COMMON NEUROLOGIC PROBLEMS 0195-5616/00 $8.00 + .

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VESTIBULAR DYSFUNCTION
William B. Thomas, DVM, MS

The function of the vestibular system is to transduce the forces of

gravity and movement into neurologic signals that the brain can use to
determine the position of the head in space and to coordinate head
movements with the motor reflexes responsible for postural and ocular
stability. Not surprisingly, lesions of the vestibular system commonly
result in abnormal posture of the head and body, gait imbalance, and
abnormal eye movements. 6 This article reviews the physiology of the
vestibular system and discusses the management of common vestibular
disorders in the dog and cat.

CLINICAL ANATOMY AND PHYSIOLOGY

The two functional components of the vestibular system are the

peripheral component located in the inner ear and the central component
located in the brain stem and cerebellum.

Peripheral Component

The membranous labyrinth and the vestibular portion of cranial

nerve VIII make up the peripheral vestibular structures. The membra-
nous labyrinth is a series of fluid-filled tubes and chambers consisting
of the cochlea, which is involved in hearing, and the utricle, saccule,
and semicircular canals, which are involved in vestibular function. These
structures are encased in the petrous temporal bone dose to cranial

From the Department of Small Animal Clinical Sciences, University of Tennessee, Knox-
ville, Tennessee

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 30 • NUMBER 1 • JANUARY 2000 227

228 THOMAS

nerve VII and sympathetic innervation to the face. The saccule and
utricle are primarily responsible for detecting gravity and linear accelera-
tion, and the semicircular canals detect rotation. 27, 54

Central Component

The vestibular portion of cranial nerve VIII synapses on the vestibu-

lar nuclei located in the medulla oblongata and on neurons in the rostral
portion of the cerebellum. The vestibular nuclei are connected via the
medial longitudinal fasciculus to the nuclei of cranial nerves III, IV, and
VI to control eye movements. This system helps to maintain conjugate
gaze when the head moves. The vestibular nuclei are also connected via
descending pathways to the neurons in the spinal cord that provide tone
in muscles of the neck, trunk, and limbs which oppose gravity to
maintain upright posture. 27• 54

Function of the Utricle and Saccule to Detect Gravity

and Linear Acceleration

Located within each utricle and saccule is a sensory area called a

macula. Each macula contains specialized hair cells that generate nerve
impulses involved in vestibular function. The hair cells have cilia pro-
jecting into a gelatinous substance containing calcium carbonate crystals
called stataconia or otoliths. 27
Under normal resting conditions, nerve fibers leading from the
hair cells continuously transmit impulses at a constant rate. When the
orientation of the head changes, the weight of the stataconia bends the
cilia, which alters the nerve impulses. When the cilia are bent in one
direction, the rate of nerve impulses increases, and when the cilia are
bent in the opposite direction, the rate of nerve impulses decreases. In
each macula, different hair cells are oriented in different directions so
that a different pattern of stimulation occurs with different head posi-
tions. The specific patterns of stimulation apprise the brain of the posi-
tion of the head with respect to gravity. 27
The vestibular neurons in the brain stem use these nerve impulses
to help maintain normal upright posture. For example, when the head
is in the horizontal position, the input from each side is equal. When
the head tilts to the left, hair cells in the left inner ear are excited and
those in the right inner ear are inhibited. This results in stimulation of
the left vestibulospinal pathways to activate antigravity muscles on the
left side of the neck, trunk, and limbs, which returns the head and body
to a level position. A lesion in the left inner ear abolishes neuronal input
from the left, although the baseline activity from the right remains. The
result is stimulation of the right vestibulospinal tracts, increasing tone
to the antigravity muscles on the right. This causes the head and body
to tilt or lean to the left towards the side of the peripherallesion.27, 50
 VESTIBULAR DYSFUNCTION 229

The cerebellum is also important in vestibular function. Portions of

the cerebellum provide tonic inhibition to the vestibular nuclei via the
caudal cerebellar peduncles. A lesion in the left cerebellar peduncle, for
instance, causes decreased inhibition of the left vestibular nuclei. The
excess activity from the left vestibular nuclei activates the left vestibulo-
spinal tract, causing the head and body to lean to the right. This is called
a paradoxic vestibular syndrome, because the head tilt is to the side
opposite the lesion.
When the head suddenly moves, that is, when the head is acceler-
ated, the stataconia, which have greater inertia than the surrounding
fluid, bend the hair cells cilia in a certain pattern depending on the
direction of movement. The resulting pattern of nerve impulses is relayed
to the brain, providing a sense of head acceleration (linear acceleration).
This causes the vestibulospinal tracts to activate the muscles necessary
to maintain normal head and body posture during linear accel-
eration_27, 50

