Vertigo

Daune L. MacGregor
Pediatrics in Review 2002;23;10
DOI: 10.1542/pir.23-1-10

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Article neurology

Vertigo
Daune L. MacGregor,
Objectives After completing this article, readers should be able to:
MD*
1. Describe the pathophysiologic processes that result in vertigo.
2. Delineate which aspects of the general and neurologic examination are particularly
important in diagnosing vertigo.
3. Determine which presentations of vertigo with hearing loss or associated neurologic
symptoms require referral to an otolaryngologist for vestibular function testing.
4. Describe appropriate management of vertigo.

Definitions
“Dizziness” is a common complaint that implies a sense of disorientation, usually an
altered perception of position in the environment. It may be due to lightheadedness or
faintness (eg, the adolescent who has orthostatic hypotension), occur in association with a
variety of acute medical disorders (eg, the febrile child who has vomiting and dehydration),
or have a psychosomatic origin (eg, depression, anxiety, or exhaustion).
Dizziness is formally classified into four categories: vertigo, presyncope, dysequilib-
rium, and light-headedness. Vertigo is defined as an illusion of movement, most often a
sensation of rotation or, less frequently, linear displacement or tilt. Vertigo is the key
symptom of vestibular pathology and usually the result of abnormalities of the labyrinth,
although it also may be symptomatic of other neurologic disease (eg, seizures or mi-
graines). It typically is accompanied by symptoms of varying degree, including nausea,
vomiting, pallor, and perspiration. There is no loss of consciousness.

Epidemiology
The prevalence of vertigo in children is unknown. A recently published study of Scottish
school children reported that 15% had experienced at least one episode of dizziness in a
1-year period. Almost 50% were assessed as having “paroxysmal vertigo” with accompa-
nying symptoms frequently suggestive of migraine (pallor, nausea, phonophobia, and
photophobia).

Pathogenesis and Etiology

The etiology of vertigo may be due to abnormalities of the vestibular, visual, or proprio-
ceptive systems. The labyrinth (the paired organs of equilibrium) consists of three
semicircular canals stimulated by angular acceleration and the utricle and saccule stimu-
lated by gravitational forces and vertical acceleration. Impulses pass via the vestibular nerve
to the vestibular nuclei in the brainstem and then ascend in the medial longitudinal
fasiculus (to the cranial nerves for eye movement) and descend in the vestibulospinal tracts
(excitatory stimuli to the extensor muscles of the head, extremities, and trunk for
maintenance of upright posture). The cerebellum receives afferent impulses and functions
as a center for integrating oculovestibular and postural responses. Cortical vestibular
representation is at the level of the posterior temporal gyrus.
Vestibular function is assessed by evaluating the oculovestibular reflex and intensity of
nystagmus produced by rotatory and caloric stimulation of the labyrinth. The oculoves-
tibular reflex permits ocular fixation on stationary objects while the head and body are in
motion.

*Professor of Paediatrics (Neurology), Clinical Director, Division of Neurology, Department of Paediatrics, Hospital for Sick
Children, University of Toronto, Toronto, Ontario, Canada.

