Migraine and Vertigo Claire is a 48-year-old female with progressive hearing loss in the right ear for the past year and a three- to four-month history of recurrent severe episodes of vertigo, nausea, diaphoresis, and unsteadiness. She notes that the spells occur spontaneously and typically last hours, with symptoms exacerbated by movement. She ... Features
Free
Features  |   October 01, 2009
Migraine and Vertigo
Author Notes
  • Jaynee A. Handelsman, PhD, CCC-A, is the assistant director of the Vestibular Testing Center in the Department of Otolaryngology-Head and Neck Surgery at the University of Michigan Health System. She has provided oversight of clinical programs in the evaluation and management of patients with balance system disorders for more than 15 years. Her ongoing clinical research examines the impact of aminoglycosides on vestibular system function. Contact her at jaynee@med.umich.edu.
    Jaynee A. Handelsman, PhD, CCC-A, is the assistant director of the Vestibular Testing Center in the Department of Otolaryngology-Head and Neck Surgery at the University of Michigan Health System. She has provided oversight of clinical programs in the evaluation and management of patients with balance system disorders for more than 15 years. Her ongoing clinical research examines the impact of aminoglycosides on vestibular system function. Contact her at jaynee@med.umich.edu.×
Article Information
Balance & Balance Disorders / Features
Features   |   October 01, 2009
Migraine and Vertigo
The ASHA Leader, October 2009, Vol. 14, 14-17. doi:10.1044/leader.FTR1.14132009.14
The ASHA Leader, October 2009, Vol. 14, 14-17. doi:10.1044/leader.FTR1.14132009.14
Claire is a 48-year-old female with progressive hearing loss in the right ear for the past year and a three- to four-month history of recurrent severe episodes of vertigo, nausea, diaphoresis, and unsteadiness. She notes that the spells occur spontaneously and typically last hours, with symptoms exacerbated by movement. She says she feels exhausted for a day or two following each episode. Claire cannot identify any specific triggers of her spells, although she notes occasional sensitivity to light and sound as well as blurred vision coincident with the spells. Previously, she has had occasional headaches. Claire reports episodic tinnitus, aural fullness, and hearing loss in the right ear only, but has no previous middle-ear pathology or otologic surgery. During her episodes, her moderately disabling symptoms interfere with both work and social activities.
Given Claire’s symptoms, what possible diagnoses would be considered in the differential, and what additional pieces of information would you need to make a diagnostic decision? How might the response to treatment be used to provide more information about the accuracy of the initial diagnosis?
Although the link between migraine and vertigo has been discussed in the literature since the late 1800s, systematic studies of the relationship between vertigo and migraine did not begin until the 1980s. Over the past few decades, various groups have described the clinical features of migrainous vertigo (MV) through large case series (Neuhauser, Leopold, von Brevern, Arnold, & Lempert, 2001; Vukovic, Plavec, Galinovic, Lovrencic-Huzjan, Budisic, & Demarin, 2007), yet a clear understanding of the pathophysiology of the syndrome is lacking. Furthermore, although anecdotal accounts report the effects of various treatments on MV, appropriately controlled studies are scarce. Part of the problem is the lack of internationally accepted diagnostic criteria and consistent nomenclature for MV. Various terms, including “migraine-related vestibulopathy,” “vestibular migraine,” “migraine-related dizziness,” and “benign recurrent vertigo” have been used to describe the diagnosis in patients who have vertigo thought to be caused by migraine.
In a clinical environment, the goal is to determine the origin of symptoms for a patient in order to provide appropriate treatment. Because dizziness and vertigo rank among the most common symptoms reported in the general population, and because they are frequently seen in patients with migraine, clinicians must determine whether the patient has MV (vertigo that is caused by migraine) or whether the dizziness is due to an unrelated cause. The clinician’s ability to make that diagnostic distinction is complicated by the vestibular and non-vestibular disorders, such as Meniere’s disease (MD) and benign paroxysmal positional vertigo (BPPV), that often co-occur with migraine but for which the pathophysiologic link is not clear. This discussion will provide an overview of current knowledge about the relationship between vertigo and migraine.
