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J. Gurberg et al.
Table 10.2
indications for
vestibular testing
Table 10.3 Vestibular testing ages for senior author’s testing lab. Note that ages vary widely
between different pediatric vestibular testing centers
Minimum age Tests
6months
3years • Vestibular-evoked myogenic potentials (VEMP), ocular
4years • Video head impulse testing (VHIT), horizontal canals
6years • Video head impulse testing (VHIT), vertical canals
10years • Caloric test
List of
• Differentiate vestibular from nonvestibular conditions
• Differentiate peripheral from central vestibular dysfunction
• Determine if vestibular loss is unilateral versus bilateral
• Conrm a suspected diagnosis
• Quantify degree and etiology of imbalance
• Planning vestibular rehabilitation strategies
• Assessing response to vestibular rehabilitation
• Evaluate for functional disorder
• Evaluate for ctitious disorder (malingering)
• Vestibular-evoked myogenic potentials (VEMP), cervical
• Videonystagmography (VNG)
• Rotary chair
• Computerized dynamic posturography (sensory organization test)
• Subjective visual vertical, static
• Subjective visual vertical, dynamic
many adult vestibular testing centers will not test young children. Fortunately, the
number of pediatric vestibular testing centers is steadily growing and some adult
centers are willing to test younger patients with encouragement. In addition to the
tests summarized below, audiometry is also a key component of the assessment of
most pediatric patients with vestibular complaints, though it is not routinely necessary in adolescents with specic complaints of dizziness/vertigo in the absence of
audiological or otological concerns. Age ranges for each test vary with each testing
center. The ages at which each test can be performed at the senior author’s lab are
summarized in Table10.3, though the tests available and ages at which they can be
done varies greatly between different testing centers. Note that both the rotary chair
and caloric tests only assess the lateral canal VOR, but the latter test is avoided in
children when possible, as it can induce nausea/vomiting and can be difcult for
young children to tolerate. It should also be noted that the interpretation of vestibular testing results is beyond the scope of this chapter and can be found in other
resources on this topic [11, 16, 22–25].
• Videonystagmography (VNG): Video-goggles are used to assess for spontaneous,
gaze-evoked, optokinetic, and positional nystagmus, as well as pursuits and sac-
cades. Caloric testing is included in the adult VNG battery, but it is often avoided
in children. In the absence of spontaneous nystagmus or BPPV, the yield of VNG
in children is generally low. Horizontal and/or torsional nystagmus without xa-
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185
tion suggests an uncompensated peripheral vestibular loss, while vertical or
direction-changing nystagmus, particularly when present with and without xa-
tion, suggest a central cause. Abnormal saccades and pursuits also suggest a
central vestibular and/or oculomotor disorder.
• Caloric Test: Caloric testing typically involves sequential, binaural, bithermal
(warm and cold) water irrigation of the ear canals, though variations of increased
tolerance but decreased sensitivity are available (e.g., air, monothermal, monau-
ral). A reduced vestibular response (or unilateral weakness) score is calculated,
which indicates impairment of the ipsilateral horizontal canal if greater than a
designated set value (usually 20%). This test is often difcult to perform in
young children and can induce nausea/vomiting, so it is generally avoided in
pediatric patients whenever possible. Ice water calorics can be helpful to conrm
a suspected diagnosis of vestibular areexia in children with congenital hear-
ing loss.
• Rotary Chair Test: This test evaluates the horizontal canal VOR and is the gold
standard for diagnosing bilateral vestibular loss. The child is rotated side-to-side
in an arc at varying frequencies in a dark room or cylindrical enclosure. The VOR
response is tracked using an infrared camera in young children and with VNG
goggles in older children (typically 4years of age and older). Computer software
calculates VOR gain, phase lead, and asymmetry scores, which can collectively
be used to determine if a child has VOR impairment of the lateral canal on the
left and right sides. Young children can sit in a parents lap or in a car seat for this
test. An infrared camera mounted to the chair can be used in children who are too
small to wear goggles.
