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9 Vestibular Ototoxicity
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generally are not much help in these circumstances after the acute phase of vertigo has resolved. Furthermore prolonged use of meclizine may result in other
centrally mediated causes of imbalance and could complicate the treatment.
Benzodiazepines are not the treatment of choice. They are reported to
adversely affect eye movements through reduction of saccadic velocity, increase
in saccadic duration, impairment of slow pursuit, decrease in VOR gain, and
increase in VOR time constant. They are also addictive.
Patients suffering from severe vestibular toxicity become visually and
proprioceptor- dependent. They need visual cues to navigate and depend excessively on proprioception to walk. While they are able to see, walking is feasible.
It is in the dark that such patients experience major difculties.
Surgical options for this debilitating disorder are limited. Some have proposed either chemical (intratympanic gentamicin) or surgical labyrinthectomy to
treat an ear that may be sending variable or abnormal balance signals to the
brain, in the hopes that a better ear will allow improved vestibular compensation.
However, such a procedure may in fact reduce the remaining vestibular function
in a patient and make symptoms worse.
The question then arises: when both ears are affected, what treatment options
exist? At present, the primary treatment used is vestibular therapy to help the
patient compensate for the vestibular loss, both by utilizing any remaining vestibular function and by coordinating proprioception and vision into the patient’s
overall balance.
One future avenue of treatment that holds great promise is the vestibular
implant [8]. It is similar to the cochlear implant in that it is a surgically inserted
device in the vestibular end organs (at present limited to the semicircular canals)
and restores VOR in these patients. The device is currently in clinical trials [9].
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Overview
The diagnosis and effective treatment of ototoxicity are challenging. A stringent,
practical protocol that encompasses all elements aimed at proling the effects of
ototoxicity is vital.
Ototoxic drugs usually adversely affect both the cochlea and the vestibular systems simultaneously. Currently, over 600 categories of drugs that have the potential
to cause ototoxicity have been listed. Aminoglycoside antibiotics, platinum-based
chemotherapeutic agents, loop diuretics, macrolide antibiotics, and antimalarials
are the commonly used medications that have documented ototoxic effects. On
questioning the patient, it has often been found that the exact time of commencement of symptomatology is frequently unclear. High interindividual variability in
symptomatology is often found because of differences in genetic factors, pharmacokinetics, the metabolic status of the individual, and comorbid medical conditions.
Ototoxicity affecting the cochlea follows a relatively predictable pattern. The
basal turn of the cochlea is involved rst, involving its outer hair cells (responsible
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for high frequencies), and as ototoxicity progresses, it involves the apical portion,
which is responsible for the lower speech frequencies.
Although ototoxic-induced hearing loss is not a life-threatening condition, it can
have a severely negative impact on communication and health-related quality of life
issues, with signicant adverse vocational, educational, and social consequences. It
has been reported that in children, even mild hearing loss can severely impair speech
and language acquisition and retard cognitive and social development. This, in turn,
leads to poor scholastic performance and lowered psychosocial functioning. The
goal of the management of ototoxicity is to minimize or prevent these complications
and plan appropriate rehabilitation measures.
C. de Souza et al.
Preventive Measures
When administering a medication that is potentially ototoxic, especially if it is to be
given as a course, it is prudent to get baseline measures of the cochlear and vestibular systems before starting treatment.
Baseline audiometric tests like pure tone, speech, and immittance audiometry
need to be documented.
The question arises as to whether baseline vestibular testing should be carried
out. If the patient is without vestibular symptoms, then perhaps rotatory chair testing can be performed. And ndings were noted and documented. At this time, there
are no clear protocols for pretreatment. Caloric testing can also be considered if the
patient does not present with perforations or infections of the ear.
All aspects of treatment should and must be carefully explained to the patient in
detail. The patient should be made aware of what the symptoms are that could herald the onset of either cochlear or vestibular toxicity.
Then should the patient present with symptoms, tests can be performed using the
baseline as a comparison to determine the level of toxicity.
Some reports have described calcium as a competitive inhibitor of gentamycin.
It was thought that an oral suspension of calcium could possibly be used as an oral
supplement to avoid or ameliorate potential ototoxicity. It, in turn, could likely
affect the efcacy of gentamycin. Thus, the pros and cons need to be carefully
weighed before initiating it.