Function of the Semicircular Canals to Detect Head

Rotation

There are three semicircular canals in each inner ear. The canals are
named according to their position in space (horizontal, rostral-vertical,
caudal-vertical); each canal lies approximately at a right angle to the
others, with one for each plane of the body. The canals are filled with
fluid called endolymph. At one end of each canal is an enlargement
(ampulla) containing the crista ampullaris. The crista ampullaris contains
the specialized hair cells responsible for transducing rotational move-
ment into neuronal impulses. These hair cells have cilia that project into
the endolymph in the canals. Under normal resting conditions, the hair
cells continuously emit neuronal discharges at a constant rate. 27, 50
When the head begins to rotate in any direction (angular accelera-
tion), the endolymph in the semicircular canals, because of its inertia,
tends to remain stationary, while the canals themselves rotate. The result
is a relative flow of fluid in the direction opposite to the rotation of the
head. This flow of fluid bends the hair cell cilia, changing the rate of
neuronal discharges. Flow of fluid in one direction increases, or stimu-
lates, neuronal activity, and flow in the opposite direction decreases, or
inhibits, neuronal activity. After a few seconds of head rotation, the fluid
"catches up" with the moving canals, the hair cell cilia return to their
resting position, and the neuronal impulses return to baseline activity.
The opposite happens if the head rotation is stopped. The endolymph
tends to continue to flow, while the canals themselves stop. Now, the
cilia are bent in the opposite direction, causing the exact opposite pattern
of neural discharges. After another few seconds, the endolymph stops
and the system returns to the resting state. 27
The most effective stimulus for each semicircular canal is rotation
of the head in the plane of the canal. Because each canal is oriented in a
230 THOMAS

different plane, rotation of the head in any direction stimulates at least

one canal. Furthermore, each semicircular canal on one side is function-
ally paired with a canal on the other side by their common position in
a parallel plane. Movement in one plane stimulates the hair cells of the
appropriate canal on one side and inhibits the hair cells on the other
side. The brain uses these patterns of neural impulses to detect when
the head is beginning to rotate. Although the macula and saccule can
detect an abnormal head position once it has occurred, the semicircular
canals can detect the initial rotation of the head. This allows the brain
to activate the appropriate antigravity muscles to prevent an abnormal
posture before it occurs.27, 50

Function of the Vestibular System to Coordinate

Eye Movements

The visual system performs optimally when images are held steady
on the retina. Even small movements of the head must be compensated
for to avoid images "slipping" on the retina. Normally, rotation of the
head induces a compensatory eye movement in the direction opposite
that of head movement. This serves to stabilize images on the retina.
The stimulus for this eye movement is vestibular information from the
semicircular canals. Signals from the vestibular neurons are relayed to
the appropriate motor nuclei of cranial nerves III, IV, and VI, which
control the extraocular muscles. This response is called the vestibula-
ocular reflex. 27' 50
For example, rotation of the head to the left causes the endolymph
in the left horizontal canal to flow in the direction causing increased
activity of the hair cells, while in the right horizontal canal, the endo-
lymph flows in the direction causing decreased activity. This results in
contraction of the right lateral rectus muscle and the left medial rectus
muscle, causing the eyes to move to the right. This is the "slow phase"
of the vestibula-ocular reflex. The presence of a slow compensatory eye
movement induced by head rotation (the so-called "doll's eye maneu-
ver") implies normal function of the vestibula-ocular pathways. 27, 50
With continued head rotation, the tension in the ocular muscles
becomes too great to allow further eye movement and the slow phase
of the vestibula-ocular reflex is interrupted by a corrective fast move-
ment in the direction of the head tum, the "fast phase" of the vestibula-
ocular reflex. The fast phase is a type of saccadic eye movement induced
by visual stimulus, usually an image in the visual periphery, and is
controlled by higher brain centers and not the vestibular system. 53 At
the end of the corrective fast movement, the slower compensatory move-
ment is resumed, with the eyes now pointing in a new direction. The
alternation of slow compensatory movements with fast jerks back to-
wards the central position is called nystagmus. It is customary to refer
to a nystagmus as occurring in the direction of the fast phase of move-
 VESTIBULAR DYSFUNCTION 231