• Video Head Impulse Test (VHIT): VHIT objectively evaluates the HIT using
VNG goggles with an accelerometer. It can evaluate each semicircular canal
individually and is generally better tolerated than caloric or rotary chair testing,
but is of limited sensitivity for mild vestibular losses [23]. Younger children
(<4years of age) typically cannot wear VHIT goggles, but a newer variation of
VHIT that uses an external camera without goggles is now available, though it is
not yet approved for use in the United States as of the time of this writing.
• Vestibular-Evoked Myogenic Potential (VEMP) Test: VEMP uses auditory stim-
uli to induce an electromyographic response in either the sternocleidomastoid
muscle (cVEMP) or the extraocular muscles (oVEMP). The cVEMP assesses the
integrity of the saccule and inferior vestibular nerve, while the oVEMP response
assesses the integrity of the utricle and superior vestibular nerve [25]. It should
be noted that the oVEMP is a newer test than cVEMP, and its role in vestibular
testing remains somewhat controversial. Cervical VEMP can be reliably per-
formed by an experienced examiner at any age, but children generally need to be
a bit older (at least 3years of age) to reliably complete ocular VEMP testing.
• Subjective Visual Vertical (SVV) Test: The patient straightens a tilted line in dark-
ness to their perceived true vertical. A deviation of >2° to one side averaged over
multiple trials suggests an ipsilateral peripheral vestibular loss involving the
utricle [22, 26]. Although abnormalities on SVV can also be indicative of acute
central vestibular losses (mostly cerebrovascular accidents), such events are very
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J. Gurberg et al.
rare in children, making this test a more consistent assessment of peripheral ves-
tibular function in children than in adults. This test requires active participation
of the patient and is generally difcult for children younger than 7years of age
to perform reliably. Dynamic variations of this test exist, which increase its sen-
sitivity and specicity, but are very difcult for children and even many adoles-
cents to tolerate.
• Computerized dynamic posturography (CDP): Sway is evaluating using a force
plate during different balance conditions allowing objective evaluation of bal-
ance compared to age-specic norms and a breakdown of balance impairment
into visual, vestibular, and somatosensory components. Children less than 4years
of age are often unable to t into the harness or follow the instructions for this test.
Pediatric Vestibular Disorders
The relative prevalence of causes of pediatric dizziness and imbalance varies
between studies, though it is well-accepted that migraine represents the most common cause. Table10.4 shows a list of the most common causes from a recent study
of >1000 patients seen for dizziness and/or imbalance at the senior author’s pediatric vestibular program [17]. Notably, although the majority of cases in this study
were found to be migraine in origin, a large proportion were also due to peripheral
vestibular dysfunction and other causes. Of particular note is that BPPV may be
more common in children than previously recognized. Also notable is the fact that
there are many nonvestibular causes of dizziness and imbalance in children, as well.
This study also found that nearly half of patients had more than one concurrent
causative diagnosis. In particular, the diagnoses of vestibular migraine, BPPV, and
persistent postural perceptual dizziness (PPPD) were found to frequently cluster
together in many patients, with BPPV and PPPD likely being secondary phenomena
to vestibular migraine, especially in adolescent females. For the purposes of organization in this chapter, the different diagnoses will be broken down into otological
disorders, neurological disorders, autonomic dysfunction, and functional/psychological disorders. Notably, many optometric/ophthalmologic conditions can also
Table 10.4 Relative
prevalence of most common
causes of pediatric dizziness
(in patients without history of
concussion (n=757)) [17]
Diagnosis %
1. Vestibular migraine 31.0
2. Benign paroxysmal positional vertigo (BPPV) 19.9
3. Primary dysautonomia 14.0
4. Persistent postural perceptual dizziness
(PPPD)
5. Panic/anxiety disorder 11.6
6. Benign paroxysmal vertigo of childhood
(BPVC)
7. Acute vestibular syndrome/vestibular neuritis 6.5
12.7
7.7
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cause dizziness and imbalance, but are beyond the scope of this chapter. Only the
most common causes of pediatric dizziness and imbalance are included in this chapter, and this list is by no means exhaustive.