Still, some other researchers have described using probenecid to reduce the level
of perilymph penetration of furosemide, resulting in diminished cochlear toxicity.
Fosfomycin has also been reported as being able to reduce the effects of cisplatin
ototoxicity.
There are several animal and invitro studies that have reported the efcacy of
otoprotective agents that can possibly prevent ototoxicity. Unfortunately, many of
these studies lack appropriate control groups, positive clinical ndings and longitudinal outcomes, and multicenter, large-scale clinical trials that would validate their
results and recommendations. Agents designated as otoprotective medications such
as sodium thiosulfate, amifostine, and N-acetylcysteine have been investigated for
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cisplatin otoprotection. While systemic administration of these agents has been
described as having the ability to reduce cisplatin-induced hearing loss, it was also
found that they simultaneously reduce cisplatin’s tumoricidal efcacy. Therefore, in
an attempt to achieve otoprotection while simultaneously achieving tumoricidal
activity, the administration of sodium thiosulfate was delayed for several hours following cisplatin administration. In addition, intra-tympanic administration of these
agents was performed. There are reports of intratympanic administration of
N-acetylcysteine, which adequately demonstrated otoprotection following the
administration of cisplatin-induced ototoxicity. Intratympanic dexamethasone also
yielded positive results following the administration of cisplatin.
Cisplatin-induced ototoxicity causes permanent hearing loss in pediatric and adult
cancer survivors. Understanding the mechanisms that cause cisplatin-induced hearing loss and the development of treatment modalities to reduce and possibly reverse
cisplatin ototoxicity have been impeded by animal models that are not ideal. In a
clinical setting, cisplatin is frequently administered in multidose, multicycle protocols. However, many studies conducted on animal models used single injections of
high-dose cisplatin. This does not reect the manner in which cisplatin is administered in clinical protocols. When these rodents were subjected to similar protocols
that occur in real-life clinical settings, there was signicant mortality that again presented a major impediment to understanding the mechanisms of ototoxicity.
A Cochrane review of three randomized, controlled trials of amifostine agents
reported that no conclusions could be drawn about their efcacy in otoprotection
against cisplatin-induced ototoxicity in children. At this time, no medications have
been approved by the US Food and Drug Administration that could play a role in the
prevention of drug-induced ototoxicity during curative cancer treatment. More clinical research and trials are needed to study the otoprotective prole of these
medications.
Recent studies have demonstrated the successful promotion of cochlear gene
therapy, adeno-associated virus-mediated delivery of brain-derived neurotrophic
factors, and stem cells in animal models. These future therapeutics hold promise for
the prevention and treatment of ototoxicity, though much work needs to be done to
document their efcacy and feasibility in humans.
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Drug Metabolizing Genes andIts Association withOtotoxicity
Well-dened, clear associations have been established between chemotherapy and
ototoxicity. Inter-individual variabilities have also been found in the development of
chemotherapy-related hearing loss [10]. These interindividual variations can likely
be explained by individual genetic variations toward the effects of chemotherapy,
which in turn can potentially exacerbate the compound’s ototoxic effects.
Understanding these genetic variants as a way to predict which patients are most
susceptible to ototoxicity could thus provide important information for clinical
decision-making.
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C. de Souza et al.
Candidate gene pharmacogenetic studies have explored the relationship between
drug-induced hearing loss and several genotypes such as thiopurine methyltransferase, ATP-binding cassette transporter C3 (ABCC3), glutathione-S-transferase
subclasses (GSTP1, GSTM1, and GSTT1), catechol-O-methyltransferase, and
megalin [11–17].
These are results that are largely inconsistent. It was found that mutations in the
mitochondrial DNA, such as the A1555G mutation, have been associated with
increased susceptibility to aminoglycoside-related ototoxicity [18]. A recent
genome-wide association study has identied the association between cisplatininduced hearing loss and genetic variants such as superoxide dismutase 2 (SOD2)
and Acylphosphatase-2 (ACYP2) ([19]).
Conclusions
1. Ototoxicity involves both the cochlea and the vestibular system.
2. There are no universally accepted, clearly dened protocols to evaluate and man-
age ototoxicity.
3. Most of the patients who are exposed to potentially ototoxic agents are obtunded
and thus cannot complain of dizziness or hearing loss. When they do complain,
ototoxicity is advanced, making treatment measures difcult.