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 neurology vertigo

Nystagmus is the observed Table 1. Clinical Presentations of Vertigo

movement of the eye in response to
stimulation of the labyrinth, retro- Peripheral Central
cochlear vestibular, or central
Occurrence Episodic, sudden onset Constant
vestibulo-ocular pathway. It is clas- Direction of spinning/ Unidirectional Variable
sified as spontaneous or induced by nystagmus
direction and by fatigability. The Nystagmus axis Horizontal, rotary Horizontal, vertical, oblique, or
direction of nystagmus is desig- rotary
Nystagmus type Slow and fast phase Irregular or equal phase
nated by the fast component (ocu-
Hearing loss, tinnitus Possible No
lar realignment). The slow compo- Loss of consciousness No Possible
nent represents the oculovestibular Other neurologic signs/ No Cranial nerve deficits, cerebellar
response. symptoms and pyramidal signs frequent
Vertigo may be due to periph- Modified from Cohen NL. Med Clin North Am. 1991:75:1251–1260.
eral vestibular disease or central ves-
tibular dysfunction. When not asso-
ciated with actual movement, the cause of vertigo is ined while continuous positive and then negative pres-
found in the peripheral system in 85% of cases. Use of the sure is applied. Normally, there should be no drift of the
term “peripheral” implies that the problem occurs either eyes. In the presence of perilymphatic fistula, the eyes
in the end organ (semicircular canals or utricle) or in the may drift slowly away from the ear with positive pressure
peripheral nerve. and back toward the ear with negative pressure.
The clinical presentations differ and allow for localiza- An important sign is the presence of spontaneous or
tion of the vertiginous symptomatology (Table 1). induced nystagmus. Endpoint or physiologic nystagmus
is seen in normal children at a 40-degree deviation of the
Clinical Aspects eyes. Because visual fixation may inhibit mild vestibular
The medical history is the initial and most important step nystagmus, otolaryngologists use Frenzel glasses (⫹10
in evaluation of the child who complains of dizziness or diopters) both to magnify the eyes and to prevent fixa-
vertigo. Young children may not have the capacity or tion suppression.
vocabulary to describe the sensation of vertigo, but they
can use “playground synonyms” such as spinning, swing- Balance Testing
ing, sliding, or like “a merry-go-round.” The key symp- Clinical testing in the office or emergency department
tom is a sensation of motion that is either rotatory or may provide much information about the child or ado-
linear. lescent who has vertigo. Simple tests of balance include
The associated aural and neurologic symptoms must the Romberg and Unterberger-Fukuda test (stepping or
be sought carefully. Are there other symptoms of hearing marching test). The Romberg test evaluates propriocep-
loss (that may fluctuate), fullness, pressure, or ringing? Is tive function. A variation of the original examination—
there objective evidence of a hearing disorder? If tinnitus the tandem Romberg test— can be performed by having
or ringing is present, is it continuous, intermittent, or the child place one foot directly in front of the other with
pausitile? Are there symptoms of cortical or brainstem the arms either at the sides or crossed in front. Vision is
disorders such as headache, visual changes, seizures, or allowed and then excluded. The Unterberger-Fukuda
loss of consciousness? test is performed with the arms placed straight out in
front at shoulder height. Vision is excluded, and the child
Physical Examination is instructed to maintain the original position and march
The complete physical examination should focus on neu- in place. A total of 50 marching steps should be taken.
rologic evaluation of the cranial nerves and cerebellar Normally, patients either will remain in place, step for-
function (past-pointing and tandem gait). The auditory ward up to 50 cms, or turn within approximately 30
canal and tympanic membranes must be examined to degrees of center. Patients who have chronic peripheral
evaluate for evidence of middle ear infection, malforma- vestibular lesions will march slowly toward the side of the
tions, cholesteatoma, or a perilymphatic fistula. A fistula lesion.
test can be performed in a cooperative child with a The Hallpike-Dix maneuver should be used during
pneumatic otoscope or tragal pressure. The child is in- the neurologic examination to elicit paroxysmal posi-
structed to look straight ahead, and the eyes are exam- tional nystagmus. The child is placed in a sitting position