Diagnostic Criteria
To understand this relationship, it is helpful to begin with a definition of terms. Vertigo is the sensation of movement when there is none and can involve the perception of self-movement or of the environment shifting. Migraine is a clinical syndrome whose diagnostic criteria are specified by the International Headache Society (IHS, 2006). Headache is the symptom that most people attribute to migraine, but there are several types of migraine, some of which do not include headache. Vertigo is not included as a symptom in the IHS classification of migraine in adults except as it relates to basilar migraine, which includes vertigo as an aura in 60% of patients (Sturzenegger & Meienberg, 1985). According to published case series papers, fewer than 10% of patients who have MV fulfill the criteria for basilar migraine (Dieterich & Brandt, 1999; Neuhauser et al., 2001). As a result, most adult patients with MV cannot be classified using current IHS criteria. Proposed operational diagnostic criteria of MV include two separate diagnostic categories: definite MV and probable MV (Neuhauser, Leopold, von Brevern, Arnold, & Lempert, 2001). The proposed criteria treat MV as an episodic vestibular disorder and provide a framework for careful definition of the core syndrome (Table 1 [PDF]). Specifically, the distinction between vertigo—which is typically associated with vestibular disorders—and nonspecific lightheadedness, giddiness, and pre-syncope—which are not typically vestibular in origin—is important. However, some patients have trouble describing their symptoms. Additionally, not all patients with mild vestibular system dysfunction experience true vertigo.
Epidemiologic Associations of Migraine and Vertigo
Migraine as a clinical syndrome can occur at any age and reportedly affects about 16% of the adult population (Lempert & Neuhauser, 2005). Dizziness is one of the most common complaints in medicine, with an estimated lifetime prevalence of roughly 20%–30% (Kroenke & Price, 1993; Yardley, Owen, Nazareth, & Luxon, 1998). Given the relatively high frequency of occurrence of these two symptoms, coincidence alone would predict that large numbers of people would have both migraine and dizziness. The literature suggests that the association between the two is actually much higher than predicted by chance alone (Neuhauser, Radtke, von Brevern, Feldmann, Lezius, Ziese, & Lempert, 2006). For example, in a study that compared the lifetime prevalence of migraine, vertigo, and MV in 200 consecutive patients seen in a dizziness clinic, 200 age- and gender-matched controls from an orthopedic clinic, and 200 patients with migraine who were seen in the authors’ headache clinic, the prevalence of migraine (using IHS criteria) was 1.6 times higher in the dizzy patients than in controls (Neuhauser et al., 2001). The lifetime prevalence of definite MV was 7% in the dizziness group and 9% in the migraine clinic group.
The same group conducted a large population study using structured telephone interviews to determine the prevalence and incidence of vestibular vertigo in the general population and to describe its characteristics (Neuhauser et al., 2005). They reported a lifetime prevalence of dizziness or vertigo in 29.5% of the population. Of the people who reported moderate to severe symptoms, only 24% described their symptoms as including vestibular vertigo, whereas the others described non-vestibular dizziness or dizziness of undetermined origin. Overall, the lifetime prevalence of vestibular vertigo was approximately 7%.
A more recent study also investigated the lifetime prevalence of vertigo and dizziness in patients with migraine headache compared with controls (Vukovic et al., 2007). Both groups were asked about the nature, onset, and frequency of their dizziness symptoms. Those with headaches also were asked about the temporal association between dizziness and migraine headache. The study found that 51.7% of the migraine patients reported dizziness or vertigo of at least moderate severity at some point, whereas 31.5% of the control group reported moderate to severe dizziness. Additionally, examination of the age of symptom onset across groups showed that vertiginous symptoms began earlier in life in those with migraine than in the controls. Finally, of the migraine patients with vertigo, 23.2% met the criteria for definite MV.