4. There are a few medications available to ameliorate ototoxicity. However, they
adversely affect the effectiveness of the medication that causes ototoxicity.
References
1. Handelsman JA.Vestibulotoxicity: strategies for clinical diagnosis and rehabilitation. Int J
Audiol. 2018;57(sup4):S69–77. https://doi.org/10.1080/14992027.2018.1468092.
2. Black FE, Pesznecker SC.Vestibular ototoxicity. Clinical considerations. Otolayngol Clin N
Am. 1993;26(5):713–36.
3. Black FO, Gianna-Poulin C, Pesznecker SC. Recovery from vestibular ototoxicity. Otol
Neurotol. 2001;22(5):662–71.
4. Ganesan P, Schmiedge J, Manchaiah V, Swapna S, Dhandayutham S, Kothandaraman
PP. Ototoxicity: a challenge in diagnosis and treatment. J Audiol Otol. 2018;22(2):59–68.
https://doi.org/10.7874/jao.2017.00360. Epub 2018 Feb 26. PMID: 29471610; PMCID:
PMC5894487.
5. Llorens J, Callejo A, Greguske EA, Maroto AF, Cutillas B, Martins-Lopes V.Physiological
assessment of vestibular function and toxicity in humans and animals. Neurotoxicology.
2018;66:204–12. https://doi.org/10.1016/j.neuro.2018.02.003. Epub 2018 Feb 8. PMID:
29428870.
6. Longridge NS, Mallinson AI.The dynamic illegible E (DIE) test: a simple technique for assessing the ability of the vestibular ocular reex to overcome vestibular pathology. J Otolaryngol.
1987;16:97–100.
https://doi.org/10.1097/00129492- 200109000- 00018.
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7. Halmagyi GM, Curthoys IS.A clinical sign of canal paresis. Arch Neurol. 1988;45:737.
8. Guyot JP, Perez Fornos A.Milestones in the development of a vestibular implant. Curr Opin
Neurol. 2019;32(1):145–53. https://doi.org/10.1097/WCO.0000000000000639.
9. Guyot JP, Guinand N, Perez Fornos A.Tribute to Bernard Cohen- whose pioneering work
made the vestibular implant possible. Front Neurol. 2020;11:452. https://doi.org/10.3389/
fneur.2020.00452.
10. Ross CJ, Katzov-Eckert H, Dubé MP, Brooks B, Rassekh SR, Barhdadi A, et al.
CPNDS.Consortium genetic variants in TPMT and COMT are associated with hearing loss in
children receiving cisplatin chemotherapy. Nat Genet. 2009;41:1345–9.
11. Choeyprasert W, Sawangpanich R, Lertsukprasert K, Udomsubpayakul U, Songdej D,
Unurathapan U, et al. Cisplatin-induced ototoxicity in pediatric solid tumors: the role of
glutathione S-transferases and megalin genetic polymorphisms. J Pediatr Hematol Oncol.
2013;35:e138.
12. Oldenburg J, Kraggerud SM, Cvancarova M, Lothe RA, Fossa SD.Cisplatin-induced longterm hearing impairment is associated with specic glutathione s-transferase genotypes in
testicular cancer survivors. J Clin Oncol. 2007;25:708–14.
13. Palodetto B, Postal M, Grignoli CR, Sartorato EL, Oliveira CA.Inuence of glutathione s transferase on the ototoxicity caused by aminoglycosides. Braz J Otorhinolaryngol. 2010;76:306–9.
14. Peters U, Preisler-Adams S, Hebeisen A, Hahn M, Seifert E, Lanvers C, etal. Glutathione
S-transferase genetic polymorphisms and individual sensitivity to the ototoxic effect of cisplatin. Anticancer Drugs. 2000;11:639–43.
15. Pussegoda K, Ross CJ, Visscher H, Yazdanpanah M, Brooks B, Rassekh SR, etal. Replication
of TPMT and ABCC3 genetic variants highly associated with cisplatin-induced hearing loss in
children. Clin Pharmacol Ther. 2013;94:243–51.
16. Riedemann L, Lanvers C, Deuster D, Peters U, Boos J, Jürgens H, etal. Megalin genetic polymorphisms and individual sensitivity to the ototoxic effect of cisplatin. Pharmacogenomics
J. 2008;8:23–8.
17. Yang JJ, Lim JY, Huang J, Bass J, Wu J, Wang C, etal. The role of inherited TPMT and COMT
genetic variation in cisplatin-induced ototoxicity in children with cancer. Clin Pharmacol Ther.
