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drugs, opiate receptor agonists (e.g., loperamide), reduce intestinal mobility and
delay transit time, thereby prolonging course of illness. Toxic side effects of these
medications include lethargy and paralytic ileus. Antisecretory drugs like bismuth
subsalicylate have limited efficacy and have potential for salicylate toxicity.
Adsorbents (e.g., hydrated aluminomagnesium silicates and kaolin-pectin), while
having potential to bind digestive mucus and reduce water loss, have not been
shown to reduce diarrheal duration, frequency, or volume.
Suggested Readings and Key References
Bryant K, McDonald LC. Clostridium difficile infection in children. Pediatr
Infect Dis J 2009;28:145–146.
Centers for Disease Control and Prevention. Delayed onset and diminished
magnitude of rotavirus activity—United States, November 2007–May 2008.
MMWR Morb Mortal Wkly Rep 2008;57(25):697–700.
Denno DM, Shaikh N, Stapp JR, et al. Diarrhea etiology in a pediatric emergency
department: a case control study. Clin Infect Dis 2012;55:897–904.
Freeman SB, Williamson-Urquhart S, Farion KJ, et al. Multicenter trial of a
combination probiotic for children with gastroenteritis. N Engl J Med
2018;379:2015–2026.
Gerber A, Karch H, Allerberger F, et al. Clinical course and the role of Shiga
toxin-producing Escherichia coli infection in hemolytic-uremic syndrome in
pediatric patients, 1997–2000 in Germany and Austria: a prospective study. J
Infect Dis 2002;186:493–500.
Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration
scale for children with acute gastroenteritis. Pediatrics 2008;122:545–549.
Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in
the diagnosis of dehydration in children. Pediatrics 1997;99:E6.
Lochhead A, Jamjoom R, Ratnapalan S. Intussusception in children presenting to
the emergency department. Clin Pediatr (Phila) 2013;52(11):1028–1033.
Schnadower D, Tarr PI, Casper TC, et al. Lactobacillus rhamnosus GG versus
placebo for acute gastroenteritis in children. N Engl J Med 2018;379:2002–
2014.

Shane AL, Mody RK, Crump JK, et al. 2017 Infectious Disease Society of
America Clinical Practice Guidelines for the Diagnosis and Management of
Infectious Diarrhea. Clinical Infectious Diarrhea 2017;65(12):e45–e80.
Vecchio AL, Vandenplas Y, Benninga M, et al. An international consensus report
on a new algorithm for the management of infant diarrhea. Acta Paediatrica
2016;105:e384–e389.


CHAPTER 24 ■ DIZZINESS AND VERTIGO
SOFIA CHAUDHARY, THERESA A. WALLS

INTRODUCTION
Dizziness can be a vague term that patients use to describe nonvertiginous
disturbances (pseudovertigo) such as lightheadedness, presyncope, intoxication,
ataxia, visual disturbances, unsteadiness, weakness, stress, anxiety,
hyperventilation, depression, and fear. True vertigo is the perception that the
environment is rotating relative to the patient or that the patient is rotating relative
to the environment. It can be immensely disturbing, even frightening, to patients
and their families. Preverbal children, unable to articulate the sensation, may be
irritable, may vomit, or may prefer to lie still. Even older children and adults may
have difficulty describing the sensation of vertigo.
Patients may present with dizziness as an isolated complaint or as part of a
constellation of symptoms related to an underlying illness. When evaluating a
child complaining of dizziness, the practitioner should listen carefully to the
details of the history as these may allow distinguishing true vertigo from
pseudovertigo. The key element in the history that strongly suggests true vertigo
is the subjective sense of rotation. Often, the best response to a chief complaint of
being dizzy is to say, “Tell me what you mean by ‘dizzy.’” Initial vague
complaints often become more concrete, and the underlying diagnosis may
become increasingly clear.

PATHOPHYSIOLOGY
True vertigo arises from a disturbance in either the peripheral or central
components of the vestibular system. The two peripheral sensory organs of the
system (together known as the labyrinth) are the semicircular canals (stimulated
by rotary motion of the head) and the vestibule (stimulated by gravity). Both
organs lie near the cochlea within the petrous portion of the temporal bone. The
proximity of the vestibule and cochlea explains the frequent association of vertigo
with hearing impairment.
Afferent impulses from these organs travel via the vestibular portion of the
eighth cranial nerve to the vestibular nuclei in the brainstem and in the
cerebellum. Efferent impulses travel through the vestibulospinal tract to the
peripheral muscles (helping to maintain balance and position sense) and also
within the medial longitudinal fasciculus to cranial nerves III, IV, and VI


(accounting for the oculovestibular reflexes). Almost all patients complaining of
true vertigo should have nystagmus, at least when the vertiginous symptoms are
peaking. The fast component of the nystagmus is almost always in the same
direction as the perceived rotation.

