M D C ANAGEMENT OF

CHAPTER 58
MANAGEMENT OF
DIZZINESS IN CHILDREN
LYDIA EVIATAR, MD
Dizziness is a fairly common complaint in children, who often use the term indiscriminately to describe vertigo, lightheadedness, balance difficulties, anxiety, or even headaches. As it is a nonspecific complaint, it may be caused by a variety of systemic
disorders or visual disturbances. The more specific complaint of true vertigo, best described as a spinning sensation (either of
self or of the environment), is more likely the result of a true vestibular dysfunction.
Obtaining a detailed and accurate history of the patients’
symptoms is essential. The circumstances associated with
the occurrence of vertigo and the duration, frequency, and
presence of related problems such as dysequilibrium, loss
of postural control, confusion, nausea, or vomiting need to
be assessed to reach an accurate diagnosis. Precipitating
factors may be head trauma, infection, exposure to ototoxic drugs, or abrupt changes in position. In young children, congenital anomalies of the inner ear, such as a
Mondini’s malformation or large vestibular aqueduct, may
be predisposing factors. A family history of progressive
hearing loss suggests a genetically transmitted disorder
that may be associated with vestibular dysfunction.
Systemic illnesses such as diabetes, endocrine disorders, or
severe anemia should be considered. Progressive degenerative neurologic disorders, such as Friedreich’s ataxia,
Huntington’s disease, multiple sclerosis, or Refsum’s disease, are associated with vestibular neuropathy and may
present with dizziness. Arnold-Chiari malformation and
vertebrobasilar insufficiency with or without pontomedullary or cerebellar infarcts are also associated with
dizziness or vertigo.
Neurovestibular Examination
The neurovestibular examination (Table 58-1) should test
the integrity of the equilibrium system. Maintenance of
equilibrium depends on appropriate information from the
visual, proprioceptive, and vestibular systems regarding
Current Management in Child Neurology, Third Edition
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the position of the body in space and the normal function
of the pyramidal and extrapyramidal systems that enable
the body to correct its position in response to a change in
the center of gravity. The appropriate central integration
of sensory input is essential for adequate postural control
and, according to more recent investigations, is not fully
developed until 15 years of age. An acute visual, vestibular, or proprioceptive disturbance will cause a mismatch to
previously stored sensory information and present as dizziness and problems with postural control.
The neurologic evaluation should be adapted to the
patient’s age and level of maturation. In infants younger
than 6 months of age, head tilt, delayed head control, and
delayed postural control may be due to vestibular dysfunction. By 6 months, head control should be well established and good symmetric righting reflexes indicate a
functional vestibular system. An asymmetric reflex suggests a unilateral lesion when no motor deficit is present.
By 4 years, the child’s brain is mature enough to have established equilibrium responses that can be tested clinically or
by posturography (Foudriat et al, 1993).
The neurologic evaluation should assess the presence of
cranial nerve deficits, the integrity of extraocular movements,
and the presence of spontaneous, gaze-induced (30° lateral,
upward, and downward gaze), or positional nystagmus. The
Dix-Hallpike maneuver involves looking for nystagmus
induced by abruptly changing the patient’s position from
sitting with a lateral head deviation of 45° to reclining with
the head hanging off the examining table and maintained in
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Management of Dizziness in Children / 371
the same lateral position. This maneuver is repeated with the
head to the right, to the left, and hyperextended in the midline position. It will elicit positional-induced nystagmus and
is positive in paroxysmal positional nystagmus and other
peripheral labyrinthine disorders (ie, labyrinthitis, neuronitis,
Meniere’s disease, and perilymphatic fistula). This positionalinduced nystagmus has a brief latency (< 10 s), fatigues with
repeated maneuvers, and is most intense when the affected
ear is down. The patient will also complain of being most
uncomfortable with the affected ear down, which is a typical
symptom of a peripheral vestibular lesion (Table 58-2).
Nystagmus due to peripheral lesions may be inhibited by
fixation. The use of Frenzel goggles (10+ diopters) during
this test eliminates fixation and facilitates eye observation by
the examiner. It is important to look for latency and duration
of response as well as habituation with repeated positioning,
as these features help differentiate between central and
peripheral lesions (Table 58-3).
A central nystagmus is not inhibited by fixation, is not
positional, and does not fatigue. Dizziness due to central
vestibular disorders, such as cerebellopontine lesions, is
usually associated with hearing loss and often with other
cranial nerves deficits. With posterior fossa lesions, cerebellar signs and pyramidal signs may be present, affecting
gait and coordination.