These studies support the notion that dizziness and vertigo are common findings in the general population and that the prevalence of vertigo is higher among people who have migraine than in control subjects, but the specific estimates of prevalence vary, due in part to the inclusion criteria used. Specifically, when subjects are asked about vertigo rather than dizziness, the prevalence is lower. Additionally, because many studies are retrospective, the data rely on the memory of symptoms, which may contribute to the variability.
Clinical Features
Migrainous vertigo is clinically heterogeneous and can present with any combination of spontaneous vertigo, positional vertigo, or head motion intolerance. The average age at onset of vertigo in migraine is 37.7 years for women and 42.4 years for men, and women are diagnosed with MV five times more often than men. In people with MV, the onset of migraine headache typically predates vestibular symptoms by 8.4 years. Vertiginous symptoms vary in duration, with approximately half of patients reporting episodes that typically persist from seconds to a full day, with about 25% having symptoms for one or more days per episode (Furman, Marcus, & Balaban, 2003).
In a prospective study aimed at describing the clinical spectrum of acute MV, von Brevern and colleagues evaluated 20 symptomatic patients with acute MV using video-oculography to record eye movements (von Brevern, Zeise, Neuhauser, Clarke, & Lempert, 2005). They also completed a neuro-otologic examination and hearing testing.
Pathological nystagmus was present in 70% of the patients, and all but one had unsteadiness of stance and gait during the symptomatic period. No patient had changes in hearing coincident with the vertigo. The symptoms reported by subjects included spontaneous vertigo, positional vertigo, and vestibular head motion intolerance. The progression from spontaneous vertigo to positional vertigo to head motion intolerance also was reported in some patients. All patients except one reported migrainous symptoms during the observed episode, with photophobia and headache being the most common.
There also is evidence that MV can mimic benign paroxysmal positional vertigo (BPPV). Von Brevern and colleagues (2004) compared true BPPV with episodic positional MV or pseudo-BPPV. For their study, they modified the previously reported criteria for definite migrainous and probable MV in such a way that vestibular symptoms were episodic positional vertigo <1 minute duration. Of the 10 subjects who fulfilled the criteria for MV and presented with pseudo-BPPV, seven reported that the duration of the episodes never exceeded a few hours or days, whereas symptoms typically persist for weeks to months in BPPV without therapy. Additionally, the four subjects who were evaluated during a symptomatic period had positional nystagmus that was not typical of BPPV. The authors concluded that MV is a widely neglected differential diagnosis of positional vertigo.
Pathophysiology
The pathophysiology of migraine, thought to be a genetically based neurological disorder in which certain triggers initiate a series of events, is becoming better understood. According to a review by Goadsby, Lipton, and Ferrari (2002), current models include functional changes occurring in the trigeminal nerve system causing imbalances in brain chemicals, such as serotonin, that regulate pain. As a result, the trigeminal nerve releases chemicals that irritate and cause swelling of blood vessels on the surface of the brain, sending pain signals to the brainstem. Additionally, a cortical-spreading depression-like mechanism has been proposed for explaining auras.
The pathophysiology of MV is less understood, although there are obvious links between central vestibular pathways and proposed mechanisms involved in migraine (Furman et al., 2003). In their review of the possible mechanisms of MV, the authors indicate that the inner ear also is a logical contributor to MV. Specifically, the short-duration vertigo symptoms in MD may be related to vasospasm-induced ischemia, and that repeated transient ischemia could lead to the irreversible damage that is eventually seen in MD. There also is speculation that MV is a manifestation of specific genetic abnormalities causing channelopathies that affect central or peripheral processing. It is noteworthy that research to date does not support a major role in MV for the genetic mutations that are already identified to be involved with two migraine syndromes (von Brevern, Ta, Shankar, Wiste, Siegel, Radtke, Sander, & Escayg, 2006).