Pediatrics in Review Vol.23 No.1 January 2002 11

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neurology vertigo

midway on a flat examining table

and instructed to look straight Table 2. Acute Paroxysmal Vertigo
ahead at all times. The examiner
first turns the head to the side, and Hearing Loss No Hearing Loss
the patient then quickly is placed ● Labyrinthitis ● Infants—benign paroxysmal vertigo or torticollis
backwards with the head over the ● Menière disease ● Adolescents—vestibular neuronitis
end of the table. The response in ● Perilymphatic fistula ● Labyrinthine concussion
● Vascular occlusion ● Paroxysmal positional vertigo
patients who have a positional ver-
● Temporal bone fracture ● Migraine
tigo is horizontal rotary nystagmus ● Seizures
with the fast phase to the down- ● Subclavian steal
ward ear. The onset of the nystag-
Modified from Eviatar L. Otolaryngol Clin North Am. 1994;27:557–571.
mus is delayed with typically a 1- to
2-second latency that lasts for 10 to
20 seconds and is associated with a Other testing used by otolaryngologists in specific
sensation of rotational vertigo. With this positioning circumstances includes rotating chair tests, vestibular
maneuver, nystagmus and vertigo occur with the affected autorotation test (physiologic stimuli of high frequency
ear down. If a diagnosis of benign paroxysmal positional produced by active head oscillations), and posturography
vertigo is considered clinically, the Hallpike-Dix maneu- (sway movement testing).
ver is not recommended because it may interfere with
immediate bedside treatment of this disorder.
Diagnostic Approach and Specific Common
Disorders
Laboratory Testing Acute-onset vertigo or paroxysmal episodes of vertigo
All patients who have symptoms of vertigo must undergo
can be approached clinically based on the presence or
hearing testing or, in infants, auditory brainstem evoked
absence of hearing loss (Table 2). If vertigo is continuous
response testing. Additional pediatric investigations de-
and unremitting, assessment can be based on the pres-
pend on the characteristics of the vertigo and accompa-
ence or absence of neurologic abnormalities (Table 3).
nying symptoms in the individual patient. Children who
have persistent nonspecific vertigo require a complete
blood count, glucose tolerance test, and measurement of Acute Paroxysmal Vertigo With Hearing Loss
electrolytes, calcium, phosphorous, magnesium, and LABYRINTHITIS. The diagnosis of labyrinthitis is based
thyroid function. Certain patients may require testing for on a history of infection preceding the onset of vertigo
sickle cell disease. Patients who have sensorineural hear- and the presence of hearing impairment. The child usu-
ing loss or neurologic findings should receive computed ally is most comfortable lying on the unaffected side. Any
tomography with thin cuts through the temporal bones, movement causes severe vertigo, nausea, and vomiting.
magnetic resonance imaging (⫾ gadolinium), or angiog- These episodic symptoms usually subside after several
raphy. If there is a history of associated loss of conscious- days.
ness, an electroencephalographic study should be ob-
tained. PERILYMPHATIC FISTULA. This condition is much
more frequent in children than had been recognized in
Special Vestibular Function Testing the past and often is caused by minor head trauma. There
Based on the course of the symptoms, the physical exam- is a sudden onset of hearing loss and vertigo from rupture
ination, and the results of the previously noted investiga- of the round or oval window into the vestibule that
tions, the child may require referral to an otolaryngolo- results in the creation of a fistula. An abrupt change in
gist for additional vestibular testing. Caloric testing is the barometric pressure (eg, decompression syndrome) also
definitive procedure for identification of vestibular pa- can result in a similar rupture.
thology. Electronystagmography is a collection of exam-
inations for the saccadic, optokinetic, and smooth pur- MENIÈRE DISEASE. Menière syndrome is very uncom-
suit systems and of nystagmus induced by warming and mon in children. Symptoms consist of vertigo, fluctuat-
cooling the labyrinth. These tests are nonspecific and do ing hearing loss, a sensation of pressure in the ear, and
not provide a diagnosis, but when results are abnormal, tinnitus. Recurrent episodes of vertigo and tinnitus are
they are suggestive of vestibular dysfunction. common, with progressive hearing loss after each event.