2013;94:252–9.
18. Fernandez K, Wafa T, Fitzgerald TS, Cunningham LL.An optimized, clinically relevant mouse
model of cisplatin-induced ototoxicity. Hear Res. 2019;375:66–74. https://doi.org/10.1016/j.
heares.2019.02.006. Epub 2019 Feb 22.
19. Hagleitner MM, Coenen MJ, Patino-Garcia A, de Bont ES, Gonzalez-Neira A, Vos HI, etal.
Inuence of genetic variants in TPMT and COMT associated with cisplatin induced hearing
loss in patients with cancer: two new cohorts and a meta-analysis reveal signicant heterogeneity between cohorts. PLoS One. 2014;9:e115869.
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Chapter 10
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Balance andVestibular Disorders
inChildren andAdolescents
JoshuaGurberg, HenriTraboulsi, andJacobR.Brodsky
Introduction
Children with vestibular dysfunction will most commonly present with dizziness or
imbalance, though a multitude of other symptoms and clinical presentations may
also occur. Pediatric vestibular medicine is an area that has received little attention
until quite recently. However, this new eld of clinical practice and research has
begun to grow rapidly as a result of increasing awareness of the signicant negative
impacts that vestibular dysfunction can have on children’s development and quality
of life. Awareness of the importance of addressing vestibular function in the congenital hearing loss and concussion populations has played a major role in fuelling
the recent expansion of this eld. The establishment of numerous dedicated pediatric vestibular programs around the world in recent years has led to increasing awareness of the signicant prevalence of vestibular disorders in children and has allowed
research in this area to expand exponentially.
J. Gurberg
Department of Otolaryngology—Head & Neck Surgery, Pediatric Surgery, Montreal
Children’s Hospital, Montreal, QC, Canada
e-mail: joshua.gurberg@muhc.mcgill.ca
H. Traboulsi
Division of Pediatric Otolaryngology, Department of Surgery, Texas Children’s Hospital,
Baylor College of Medicine, The Woodlands, TX, USA
e-mail: hxtrabou@texaschildrens.org
J. R. Brodsky (
Department of Otolaryngology and Communication Enhancement, Boston Children’s
Hospital, Boston, MA, USA
Department of Otolaryngology, Harvard Medical School, Boston, MA, USA
e-mail: Jacob.Brodsky@childrens.harvard.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
B. T. Crane et al. (eds.), Disorders of the Vestibular System,
https://doi.org/10.1007/978-3-031-40524-2_10
*)
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Dizziness and imbalance impact approximately 2.0% and 3.7% of children in the
United States, respectively [1]. Other studies have found similar prevalences in other
countries [2, 3]. However, awareness of the most common causes of vestibular symptoms in children and their appropriate work-up and management is greatly lacking.
Data from the 2016 United States National Health Interview Survey demonstrated
that 5.6% of a nationally-representative cross-sectional sample of 9247 children had
reported symptoms of dizziness and/or imbalance [1]. However, none of those children were given a causative diagnosis of migraine by their health care providers,
despite overwhelming evidence from the medical literature that migraine is the most
common cause of pediatric dizziness [1, 4–13]. Thus, it is important that any pediatric provider that could be involved in the evaluation of children with dizziness or
imbalance be aware of the general work-up and most common diagnoses to cause
vestibular symptoms in children. Although migraine is the most common cause of
dizziness in children, peripheral vestibular disorders are also quite common causes
of dizziness and/or imbalance in children, as summarized in further detail later in this
chapter, and vestibular impairment is particularly common in children with congenital hearing loss. Thus, pediatric otolaryngologists should also become familiar with
how to appropriately manage these patients. Pediatric vestibular disorders are treatable, but only if the provider knows what they are treating and how best to manage it.
