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

Migraine-Associated Vertigo

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

Introduction

Background

Migraine is a disease characterized by periodic headaches, but patients often experience other symptoms, including dizziness. In some patients, dizziness can be the only symptom.

Since the 19th century, repeated references have been made to the clinical association of migraine and dizziness. Over the years, several syndromes have been reported of episodic vertigo associated with migraine. Some of these syndromes include benign paroxysmal vertigo of childhood and benign recurrent vertigo in adults. Some authors have even suggested an association between migraine and Ménière disease.

In 1984, Kayan and Hood reported a significant increase in the frequency of vertigo in people with migraines versus people with tension headaches.¹ Vertigo is also a known symptom of basilar artery migraine, which is a special form of migraine (see the International Headache Society classification of migraine, below). Although the definition of migraine-related vertigo and the continuum of the symptom complex remains poorly defined, the relationship is clearly more than a chance association.

One well-controlled study evaluated 200 patients from a migraine clinic, a dizziness clinic, and a control group from an orthopedic clinic. The group presenting with vertigo showed a higher lifetime prevalence of migraine (38%) than a similar group of patients in the control group (24%, P < 0.01). Similar findings have been seen in studies evaluating migraine patients. Vertigo, as well as chronic nonspecific symptoms of vestibular system dysfunction, can be related to all forms of migraine.

The manifestations of migraine-associated vertigo are quite varied and may include episodic true vertigo, positional vertigo, constant imbalance, movement-associated dysequilibrium, and/or lightheadedness. Symptoms can occur prior to the onset of headache, during a headache, or, as is most common, during a headache-free interval. As such, many patients who experience migraines have vertigo or dizziness as the main symptom rather than headache. For this reason, this article is devoted to the description of migraine-associated vertigo.

Migraine headaches are recurrent headaches often accompanied by nausea and light sensitivity separated by symptom-free intervals. The headaches typically have a throbbing quality, are relieved after sleep, and may be accompanied by visual symptoms, dizziness, or vertigo. Patients often have a family history of migraine. Migraine can be divided into 2 categories, migraine without aura (common migraine, 90% of migraine headache cases) and migraine with aura (classic migraine, 10% of cases).

Basilar migraine, also known as Bickerstaff syndrome (1961), is an important variant of migraine with aura. Bickerstaff syndrome consists of 2 or more symptoms (ie, vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields of both eyes, diplopia, bilateral paresthesias or paresis, decreased level of consciousness) followed by a throbbing headache.

• Migraine without aura (formally called common migraine)
  • Headache attacks last 4-72 hours untreated. In children younger than 15 years, headache may last 2-48 hours.
  • Headache has at least 2 of the following characteristics:
    • Unilateral location
    • Pulsating quality
    • Moderate or severe intensity that inhibits or prohibits daily activities
    • Aggravation by walking up stairs or similar routine physical activity
  • During headache, at least 1 of the following occurs:
    • Nausea and/or vomiting
    • Photophobia and phonophobia
  • At least 1 of the following occurs:
    • History and physical examination findings do not suggest another disorder.
    • History and physical examination findings do suggest another disorder, but the other disorder is ruled out by appropriate investigations (eg, MRI or CT scanning of the head).
• Migraine with aura (formally called classic migraine)
  • Aura with at least 2 attacks of the following:
    • One reversible aura symptom indicating focal CNS dysfunction (ie, vertigo, tinnitus, decreased hearing, ataxia, visual symptoms in one hemifield of both eyes, dysarthria, double vision, paresthesias, paresis, decreased level of consciousness)
    • Aura symptom that develops gradually over more than 4 minutes or 2 or more symptoms that occur in succession
    • No aura symptom that lasts more than 60 minutes unless more than one aura symptom is present
    • Headache occurring before, during, or up to 60 minutes after aura is completed
  • Headache - Same as that for migraine without aura
• Migraine with prolonged aura - Fulfills criteria for migraine with aura but the aura lasts more than 60 minutes and less than 7 days
• Basilar migraine (replaces basilar artery migraine) - Fulfills criteria for migraine with aura but 2 or more aura symptoms of the following types occur: vertigo, tinnitus, decreased hearing, ataxia, visual symptoms in both hemifields of both eyes, dysarthria, double vision, bilateral paresthesias, bilateral paresis, and decreased level of consciousness
• Migraine aura without headache (replaces migraine equivalent or acephalic migraine) - Fulfills criteria for migraine with aura but no headache occurs
• Childhood periodic syndromes that may be precursors to or be associated with migraine
• Benign paroxysmal vertigo of childhood
  • Brief sporadic episodes of dysequilibrium, anxiety, and often nystagmus or vomiting
  • Normal neurologic examination findings
  • Normal findings on electroencephalography
• Migrainous infarction (replaces complicated migraine)
  • Patient has previously fulfilled criteria for migraine with aura.
  • The present attack is typical of previous attacks, but neurologic deficits are not completely reversible within 7 days and/or neuroimaging demonstrates ischemic infarction in relevant area.
  • Other causes of infarction are ruled out by appropriate investigations.

