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differences in the majority of neuro-otological tests. However, VM patients had
signicantly increased emetic response (more likely to have nausea and/or vomiting) during caloric testing compared to patients with other causes of dizziness [98].
The majority of patients with VM have normal electronystagmography results.
In some studies there have been a number of patients with a unilaterally reduced
vestibular response, abnormal directional preponderance on rotational chair testing, reduced vestibular response on caloric testing [12], increased postural sway
[99, 100] or reduced amplitudes of vestibular myogenic evoked potentials [101,
102]. These results suggest that there is both peripheral and central vestibular
dysfunction present in VM.However, none of these results are sensitive or specic for the diagnosis of VM.It has been considered that testing of combined
stimuli to assess vestibular- visual processing may reveal abnormalities more
consistent with the VM diagnosis. Testing of visually enhanced vestibulo-ocular
reex (VVOR) has been analyzed in migraine patients with vestibular symptoms.
In VVOR testing the rotational chair evaluation of the vestibulo-ocular reex is
performed in a lighted setting with an optokinetic visual stimulus to produce eye
motion. VVOR gain (nystagmus velocity relative to chair rotation speed) has
been found to be elevated in patients with VM [103]. There are no other consistent responses to caloric or vestibular testing in these patients [93, 94]. Thus,
proper diagnosis relies primarily on the astute clinician interpreting the patient’s
clinical symptoms.
Patients and their symptoms can be evaluated with the Dizziness Handicap
Inventory (DHI) [104] a survey used in vestibular disorders to evaluate patient
symptoms and handicap. The average DHI score in a UCSF population of patients
with VM was 49. Recently, a validated disease specic survey from UCSF was
developed specically for use in VM.The Vestibular Migraine Patient Assessment
Tool and Handicap Inventory (VM-PATHI) was validated in 2020 to measure
disease severity in vestibular migraine patients [105]. The VM-PATHI is available on the UCSF Balance and Falls website (
https://ohns.ucsf.edu/balance- falls/
vestibular- migraine). The survey covers cognition, emotional disturbance, dis-
equilibrium symptoms, anxiety, motion sensitivity and headache equivalents
(Fig.11.2). The survey was developed in three phases: in the rst phase a library
of questions for inclusion were developed with experts in neurotology, neurology, audiology and biostatistics, with the aim of high face and content validity.
In the second phase the questions were trialed in a small cohort to determine
readability and ease of use. In the nal phase it was administered to a large group
of patients to determine reliability, internal consistency, test-retest liability, and
was given to controls to assess discriminant validity. It was also compared against
the DHI and quality of life measure (Short Form-36). The nal, validated survey
has 25 questions about symptoms that are scored on a Likert scale ranging from
“no problem” to “problem as bad as it can be.” For the nal survey, Cronbach’s a
was 0.92 and test retest reliability was high (r=0.90, p<0.001) [105]. The survey is responsive to treatment as well.
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D. M. Gillard and J. D. Sharon
Cognition Emotional Disturbance
-Productivity at work
-Difficulty concentrating
-Trouble remembering things
-Fatigue
-Photophobia
-Fear of Falling
-Anxiety
-Lightheadedness
-Dizziness with busy visual
scenes
-Sadness
-Social avoidance
-False sensation of
movement
Motion SensitivityAnxiety
-Spinning vertigo
-Nausea
Disequilibrium
-Phonophobia
-Imbalance
-Difficulty with stairs
-Dizziness with motion
-Difficulty walking
Headache Equivalents
-Head pressure-Motion sickness-Stress
-Ear pressure
-Headache
Fig. 11.2 VM-PATHI questionnaire factors. Principal component analysis of VM-PATHI data
showed six natural groupings within the data set [105]
Differential Diagnosis
It is important to distinguish VM from other common causes of vertigo, while recognizing that sometimes, vestibular disorders can coexist. Symptoms of VM overlap with almost every other cause of dizziness, including benign paroxysmal
positional vertigo (BPPV), Meniere’s disease, superior canal dehiscence syndrome
(SCDS), mal de debarquement syndrome (MdDS), vestibular neuritis, persistent
postural perceptual dizziness (PPPD), and bilateral vestibular hypofunction (BVH).