Treatment
Treatment of migraine-related dizziness usually entails migraine prevention, although very little objective evidence from controlled studies is available to determine the relative effectiveness of various treatment strategies. Migraine prevention should be a multi-tiered approach that involves avoiding possible triggers, maintaining a healthy lifestyle with regular exercise and balanced meals, and getting plenty of sleep. In some cases, otologic treatments for presumed MD (e.g. low-salt diet and diuretics) may be helpful.
Prophylactic migraine medications can be used if these measures alone are not enough. Although the mechanism of action of these medications is not completely understood, they are thought to work by affecting the balance of certain chemicals in the brain. The major groups of medication used for migraine prevention include beta-blockers, calcium channel blockers, tri-cyclic antidepressants, and anti-epileptic (anti-seizure) medicines. Typically, response to treatment should be evaluated after three months, with a greater than 50% reduction in attack frequency as a realistic goal.
As each patient with migraine is unique, it is impossible to determine which medication will work for an individual patient. In addition, because each of these medications has side effects and possible drug interactions, the choice of medication should be discussed carefully with the patient’s primary health care provider.
Vestibular rehabilitation may be another treatment for some patients with migraine. Wrisley, Whitney, and Furman (2002) studied treatment outcomes in patients with a history of migraine and a diagnosis of an unrelated vestibular disorder and patients with a vestibular disorder without migraine. Both groups demonstrated improvement on subjective and objective (dynamic gait index) measures of handicap following a course of treatment, although the migraine group demonstrated worse scores on all measures than did the subjects without a migraine history. The researchers concluded that vestibular physical therapy was beneficial to all subjects, and vestibular rehabilitation may be a valid treatment option for patients with ongoing symptoms secondary to MV.
Meniere’s Disease
The relationship between MV and MD has been studied by many in an effort to determine the proportion of patients with MD who have a history of migraine and to examine the prevalence of MD in patients diagnosed with migraine. It is clear that patients with MD have an increased lifetime prevalence of migraine, and that as many as 45% of patients with MD have at least one migrainous symptom (e.g., headache, photophobia, phonophobia) during vertiginous attacks. The co-morbidity between MD and MV may be a result of a common pathogenesis or MV interactions such that migraine can lead to MD or MD can trigger migraine. It is likely that development and implementation of a standard diagnostic approach to MV may help differentiate these possibilities.
Another potential explanation is that overlap in the symptom presentations of the two syndromes may lead to misdiagnoses. Consider, for example, the clinical vignette that opens this article. To investigate that hypothesis, Boismier and Disher (2001) studied patients who were diagnosed with MD but who failed to respond to medical management (low-salt diet and diuretic). When the patients were treated with migraine medications (i.e., verapamil, propranolol, or amitriptyline), their symptoms resolved. This finding supports the inadequacies of the diagnostic criteria that are used to differentiate MD from migraine. Furthermore, it supports the use of initial treatment outcomes, both positively and negatively, to adjust the diagnosis.
Migraine and Benign Paroxysmal Positional Vertigo
As noted earlier, migrainous vertigo can mimic benign paroxysmal positional vertigo. Roberts, Gans, and Kastner (2006) presented a case report of a patient who presented with positional vertigo that was initially thought to be horizontal canal BPPV. She was treated with a particle repositioning maneuver for cupulolithiasis of the horizontal canal, which did not result in decreased symptoms or in a change in nystagmus. When the patient noted that she had a migrainous headache with a week-long bout of vertigo, the authors concluded that she was experiencing migraine positional vertigo (MPV) rather than horizontal canal BPPV. She was referred to a neurotologist who prescribed Topamax, which resulted in complete resolution of her symptoms. This finding reinforces the need for clear diagnostic criteria, as well as the importance of a thorough case history and clinical examination. Furthermore, using initial treatment outcomes to refine a diagnosis and treatment plan may be warranted.