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Otological
Sensorineural Hearing Loss
A large proportion of children with sensorineural hearing loss (SNHL) have vestibular impairment with associated imbalance and motor delay [27–30]. Many
causes of pediatric hearing loss are known to cause signicant vestibular impairment, while many that have previously been thought to not cause vestibular impairment are now being found to have vestibular impacts in many cases. This is also
important to consider, because cochlear implantation can have variable impacts on
vestibular function and balance in children [31, 32]. It should also be noted that
Ménière’s disease is very rare in children, despite being one of the most common
causes of vertigo in adults. Some of the most common congenital hearing loss disorders to cause concurrent vestibular impairment are summarized below.
• Enlarged vestibular aqueduct (EVA) syndrome: An enlarged vestibular aqueduct
is the most common inner ear malformation associated with sensorineural hearing loss [33]. Although less common than hearing loss, a vestibular decit can be
present with EVA2. Children can present with imbalance and poor coordination.
EVA is often an isolated nding, but can also be associated with other ear anomalies, or part of syndromes. It can be sporadic or due to mutations in the SLC26A4
gene, which causes Pendred syndrome when mutations are homozygous. Patients
with EVA can have progressive or uctuating hearing loss and sometimes also
have episodic vertigo.
• Usher syndrome: There are three types of Usher syndrome, which are all characterized by SNHL and retinal degeneration. Type 1 is associated with congenital
vestibular areexia, type 2 typically has no (or minimal) vestibular dysfunction,
and type 3 has variable and often late-onset vestibular dysfunction [34].
• CHARGE syndrome: The acronym for CHARGE refers to its most common
associated anomalies of eye Colobomas, Heart defects, choanal Atresia, growth
Retardation, Genitourinary anomalies, and Ear anomalies. It is most commonly
due to a mutation in the CHD7 gene. Imbalance and vestibular dysfunction is
common due to the presence of inner ear anomalies (often completely absent
semicircular canals) in addition to the possible presence of cerebellar anomalies.
CHARGE patients also frequently have SNHL that can be severe to profound [35].
• Congenital cytomegalovirus (CMV): Perinatal infection with CMV can cause
either isolated SNHL or a constellation of multiple anomalies, including global
developmental delay, microcephaly, and visual impairment. Peripheral vestibular
impairment is relatively common in congenital CMV, particularly in the setting
of SNHL, and cerebellar dysfunction can also occur, further impacting balance [36].
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• Cogan’s syndrome: This rare auto-inammatory condition typically presents in
adolescence and causes progressive uveitis that can result in blindness along
with SNHL and vestibular impairment with associated vertigo. It can often be
rapidly progressive, but can be treated with immune-modulator therapy, so
prompt evaluation by an Ophthalmologist and Rheumatologist is essential whenever this condition is suspected [37].
Middle Ear Dysfunction
Recurrent acute and/or chronic otitis media has been demonstrated to negatively
impact balance in children, though the exact mechanism for this effect is yet to be
denitely established [38, 39]. Tympanostomy tube insertion typically yields resolution of balance impairment, but there is increasing evidence that long-standing
middle ear effusions can have more long-standing impacts on vestibular function
[40]. Middle ear dysfunction can also rarely lead to complications that can further
impact balance and vestibular function, such as labyrinthitis (see below), cholesteatoma with labyrinthine stula, or meningitis.
Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is due to the displacement of otoconia from the utricle into one or more of
the semicircular canals. This causes episodic vertigo with movements of the head
within the plane of the affected canal. Although less common than in the adult
population, BPPV has been found to be more common than previously thought in
children, and may impact as many as one in ve children with dizziness and as
many as one in three with postconcussive dizziness [16, 17, 20, 21, 41]. However,
it should be noted that BPPV in children and adolescents is frequently a secondary
condition, particularly in conjunction with concussion, vestibular migraine, and
acute vestibular syndrome (vestibular neuritis). Children seem to more commonly
have superior canal, lateral canal, and multiple canal involvement compared to
adults [20, 21]. Diagnostic maneuvers are used to diagnose the condition and to
determine the affected canal(s), and then therapeutic maneuvers can be performed
in the ofce to treat it. This can often be done with an appropriately-trained vestibular physical therapist, if the treating clinician does not have adequate experience
to do so.