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 neurology vertigo

BENIGN PAROXYSMAL POSI-

Table 3. Continuous Vertigo TIONAL VERTIGO. Benign paroxys-
mal positional vertigo has been de-
No Neurologic scribed in children as young as 11
Neurologic Abnormalities Abnormalities years of age. The cause has been
● Acoustic neuroma (neurofibromatosis type II) ● Metabolic disease** determined to be the presence of
● Posterior fossa tumour ● Tension-type headache free-floating debris in the posterior
● Drug-induced* ● Panic and anxiety disease semicircular canal. This type of ver-
● Cholesteatoma ● Depression
● Cerebral infarction ● Severe anemia tigo has been related to head
● Demyelinating disease (multiple sclerosis or ● Sickle cell disease trauma or vestibular neuronitis. In a
central nervous system Lyme disease) ● Polycythemia proportion of patients, no cause can
● Vertebrobasilar insufficiency ● Hyperviscosity syndromes be found. Benign paroxysmal posi-
● Cardiac dysrhythmias tional vertigo is provoked by a
*Aminoglycosides, ethacrynic acid, furosemide, isoniazid, quinine, acetylsalicyclic acid, diphenyl- change in position and lasts for sec-
hydantoin
**Diabetes mellitus, endocrine disorders (Addison disease, thyroid disease)
onds.
Modified from Eviatar L. Otolaryngol Clin North Am. 1994;27:557–571.
MIGRAINE AND SEIZURES. Basi-
lar artery migraine presents primar-
Acute Paroxysmal Vertigo Without Hearing ily in adolescent girls with recurrent stereotypic attacks of
Loss brainstem and cerebellar dysfunction. The clinical fea-
VESTIBULAR NEURONITIS. This disorder primarily oc- tures can include ataxia, dysarthria, vertigo, and tinni-
curs in adolescents following respiratory infection. tus. There are variable bilateral visual complaints. Al-
Symptoms include vertigo, nausea, and vomiting with ternating hemiplegia and paresthesias of the face and
postural instability. Episodes are self-limited but tend to limbs can occur, and there can be alteration of con-
recur with decreasing intensity. Diagnosis is made by sciousness. A severe pounding or pulsatile headache
electronystagmography and thermal caloric testing. will follow.
Vertigo also may be the aura preceding a generalized
BENIGN PAROXYSMAL VERTIGO AND TORTICOLLIS. seizure or present as an actual ictal phenomenon (partial
Benign paroxysmal vertigo presents initially between complex seizure). Vestibulogenic seizures are very rare
1 and 2 years of age, with symptoms recurring to the age and represent a form of reflex sensory epilepsy (induced
of 4 years. The child presents suddenly with extreme by spinning).
unsteadiness and may be unable to remain upright. Nys-
tagmus may be present, but other symptoms such as
vomiting are uncommon. The child is fully conscious Management and Prognosis
throughout the entire episode. Many children develop The treatment of vertigo depends on the duration and
migraine later in life. The diagnosis is supported by a discomfort of the symptom and the underlying pathol-
family history of migraine. ogy. Acute vertigo can be treated symptomatically and
Another migraine variant seen in infants is paroxysmal with reassurance. Antiemetics can be given rectally or
torticollis. A child who has this rare form of migraine will intramuscularly. Vestibular sedation or suppressant
tilt his or her head to one side for several hours (and medication is also useful (meclizine, dimenhydrinate,
infrequently for up to several days). There may be asso- promethazine, and diazepam). Persistent severe nausea
ciated vomiting. These episodes usually cease by 2 years and vomiting may require administration of prochlor-
of age, with many children developing typical migraine perazine or metoclopramide.
headaches by early childhood. Most children who have acute vertigo recover spon-
taneously over a period of several weeks to months.
LABYRINTHINE CONCUSSION. Head trauma with or Symptomatic recovery is due to vestibular compensation
without temporal bone fracture can produce labyrinthine and central plasticity (reorganization of vestibular cir-
concussion. There is severe vertigo, with unsteadiness cuits). In some children and adolescents, symptoms re-
and falling toward the affected side. These symptoms cur, often in association with physical or psychological
may persist, but they gradually diminish in intensity over stress. Medications producing vestibular sedation
a 4- to 6-week period. should not be prescribed for long-term daily use be-

Pediatrics in Review Vol.23 No.1 January 2002 13

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neurology vertigo

Figure. Epley particle repositioning maneuver.

cause they may interfere with the normal compensa- scribed, with balance and gait training during dynamic
tion process. tasks that precipitate the patient’s symptoms. These ex-
A specific treatment for benign paroxysmal positional ercises are practiced until an asymptomatic state is
vertigo is a bedside maneuver (Epley particle reposition- reached. Management of accompanying psychological
ing maneuver). This maneuver relocates the free floating symptoms (eg, anxiety, panic attacks, depression) de-
debris from the posterior semicircular canal into the pends on the nature of the associated symptom.
vestibule of the labyrinth. Symptomatic relief after a Surgical procedures for the treatment of vertigo rarely
single treatment session is reported in 80% to 90% of are required in childhood. Endolymphatic arachnoid
patients, although 15% to 30% may have recurrence of shunt operations are successful in 65% of patients who
symptoms. The maneuver is repeated until nystagmus no have Menière disease. Disabling vertigo due to vestibular
longer can be elicited (Figure). A modified version of the nerve or labyrinthine disorders may require vestibular
Epley maneuver can be taught to patients with instruc- nerve section. Surgery is an option for patients who have
tions to perform the activity three times a day until there severe intractable benign paroxysmal positional vertigo
are no symptoms of positional vertigo for 24 hours. using procedures to disable the posterior semicircular
Chronic or recurrent vertigo is often resistant to treat- canal.
ment, but it may respond to a course of clonazepam or Appropriate management of vertigo depends on de-
carbamazepine. Exercise regimens also have been pre- termination of the etiology and carefully tailored treat-