Pathophysiology

The pathophysiology of migraine-associated vertigo is not completely understood, however both central and peripheral defects have been observed. In 1992, Cutrer and Baloh developed the most commonly accepted theory regarding the pathophysiology of migraine-associated vertigo.² These authors propose that episodes of dizziness of a duration similar to that of a migraine aura (<60 min) that are time-locked with the headache most likely have the same pathophysiologic mechanism (eg, spreading wave of depression) as other aura phenomena.

According to the spreading depression theory, some type of stimulus (eg, chemical, mechanical) results in a transient wave front that suppresses central neuronal activity. This depression spreads in all directions from its site of origin. Neuronal depression is accompanied by large ion fluxes, including increases in extracellular K⁺ and decreases in extracellular Ca⁺⁺. These changes result in a reduction in cerebral blood flow in the areas of spreading depression. However, most patients with migraine-associated vertigo have dizziness independently of the headache.

Cutrer and Baloh suggest that when dizziness is unrelated to headache, the dizziness occurs from the release of neuropeptides (ie, neuropeptide substance P, neurokinin A, calcitonin gene–related peptide [CGRP]).² Neuropeptide release has an excitatory effect on the baseline firing rate of the sensory epithelium of the inner ear, as well as on the vestibular nuclei in the pons.

Asymmetric neuropeptide release results in the sensation of vertigo. When neuropeptide release is symmetric, the patient feels an increased sensitivity to motion due to an increased vestibular firing rate during head movements. Cutrer and Baloh also propose that CGRP and other neuropeptides may produce a prolonged hormonelike effect as these peptides diffuse into the extracellular fluid.² This may explain the prolonged symptoms in some patients with migraine-associated vertigo, as well as the typical progression of persistent spontaneous vertigo followed by benign positional vertigo then motion sensitivity.

Some authors have suggested that peripheral cochleovestibular dysfunction in migraine patients may be attributed to vasospasm of the internal auditory artery causing ischemia to the labyrinth. Furthermore, Lee et al have reported a positive association of progesterone receptor (PGR) with migraine-associated vertigo.³

Serotonin (5-HT) has also been found to be an important substrate in the development of migraine. Interestingly, 5-HT has direct effects on the firing rate of vestibular nucleus neurons. Both the serotonergic and the peptidergic pathways possibly play a role in the development of the short and prolonged periods of dizziness in migraine-associated vertigo. No single hypothesis explains the headache or dizziness process in migraine at this time. Thus, the causes of the symptoms of migraine remain controversial.