Labyrinthitis andVestibular Neuritis (Acute Vestibular Syndrome)
Vestibular neuritis typically causes acute onset vertigo with nausea, vomiting,
and imbalance that can last for several days during its acute phase. This is followed by a recovery phase that can last for weeks where patients experience
milder disequilibrium and imbalance. It is sometimes preceded by an upper
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respiratory tract infection, but this is certainly not ubiquitous. It is thought to be
viral in origin, but this has still not been denitely established as the etiology of
all cases, and some cases may even be related to vestibular migraine, hence the
newer preferred term of “acute vestibular syndrome” [42]. Vestibular rehabilitation is the most effective treatment, though steroids have been demonstrated in
some studies to be benecial if given early on in the course of the illness [43].
Labyrinthitis causes a similar presentation to vestibular neuritis, but also causes
hearing loss that can often be permanent, but may improve gradually over time.
Labyrinthitis can sometime occur as a complication of middle ear disease, so a
thorough ear examination and appropriate management of any concurrent middle
ear dysfunction is paramount.
Neurological
Vestibular Migraine
Vestibular migraine is a migraine variant that causes episodic vertigo or motion
intolerance along with concurrent migrainous symptoms. It is the most common
cause of episodic vertigo in both children and adults and is diagnosed by clinical
criteria (Table10.5) [44]. Notably, migrainous symptoms must be present with
vertigo episodes (e.g., light or sound sensitivity, visual aura, etc.), but headaches
do not necessarily need to be concurrent with the vertigo episodes. First line treatment in pediatric patients consists of migraine hygiene (e.g., optimization of
sleep, diet, hydration, stress management), though medical therapy with rescue
medications and/or daily preventative medications is also effective and often necessary [4].
Table 10.5 Diagnostic criteria for vestibular migraine, International Classication of Headache
Disorders, third Edition [67]
A.At least ve episodes fullling criteria C and D
B.A current or past history of migraine without aura or migraine with aura
C.Vestibular symptoms of moderate or severe intensity, lasting between 5min and 72h
D. At least half of episodes are associated with at least one of the following three migrainous
features:
1. Headache with at least two of the following four characteristics:
(a) Unilateral location
(b) Pulsating quality
(c) Moderate or severe intensity
(d) Aggravation by routine physical activity
2. Photophobia and phonophobia
3. Visual aura
E.Not better accounted for by another ICHD-3 diagnosis or by another vestibular disorder
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Benign Paroxysmal Vertigo ofChildhood (BPVC)
BPVC is a pediatric migraine variant/precursor disorder that causes episodes of
room-spinning vertigo that typically last for minutes at a time [45]. There is often
no other associated symptoms and headaches do not typically occur with this condition. Episodes are also often accompanied by nystagmus, imbalance, and/or fearfulness. Children are asymptomatic between episodes. Age of onset is typically
between 3 and 6 years of age. The condition usually resolves approximately
2–3years after onset [46], but children with this condition have a higher risk of
developing migraines in adolescence or adulthood than the general population. A
family history of migraine is also common with this condition. Treatment is not usually necessary, since episodes are usually very brief and sporadic, but the medication cyproheptadine may be effective as daily preventative therapy in cases where
episodes are very frequent, prolonged, or severe [45].
Benign Paroxysmal Torticollis ofInfancy (BPTI)
BPTI causes recurrent episodes of head tilting (torticollis) that can last from hours to
days and occur every few days to weeks. It typically starts in infancy and almost ubiquitously resolves by 2–3 years of age [45]. It is typically accompanied by some
migrainous features (e.g., light or sound sensitivity, irritability, nausea) as well as
imbalance. Most children are asymptomatic between symptom ares. It does not
require treatment, but the medication cyproheptadine may be effective as daily preventative therapy in cases where episodes are very frequent, prolonged, or severe [45].
It should also be noted that EVA can present with episodic torticollis, though usually
without concurrent migrainous symptoms, and the torticollis episodes may precede
the diagnosis of hearing loss, so audiological monitoring should be considered for
children with paroxysmal torticollis, even when a migraine etiology is suspected [47].