With vestibular disorders, tandem gait with eyes closed
may elicit swaying and veering toward the affected side. A
reinforced Romberg test is more sensitive than the regular
version and helps elicit subtle vestibular findings. The stepping test, introduced by Fukuda, requires the patient to
step in place with eyes closed at the intersection of two perpendicular lines while counting to 60. With unilateral
vestibular lesions, this maneuver will elicit veering toward
the affected side by more than 45°. With bilateral vestibular dysfunction, a significant forward displacement of
more than 20 inches may be seen.
TABLE 58-2. Peripheral Vestibular Disorder
Acute onset vertigo
Head tilt or swaying toward affected side
Autonomic dysfunction
Nystagmus toward unaffected side
Positive Dix-Hallpike maneuver
Preferred position: supine, affected ear up
Improves over time
Dizziness may present as part of a preexisting condition or
as a seemingly isolated complaint (Figure 58-1). Visual disturbances causing distortion of images often are associated
with dizziness. This is especially common when the wrong
glasses are prescribed. Systemic disorders, such as diabetes,
endocrine disorders, longstanding renal insufficiency with
uremia, demyelinating disorders (eg, multiple sclerosis), and
degenerative disorders, may be associated with low-grade
constant dizziness, fluctuating in intensity, as a result of a
chronic vestibular neuropathy. Long-standing use of aminoglycosides, quinine, cisplatin, or diphenylhydantoin may
damage the vestibular nerve or the labyrinth and cause
unremitting dizziness. Unremitting dizziness may occur in
acoustic neuroma, other cerebellopontine (CP) angle lesions,
and posterior fossa tumors. There is usually progressive hearing loss and progressive involvement of other cranial nerves,
pyramidal tract signs, and cerebellar dysfunction.
Magnetic resonance imaging (MRI) of the brain with
contrast and thin cuts through the CP angle will obviate
the diagnosis. In the absence of neurologic findings,
endocrine abnormalities, or exposure to ototoxic drugs,
the possibility of anxiety or panic attacks or psychosocial
stress needs to be considered. These patients will admit
upon questioning to hyperventilation, excessive palm
sweating, palpitations, and even chest pressure during the
attacks. Many patients complaining of constant dizziness
with mild variations in intensity also have frequent
headaches. This combination of symptoms may be the
manifestation of underlying stress, anxiety, or depression.
When headaches are associated with recurrent dizziness,
one should consider vertiginous migraines. Autonomic
features are often present in vertiginous migraine.
The difference between dizziness and vertigo is very
important indeed. Whereas dizziness is a less-specific symptom associated with systemic ailments, space-occupying
lesions, or psychosocial stresses, vertigo is more likely associated with a true vestibular disorder that can be due to a
vascular, inflammatory, or degenerative process.
It is helpful to approach the diagnosis of vertigo by separating vertigo with hearing loss from vertigo without
TABLE 58-1. Clinical Neurovestibular Testing
TABLE 58-3. Central Vestibular Disorder
Neurologic examination adapted to child’s age
Righting and equilibrium responses
Reinforced Romberg test
Stepping test
Tandem gait, eyes closed
Dix-Hallpike maneuver
Orthostatic hypotension test
Unremitting dizziness or vertigo
Nystagmus is constant and not positional; does not habituate and is not
inhibited by fixation
Dix-Hallpike maneuver noncontributory
Cranial nerve deficits may be present
Pyramidal or cerebellar deficits may coexist
Imaging studies recommended
Differential Diagnosis
Current Management in Child Neurology, Third Edition
© 2005 Bernard L. Maria, All Rights Reserved
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Management of Dizziness in Children
Pages 370–376
372 / The Office Visit: Other Neurologic Complaints and Conditions
Nature of complaint
Chronic dizziness or vertigo
Acute paroxysmal vertigo
Hearing loss
Yes
Hearing loss
No
Yes
No
Yes
Neurologic deficits
Yes
No
Neurologic deficits
Yes
No
Fever
No
Yes
No
Age 1–4
CP angle or
posterior
fossa tumor
Cholesteatoma or
autoimmune
disorder
CP angle or
posterior
fossa tumor
Headache
Labyrinthitis
Any age
Trauma
BPV
Yes
No
Yes
Loss of
consciousness
No
Yes
Chronic
daily
headache
Endocrine
disorders,
anemia,
anxiety, or
depression
Concussion
or fistula
No
Otoxic
drugs
Yes
Syncope or
seizure
No
Nausea or
vomiting
Yes
Otoxicity
Nausea or
vomiting
Yes
No
No
Anxiety or
panic
Vestibular
neuronitis
Yes
Meniere’s
syndrome
Vascular
event
No
Vertiginous
migraine
Psychosomatic
Positional
Yes
PPV or
orthostatic
hypertension
FIGURE 58-1. Dizziness: differential diagnosis.