Frequency

United States

Migraine is an extremely common disorder worldwide. Migraine occurs in 18% of women and in 6% of men, totaling 25-28 million people in the United States alone. The disease is most prevalent in women of childbearing age, with an approximate prevalence of 25% in 35-year-old women. Overall, episodic vertigo occurs in about 25-35% of all migraine patients. Using these figures, roughly 3.0-3.5% of people in the United States have episodic vertigo and migraine. Comparatively, the prevalence of Ménière disease (a peripheral vestibular disorder with symptoms overlapping that of migraine-associated vertigo) is estimated to be 0.2% of the US population.

Sex

The epidemiology of migraine-associated vertigo corresponds to that of migraine in general. Migraine is present in 18% of females and in 6% of males aged 12-80 years. Peak ages are 30-45 years.

Clinical

History

As with any type of dizziness evaluation, the history is the most important means to diagnose migraine-associated vertigo. Patients with migraine-related vestibulopathy typically experience a varied range of dizzy symptoms throughout their life and even within individual attacks. These symptoms may be solitary or may be a combination of vertigo, lightheadedness, or imbalance. At the time of presentation, dizziness symptoms may have been present for a few weeks or for several years. Vertigo may occur spontaneously, provoked by head motion or provoked by visual stimuli. Symptoms may last for a few minutes or may be continuous for several weeks or months. In women, dizziness may often occur during the menstrual cycle.

• Patients with migraine-associated vertigo often provide a long history of motion intolerance during car, boat, or air travel or all 3. Some patients are very sensitive to motion of the environment and to busy environments. Vertigo, which is an illusion of movement of the environment or of the patient in relation to the environment, is the most common type of dizziness reported. Vertigo is present at some time in approximately 70% of patients. The attacks of vertigo may awaken patients and are usually spontaneous, but they may be provoked by motion.
• The duration of the vertigo can also be quite variable. When vertigo is present, it may be indistinguishable from the spontaneous vertigo of Ménière disease. One clue that the vertigo is not of the Ménière type is that the vertigo of migraine-associated vertigo may last longer than 24 hours. In fact, a rocking sensation may be a continuous feeling for many weeks to months. In contrast, the vertigo of Ménière disease typically does not last longer than 24 hours. (For further information regarding migraine-associated vertigo and Ménière disease, see Differentials and Table 1). The frequencies of different durations of vertigo spells in migraine-associated vertigo are as follows:
  • A duration of seconds (7%)
  • A duration of minutes to up to 2 hours (31%)
  • A duration of 2-6 hours (5%)
  • A duration of 6-24 hours (8%)
  • A duration longer than 24 hours (49%)
• Unexplained sensorineural hearing loss has been variously reported in 0-31% of unselected patients with migraine. Changes in sensorineural hearing are rarely a significant feature of migraine-related vertigo and help to differentiate it from other causes of vertigo, especially Ménière disease. Up to 80% of patients with basilar migraine have been reported to have sensorineural hearing loss. The hearing loss of basilar migraine often affects the lower frequencies and may be bilateral. Fluctuation is also possible, similar to the sensorineural hearing loss of Ménière disease. Unlike in Ménière disease, the sensorineural hearing loss rarely progresses.

 [#targettable1]Table 1. A Comparison of the Symptoms of Migraine-Associated Vertigo and Ménière Disease 

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Table

Symptom	Migraine-Associated Vertigo	Ménière Disease
Vertigo	May last >24 h	Lasts £24 h
Sensorineural hearing loss	Very uncommon; when present, often low frequency; very rarely progressive; may fluctuate in cases of basilar migraine	Nearly always progressive; most often unilateral; may be bilateral; fluctuation is common
Tinnitus	May be unilateral or bilateral; rarely obtrusive	May be unilateral or bilateral; often of significant intensity
Photophobia	Often present; may or may not be associated with dizziness	Never present unless a concurrent history of migraine exists

Symptom	Migraine-Associated Vertigo	Ménière Disease
Vertigo	May last >24 h	Lasts £24 h
Sensorineural hearing loss	Very uncommon; when present, often low frequency; very rarely progressive; may fluctuate in cases of basilar migraine	Nearly always progressive; most often unilateral; may be bilateral; fluctuation is common
Tinnitus	May be unilateral or bilateral; rarely obtrusive	May be unilateral or bilateral; often of significant intensity
Photophobia	Often present; may or may not be associated with dizziness	Never present unless a concurrent history of migraine exists