J. Gurberg et al.
Autonomic Dysfunction
Autonomic dysfunction (a.k.a., dysautonomia) is a common cause of dizziness
symptoms in the adolescent age group [17], and is typically a secondary phenomenon that can be triggered by multiple different primary conditions, including cardiac conditions, dehydration, nutritional deciencies, acute/chronic infection,
endocrine disorders, anemia, electrolyte deciency, and anxiety. Thus, a thorough
medical work-up may be warranted when dysautonomia is suspected and a clear
source is not evident. Hemodynamic intolerance is a common primary cause of
dysautonomia symptoms that are sensitive to orthostatic changes and physical exertion [48]. This is particularly common after concussion [17, 49]. In many adolescents this may also be due to postural orthostatic tachycardia syndrome (POTS),
which may require a work-up by a cardiologist to diagnosis and treat. Anxiety and/
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or chronic stress are also common triggers of autonomic dysregulation, so chronic
dizziness from other causes can often trigger secondary dysautonomia leading to
different types of dizziness in a single patient [17]. The dizziness with dysautonomia is typically a lightheadedness, though room-spinning vertigo is sometimes also
described. Concurrent symptoms during episodes include tunnel vision, tinnitus,
decreased hearing, paresthesias in the hands/feet, chest tightness, palpitations, cognitive impairment, and sometimes syncope. With POTS or hemodynamic intolerance, the rst-line treatment is optimizing hydration and increasing salt/electrolyte
intake. Physical therapy with orthostatic/hemodynamic retraining as well as reconditioning therapy can also be benecial [50]. When these treatments are unsuccessful, then medications to increase peripheral vascular tone can be helpful, such as
midodrine or udrocortisone, which are typically prescribed by a cardiologist.
Treatments for secondary autonomic dysfunction are specic to the causative condition (e.g., anxiety management, correction of hormone/electrolyte derangements,
etc.) and are typically outside of the realm of practice of the pediatric
otolaryngologist.
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Functional/Psychological
Panic Disorder
Panic attacks are a relatively common cause of episodic vertigo, and can occur in
patients without a known history of baseline anxiety. These episodes are typically
similar to the episodes seen in autonomic dysfunction, as summarized in the above
section, though are typically also accompanied by hyperventilation with associated
carbon dioxide retention, which can exacerbate the dizziness symptoms. Treatments
for panic attacks include psychological therapies (e.g., cognitive behavioral therapy,
biofeedback) and medical therapies (e.g., serotonin reuptake inhibitors, beta blockers, etc.).
Persistent Postural Perceptual Dizziness (PPPD)
PPPD is a functional neurological disorder (FND) that causes chronic dizziness that
is reported as being either constant or intermittent throughout the majority of the day
along with frequent symptom ares associated with particular triggers [51–53].
Common triggers include standing/walking and head movements. Additionally,
patients are highly sensitive to settings that incorporate a degree of “visual ow”
(e.g., grocery stores, shopping malls, hallways, etc.) and big, open spaces. Patients
typically also report a constant fear of falling, but rarely exhibit any actual falls. It is
typically triggered by an initial precipitating vestibular disorder (e.g., BPPV, vestibular migraine, concussion), and often can occur concurrently with the ongoing primary
vestibular condition. The diagnostic criteria for this condition are summarized in
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Table 10.6
dizziness [53]. Patients must meet all ve of criteria A through E
Criteria Additional details
A. One or more symptoms of dizziness,
B. Persistent symptoms occur without
C. The disorder is precipitated by
D. Symptoms cause signicant distress or
E. Symptoms are not better accounted for
Bárány Society consensus criteria for the diagnosis of persistent postural perceptual
1. Symptoms last for prolonged (hours-long)
unsteadiness, or nonspinning vertigo are
present on most days for 3months or
more.
specic provocation, but are exacerbated
by three factors:
conditions that cause vertigo,
unsteadiness, dizziness, or problems
with balance including acute, episodic,
or chronic vestibular syndromes, other
neurologic or medical illnesses, or
psychological distress.
functional impairment.
by another disease or disorder.
periods of time, but may wax and wane in
severity.
2. Symptoms need not be present continuously
throughout the entire day.
1. Upright posture.
2. Active or passive motion without regard to
direction or position.