BPV = benign paroxysmal vertigo; CP = cerebellopontine; PPV = paroxysmal positional vertigo.
hearing loss and to proceed with a specific line of questioning that will lead to the correct diagnosis. A comprehensive pediatric “dizziness” questionnaire was designed by
the author and tested on 62 patients with dizziness. The
sensitivity of the questionnaire in reaching the correct
diagnosis was calculated at 92%.
Acute Paroxysmal Vertigo with
Hearing Loss
Labyrinthitis
The acute onset of vertigo, nausea, and vomiting, aggravated by head motion and associated with fever and hearing loss, is typical of an acute labyrinthitis. The attacks
may last several days and are associated with severe equilibrium disturbances and autonomic disturbances. Acute
labyrinthitis is probably the most common etiology of vertigo and hearing loss in young children who present with
fever and bacterial or viral otitis media. Immediate, aggressive treatment of the otitis is required. Meclizine, diphenhydramine, or a scopolamine patch will alleviate the verCurrent Management in Child Neurology, Third Edition
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No
Unknown
tigo. Intravenous fluids may be required to overcome dehydration resulting from vomiting and antiemetics are helpful in stopping vomiting.
Meniere’s Disease
Meniere’s disease presents in a similar fashion to
labyrinthitis but without fever. It is accompanied by tinnitus, ear pressure, and fluctuating hearing loss. The attacks
are recurrent and associated with progressive hearing loss.
Fortunately, the condition is very rare in children.
Treatment consists of diuretics for the alleged labyrinthine
hydrops and symptomatic treatment for vertigo with
meclizine, diphenhydramine, or scopolamine patch.
Perilymphatic Fistula
Head trauma, barotrauma, and exertion may cause a rupture of the round or oval window, leading to a perilymphatic fistula presenting with episodes of vertigo and progressive sensorineural hearing loss (SNHL). As in the
previously described peripheral vestibular disorders, the
vertigo is usually positional and the attacks may be associated with nystagmus. Nystagmus can often be elicited by
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Management of Dizziness in Children / 373
increasing pressure in the ear canal with a pneumatic otoscope. It can be observed with the naked eye or recorded
by electronystagmography. Exploratory ear surgery may be
required to identify and correct the leak, localized at the
oval or the round window. Early corrective surgery may
salvage hearing and control the vertigo. Congenital anomalies of the inner ear may be predisposing factors and highresolution computed tomography (CT) of the temporal
bone may establish the diagnosis.
Head Trauma
Head trauma can cause temporal bone fracture resulting in
SNHL and vestibular damage, or it may cause a labyrinthine
concussion without hearing loss. Auditory brainstem
evoked potentials are helpful in detecting brainstem
involvement. Steroids have been advocated for reduction of
immediate posttraumatic swelling and promoting healing of
the cochlear and vestibular nerves. Subsequent vestibular
rehabilitation is helpful in promoting adaptation to the
acute vestibular trauma.
Vascular Occlusion
Vascular occlusion of the labyrinthine artery may occur in
hypercoagulable states, such as sickle cell disease.
Treatment focuses on the underlying condition. Traumatic
vertebral artery aneurysmal dissection may cause
embolization of brainstem and cerebellum, and acute
vertigo. Initial treatment with heparin is indicated to prevent further embolization, followed, in time, by surgical
correction of the aneurysm.
Autoimmune Disorders
Autoimmune disorders, such as Cogan’s syndrome, may
cause hearing loss and acute labyrinthine dysfunction. The
mechanism is an autoimmune process affecting the
cochlea and labyrinth, resulting in elevated anticochlear
antibodies. Checking for presence of anticochlear antibodies is recommended. The recommended treatment is
intravenous immunoglobulin G or steroids, which are
reported to substantially ameliorate the symptoms.
Paroxysmal Vertigo without
Hearing Loss
Paroxysmal vertigo without hearing loss should be evaluated according to the patient’s age.