DIFFERENTIAL DIAGNOSIS
As discussed earlier, dizziness is best divided into vertiginous conditions (true
vertigo) and nonvertiginous conditions (pseudovertigo). Table 24.1 lists the
differential diagnosis of true vertigo and highlights the life-threatening causes.
Table 24.2 lists the most common causes of vertigo. Table 24.3 lists numerous
nonvertiginous conditions that may initially be described as dizziness. Because
the spectrum of nonvertiginous conditions is so broad, the following discussion
will concentrate on true vertigo.
Vertigo follows a dysfunction of the vestibular system within the semicircular

canals, vestibule, or vestibular nerve (peripheral vertigo), or within the brainstem,
cerebellum, or cortex (central vertigo). It can also be divided into conditions in
which hearing is impaired (usually peripheral causes) and into conditions in
which hearing is spared (usually central causes) ( Table 24.1 ). Finally, vertigo
can be divided into acute (usually infectious, postinfectious, traumatic, or toxic)
and chronic-recurrent groups (usually caused by seizures, migraine, or benign
paroxysmal vertigo of childhood).

Infections
Both acute and chronic bacterial and viral infections of the middle ear, with or
without associated mastoiditis, may cause vestibular and auditory impairment
(see Chapters 34 Hearing Loss and 58 Pain: Earache ). Severe, untreated, acute
suppurative otitis media with effusion may extend directly into the labyrinth.
Even without direct invasion of pathogens, inflammation can cause labyrinthitis.
Chronic and recurrent otitis media can produce a cholesteatoma of the
tympanic membrane, an abnormal growth of keratinizing squamous epithelium
caused by repeated cycles of perforation and healing. Cholesteatomas can erode
the temporal bone and the labyrinth, producing a draining fistula from the
labyrinth that presents as vertigo, nausea, and hearing impairment. Computed
tomography (CT) scan or magnetic resonance imaging (MRI) shows destruction
of the temporal bone.
Viral infections can directly affect the labyrinth or the vestibular nerve;
together these conditions are known as vestibular neuronitis. Known pathogens
include mumps, measles, and the Epstein–Barr virus. Herpes zoster infection of
the ear canal and facial palsy (Ramsay Hunt syndrome) may also involve the


eighth nerve. More commonly, a nonspecific upper respiratory tract infection may
precede the illness. Onset is usually acute and can be severe. Nystagmus is
usually present. Patients prefer to lie motionless with their eyes closed. Recovery

is from 1 to 3 weeks. Early use of prednisone may shorten the course.

Migraine
Vertigo may be a prominent feature of classic migraine, or of a migraine
equivalent, in which there is no associated headache (see Chapters 59 Pain:
Headache and 97 Neurologic Emergencies ). Nearly 20% of children with
migraine may have vertiginous symptoms during their aura. Basilar migraine
presents as a throbbing occipital headache following signs and symptoms of
brainstem dysfunction (including vertigo, ataxia, tinnitus, and dysarthria). Vertigo
from migraine equivalent (without pain) is typically seen in patients with a family
history of migraine headache and is associated with other transient neurologic
complaints (e.g., weakness, dysarthria).
TABLE 24.1
CAUSES OF VERTIGO IN CHILDREN
Peripheral causes

Central causes

Ingestions a , b
Temporal bone fracture a , b
Suppurative or serous labyrinthitis b
External ear impaction (especially cerumen)
Ramsay Hunt syndrome (Varicella zoster
infection)
Cholesteatoma b
Perilymphatic fistula b
Vestibular neuronitis
Benign paroxysmal vertigo
Posttraumatic vestibular concussion
Ménière disease b

Tumor a
Meningitis a , b
Encephalitis a
Trauma a
Stroke a , b
Increased intracranial pressure

a Life-threatening
b May

causes of vertigo.
have associated hearing impairment.

a

Multiple sclerosis
Seizure (usually complex
partial)
Migraine
Motion sickness
Paroxysmal torticollis of
infancy