylactic medical therapy should be used when migraine-associated vertigo occurs several times a month, is continuous over several weeks or months, or has severely affected the patient's lifestyle. First-line prophylactic medications include calcium channel blockers (verapamil), tricyclic antidepressants (nortriptyline), and beta-blockers (propranolol). Second-line treatment includes topiramate, valproic acid, venlafaxine, and methysergide. Acetazolamide has also been reported as an effective treatment by several authors.

The actual mechanism of action for migraine control with these medications is unknown. However, the calcium channel blockers, tricyclic antidepressants, beta-blockers, and methysergide are believed to block the release of neuropeptides into dural blood vessel walls because of their antagonist effect on 5-HT2 receptors.

One class of prophylactic medication does not seem to be more effective than the others. Therefore, unless contraindicated, verapamil is often used initially because this medication has the lowest side effect profile among the prophylactic medications. If dizziness is not controlled with one class of medication, another class should be used. If dizziness is controlled with one of these medications, the drug should be administered continuously for at least 1 year (except for methysergide, which requires a 3- to 4-wk drug-free interval at 6 mo). The medication can be restarted for another year if the dizziness returns after discontinuing therapy.

Calcium channel blockers

This agent inhibits 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.

Adult

Starting dosage: 120-240 mg/d; not to exceed 480 mg/d; start at closest dosage in equivalent weight in pounds; titrate upward until symptoms relieved or severe constipation develops; clinical response usually observed in 2-8 wk after maximum tolerated dose started

Pediatric

Not established

Verapamil 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 verapamil levels; verapamil may increase theophylline levels

Documented hypersensitivity; systolic pressure of <90 mm Hg; cardiac conduction abnormalities; gastrointestinal obstruction; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension

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

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver function periodically

Tricyclic antidepressants

Mechanism of action is unknown. These agents inhibit the activity of such diverse agents as histamine, 5-HT, and acetylcholine.


Nortriptyline (Aventyl, Pamelor)

By inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, this drug increases the synaptic concentration of these neurotransmitters in the central nervous system.
Pharmacodynamic effects such as the desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play a role in its mechanisms of action.

Adult

10 mg/d PO for 1 wk initially; if tolerated, increase in 10- or 25-mg increments; not to exceed 100 mg/d; may have some benefit in 7-10 d but most require 4-8 wk at therapeutic dosages to observe beneficial effects. Alternatively, it can be started 25mg/d qhs for 3 weeks with increase in 25mg increments every 3 weeks up to 75mg/d.

Pediatric

Not established

Cimetidine may increase nortriptyline levels when used concurrently; nortriptyline may increase prothrombin time in patients stabilized with warfarin

Documented hypersensitivity; history of cardiac disease/arrhythmia; closed-angle glaucoma; thyroid disease; ileus; urinary retention

Pregnancy

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

Precautions

Drowsiness, dry mouth, constipation, and photosensitivity are common side effects; urinary retention also possible; when discontinued, dosage should be tapered over 2 wk to prevent rebound cholinergic effects

Beta-adrenergic blockers

These agents are effective in prophylactic therapy, possibly by blocking vasodilators, decreasing platelet adhesiveness and aggregation, stabilizing the membrane, and increasing the release of oxygen to tissues.


Propranolol (Inderal, Betachron ER)

Controls cardiac and psychomotor manifestations within minutes.

Adult

20 mg PO q12h; increase in 20-mg increments q3-7d, depending on patient tolerance and heart rate; not to exceed 240-320 mg/d; use long-acting propranolol (80-120 mg cap) once appropriate dosage found; effect usually observed at 4 wk, but a 3-mo trial at max tolerated dose should be administered before considering patient a nonresponder

Pediatric

1 mg/kg/d PO divided bid initially; increase to maintenance dose of 2-4 mg/kg/d PO divided bid; not to exceed 16 mg/kg/d

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities; orthostatic hypotension; occlusive peripheral vascular disease

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

Adverse effects include fatigue (tends to diminish over the course of a few wk), 10% incidence of impotence, and depression; withdrawal should be tapered over a 2-wk period to prevent rebound headache or angina in patients with preexisting coronary artery disease

Ergot alkaloids and derivatives

These agents are direct vasoconstrictors of smooth muscle in cranial blood vessels. Their activity depends on the CNS vascular tone at the time of administration.


Methysergide (Sansert)

Causes constriction of peripheral and cranial blood vessels.

Adult

2 mg/d PO initially; increase in 2-mg increments q3-4d to maximum of 4-8 mg/d in divided doses for up to 6 mo; a drug-free interval of 3-4 wk should follow each 6-mo course of treatment; dosage should be gradually reduced in 2- to 3-wk period prior to beginning of drug-free interval to prevent rebound headaches; if improvement does not occur within 3 wk of initiation of treatment, methysergide should be weaned and discontinued

Pediatric

Not established

Documented hypersensitivity; angina; coronary artery disease; hypertension; peptic ulcer disease; peripheral vascular disease; pregnancy; pulmonary disease; renal disease; rheumatoid arthritis; thrombophlebitis; valvular heart disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Nausea/vomiting, diarrhea, heartburn, and abdominal pain are common adverse effects (may be minimized with food ingestion); retroperitoneal fibrosis, pulmonary fibrosis, or fibrosis of cardiac tissue rare (drug withdrawal usually reverses these conditions)

Anticonvulsants

Anticonvulsants, particularly those that interact with the GABA-ergic system, seem to have a positive effect in reducing migraine attacks.