The link between migraine and dizziness has been well established, and migrainous vertigo is a syndrome that is becoming better understood. However, the progression of knowledge about the etiology of MV is limited by the absence of internationally accepted diagnostic criteria for the condition. Although functional criteria have been proposed and some researchers have been using them, others have been using criteria that are more broadly defined. As a result, comparison of the data across studies is problematic.
In a patient-care environment, the goal of the clinician is to arrive at a diagnosis to determine a treatment plan. Does Claire have MV or MD? The clinical profile does not clearly eliminate or support either choice, so the diagnostic process likely will include evaluating the outcomes of initial treatment. However, additional acceptance of consistent criteria for MV by researchers and clinicians should result in better understanding of the pathophysiology of the syndrome to evaluate effectiveness. Given the high lifetime prevalence of migraine, dizziness, and MV, additional research in this area is clearly warranted.
Find Out More

Dizziness and Migraine

References
Boismier, T. & Disher, M. (2001). Spontaneous vertigo and headache: endolymphatic hydrops or migraine? ENT Journal, (88), 881–885.
Boismier, T. & Disher, M. (2001). Spontaneous vertigo and headache: endolymphatic hydrops or migraine? ENT Journal, (88), 881–885.×
Dieterich, M. and Brandt, T. (1999). Episodic vertigo related to migraine (90 cases): vestibular migraine? Journal of Neurology, 246, 883–892. [Article] [PubMed]
Dieterich, M. and Brandt, T. (1999). Episodic vertigo related to migraine (90 cases): vestibular migraine? Journal of Neurology, 246, 883–892. [Article] [PubMed]×
Furman, J.M., Marcus, D.A., & Balaban, C. (2003). Migrainous vertigo: development of a pathogenic model and structured diagnostic interview. Current Opinion in Neurology, 16(1), 5–13. [Article] [PubMed]
Furman, J.M., Marcus, D.A., & Balaban, C. (2003). Migrainous vertigo: development of a pathogenic model and structured diagnostic interview. Current Opinion in Neurology, 16(1), 5–13. [Article] [PubMed]×
Goadsby, P.J., Lipton, R.B., & Ferrari, M.D. (2002). Drug therapy: migraine—current understanding and treatment. New England Journal of Medicine, 346, 257–270. [Article] [PubMed]
Goadsby, P.J., Lipton, R.B., & Ferrari, M.D. (2002). Drug therapy: migraine—current understanding and treatment. New England Journal of Medicine, 346, 257–270. [Article] [PubMed]×
Harker, L.A. and Rassekh, C. (1988). Migraine equivalent as a cause of episodic vertigo. Laryngoscope, 98, 160–164. [PubMed]
Harker, L.A. and Rassekh, C. (1988). Migraine equivalent as a cause of episodic vertigo. Laryngoscope, 98, 160–164. [PubMed]×
International Headache Society Classification Subcommittee. (2006). IHS Classification ICHC-II. http://ihs-classification.org/en/.
International Headache Society Classification Subcommittee. (2006). IHS Classification ICHC-II. http://ihs-classification.org/en/.×
Kayan, A. and Hood, J.D. (1984). Neuro-otological manifestations of migraine. Brain, 107, 1123–1142. [Article] [PubMed]
Kayan, A. and Hood, J.D. (1984). Neuro-otological manifestations of migraine. Brain, 107, 1123–1142. [Article] [PubMed]×
Lempert, T. & Neuhauser, H. (2005). Migrainous Vertigo. Neurologic Clinics, 23, 715–730. [Article] [PubMed]
Lempert, T. & Neuhauser, H. (2005). Migrainous Vertigo. Neurologic Clinics, 23, 715–730. [Article] [PubMed]×
Neuhauser, H.K. (2007). Epidemiology of Vertigo. Current Opinion in Neurology, 20(1), 40–46. [Article] [PubMed]
Neuhauser, H.K. (2007). Epidemiology of Vertigo. Current Opinion in Neurology, 20(1), 40–46. [Article] [PubMed]×
Neuhauser, H., Leopold, M., von Brevern, M., Arnold, G., & Lempert, T. (2001). The interactions of migraine, vertigo, and migrainous vertigo. Neurology, 56, 436–441. [Article] [PubMed]
Neuhauser, H., Leopold, M., von Brevern, M., Arnold, G., & Lempert, T. (2001). The interactions of migraine, vertigo, and migrainous vertigo. Neurology, 56, 436–441. [Article] [PubMed]×
Neuhauser, H., Radtke, A., von Brevern, M., Feldmann, M., Lezius, F., Ziese, T., & Lempert, T. (2006). Migrainous vertigo: Prevalence and impact on quality of life. Neurology, 26, 1028–1033.