Like BPPV, VM can cause positional vertigo and nystagmus. Vestibular symptoms in VM generally have longer duration than in BPPV. Although the duration of
vertigo attacks are variable they generally last minutes to hours to days. In BPPV,
acute episodes of vertigo are short, generally lasting under a minute. However, in
both disorders patients can report mild dizziness or disequilibrium symptoms
between attacks which can confound the clinical picture. While the acute nystagmus in VM can be variable it is usually low velocity and low intensity. It can be
horizontal, vertical, or torsional [106]. On the other hand, BPPV nystagmus, when
affecting the posterior canal, is torsional upbeating, provoked by the Dix–Hallpike,
brief latency, and self-limited. The nystagmus of VM can be worsened or provoked
by head movement, generally lasts much longer, and does not tend to fatigue.
However, the picture is often complicated by the fact that there is an increased risk
of BPPV in patients with migraine [107, 108]. It is important for the clinician to
ask patients presenting with dizziness about migrainous features, even when the
diagnosis of BPPV seems clear. Furthermore, those with VM should still be
screened for BPPV.
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VM often has overlapping symptoms with Meniere’s disease. In vestibular
migraine otologic complaints are common, including tinnitus, aural fullness and
subjective hearing loss. In addition, the duration of vertigo can be similar: minutes
to hours. Audiometry is the single most helpful test in trying to distinguish Meniere’s
disease and VM.Vestibular testing in Meniere’s is not always abnormal, however a
unilateral caloric weakness with preserved video head impulse testing is considered
a hallmark of the disease. More recent studies have shown that VM can progress to
objective hearing loss as well [109]. This hearing loss with VM is more likely to be
bilateral and low frequency if present, while hearing loss in Meniere’s is unilateral
and uctuating. However, attempts at complete disentanglement of VM and
Meniere’s may be misguided: there is signicant overlap between them. About half
of Meniere’s patients meet the criteria for migraine [110], far more than expected by
chance. Practically, some Meniere’s patients, especially those with migrainous history or migrainous symptoms during attacks, do respond to migraine medications.
Vestibular paroxysmia also presents with recurrent vertiginous symptoms.
Episodes are recurrent (multiple times per day), spontaneous, and brief (typically
under a minute). It is believed to be caused by pressure induced dysfunction of the
vestibulocochlear nerve, related to compression by the anterior inferior cerebellar
artery [111]. Clinically, the attacks are more brief than seen in VM although the frequent recurrences can make it hard to distinguish from the more persistent vestibular
symptoms of VM.Vestibular paroxysmia can generally be identied with MR imaging showing compression of the eighth cranial nerve. However, MR ndings of blood
vessels impinging the eighth nerve are fairly common, so they need to be correlated
with symptoms and response to medications to diagnose vestibular paroxysmia.
Superior semicircular canal dehiscence syndrome (SCDS) should also be considered in the differential for VM. SCDS is caused by a deciency in the bony labyrinth
and presents with vertigo, disequilibrium, conductive hyperacusis, autophony, conductive hearing loss, pulsatile tinnitus and aural fullness [112]. The vertigo in SCDS
can be triggered by loud noises (Tulio’s phenomenon) or pressure (Hennenbert’s
sign) [113]. SCDS patient’s often also report aural fullness, dizziness between acute
vertigo episodes, brain fog, and phonophobia. All subjective SCDS symptoms can
be seen with vestibular migraine, including pulsatile tinnitus [87]. Therefore, practitioners are advised to keep a high index of suspicion for SCDS, and consider
workup with VEMP and CT scan when appropriate. When migraine and SCDS are
both present, treatment outcomes for SCDS are worse [114].
Mal de Debarquement Syndrome (MdDS) is another disease that can present
with chronic dizziness or imbalance. It is characterized by a persistent sensation of
motion and imbalance often described as a sensation of rocking or swaying. It is
also associated with ear fullness, hyperacusis, fatigue, poor concentration and visual
disturbances [115, 116]. When symptoms clearly are precipitated by sea travel,
resulting in chronic rocking, MdDS is the preferred diagnosis. However, pathophysiology is not completely understood, and many with MdDS respond to migraine
treatment, suggesting there is overlap [117]. Again, like the other disorders on the
differential, patients with migraine have an increased risk of developing
(MdDS) [115].