3. Exposure to moving visual stimuli or complex
visual patterns.
1. When the precipitant is an acute or episodic
condition, symptoms settle into the pattern of
criterion A as the precipitant resolves, but they
may occur intermittently at rst, and then
consolidate into a persistent course.
2. When the precipitant is a chronic syndrome,
symptoms may develop slowly at rst and
worsen gradually.
Table10.6. PPPD is a relatively new umbrella term that incorporates a number of
vestibular FND conditions that previously went by other names, including chronic
subjective dizziness, space motion discomfort, visual vertigo, and phobic postural
vertigo. In the pediatric age group it most commonly impacts adolescents, particularly females [51]. Pre-existing anxiety or depression are risk factors for developing
PPPD, but it can also occur in people without any pre- existing mental health conditions. However, secondary anxiety from the chronic dizziness and confusion between
visual and vestibular inputs to maintain equilibrium is ubiquitous. Treatment for
PPPD includes habituation-based vestibular physical therapy, cognitive behavioral
therapy, and often also selective serotonin reuptake inhibitor (SSRI) or serotonin norepinephrine reuptake inhibitor (SNRI) medications. It is a challenging condition to
treat and requires close, long-term follow-up to achieve successful recovery.
Vestibular Rehabilitation
Vestibular rehabilitation is a core, workhorse treatment approach in the management
of a majority of vestibular conditions that affect children and adolescents. Vestibular
rehabilitation is typically conducted by a specially-trained physical therapist, though
some occupational therapists also are appropriately trained in this area, as well. It
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involves a multitude of different strategies that must be tailored to the specic
condition(s) that a given patient is aficted by, as well as a given patient’s functional
limitations, symptoms, triggers, and goals [16]. For this reason, a comprehensive
evaluation prior to treatment is of the utmost importance, which should include an
in-depth review of the medical history, developmental history, symptoms, and available vestibular testing. While the otolaryngologist’s assessment will focus more on
the vestibular and the oculomotor systems, the physical therapist has the appropriate
tools for a detailed assessment of the balance system as a whole, including the musculoskeletal system and the patient’s gait. Symptom questionnaires [54, 55] as well
as balance and gait assessment tools [56, 57] are available for use in children, and
are useful to monitor response to treatment. A course of vestibular rehabilitation
typically lasts for a few weeks, but may be shorter or longer, depending on what is
being treated and the patient’s response. Usually, the patient has weekly sessions
with the therapist along with exercises to work on at home in between the visits.
General categories of vestibular rehabilitation treatment approaches are summa-
rized below:
• Restoration—The goal of this approach is to restore an impaired vestibular system. This approach be used when residual function is present. This approach is
primarily effective for partial, incompletely compensated, unilateral, peripheral
vestibular losses. Much of this approach focuses on vestibulo-ocular reex
retraining exercises with combinations of visual xation/tracking with head and/
or body movements.
• Adaptation—The goal of this approach is to induce long-term changes in the
neuronal response to head movements with the goal of reducing symptoms and
normalizing gaze and postural stability. This approach is typically done in conjunction with restorative therapy and includes vestibulo-ocular reex training
and postural/balance retraining.
• Habituation—This approach is primarily used for treating PPPD and similar
conditions and consists of gradual, systematically increasing exposure to provocative stimuli to facilitate tolerance to such triggers. Common triggers involved
in habituation therapy include position changes, head movements, and visual
ow stimuli.
• Substitution—This approach is typically reserved for patients with severe or complete bilateral vestibular loss (areexia). The child is trained to use nonvestibular
sensory systems to maintain balance and visual stability, including proprioception, vision, smooth pursuit, saccades, and/or assistive devices. Patients with bilateral vestibular areexia can be especially challenging to rehabilitate, particularly
since many of them may also have conditions that predispose them to concurrent
visual compromise (e.g., CHARGE, Usher, CMV, etc.). Thus, this type of rehabilitation is often done over many months or years, in contrast to the other therapeutic approaches above that can often be highly effective in a matter of weeks.
• Repositioning maneuvers—Many vestibular physical therapists are also experienced in performing repositioning maneuvers to treat BPPV, as discussed in further detail in the section on BPPV above.
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