J. Gurberg et al.
Embryology, Anatomy, Physiology, andDevelopment
In order to understand how best to evaluate and treat pediatric vestibular disorders, it
is important to rst have at least a general understanding of the development of the
vestibular system. Embryologically speaking, the semicircular canals and otolith
organs develop as part of the inner ear. This begins at 3weeks gestational age (GA)
when a focus of ectoderm, the otic placode, invaginates in the region of the embryonic
hindbrain to form the otic pit and eventually the otic vesicle, which will form the
membranous labyrinth [14]. At 5weeks GA, the otic vesicle develops into an otocyst
and is divided into cranial, intermediate, and caudal portions. The intermediate portion, or “utriculosaccular area,” is comprised of a saccular and utricular region, which
form the vestibule and semicircular canals, respectively. At 6weeks GA, the superior
semicircular canal, utricle, and saccule develop, followed by the posterior canal, and
nally the lateral canal at 21–23weeks. This order of canal development explains why
lateral canal dysplasia is the most common vestibular end organ anomaly, since it is
the last to complete its development. Between 19 and 23weeks GA, the membranous
labyrinth is surrounded by the osseous labyrinth through ossication of the surrounding precartilage, which is derived from embryonic mesoderm and neural crest cells.
The sensory epithelia of the vestibular system are the three cristae within the
ampullated ends of the semicircular canals and the maculae of the otolith organs [14,
15]. These structures begin to develop at 3 weeks GA from otocyst ectoderm. By
7weeks GA, otoconia and vestibular hair cells have begun to develop in these sensory
regions, which rst become active at 8–9weeks. The vestibulocochlear nerve, which
innervates these structures, develops from a collection of neural crest cells known as
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fascioacoustic primordium at 5weeks gestation. The vestibulocochlear ganglia arise
from otocyst ectoderm as well as neural crest cells and are divided into a superior
division, innervating the superior semicircular canal, lateral semicircular canal, and
the utricle, and an inferior division innervating the posterior semicircular canal and
saccule. The remaining portion makes up the spiral ganglion of the cochlea. The vestibular system begins sensing linear and angular acceleration as early as 32week GA.
The vestibulo-ocular reexes are functional at birth as evidenced by the presence
of primitive newborn reexes such as the dolls eye response. The absence of such
reexes may indicate a deciency in the vestibular system. This system is also
essential in normal motor development. The child should be able to lift their head
by 3–4months of age, sit by 6–7months, pull to stand at 9months, and walk at
12–14months [16]. Failure to meet these milestones may indicate a problem with
the vestibular system, though these delays can also be due to other areas of dysfunction. As the child meets these milestones and interacts more with his or her environment, the vestibular system continues to develop until fully mature at 15years of age.
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History
The history and physical examination are generally the highest yield component of
the medical evaluation in establishing a diagnosis and treatment plan for pediatric
patients with vestibular symptoms. A common misconception is that most children
are unable to provide an effective history regarding vestibular symptoms. We have
anecdotally found that this is often not the case. Many children can actually provide
a very helpful history, if the provider knows what to ask. Some general guidelines
are provided in the following paragraphs to help optimize the efcacy and efciency
of this sometimes-challenging assessment.
Firstly, it should be noted that there are generally two major categories of pediatric patients that present with vestibular complaints [1, 17]. Younger children more
often present with imbalance or motor delay, often in the setting of congenital hearing loss, otitis media, or global developmental delay. Older children (grade school
through adolescence) more often present with complaints of dizziness or vertigo,
sometimes accompanied by imbalance, often in the setting of concussion or
migraine. Although these categories are not mutually exclusive, it can be helpful to
think in these general terms when acquiring the history, since the diagnoses to consider differ signicantly between these two groups.
For young children with imbalance, it is particularly important to ask about
motor milestones, as summarized above, as well as about speech development and
signs of hearing loss or otitis media [16]. Vision plays a particularly important role
in balance in young children, so it is also essential to ask about signs/symptoms of
visual impairment and to conrm that an optometric/ophthalmologic evaluation has
been completed. Birth history is also important to discuss, including any perinatal
infections that could suggest a diagnosis of neonatal cytomegalovirus infection or
meningitis, signicant hyperbilirubinemia that could have resulted in kernicterus,
and perinatal antibiotic exposure that could have resulted in vestibulo/ototoxicity.
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J. Gurberg et al.