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Persistent postural-perceptual dizziness (PPPD) is another important cause to
consider in a patient with chronic vertigo. PPPD patients present with vertigo that is
often not described as the classic spinning vertigo variant. They also often report a
feeling of unsteadiness. These symptoms are often exacerbated by upright posture,
active or passive motion or exposure to moving visuals or other complex visual stimuli [118]. It is thought that anxiety and hypervigilance help perpetuate PPPD symptoms [119]. Under current Barany society diagnostic criteria, PPPD is a chronic
disorder (symptoms are present on most days), whereas vestibular migraine is an
episodic disorder (attacks last 5min to 72h). However, in the author’s experience,
many patients with VM have chronic symptoms. Migraine headache is well recognized to have both episodic and chronic variants, and therefore we believe that VM
has episodic variants (with periods of feeling normal), and chronic variants (symptoms present most or all days). The chronic variant can be difcult to separate from
PPPD, and since the pathophysiology of PPPD explains a maladaptive response to a
vestibular challenge, both disorders would be expected to coexist some of the time.
Basilar artery migraine is another migraine syndrome with additional vestibular
symptoms such as vertigo, tinnitus and hyperacusis. However, this syndrome also
presents with additional transient brainstem symptoms including dysarthria, ataxia,
diplopia and decreased consciousness.
Postconcussive syndrome can be symptomatically identical to vestibular
migraine, with dizziness, headache, photophobia, phonophobia, difculty concentrating, and brain fog. The main distinguishing factor is a history of head trauma.
Since treatment options for postconcussive syndrome can be limited, the authors
will try to treat postconcussive dizziness with migraine medications, with variable
success [120].
Other important diseases that should be included in the differential for VM
include the following: vertebrobasilar TIA or stroke, basilar artery thrombosis, vertebral artery dissection, orthostatic hypotension, peripheral neuropathy, multiple
sclerosis, vestibular neuritis, bilateral vestibular loss, seizures and cerebellopontine
angle tumors.
Research shows that patients with VM are often misdiagnosed. In a study using
2008 NIHS data 54% of patients with VM had seen a provider for their complaints,
with an average of 2.1 providers seen [20]. However, despite frequent provider visits, 91% of those that met study criteria for VM did not have a VM diagnosis. The
most common dizziness diagnosis received in these patients was “other health problem,” followed by medication side effects and inner ear infection. Only 2.4% of this
cohort had a diagnosis of migraine [20].
D. M. Gillard and J. D. Sharon
Treatment
Currently, the treatment paradigm for VM generally follows the approach and management of migraine headache. Conservative management of VM consists of stress
reduction, good sleep hygiene, following a regular schedule, treating anxiety,
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avoiding dietary triggers, stabilizing hormone uctuations and avoidance of visual
triggers. Common foods that are avoided include red wine, chocolate, caffeine, processed meats, aged cheeses, tree nuts, bananas, and avocados. There is limited evidence for this, although anecdotally some patients do seem to respond to dietary
restriction. Over-the-counter dietary supplements have been used for treatment
including magnesium, riboavin, feverfew, butterbur, and Coenzyme-Q10. There is
reasonable evidence that magnesium supplementation is helpful with treating
migraine headaches [121].
If conservative management is not successful for treating VM, a variety of prophylactic medications can be used to decrease the frequency and severity of vestibular migraine. Common medications used for classical migraine prophylaxis are used
for VM, including tricyclic antidepressants such as nortriptyline, mixed reuptake
inhibitors, like venlafaxine, antiepileptics, including topiramate, beta-blockers,
such as propranolol and calcium channel blockers such as verapamil [122]. Initial
choice of medication is based on several factors, including concurrent medications,
comorbidities, and side effect prole (Table11.3). The decision to start a daily medication is based on the frequency and severity of attacks. Dosing is increased until
side effects occur, or acceptable therapeutic response is achieved. If no response is
seen at reasonable doses, then another medication is tried. For partial responses,
Table 11.3 Commonly used oral vestibular migraine prophylactic agents (disclaimer—table is
incomplete, consult a drug compendia for full information)
Medication Side effects Contraindications Monitoring
Nortriptyline Weight gain,
sedation, dry
mouth
Topiramate Tingling in
hands/feet,
cognitive
changes,
fatigue, weight
loss
Propranolol Low BP,
worsened
depression
Verapamil Low BP Hypotension, cardiac
Venlafaxine Nighttime
sweating,
elevated BP,
weight loss,
sexual
dysfunction
Recent myocardial
infarction, MAOI use,
Sjogren’s
H/o kidney stones,
acid/base disorders,
kidney failure,
glaucoma. May worsen
balance
Cardiac disease,
asthma, diabetes,
hypotension
disease
MAOI use CMP/lipids annually,
None routinely, but
consider EKG (QT
prolongation), BMP
(SIADH), or psych eval
(worsening depression/
suicidality) as indicated
BMP annually and with
dose changes, annual
ophtho exam
EKG, BP Anxiety,
EKG, BP HTN
suicidality
Also helpful
for
Insomnia,
anxiety,
depression
Weight loss,
seizures
tremor, HTN
Anxiety,
depression,
weight loss
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D. M. Gillard and J. D. Sharon
doses can be increased. For partial responses with dose-limiting side effects, combinations of medications can be helpful.