Benign Paroxysmal Vertigo
Infants and children younger than the age of 5 years may
experience a sudden spinning sensation and loss of equilibrium and hold on to the nearest support, usually their
mother, until the vertigo subsides. The attack may last
minutes to hours, during which the child appears
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diaphoretic and pale, with nystagmus often present. Head
tilt nausea and vomiting are occasionally present. There is
no confusion or automatism during the episode and no
confusion or sleepiness after it, as observed with partial
complex seizures. Equilibrium is definitely impaired during the attack and the child refuses to move. The neurologic examination between attacks is entirely normal. The
condition is called benign paroxysmal vertigo (BPV). There
is usually a strong family history of migraine and 50% of
these children develop migraine attacks in adolescence.
Because the episodes are usually brief, treatment is not
indicated, but reassuring the child and the family regarding the benign nature of the condition is very helpful.
Children should have a brain MRI and electroencephalogram (EEG) at the time of the first attack to exclude a
space-occupying lesion or partial complex seizures.
Paroxysmal Torticollis or Tortipelvis
Paroxysmal torticollis and paroxysmal tortipelvis also are
manifestations of acute vestibular dysfunction in young
children. The etiology of these conditions is not fully
understood. They are considered migraine equivalents
because of the strong association with migraine later in life.
Because of the brief duration of the episodes, treatment is
usually futile. Children who exhibit poor balance between
attacks benefit from physiotherapy.
Vestibular Neuronitis
In older children and in adolescents, an acute episode of
vertigo, often preceded by an upper respiratory infection
and associated with nausea, vomiting, and dysequilibrium,
is termed vestibular neuronitis. The condition lasts from a
few days to several weeks, with decreasing duration and
intensity over time. Episodes may recur months and even
years later, usually with decreased severity and duration.
Acute treatment consists of hydration, bed rest, and symptomatic treatment of the vertigo with meclizine, scopolamine, or diphenhydramine, and antiemetics (Table 58-4).
A prospective longitudinal study of 21 children with
vestibular neuronitis provides data on the natural history
of the condition. It shows progressive decline of symptoms.
Complete recovery was documented in all the children
studied after 5 years (Taborelli et al, 2000). Symptoms that
persist beyond 2 or 3 weeks of treatment with antivertigo
medication are helped with physiotherapy aimed at correcting the sensory mismatch and promoting habituation.
This is achieved by encouraging the patient to repeatedly
assume the most uncomfortable position (affected ear
down) while using visual and proprioceptive cues during
the procedure. This maneuver helps the patient to compensate for the vestibular loss and promotes central reorganization of postural control, leading to progressive resolution of the dizziness.
Management of Dizziness in Children
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374 / The Office Visit: Other Neurologic Complaints and Conditions
TABLE 58-4. Treatment of Dizziness
Acute vertigo and autonomic symptoms
Intravenous hydration
Diazepam IV 0.05–0.15 mg/kg/dose or PO 0.12–0.8 mg/kg/dose
Meclizine PO 25–100 mg/dose/d
Prochlorperazine IM 0.05–0.15 mg/kg/dose or PO 0.4 mg/kg /dose
in 3–4 doses
Diphenhydramine IV or IM 5 mg/kg/d in 3–4 doses; adolescents: transdermal scopolamine 1.5 mg
Hydrops or Meniere’s disease: diuretics (diazides or Diamox®)
Bacterial labyrinthitis: antibiotics
Autoimmune disorders: steroids
Subacute or chronic vertigo
Meclizine 25–100 mg/d
Treat underlying disorder:
Migraine: nonsteroidal antiinflammatory drugs for subacute episode
Chronic migraine: amitriptyline 10–75 mg/d, propanolol 10–20 mg bid, or
divalproex sodium (Depakote®) 1 or 2 capsules of 125 mg bid or ER
250 mg bid
Vertiginous seizures: carbamazepine 25 mg/kg/d or as per EEG
CP angle or posterior fossa tumor: surgery
Cholesteatoma: surgery
Perilymphatic fistula: surgery
Orthostatic hypotension: increase fluid and salt intake or mineralcorticoids
Paroxysmal positional vertigo: physiotherapy, ie, positioning maneuvers
Panic or anxiety attacks: psychiatric counseling; alprazolam 2–4 mg/d or
paroxetine 10–40 mg/d
bid = twice daily; CP = cerebello-pontine; EEG = electroencephalogram;
ER = extended release; IM = intramuscularly; IV = intravenously; PO = orally.