Table 10.1
Dizziness
character
Episode
duration
Provoking
factors
Associated
symptoms
PPPD persistent postural perceptual dizziness, BPPV benign paroxysmal positional vertigo, BPVC
benign paroxysmal vertigo of childhood
Dizziness history factors and common associated diagnoses
Lightheadedness/
Disequilibrium
Vertigo • Vestibular migraine
Seconds–minutes • BPPV
Hours • Vestibular migraine
Days to weeks • Acute vestibular syndrome/vestibular neuritis
Weeks to months (or
“constant”/chronic)
Position changes/head
movements
Visual ow • PPPD
Stress • Vestibular migraine
Lack of sleep, diet changes,
menses
Headache, photophobia,
phonophobia, visual aura
Tunnel vision, paresthesias,
tinnitus
Nausea/vomiting • Vestibular migraine
Hearing loss • Labyrinthitis
• Hemodynamic intolerance/dysautonomia
• Panic disorder/anxiety
• PPPD
• Acute vestibular syndrome (recovery phase)
• BPPV
• BPVC
• Acute vestibular syndrome (acute phase)
• BPVC
• Hemodynamic intolerance/dysautonomia
• Panic disorder/anxiety
• PPPD (symptom ares)
• PPPD
• BPPV
• Hemodynamic intolerance/dysautonomia
• Vestibular migraine
• Acute vestibular syndrome/vestibular neuritis
• PPPD
• PPPD
• Panic disorder/anxiety
• Vestibular migraine
• Vestibular migraine
• Panic disorder/anxiety
• Hemodynamic intolerance/dysautonomia
• PPPD
• Acute vestibular syndrome/vestibular neuritis
The history can be more challenging with children and adolescents presenting
for evaluation of dizziness or vertigo. Both the child and the parent should participate in the discussion, whenever possible, as characterization of the subjective features of the symptoms is paramount. A structured intake questionnaire for vestibular
patients can greatly improve efciency in a busy clinic. The highest yield questions
for these patients pertain to the character, timing, and provoking factors for the dizziness, as well as any associated symptoms. Table10.1 outlines which of the most
common causes of pediatric dizziness should be considered when particular
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responses are given regarding each of these factors. Parents may make inaccurate
assumptions about what the child is experiencing, so direct involvement of the
patient in the interview can be very helpful, when feasible.
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Physical Examination
Cooperation with examination and testing of younger children can be enhanced by
saving invasive components for the end and by using games and light-up toys. The
examination should include assessment of the ears, eyes, neurological function, balance, vestibulo-ocular reex (VOR), and nystagmus. Gait and stance can often be
observed during the interview in younger children, and older children should also be
evaluated with eyes closed in Romberg, tandem, and one-leg stance positions. The
single leg stance with eyes closed is a particularly useful screen for vestibular
impairment, as it reduces the child’s ability to rely on other systems (vision and
proprioception) to balance and forces them to use their vestibular inputs. Cushing
and colleagues demonstrated that inability to maintain a single-leg stance with eyes
closed for >3s is highly sensitive and specic for predicting bilateral vestibular loss
in children >3years old with bilateral sensorineural hearing loss [18, 19]. The head
impulse test (HIT) can be facilitated in toddlers and infants by having an assistant
hold a light-up toy, sticker, or smartphone/tablet as a target for the child to focus on
while the examiner performs the head thrusts. The presence of spontaneous nystagmus without xation suggests that an uncompensated vestibular loss is present.
Assessment of spontaneous and gaze-evoked nystagmus ideally should be performed both with and without xation (using Frenzel or videonystagmography
goggles), whenever possible, since visual xation on a target will typically suppress
nystagmus from peripheral vestibular dysfunction. Thus, if Frenzel or videonystagmography (VNG) goggles are not available, then it should be noted that nystagmus
of peripheral etiology cannot be denitively ruled out. Evaluation of positional nystagmus should include bilateral Dix–Hallpike maneuvers, bilateral supine head-roll
maneuvers, and a midline head-hang maneuver, as benign paroxysmal positional
vertigo (BPPV) can affect any of the semicircular canals in pediatric patients [20,
21]. Providers should have a low threshold for performing positional testing, as
BPPV in children is likely much more common than previously thought, but is often
missed. VNG goggles should also be used for diagnostic positional maneuvers, if
available, as their use signicantly increases the sensitivity of this evaluation.
Vestibular Testing
Indications for vestibular testing in children and adolescents are summarized in
Table10.2. Vestibular testing alone will not yield a diagnosis without a careful history and physical examination. Pediatric vestibular testing can be challenging, and
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