Acute attacks should also be treated symptomatically. Helpful medications
include antiemetics (e.g., ondansetron, phenergan), and vestibular suppressants
(e.g., meclizine, benzodiazepines). It’s currently unknown if migraine abortives like
triptans are effective in reducing vestibular migraine symptoms, they can be tried
as well.
It has been difcult to determine whether or not treatments are truly effective for
VM.In a 2002 retrospective chart review of 81 VM patients by Repleog etal. [20,
123], 16% of patients had improvement with dietary changes alone, while 66% of
VM patients had complete or signicant symptomatic improvement with medications and 29% had partial symptomatic improvement. In this study patients underwent a stepwise treatment approach which started with dietary changes, then a
tricyclic antidepressant and then another migraine prophylactic agent if that did not
improve symptoms signicantly. In another retrospective chart review study of 32
patients [124], caffeine cessation was effective for 15% of patients, while nortriptyline was effective for 47% of patients who failed caffeine avoidance. In a 2013
randomized prospective trial comparing betahistine and as needed paracetamol plus
or minus unarizine, the unarizine arm had signicantly better vertigo control,
while there was no difference in headache control between groups [125]. In a 2015
randomized prospective trial of venlafaxine versus propranolol, both treatment arms
had signicant improvement in VM symptoms. There was no difference seen in
treatment efcacy based on DHI [125, 126]. It is important to note that this study
did not have a placebo-controlled arm. Although there are a variety of studies, the
majority are not randomized clinical trials and they often do not compare validated
outcome measures to determine efcacy for treatment of vestibular symptoms in VM.
There have also been several investigations into the efcacy of abortive medications for VM treatment, with varying rates of success. Zolmitriptan was studied in a
randomized placebo controlled trial, and did outperform placebo, but there were
very few vestibular migraine attacks so the study did not achieve adequate power for
proper analysis and rm conclusions [125–127]. Sumatriptan improved both vertigo and migraine symptoms in a patient survey [128]. Almotriptan was shown to be
benecial in reducing vertigo during acute VM attacks in an open label, uncontrolled retrospective study of 18 subjects [128, 129]. Rizatriptan was investigated in
a small study of ten subjects, half with vestibular migraine and half with migraine
without dizziness. Subjects were pretreated with either rizatriptan or placebo, and
then exposed to several stimuli intended to provoke motion sickness. Rizatriptan
was shown to decrease motion sickness in VM patients compared to those with
migraine without vertigo [130]. There are also case reports of IV methylprednisolone showing efcacy for severe VM treatment [131].
Although there have been a variety of studies, a recent 2015 Cochrane review
reported that we cannot determine if treatment for VM is effective as there are not
signicantly powered placebo controlled, randomized, clinical trials for VM treatment [132]. The author’s treatment paradigm can be seen in Fig.11.3. General treatment advice is offered in Table11.4.
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Barany criteria for VM
Physical exam
-Neuro exam including:
cerebellar, oculomotor,
cranial nerves
-Otoscopy
-Head impulse test
-Dix Hallpike Maneuver
treatments
Asymmetric hearing
loss present
Audiogram
VM diagnosis
Conservative Management: Stress reduction,
sleep hygiene, avoidance of dietary triggers,
hormone stabilization, avoidance of visual
triggers, supplements (magnesium, riboflavin,
feverfew, butterbur, Coenzyme Q-10),
symptomatic medication for acute attacks
Oral prophylactics
CGRP Blockers
Referral to headache center for
Botox, devices, nerve blocks, IV
Consider Meniere’s
Disease, obtain MRI
If anxiety large portion of
symptoms, consider
mindfulness-based
practice
Vestibular physical
therapy once motion
sensitivity symptoms are
better controlled
Obtain MRI
Vestibular Te sting
Treat for BPPV and
reassess
Treat comorbid:
-Anxiety
-Allergies
-Obstructive sleep apnea
Abnormal
neuro exam
Abnormal head
impulse test
Abnormal Dix-
Hallpike
Fig. 11.3 Algorithm for treatment of vestibular migraine. VM vestibular migraine, CGRP
calcitonin- gene-related peptide
Clinical Trials andFuture Directions
It is clear that prospective, randomized, placebo-controlled clinical trials are needed
to evaluate VM treatment. A recently completed trial, the PROVEMIG trial, was a
placebo-controlled randomized controlled trial studying the efcacy of metoprolol
for the treatment of VM.After randomizing 130 patients the trial had to be discontinued for poor patient accrual. However, there was no signicant difference in incidence of vertigo attacks between the placebo and metoprolol groups when the
available data were analyzed [133].