Migraine Variants
Vertigo may precede or accompany a headache and may
be associated with nausea or vomiting. Phonophobia and
sonophobia, characteristic of migraine, may or may not
be present. This constellation of symptoms is characteristic of the migraine variant known as vertiginous
migraine, which respond to the same medications used to
treat classic migraine.
Basilar Artery Migraine
Acute paroxysmal vertigo associated with tinnitus, acroparesthesias, perioral paresthesia, and visual obscuration
was initially described by Bickerstaf in prepubescent girls
and labeled basilar artery migraine (BAM) because the
symptoms are consistent with vasoconstriction in the vertebrobasilar territory. The condition is recognized in all age
groups and in both genders and can be a frightening experience for patients and parents alike. It may be associated
with loss of consciousness when the decreased perfusion of
the reticular activating system in the brainstem is of long
duration. Both brain MRI and EEG are indicated to rule
out a vascular malformation of the brainstem or a seizure
disorder. For suspected vascular malformations, magnetic
resonance angiography (MRA) or CT angiography may
be necessary to confirm the diagnosis. Treatment of the
acute episode is primarily with nonsteroidal antiinflamCurrent Management in Child Neurology, Third Edition
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matory agents. Ergot preparations are contraindicated for
fear of causing severe vasoconstriction in the vertebrobasilar distribution, causing stroke. Calcium channel
blockers may be effective as preventive therapy but should
be used with extreme caution.
Cyclic Vertigo
We described a group of children with cyclic vertigo. The vertigo occurred at very predictable intervals, starting early in
the morning with severe photophobia, nausea, and vomiting.
After many years of cyclic vertigo, the children developed
classic headaches. Three of nine children were subsequently
diagnosed with bipolar disorder. This presentation is most
likely another migraine variant associated with a functional
disturbance of the internal biologic clock. The treatment is
symptomatic during the episode. When attacks are frequent,
migraine prophylaxis with propranolol, valproate, or topiramate can be effective.
Motion Sickness
Most children with migraines suffer from motion sickness
and are prone to vertigo, nausea, and vomiting during passive locomotion (car rides) or motion in the surrounding
environment while they remain still. They may be especially oversensitive to optokinetic stimulation. The explanation for this disorder is not clear but may be due to the
patient’s inability to tolerate an abrupt sensory mismatch.
Habituation may be achieved by gradually increasing
exposure to longer rides and by ensuring a wide-open
visual field during rides. The use of meclizine during prolonged trips may be helpful for symptom control.
Vertiginous Seizures
Loss of consciousness or altered consciousness immediately preceded by vertigo suggests a vertiginous partial
complex seizure. Vertiginous seizures are very rare; however, dizziness may be experienced in various seizure types.
The diagnosis should rely on EEG abnormalities best
elicited after sleep deprivation or, better yet, recorded during the event itself. Treatment should be selected on the
basis of the nature of the underlying seizure disorder.
Panic Attacks
Severe panic attacks, agoraphobias, and claustrophobias
have presented as episodic vertigo. A carefully directed line
of questioning (as suggested in the “dizziness questionnaire”) will elicit the episodes of hyperventilation, palpitation, and autonomic instability that characterize these conditions and eliminate the need for extensive and costly
work-up. Management of the condition preferably should
be assigned to a psychiatrist. Antidepressant and antianxiety medication, such as paroxetine or benzodiazepines, can
be very helpful in controlling symptoms (see Table 58-4).
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Management of Dizziness in Children / 375
Orthostatic Hypotension
Vertigo associated with abrupt changes in position from
supine to sitting or standing is most likely the result of
orthostatic hypotension. This diagnosis can be easily established during the general physical examination by measuring blood pressure in the supine and standing positions and documenting a significant drop of > 20 mm Hg
of the systolic pressure during standing. Tilt testing in a
neurophysiology laboratory may provide additional confirmatory evidence. Increasing fluid and salt intake may
eliminate the orthostatic hypotension; however, corticosteroids (eg, Florinef®) need to be added in severe cases.
