Migraine-associated vertigo

Migraine-associated vertigo (MAV) is defined as vertigo or dizziness caused by migraine. Approximately 10% of the population has migraine headaches, and one-third of persons with migraine experience dizziness, so the prevalence of MAV can be estimated as approximately 3% of the population. Using stricter criteria (outlined on the following page), the prevalence has been estimated at nearly 1% of the population. By way of comparison, the prevalence of Ménière’s disease has been estimated to be 2 per 1000, or 0.2%. Thus, MAV is approximately 5 to 10 times more common than Ménière’s disease.

The literature concerning migraines in general is immense, and an exhaustive review is impractical. The literature specifically about MAV is also large, and there are several excellent recent reviews of this topic. This article focuses on the salient features of dizziness as a manifestation of migraine, concentrating on the points of diagnosis and management of interest to the otolaryngologist.

Definition of migraine-associated vertigo

Although there is no universally recognized definition for MAV, several recent studies have employed criteria originally proposed by Neuhauser and Lempert. These criteria are extensions of the definition of migraine as proposed in the International Classification of Headache Disorders (2nd Edition) ( ICHD-II ) and are as follows:

• 
  

  Definite vestibular migraine

  
  
  
  
  • 1.
    

    Episodic vestibular symptoms of at least moderate severity.

    
    
  • 2.
    

    One of the following:

    
    
    
    
    • •
      

      Current or previous history of migraine according to the ICHD‑II .

      
      
    • •
      

      Migrainous symptoms during two or more attacks of vertigo (Migrainous headache, photophobia, phonophobia, visual aura, or other aura).

    
    
    
    
  • 3.
    

    Other causes ruled out by appropriate investigations.

  
  
  
  
• 
  

  Probable vestibular migraine

  
  
  
  
  • 1.
    

    Episodic vestibular symptoms of at least moderate severity.

    
    
  • 2.
    

    One of the following:

    
    
    
    
    • •
      

      Current or previous history of migraine according to the ICHD‑II .

      
      
    • •
      

      Migrainous symptoms during vestibular symptoms.

      
      
    • •
      

      Migraine precipitants of vertigo in more than 50% of attacks (food triggers, sleep irregularities, or hormonal change)

      
      
    • •
      

      Response to migraine medications in more than 50% of attacks.

    
    
    
    
  • 3.
    

    Other causes ruled out by appropriate investigations.

  
  

Definition of migraine-associated vertigo

Although there is no universally recognized definition for MAV, several recent studies have employed criteria originally proposed by Neuhauser and Lempert. These criteria are extensions of the definition of migraine as proposed in the International Classification of Headache Disorders (2nd Edition) ( ICHD-II ) and are as follows:

• 
  

  Definite vestibular migraine

  
  
  
  
  • 1.
    

    Episodic vestibular symptoms of at least moderate severity.

    
    
  • 2.
    

    One of the following:

    
    
    
    
    • •
      

      Current or previous history of migraine according to the ICHD‑II .

      
      
    • •
      

      Migrainous symptoms during two or more attacks of vertigo (Migrainous headache, photophobia, phonophobia, visual aura, or other aura).

    
    
    
    
  • 3.
    

    Other causes ruled out by appropriate investigations.

  
  
  
  
• 
  

  Probable vestibular migraine

  
  
  
  
  • 1.
    

    Episodic vestibular symptoms of at least moderate severity.

    
    
  • 2.
    

    One of the following:

    
    
    
    
    • •
      

      Current or previous history of migraine according to the ICHD‑II .

      
      
    • •
      

      Migrainous symptoms during vestibular symptoms.

      
      
    • •
      

      Migraine precipitants of vertigo in more than 50% of attacks (food triggers, sleep irregularities, or hormonal change)

      
      
    • •
      

      Response to migraine medications in more than 50% of attacks.

    
    
    
    
  • 3.
    

    Other causes ruled out by appropriate investigations.

  
  

Pathophysiology of migraine-associated vertigo

Migraine has been recognized for centuries and has been studied intensively, yet its pathophysiology remains poorly understood. The mechanistic framework used throughout this review combines the ideas that migraine sufferers are more sensitive to many types of unpleasant sensory input and that when there is an overload of adverse sensory input, a threshold is triggered resulting in a cortical event followed by brainstem events, causing even more sensory input to be perceived as noxious, generally resulting in severe headache and temporary shutdown of the individual.