ment. Thus, rotation towards the left produces a horizontal nystagmus

to the left. 50
Damage to a single semicircular canal can result in a loss of the
baseline neural activity from the affected canal. Because the functionally
paired canal in the contralateral ear continues to exhibit baseline activity,
there is an imbalance of signals from the two canals. This pattern of
activity is interpreted as head rotation, despite the fact that the head is
motionless. This induces a nystagmus characterized by eye movements
in the plane of the damaged canal, with the slow phase towards the
damaged side and the fast phase in the opposite direction. As selective
damage to only one semicircular canal is unusual, abnormal eye move-
ment caused by a lesion in the inner ear usually has horizontal, vertical,
and rotary components because of the combined effects of altered input
from multiple damaged canals. The horizontal and rotary components
are most prominent, because the components from the two vertical
canals tend to cancel out one another. 27• 50

COMPENSATORY MECHANISMS AND

PHARMACOLOGIC THERAPY

The nervous system is able to compensate for vestibular disorders

provided that the lesion is stable or changing slowly enough. The mecha-
nisms that contribute to this recovery include the central preprogram-
ming of eye movements and postural responses and the substitution of
visual and somatosensory cues for the lost vestibular cues. The mecha-
nism most successful in contributing to recovery, however, is probably
adaptation of the vestibular system itself by modulation of activity
in the brain stem and cerebellum. 31 Experimental work indicates that
correction of vestibular dysfunction requires somatosensory feedback as
the patient attempts to use vestibular reflexes. Enforced activity that
appropriately challenges the vestibular system enhances the rate of
compensation. Conversely, a period of immobilization after an acute
peripheral vestibular lesion not only slows recovery but actually limits
the degree of vestibular function that is reached. 71 Therefore, even
though cage confinement of an animal with acute vestibular dysfunction
may be necessary to prevent injury when the patient is severely ataxic,
normal activity should be encouraged as soon as possible.
Many types of drugs, including anticholinergics, antihistamines,
and benzodiazepines, have been used to treat vestibular dysfunction
in human patients?1 Drugs with anticholinergic activity diminish the
excitability of neurons in the vestibular nuclei, suppressing both the
spontaneous firing rate and response to vestibular stimulation. The
vestibular depressant properties of antihistamines (e.g., meclizine, di-
menhydrinate) may be partly a result of their weak anticholinergic
properties. The phenothiazines also have weak anticholinergic and anti-
histaminic effects. Likewise, diazepam decreases the resting activity of
vestibular nuclei neurons. 6 These agents work by suppressing vestibular
232 THOMAS

tone from the contralateral normal vestibular apparatus, decreasing the

imbalance in vestibular input to the brain. Meclizine (25 mg orally once
daily in dogs, 12.5 mg orally once daily in cats) and diazepam (0.1-0.5
mg/kg orally every 8 hours in dogs, 1-2 mg orally every 12 hours in
cats) are sometimes helpful in decreasing signs associated with acute
vestibular lesions. Long-term use of these drugs is not indicated, how-
ever, because they may suppress the sensory imbalance in the vestibular
system that is an essential stimulus to ultimate recovery. 48, 71

SIGNS OF VESTIBULAR DISEASE

Vestibular dysfunction can occur with damage to either the periph-

eral or central components. Most disorders affect the vestibular system
in an asymmetric (unilateral) fashion, but bilateral lesions occasionally
occur. Different clinical signs depend on whether the peripheral or
central components are damaged (Table 1).

Head Tilt

Head tilt is the most consistent sign of unilateral vestibular dysfunc-

tion. This occurs as a result of the loss of antigravity muscle tone on one
side of the neck. Peripheral vestibular lesions cause a head tilt towards

Table 1. NEUROLOGIC SIGNS OF PERIPHERAL VERSUS CENTRAL VESTIBULAR

DYSFUNCTION

Sign Peripheral Central

Head tilt To the same side as the To either side
lesion
Ataxia Yes Yes
Rotation-induced Yes, may be Yes, may be asymmetric
nystagmus asymmetric
Spontaneous Horizontal or Horizontal, rotational, or
nystagmus rotational, fast phase vertical; fast phase to
away from side of either side; may change
lesion, direction not direction with head
altered with head position
position
Proprioceptive No Possible, usually same side
positioning deficits as lesion
Cranial nerve deficits Cranial nerve VII may Cranial nerves V, VI, VII, IX,
be affected, same X, or XII may be affected;
side as lesion same side as lesion
Homer's syndrome Possible, same side as Rare
lesion
Mental status Alert, may be May be disoriented,
disoriented depressed, stuporous, or
comatose
 VESTIBULAR DYSFUNCTION 233

the side of the lesion. For example, a right inner ear lesion causes the
right ear to be held lower than the left. Central lesions can cause a head
tilt to either side. Animals with bilateral vestibular disease usually do
not have a head tilt but typically stand crouched and low to the ground. 54

