Excerpt from Migraine-Associated Vertigo

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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. Vertigo also is 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 life time 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, and/or movement-associated dysequilibrium. 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.

International Headache Society classification of migraine

• 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

In 1992, Cutrer and Baloh developed the most commonly accepted theory regarding the pathophysiology of migraine-associated vertigo. 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 that occurs independent 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]). 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. 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.

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.

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