Paroxysmal Positional Vertigo
Paroxysmal positional vertigo occurs during abrupt changes
of head position while turning over abruptly in bed or causing other abrupt changes in head position. The sensation of
vertigo often is associated with a brief bout of torsional
nystagmus elicited when the affected ear is undermost. This
can be reproduced in the office by using the Dix-Hallpike
maneuver. The etiology is attributed to calcium debris
broken off the otololiths and lodging in the posterior semicircular canal. The condition is very rare in children but
may occur as the result of head trauma. Treatment consists
of head positioning exercises that will induce habituation and
may even reposition the debris in some cases. The field of
vestibular therapy using multisensory integration modalities
is rapidly expanding on the basis of extensive experiments on
vestibular compensation in adults and in children. It is a very
useful, safe, and effective treatment that is receiving progressively more recognition in clinical practice as an adjunct or a
substitute to medication.
Laboratory Testing
The therapeutic and technology assessment subcommittee
of the American Academy of Neurology recently reviewed
the vestibular testing techniques used in adults and children (Table 58-5). Most laboratory testing relies on evaluation of the vestibulo-ocular reflex (VOR). This is a short
latency reflex that generates compensatory eye movements
in response to head movements in order to maintain visual
fixation. The VOR can be evaluated during the application
of stimuli such as rotation and caloric irrigation. The most
common method of testing the VOR is electro-oculography,
also referred to as electronystagmography. The technique
measures changes in corneoretinal potential using
electrodes placed around the inner and outer canthi of the
eyes. It permits recording of the direction, amplitude, and
velocity of eye movements in different head positions and
in response to different types of vestibular stimulation.
Infrared video nystagmography uses infrared cameras
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TABLE 58-5. Laboratory Testing
Electronystagmography
Hearing test adapted to patient’s age
Auditory brainstem potentials in suspected brainstem involvement
Brain MRI with contrast in suspected central disorders
MRA or CT angiogram in vascular disorders
CBC, FBS, TFT, electrolytes, and coagulation studies
CBC = complete blood count; CT = computed tomography; FBS = fasting blood
sugar; MRA = magnetic resonance angiography; MRI = magnetic resonance
imaging; TFT = thyroid function tests.
positioned in eye goggles that detect movements of the
eyes. Most commercially available techniques record horizontal eye movements. Two methods are used for stimulation of the vestibular apparatus: rotation and caloric irrigation of the ear canals by air or water.
Caloric testing should be performed with the head positioned in such manner that the horizontal semicircular
canal is vertically placed. The caloric irrigation produces a
convection current, causing the endolymph to rise when
warmed and sink when cooled. The nystagmus during cool
irrigation is away from the ear and during warm irrigation
toward the irrigated ear. A pitfall of the technique is that a
narrow or an obstructed ear canal may reduce the intensity
of the stimulus, causing a reduced response. Using a formula developed by Yonkees, it is possible to determine the
presence of a hypoactive labyrinth (less nystagmus generated by hot and cold stimulation in one ear compared with
the other ear) or directional preponderance (the nystagmus
elicited by the caloric irrigations beats primarily in one
direction). The presence of a hypoactive labyrinth suggests
damage to the peripheral organ, as in vestibular neuronitis
or labyrinthitis. Directional preponderance is more likely
associated with a central lesion or an old peripheral lesion.
Children older than 3 years of age usually are able to tolerate a bithermal caloric irrigation, even though the procedure
requires about half an hour and may cause vertigo, especially
when performed after an acute labyrinthine insult. Rotational
testing using a sinusoidal stimulation with a computerized
rotational chair that delivers frequencies of rotation from
0.01 Hz to 0.16 Hz is more suitable for pediatric testing.
Unfortunately, the equipment is expensive and not universally
available. Rotational testing allows precise application of multiple frequencies of rotational stimuli, whereas caloric testing
is equivalent to a single very low frequency (0.003 Hz). The
disadvantage is that it tests both ears simultaneously and is not
as reliable in detecting unilateral lesions. The test is suitable for
very young children who can be tested while sitting in a
parent’s lap. Measurement of the VOR in rotational testing is
expressed in terms of gain (eye velocity relative to head velocity) and phase (timing of eye motion relative to head motion).
A perfect VOR function will present a gain of 1 and a phase
shift of 180°. The VOR is less efficient during very low
Management of Dizziness in Children
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376 / The Office Visit: Other Neurologic Complaints and Conditions
frequencies of head movement and is best at rotations of 1 to
6 Hz, which closely simulate head motion during locomotion.
The VOR may show asymmetry in cases of substantial
unilateral labyrinth hypofunction. The rotational test is
best suited for assessment of ototoxicity.