Ataxia and Gait Disturbance

Vestibular lesions often cause ataxia characterized by a base-wide

stance and swaying of the trunk and head. Animals with unilateral
lesions often lean, fall, or roll to one side. Affected animals commonly
fall when they shake their head. With bilateral vestibular disease, the
patient falls to either side and often moves the head widely from side
to side. Peripheral lesions do not cause weakness or deficits in proprio-
ceptive positioning. Such deficits indicate a central lesion that is affecting
ascending proprioceptive or descending motor pathways. 54 The presence
or absence of proprioceptive positioning deficits is the most reliable way
to discriminate between peripheral and central vestibular lesions.

Nystagmus

Nystagmus is a rhythmic movement of the eyes. Jerk nystagmus is

the most common form of nystagmus and is characterized by a fast and
slow phase. As discussed previously, the direction of the nystagmus
refers to the direction of the fast phase and may be horizontal, vertical,
rotational, or a combination of these three directions. Physiologic nystag-
mus is nystagmus that occurs in normal animals, and pathologic nystag-
mus implies an underlying abnormality. 6

Physiologic Nystagmus
In normal alert patients, rotation of the head initially induces nys-
tagmus in the plane of rotation. This is the normal vestibula-ocular
reflex and is characterized by a slow phase in the direction opposite that
of the head rotation and a fast phase in the same direction as the head
rotation. For example, rotation of the head to the left in the horizontal
plane causes a horizontal nystagmus with the fast phase to the left.
Vestibular disease may cause an asymmetric rotation-induced nystagmus
when the head is moved in different directions. Animals with bilateral
vestibular disease lack rotation-induced nystagmus, as the stimulus for
this reflex is vestibular activation. 54
There are two other types of physiologic nystagmus. Caloric-in-
duced nystagmus induces flow of the endolymph in the semicircular
canals by creating a thermal gradient from one side of the horizontal
canal to the other. The test for physiologic nystagmus consists of irrigat-
ing the ear canal with warm (44°C) or iced (approximately 0°C) water
and observing for the induced nystagmus. Asymmetry in the response
234 THOMAS

when each ear is irrigated suggests vestibular dysfunction. 6 Results in

animals vary greatly; thus, this test is rarely used in veterinary medicine.
Optiokinetic nystagmus is induced by moving a striped pattern across
the patient's visual field. Normally, there is a slow following eye move-
ment in the direction of the stripe movement that is regularly interrupted
by fast movements in the opposite direction. The stimulus for this
reflex is visual and not vestibular. Absent or asymmetric opticokinetic
nystagmus usually indicates blindness or central nervous system dis-
ease, although acute peripheral vestibular lesions also can cause an
asymmetric response. 6 This test is uncommonly used in veterinary medi-
cine.

Pathologic Nystagmus
Spontaneous Nystagmus. Spontaneous nystagmus is nystagmus
that occurs when the head is in the normal position and not moving. A
unilateral acute peripheral lesion often causes spontaneous nystagmus
with horizontal and rotational components. The fast phase is directed
away from the side of the lesion. Spontaneous nystagmus resulting from
a peripheral lesion is strongly inhibited by visual fixation. Unless the
patient is seen within the first few days of the occurrence of the lesion,
spontaneous nystagmus is often absent because of compensation. Spon-
taneous nystagmus of central origin is usually purely vertical, horizontal,
or rotational, as pathways for these vestibulo-ocular movements separate
beginning at the vestibular nuclei. 6 Vertical spontaneous nystagmus indi-
cates a central lesion. Spontaneous nystagmus is usually not a feature of
bilateral vestibular disease.
Positional Nystagmus. Positional nystagmus refers to nystagmus
that is present only when the head is placed in an unusual position, for
example, extended or upside down. Because spontaneous nystagmus
often resolves within several days, the examiner should always attempt
to induce positional nystagmus by extending the head and placing the
patient in left lateral, right lateral, and dorsal recumbency. The presence
of positional nystagmus indicates vestibular dysfunction but does not
further localize the lesion, as it can occur with central or peripheral
lesions. 6 Nystagmus that changes direction with differenthead positions
is most commonly seen with central lesions, however. Positional nystag-
mus is usually absent with bilateral lesions. .
Pendular Nystagmus. Pendular nystagmus refers to nystagmus that
does not have a fast and slow phase-the eyes move with equal speed
in either direction. Spontaneous pendular nystagmus is often caused by
a congenital abnormality in the visual pathways, most commonly in
oriental breeds of cats such as the Siamese and Himalyan. 34 It is im-
portant to recognize pendular nystagmus and realize that it is not a sign
of vestibular disease.
In summary, the presence of either spontaneous or positional jerk
nystagmus is always abnormal and usually indicates vestibular dysfunc-
tion. With peripheral vestibular disease, the nystagmus is either hori-
 VESTIBULAR DYSFUNCTION 235