Valproic acid (Depakote, Depakene, Depacon)

Chemically unrelated to other drugs that treat seizure disorders. Although mechanism of action not established, activity may be related to increased brain levels of GABA or enhanced GABA action. Valproate may also potentiate postsynaptic GABA responses, affect potassium channel, or have a direct membrane-stabilizing effect.

Adult

250 mg PO bid initially; titrate weekly to maximum 500 mg bid; use ER form (500-mg tab) once appropriate dosage found; titrate to maintain blood level at 75-100 µg/mL; effect may usually be observed at 4 wk

Pediatric

10-15 mg/kg/d PO for children > 2 y; increase dose by 5-10 mg/kg/d at weekly intervals to maximum 60 mg/kg/d depending on patient's symptoms; divide doses >250 mg/kg/d into bid/qid

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 test results); may increase zidovudine levels in HIV seropositive patients

Documented hypersensitivity; hepatic disease; pancreatitis; thrombocytopenia; bone marrow suppression

Pregnancy

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

Precautions

Drowsiness, ataxia, anorexia, nausea, and vomiting may occur; 10% incidence of dose-related hand tremor reported; 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 occurs; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness


Topiramate (Topamax)

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

Adult

Slowly titrate upward at a minimum of 1 wk intervals as follows:
Week 1: 25 mg PO qhs
Week 2: 25 mg PO bid
Week 3: 25 mg PO qAM and 50 mg PO qhs
Week 4: 50 mg PO bid
Week 5: 50 mg PO qAM and 75 mg PO qhs
Week 6: 75 mg PO bid

Pediatric

Not established

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

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 over that of an untreated population (the risk may be reduced with increased 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; the 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, non–anion gap metabolic acidosis, 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

More on Migraine-Associated Vertigo

Overview: Migraine-Associated Vertigo
Differential Diagnoses & Workup: Migraine-Associated Vertigo
Treatment & Medication: Migraine-Associated Vertigo
Follow-up: Migraine-Associated Vertigo
References

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Further Reading

Keywords

migraine-associated vertigo, migraine associated vertigo, migraine, vertigo, migraine vertigo, headaches, dizziness, benign paroxysmal vertigo of childhood, benign recurrent vertigo in adults, basilar artery migraine, basilar migraine, Bickerstaff syndrome, episodic true vertigo, positional vertigo, constant imbalance, movement-associated dysequilibrium, common migraine, migraine without aura, classic migraine, migraine with aura, migraine with prolonged aura, migraine aura without headache, migraine equivalent, acephalic migraine, migrainous infarction, complicated migraine, familial hemiplegic migraine, migraine headaches, migraine headache, migraines

Contributor Information and Disclosures

Author

Aaron G Benson, MD, Clinical Adjunct Professor, Division of Neurotology, Department of Otolaryngology Head and Neck Surgery, University of Michigan; Consulting Staff, Toledo Ear, Nose and Throat, Inc
Aaron G Benson, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Davin W Chark, MD, Staff Physician, Department of Otolaryngology, University of California Irvine Medical Center
Disclosure: Nothing to disclose.

Hamid R Djalilian, MD, Associate Professor of Otolaryngology, Director of Neurotology and Skull Base Surgery, University of California Irvine Medical Center
Hamid R Djalilian, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Neurotology Society, American Society of Gene Therapy, Association for Research in Otolaryngology, Chicago Medical Society, and Illinois State Medical Society
Disclosure: Mind:Set Technologies Ownership interest Other

Wayne K Robbins, DO, FAOCO, Program Director, Department of Otolaryngology-Facial Plastic Surgery, Genesys Regional Medical Center, Michigan State University
Wayne K Robbins, DO, FAOCO is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, and American Osteopathic Association
Disclosure: Nothing to disclose.

Robert A Battista, MD, FACS, Assistant Professor of Otolaryngology, Northwestern University Medical School; Physician, Ear Institute of Chicago, LLC
Robert A Battista, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Jack A Shohet, MD, Associate Clinical Professor, Department of Otolaryngology-Head and Neck Surgery, University of California Irvine; Otolaryngologist, Shohet Ear Associates Medical Group, Inc
Jack A Shohet, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Neurotology Society, American Tinnitus Association, and California Medical Association
Disclosure: Envoy Medical Consulting fee Consulting

Pharmacy Editor

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

Managing Editor

Erik Kass, MD, Chief, Department of Clinical Otolaryngology, Associates in Otolaryngology of Northern Virginia
Erik Kass, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Association for Cancer Research, American Medical Association, and American Rhinologic Society
Disclosure: Nothing to disclose.

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo  Consulting; Medvoy Ownership interest Management position

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