• A thorough headache history is also important when evaluating patients for possible migraine-associated vertigo. Many patients with recurrent headaches are unaware that their headaches may be from migraine. Therefore, the examining physician should have a thorough knowledge of the strict diagnostic criteria for migraine diagnosis (see the International Headache Society classification of migraine, in Background).
• Patients may or may not have a history of concurrent migraine headaches. In fact, most patients have dizziness symptoms during headache-free intervals or even numerous years following their last migraine headache. Some patients with migraine-associated vertigo have never experienced a migraine headache but have a family history of migraine.
• No diagnostic tests exist for migraine-associated vertigo. The diagnosis is made by clinical history or, when the history is unclear, by a therapeutic response to treatment. A definite diagnosis of migraine-associated vertigo can be made when patients have migraine with aura that is accompanied by concurrent episodes of vertigo or when they have migraine without aura that is repeatedly associated with vertigo immediately before or during the headache.
• A probable diagnosis of migraine-associated vestibulopathy is suggested when patients experience recurrent or continuous vertigo or dizziness sensations without neurologic symptoms, when the dizziness is not time-locked to headache, when a past or family history of migraine headaches exists, and when the dizziness cannot be fully explained by other vestibular disorders. In these patients, a trial of migraine therapy can be started for both diagnostic and therapeutic purposes.
• Proposed criteria by Neuhauser and Lempert for diagnosis of definite migrainous vertigo are as follows:⁴
  • Episodic vestibular symptoms of at least moderate severity (rotational vertigo, other illusory self or object motion, positional vertigo, head motion intolerance, ie, sensation of imbalance or illusory self or object motion that is provoked by head motion)
  • Migraine according to the IHS criteria
  • At least one of the following migrainous symptoms during at least 2 vertiginous attacks: migrainous headache, photophobia, phonophobia, visual or other auras
  • Other causes ruled out by appropriate investigations
• Proposed criteria for diagnosis of probable migrainous vertigo are as follows:
  • Episodic vestibular symptoms of at least moderate severity (rotational vertigo, other illusory self or object motion, positional vertigo, head motion intolerance)
  • At least one of the following: migraine according to the criteria of the IHS; migrainous symptoms during vertigo; migraine-specific precipitants of vertigo, eg, specific foods, sleep irregularities, hormonal changes; response to antimigraine drugs
  • Other causes ruled out by appropriate investigations

Physical

Findings on a complete neurotologic examination are often normal. Horizontal rotary spontaneous nystagmus may be present during an acute attack of vertigo. Dix-Hallpike examination may elicit symptoms of vertigo or nonvertigo dizziness, each without nystagmus.

Causes

Migraine headache and migraine-associated vertigo are often triggered by certain factors. These factors include stress, anxiety, hypoglycemia, fluctuating estrogen, certain foods, and smoking.

Genetics

The genetic cause of a rare type of migraine has been discovered. Familial hemiplegic migraine, a form of migraine with aura, is associated with mutations in the CACNA1A gene located on chromosome arm 19p13. This gene codes for a neuronal calcium channel. Defects involving this gene are also involved with other autosomal dominant disorders that have neurologic symptoms (see Table 2, below). One example is that of episodic ataxia type 2 (EA2), which is also known as periodic vestibulocerebellar ataxia and acetazolamide-responsive hereditary paroxysmal cerebellar ataxia). In cases of EA2, a pH abnormality has been discovered, and it often resolves with medication (eg, acetazolamide, valproic acid, calcium channel blocker).

Table 2. CACNA1A Gene Defects Associated With Autosomal Dominant Disorders With Neurologic Symptoms*

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* Adapted from Tusa, 1999⁵

^† ENG

^‡ SCA6

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