There are several ongoing trials investigating the efcacy of various treatment
regimes. There are two ongoing trials at UCSF (the author’s institution) for VM
treatment. The rst is a mindfulness based stress reduction (MBSR) trial. MBSR is
an accepted medical therapy for a variety of conditions. The hypothesis for this trial
is that VM patients may benet from MBSR given that there are high rates of medication intolerance, high rates of comorbid anxiety and stress is one of the most
common triggers for VM.The pathophysiology of VM may involve sensory hypersensitivity, hypervigilance, catastrophizing, and functional maladaptation, which
may benet from MBSR therapies. The trial involves a single arm open label prospective trial.
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Table 11.4
• Vestibular migraine is incredibly common. All patients with dizziness should be asked
about: personal history of migraine, family history of migraine, and migrainous symptoms
during attacks.
• Patients will not volunteer information about photophobia or phonophobia during attacks—
this has to be specically inquired about.
• Medication sensitivities are very common with VM.Use low doses of medications to start,
taper on and off, and counsel appropriately.
• Treatment of anxiety, stress, sleep disorders, and allergies may be helpful.
• Audiometry is helpful in distinguishing Meniere’s disease from VM.
• Adequate time should be set aside for patient counseling about diagnosis and treatment
options.
• Vestibular testing is likely to worsen symptoms, therefore consider using it judiciously when
a concurrent issue is suspected.
• Minor brain white matter abnormalities are very commonly seen on FLAIR or T2 MRI
sequences, reassurance to patients can be very helpful regarding those ndings, which
frequently cause alarm.
• Periodic follow-up is usually necessary while nding a specic medication regimen that
works for a particular patient.
• Not all patients require pharmacologic intervention.
• Anxiety is a frequent comorbidity in this population. We nd it most helpful to consider a
disease modier that also requires treatment. Blaming anxiety for dizziness tends to be clinically
counterproductive. We nd that dizziness and anxiety often make each other worse.
• Similar to migraine headache (and despite published criteria) there are likely episodic and
chronic forms of vestibular migraine.
• Many symptoms are shared between superior canal dehiscence and vestibular migraine,
consider working up for superior canal in select cases, especially when objective ndings are
present (weber to one ear, negative bone conduction thresholds, etc.).
Clinical pearls
Another ongoing UCSF trial is the INVESTMENT Trial, INvestigating
VESTibular Migraine Emgality Treatment. This is a double-blind, placebo controlled randomized clinical trial investigating the efcacy of Galcanezumab-gnlm
for the treatment of VM, sponsored by Eli Lilly. The outcomes of the trial are to
compare the VM-PATHI, DHI, and quality of life score between treatment and placebo arms as well as to compare the denitive number of dizzy days assessed
through a daily text message between arms.
There is also a large multicenter, randomized, placebo-controlled clinical trial at
the University of California Los Angeles in conjunction with the Mayo Clinic to
study the effectiveness of rizatriptan in the treatment of VM.At the time of writing
this chapter the trial has been completed, but results are not yet available.
Conclusions
Vestibular migraine is a very common and treatable cause of dizziness. Barriers to
care exist, including underdiagnosis, lack of biomarkers, variable rates of treatment
effectiveness, high rates of comorbid anxiety and depression, and lack of high level
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studies. However, there are diagnostic criteria that are helpful in working up patients,
as well as symptom and disease specic patient-reported outcome measures that are
useful for tracking outcomes. Treatment is generally similar to the treatment of
migraine headaches, with both pharmacologic and nonpharmacologic options.
When possible, care from a multidisciplinary team can improve the patient experience and care outcomes. More work is required to understand pathophysiology,
improve diagnostics, and to understand the effectiveness of different treatment
options.
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