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 neurology vertigo

ment plans specific to the vestibular or central disorder Eviator L. Dizziness in children. Otolaryngol Clin North Am. 1994;
producing the vertigo. 27:557–571
Fife TD, Tusa RJ, Furman DS, et al. Vestibular testing techniques in
adults and children. Neurology. 2000;55:1431–1441
Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl
J Med. 1999;341:1590 –1596
Suggested Reading Linstrom CJ. Office management of the dizzy patient. Otolaryngol
Baloh RW. Vertigo. Lancet. 1998;352:1841–1846 Clin North Am. 1992;25:745–780
Cohen NL. The dizzy patient: update on vestibular disorders. Med Luxon LM. Vertigo. New approaches to diagnosis and manage-
Clin North Am. 1991;75:1251–1260 ment. Br J Hosp Med. 56:519 –520, 537–543
Derebery MJ. The diagnosis and treatment of dizziness. Med Clin Russell G, Abu-Arafeh I. Paroxysmal vertigo in children—an epidemi-
North Am. 1999;83:163–177 ological study. International J Ped Otorhin. 1999;49:S105–S107

Pediatrics in Review Vol.23 No.1 January 2002 15

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neurology vertigo

PIR Quiz
Quiz also available online at www.pedsinreview.org.

5. A 12-year-old child complains of dizziness and a feeling of the room “spinning around him” for the past
12 hours. He has had a cough and runny nose for 3 days. The symptoms improve when he lies on the left
side and worsen when he attempts to move from one place to another. Physical examination shows an
intact sensorium. Funduscopic examination results are normal, and external ocular movements are intact.
Tympanic membranes are normal. Sense of position and vibration and deep tendon reflexes are normal.
Hearing is impaired in the right ear. No tremors are noted, and finger-to-nose test results are normal.
Which of the following structures is most likely to be affected?
A. Cerebellum.
B. Labyrinth.
C. Midbrain.
D. Optic nerves.
E. Posterior columns.

6. A previously well 2-year-old child presents with marked unsteadiness for the past 12 hours. He now is
unable to stand or walk. There is no history of vomiting, and the child otherwise appears well. His mother
has had episodes of migraine for several years. Physical examination reveals no abnormalities other than
extremely unsteady gait and posture. Which of the following is the most likely diagnosis?
A. Benign paroxysmal vertigo.
B. Cerebellitis.
C. Guillain-Barré syndrome
D. Medulloblastoma.
E. Transverse myelitis.

7. A 5-year-old boy presents with a 2-week history of unsteady gait. He has had early morning headaches for
the past 3 months. He often complains of double vision, and his mother notes that he seems to bump into
objects while walking. For the past week, he has been drooling and appears to have difficulty swallowing.
Physical examination shows mild left-sided facial weakness and weakness of the extremities. Which of the
following is the most appropriate next step in management?
A. Brain stem evoked potentials.
B. Epley particle positioning maneuver.
C. Lumbar puncture.
D. Magnetic resonance imaging of the brain.
E. Test for visual refraction errors.

8. A 12-year-old boy presents with a feeling of dizziness and a sensation of objects spinning around him for
1 day. He also complains of hearing loss in the right ear. The symptoms started shortly after he was struck
by a baseball during a game. Physical examination shows normal ear canals and tympanic membranes.
Pneumatic otoscopy of the right ear reveals drifting of the eyes to the left with positive pressure and
drifting back to the right with negative pressure. Which of the following is the most likely diagnosis?
A. Benign paroxysmal positional vertigo.
B. Epidural hematoma.
C. Lateral sinus thrombosis.
D. Menière syndrome.
E. Perilymphatic fistula.

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 Vertigo
Daune L. MacGregor
Pediatrics in Review 2002;23;10
DOI: 10.1542/pir.23-1-10

Updated Information & including high resolution figures, can be found at:
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