Posturography uses a computerized moving platform to
elicit postural reactions to abrupt changes in the center of
gravity with and without visual and proprioceptive clues.
The computer analyzes body sway and compensatory postural reactions. The test requires special equipment and has
had limited practical use because of its high cost, difficulty
administering it in young children, and limited standardization in children. Several studies on posturography from Japan
and the United States are available and describe a delay in
acquiring mature integrated postural reactions in children
younger than 15 years of age. However the studies were performed with equipment designed and used for adults, which
may account for some of the alleged delays. The limited number of children studied and the discrepancies between the
results published from various centers underlie the difficulty
in using these tests for routine diagnostic purposes.
Indications for Vestibular Testing
Vestibular testing is especially helpful in disorders of the
peripheral organ (ie, labyrinthitis, vestibular neuronitis,
posttraumatic vertigo, perilymphatic fistula, Meniere’s disease, or vestibular schwannoma). A hypoactive labyrinth
will confirm damage to the peripheral organ. Repeated
testing may provide a measure of the degree of recovery
over time. Drug ototoxicity can be carefully assessed and
monitored with rotational testing. Testing also is indicated
in balance disorders when it is important to differentiate
between poor balance resulting from visual, vestibular, or
proprioceptive disorders. Although the history and clinical testing will give a definite clue concerning the disorder’s
etiology, vestibular testing helps confirm the diagnosis.
Children with acquired or congenital hearing loss also
will benefit from testing, as the cochlea and labyrinth are in
close proximity and may be affected by the same noxious
agents. A child with poor bilateral labyrinthine function
may become very disoriented in the dark or while diving
into a pool, as visual cues are missing in the dark and proprioceptive clues missing when one is immersed in water.
Testing the VOR during smooth pursuit or generation of
saccades provides information on cerebellar control of eye
motions, and suppression of nystagmus with fixation will
indicate that the lesion is peripheral and not central.
Hearing testing is essential in all suspected peripheral
lesions and suspected posterior fossa lesions, especially
vestibular schwannoma.
EEG should be performed in cases of vertigo with loss
of consciousness or loss of postural control to exclude the
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BC Decker Inc
possibility of seizures versus basilar artery migraine or vertiginous migraine.
MRI of the brain is the method of choice to rule out
posterior fossa tumors, including CP angle lesions.
When vascular anomalies are suspected, MRA is recommended.
CT of the head with thin cuts through the temporal
bone is especially helpful to demonstrate congenital anomalies of the inner ear.
Determining the etiology for and the management of
dizziness and dysequilibrium are very difficult diagnostic
dilemmas. Using a comprehensive standardized “dizziness
questionnaire” and a step-by-step diagnostic algorithm
approach will greatly facilitate finding the etiology and
instituting appropriate treatment.
Suggested Readings
Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache
1992;32:300–4.
Eviatar L, Eviatar A. Neurovestibular examination of infants and
children. Adv Otorhinolaryngol 1978;23:169–91.
Fife TD, Tusa RJ, Furman JM, et al. Assessment: vestibular testing
techniques in adults and children: report of the Therapeutics
and Technology Assessment Subcommittee of the American
Academy of Neurology. Neurology 2000;55:1431–41.
Foudriat BA, Di Fabbio RP, Anderson JH. Sensory organization
of balance responses in children 3–6 years of age: a normative study with diagnostic implications. Int J Pediatr
Otorhinolaryngol 1993;27:255–71.
Linzer M, Yang EH, Estes NA III, et al. Diagnosing syncope. Part
2: unexplained syncope. Clinical Efficacy Assessment Project
of the American College of Physicians. Ann Intern Med
1997;127:76–86.
McCabe BF, Ryu JH, Sekitani T. Further experiments on vestibular compensation. Laryngoscope 1972;82:381–96.
Taborelli G, Melagrana A, D’Agostino R, et al. Vestibular neuronitis in children: study of medium and long term followup. Int J Pediatr Otorhinolaryngol 2000;54:117–21.
Practitioner and Patient Resource
Vestibular Disorders Association (VEDA)
P.O. Box 4467
Portland, OR 97208-4467
Phone: (503) 229-7705
Fax: (503) 229-8064
E-mail: [email protected]
http://www.vestibular.org
VEDA is a nonprofit organization that provides information to
the public and health professionals about inner-ear balance disorders such as Meniere’s disease, benign paroxysmal positional
vertigo, and labyrinthitis.
Management of Dizziness in Children
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