Neuhauser, H., Radtke, A., von Brevern, M., Feldmann, M., Lezius, F., Ziese, T., & Lempert, T. (2006). Migrainous vertigo: Prevalence and impact on quality of life. Neurology, 26, 1028–1033.×
Neuhauser, H., von Brevern, M., Radtke, A., Lezius, F., Feldmann, M., Zeise, T., & Lempert, T. (2005). Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology, 65, 898–904. [Article] [PubMed]
Neuhauser, H., von Brevern, M., Radtke, A., Lezius, F., Feldmann, M., Zeise, T., & Lempert, T. (2005). Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology, 65, 898–904. [Article] [PubMed]×
Von Brevern, M., Radtke, A., Clarke, A., & Lempert, T. (2004). Migrainous vertigo presenting as episodic positional vertigo. Neurology, 62, 469–472. [Article] [PubMed]
Von Brevern, M., Radtke, A., Clarke, A., & Lempert, T. (2004). Migrainous vertigo presenting as episodic positional vertigo. Neurology, 62, 469–472. [Article] [PubMed]×
Von Brevern, M., Ta, N., Shankar, A., Wiste, A., Siegel, A., Radtke, A., Sander, T., & Escayg, A. (2006). Migrainous vertigo: mutation analysis of the candidate genes CACNA1A, ATP1A2, SCN1A, and CACNB4. Headache, 1136–1141.
Von Brevern, M., Ta, N., Shankar, A., Wiste, A., Siegel, A., Radtke, A., Sander, T., & Escayg, A. (2006). Migrainous vertigo: mutation analysis of the candidate genes CACNA1A, ATP1A2, SCN1A, and CACNB4. Headache, 1136–1141.×
Von Brevern, M., Zeise, D., Neuhauser, H., Clarke, A., & Lempert, T. (2005). Acute migrainous vertigo: clinical and oculographic findings. Brain, 128(2), 365–374. [PubMed]
Von Brevern, M., Zeise, D., Neuhauser, H., Clarke, A., & Lempert, T. (2005). Acute migrainous vertigo: clinical and oculographic findings. Brain, 128(2), 365–374. [PubMed]×
Vukovic, V., Plavec, D., Galinovic, I., Lovrencic-Huzjan, , Budisic, M., & Demarin, V. (2007). Prevalence of vertigo, dizziness, and migrainous vertigo in patients with migraine. Headache, 47, 1427–1435. [Article] [PubMed]
Vukovic, V., Plavec, D., Galinovic, I., Lovrencic-Huzjan, , Budisic, M., & Demarin, V. (2007). Prevalence of vertigo, dizziness, and migrainous vertigo in patients with migraine. Headache, 47, 1427–1435. [Article] [PubMed]×
Wrisley, D., Whitney, S., & Furman, J. (2002). Vestibular rehabilitation outcomes in patients with a history of migraine. Otology and Neurotology, 2.
Wrisley, D., Whitney, S., & Furman, J. (2002). Vestibular rehabilitation outcomes in patients with a history of migraine. Otology and Neurotology, 2.×
0 Comments
Submit a Comment
Submit A Comment
Name
Comment Title
Comment


This feature is available to Subscribers Only
Sign In or Create an Account ×
FROM THIS ISSUE
October 2009
Volume 14, Issue 13