There is good evidence that the brain of persons with migraine is hyperexcitable. Persons with migraine are more likely to experience discomfort from bright light, loud sound, smells, and motion as well as many other sensory inputs that are not disturbing to non-migraineurs. Some studies report thickening of sensory cortex. Migraine sufferers are almost always extraordinarily sensitive during their headaches but also are often more sensitive at baseline, even outside of their migraine headaches. As an example, patients with migraines often give a history of susceptibility to motion sickness. Studies have found that 45% of children with migraines and 50% of adults with migraines report a history of being highly susceptible to motion sickness. In other words, migraines are hard-wired.

The vascular theory of headache proposes that migraine aura represents vasoconstriction and cortical hypoxia. It is now believed that vascular dysregulation is only part of the pathophysiology. Migraine aura is now thought to represent a cortical neuronal process. Research on migraine aura, such as the cortical spreading depression of Leão and the changes in blood flow in the occipital cortex demonstrated in migraineurs with certain visual auras, implicates both vascular dysregulation and abnormal electrical activity.

Research regarding the pain associated with migraines as well as the response to serotonin agonists, such as triptans, implicates dysfunction of trigeminal brainstem circuits. The vasodilator peptide, calcitonin gene–related peptide (CGRP), is found in the cell bodies of trigeminal neurons. CGRP probably modulates vascular nociception and has been heavily implicated in the headache of migraine. There may be a positive feedback loop in which sensory overload triggers cortical circuitry that causes release of CGRP, which increases painful input. Triptans, acting as 5-hydroxytryptamine1B/D agonists, block these responses.

In MAV, the same general mechanisms have been proposed. Patients with MAV commonly report unusual discomfort from motion as well as visual input. Motion sickness symptoms, punctuated by dizziness attacks, may occur with or without headache.

Common historical features of migraine-associated vertigo

Although this article uses the term vertigo , patients may use a variety of descriptions for the disequilibrium that they experience. One recent study of MAV found that the most common vestibular symptom was rotational vertigo (70%), followed by intolerance of head motion (48%) and positional vertigo (42%). Intolerance of visual motion is another common complaint. Less common symptoms include a sensation of motion sickness, floating, rocking, tilting, walking on an uneven surface, and lightheadedness. The chronology is similarly variable, with onset ranging from gradual to abrupt. Neuhauser and colleagues found the most common duration to be 5 to 60 minutes (33%), followed by 1 to 24 hours (21%), seconds to 5 minutes (18%), and more than 24 hours (2%). Cutrer and Baloh proposed that the mechanism of short vertigo attacks was aura whereas longer attacks were due to processes resembling central sensitization.

MAV and migraine headaches need not be simultaneous. Neuhauser and colleagues reported that during symptoms of MAV, 45% of patients consistently have migraine headache, 48% of patients sometimes have migraine headache, and 6% of patients never have migraine headache. During MAV, 70% of patients have photophobia, 64% have phonophobia, and 36% have auras other than vertigo.

A minority of patients are able to identify triggers for MAV, and these usually are similar to triggers for other migraines. Putative triggers documented in clinical practice can be numerous, but some recur far more frequently than others. Common weather-related triggers include storm fronts (ie, rapid changes in barometric pressure) and changes of season. Common activity triggers include physical exertion, dehydration, sleep deprivation, menses, and exposure to bright light. Common dietary triggers include caffeine (or change in the pattern of caffeine intake), chocolate, alcohol, aged cheeses, monosodium glutamate, and nitrites. Although the time lapse between trigger exposure and symptom manifestation is usually on the order of minutes to hours, occasionally the trigger is delayed. For this reason, it is worthwhile for patients to spend several weeks maintaining a symptom and dietary log.

Patients with migraines also have aural complaints. Of patients with both migraines and dizziness, 66% report phonophobia, 63% report tinnitus, 32% report hearing loss, and 11% report fluctuating hearing loss and aural fullness.

Demographics and risk factors of migraine-associated vertigo

The prevalence of MAV using the criteria discussed previously has been estimated at 0.98%. Similar to migraine in general, it affects women approximately 3 times more frequently than men.

Migraine in general occurs with greater than chance frequency in association with several important otologic disorders. Approximately 10% of the general population has migraine. Approximately one-third of patients with BPPV have migraines, with a higher percentage in female (43%) than male patients (21%). Radke and coworkers reported that 56% of patients with Ménière’s disease also have symptoms meeting criteria for migraines. The mechanism for the association between otologic entities and MAV remains unclear.

Physical examination in migraine-associated vertigo

A patient who has MAV and no other illnesses typically has a normal examination. One exception to this is that patients with migraine (including MAV) may have nystagmus that, although usually not observable on direct inspection, may be discernible with video Frenzel goggle examination.