Literature Review
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Which Factors Predict Response to Acute Migraine Treatment?
Demographic variables, headache features, comorbidity, and treatment factors may predict inadequate response to acute migraine treatment at two...
Vertigo is a normal response to certain stimuli, such as looking down from heights and abnormal head movements. In addition, any dysfunction along the pathway that processes balance and gravity information (eg, the semicircular canals, acoustic nerve, and brainstem vestibular centers) can cause vertigo.
Migraine is significantly more common in patients with vertigo, and vertigo is significantly more common in migraineurs than in the general population. In addition, migraineurs are predisposed to motion sickness, which often includes vertigo. Migraineurs’ vestibular systems are more sensitive to stimuli than those of nonmigraine controls, and migraineurs experience vestibular stimulation as more unpleasant and more likely to cause emesis, compared with nonmigraine controls, Dr. Levin said.
The reasons for these correlations are unknown. It may be that heightened vestibular sensitivity in migraine is due to migraineurs perceiving all stimuli more intensely, or migraineurs may be more keenly aware of early signs of vestibulopathy. Vertigo may be a migraine trigger, or a subset of patients may have a type of migraine that includes vertigo as a key symptom, he said. This last possibility is the so-called vestibular migraine.
Vestibular migraine, which also has been known as migraine-associated vertigo, migraine-associated dizziness, and migraine-associated vestibulopathy, has been difficult to define. The current generally accepted definition requires two basic diagnostic criteria: current or previous history of migraine and migraine features (eg, headache, photophobia, phonophobia, or visual aura) with at least half of the spells of vertigo.
Vestibular migraine is estimated to affect about 1% of the general population, 7% of patients at dizziness clinics, and 9% of patients at headache centers.
The duration of vertigo in vestibular migraine varies. About a third of the episodes last for minutes, a third for hours, and a third for days. Vertigo can occur between migraine attacks, prior to them, during, or after, and it tends to be spontaneous. Vestibular migraine is common in children and more common in women than in men. It generally arises years after migraines begin.
Unsteadiness and balance problems are common in vestibular migraine, and audiologic disturbances occur in a minority of patients. Migraine with brainstem aura (formerly called basilar migraine) can include vertigo, but the diagnosis also requires at least one other brainstem symptom (eg, tinnitus or dysarthria).
When seeing patients, neurologists’ first step might be to try to distinguish between vertigo and other similar symptoms, such as presyncope, disorientation, or disequilibrium. “A sense of motion is the best indication of vertigo, though even that might be lacking,” Dr. Levin said.
Neurologists can determine whether position triggers vertigo and identify evidence of peripheral biologic problems (eg, tinnitus, changes in vision, or other focal neurologic signs and symptoms). Family history of migraine in people with episodic vertigo may be a clue that the patient has vestibular migraine versus other causes of vertigo, Dr. Levin said. A history of syncope or other signs may suggest that a patient’s symptoms are related to light-headedness instead of vertigo. Psychiatric illness, time course, drug exposure, and stroke or stroke risk factors also should be considered.
Diagnostic tests may help neurologists distinguish between vestibular migraine and other causes of vertigo. Audiograms can assess for hearing loss, and MRIs may rule out masses or other lesions. Brainstem auditory evoked responses, electronystagmography (ENG), and videonystagmography (VNG), which typically includes saccade, tracking, positional, and caloric testing, also can be useful.
One diagnostic entity that can be mistaken for vestibular migraine is mal de debarquement, which is marked by a persistent feeling of vertigo after a cruise or other motion experience. Patients with this condition also may experience symptoms such as blurred vision, inability to focus, cognitive changes, headaches, nausea, feelings of pressure, and trouble sleeping. “It can actually start sounding like migraine,” Dr. Levin said. “Strangely enough, patients may not mention their disembarkation from a trip. …You have to sometimes draw it out.”
Vestibular testing is normal in these patients, and oddly, they often feel better when they ride in a car or otherwise experience motion. Migraine treatment does not work for these patients. Benzodiazepines may help, but patients may become tolerant. Mal de debarquement tends to dampen and resolve in many patients.
Other causes of vertigo include Meniere’s disease, benign paroxysmal positional vertigo, meningeal infection or inflammation, labyrinthine or brainstem ischemia, perilymph fistula, and benign positional vertigo of childhood.
In the end, some diagnostic entities may be part of a spectrum, Dr. Levin said. Thirty-eight percent of vestibular migraines have auditory symptoms as in Meniere’s disease, and the prevalence of migraine in patients with Meniere’s disease is twice that of the general population. Many patients fit diagnostic criteria for vestibular migraine and Meniere’s disease.
The pathophysiology of vestibular migraine is unknown. Connections between vestibular nuclei in the brainstem and the trigeminal nuclei may underlie the condition. Vestibular and trigeminal nociceptive pathways may be activated in parallel. Alternatively, structural brain lesions in the temporal lobes or elsewhere may cause vestibular migraine.
Like other migraine auras, vestibular migraine may be a manifestation of focal or generalized cortical spreading depression. “There are cortical centers for vertigo,” Dr. Levin said. When these cortical centers are affected in patients with epilepsy, patients may experience “tornado seizures,” he said.
Some studies suggest that migraine treatments might help patients with vestibular migraine. Zolmitriptan and rizatriptan at the time of vertigo have been tried, with some suggestion that they may provide benefit.
The best evidence for pharmacologic prevention exists for flunarizine, propranolol, and lamotrigine. Other trials suggest that vestibular rehabilitation and combined caffeine cessation, nortriptyline, and topiramate may be effective.
Limitations of trials in vestibular migraine have included small numbers of patients, noncontrolled designs, and inconsistent definitions of vestibular migraine. In addition, case reports have suggested that benzodiazepines, cinnarizine, selective serotonin reuptake inhibitors, pizotifen, dothiepin, acetazolamide, and behavioral modification may benefit patients. Investigators are enrolling patients in a double-blind, placebo-controlled trial that will evaluate the use of metoprolol for the preventive treatment of vestibular migraine.
If occurrences of vertigo are infrequent, symptomatic vertigo treatments are Dr. Levin’s first choice. “I have had good luck with scopolamine, for example,” he said. Dopamine antagonists, neuroleptics, sedatives, and benzodiazepines are also useful symptomatic treatments for vertigo. The Epley maneuver and other canalith repositioning maneuvers may benefit some patients. For acute treatment, it makes sense to try a triptan, Dr. Levin said. “Sometimes it does work. Other times it does not, and you have to resort to symptomatic medication,” he said.
—Jake Remaly
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