zontal or rotational and the fast phase is directed away from the side of
the lesion. With central vestibular disease, the nystagmus may be in any
direction (including vertical) and may change direction with changes in
the position of the head. In other words, vertical nystagmus or nystag-
mus that changes direction with different positions of the head indicates
a central lesion. Animals with bilateral vestibular disease do not have
spontaneous or positional nystagmus.

Strabismus

Vestibular disease may cause one eye to be deviated ventrally or

ventrolaterally when the neck is extended (positional strabismus). The
ventrally deviated eye is usually on the side of the lesion. Occasionally,
a constant ventral strabismus is present with vestibular disease.

Cranial Nerve Deficits and Horner's Syndrome

Because cranial nerve VII and sympathetic innervation to the face

travel close to the inner ear, peripheral vestibular lesions may be associ-
ated with ipsilateral facial paralysis, or Homer's syndrome. Homer's
syndrome in the cat and dog is characterized by ipsilateral miosis, ptosis
(drooping of the upper lid and sometimes elevation of the lower lid),
enophthalmos, and protrusion of the third eyelid. Central vestibular
lesions also may affect other cranial nerves such as the trigeminal and
abducens nerve, but Homer's syndrome is rare.

DIAGNOSTIC ASSESSMENT

Vestibular dysfunction is usually evident as head tilt, ataxia, or

abnormal nystagmus. A detailed history is taken to determine the onset
of signs (sudden or insidious) and any progression. The client is ques-
tioned about any trauma, previous ear infection, topical or systemic
medication, or other signs of illness that the dog or cat has demonstrated
such as scratching at the ears or respiratory signs. A thorough neurologic
examination is performed, paying particular attention to any deficits in
postural reactions and cranial nerve abnormalities. Any spontaneous
nystagmus should be characterized, and an attempt should be made to
stimulate rotation-induced nystagmus and positional nystagmus. Based
on these results, the clinician is usually able to determine if the lesion
involves the peripheral or central components of the vestibular system.
This step is critical, because the diagnostic considerations and necessary
diagnostic tests depend on whether the central or peripheral components
are affected.
Ancillary diagnostic tests for patients with peripheral vestibular
disease include otoscopic examination; imaging of the tympanic bullae
236 THOMAS

with radiography, computed tomography (CT), or magnetic resonance

(MR) imaging; and thyroid function testing. Tympanometry is also useful
in assessing the middle ear, especially in animals with infection. 42 Brain
stem auditory evoked response testing is also useful in assessing the
inner ear and brain stem and sometimes helps to differentiate between
peripheral and central lesions. 58 Diagnosis of central vestibular disease
is often based on CT or MR imaging of the brain and analysis of
cerebrospinal fluid (CSF).

PERIPHERAL VESTIBULAR DISEASES

Otitis Media-lnterna

Otitis is the most common cause of peripheral vestibular disease in

the dog and is also common in the cat. 55 Otitis can cause vestibular
dysfunction by two mechanisms. Bacteria that infect the middle ear can
produce toxins that inflame the labyrinth (otitis media), or bacteria may
invade the labyrinth itself (otitis interna), often as an extension of otitis
media. Common bacterial isolates include Staphylococcus spp., Streptococ-
cus spp., and Pseudomonas spp.
Affected animals may have signs of otitis externa, including head
shaking, rubbing or scratching at the ears, and pain. Otitis media also
can occur without signs of otitis externa, however. 53 Early in the course
of otitis media-interna, there may be hyperirritability of the sympathetic
pathway to the eye, resulting in mydriasis. Frequent yawning also may
be a feature. 10• 53 Later, there may be peripheral vestibular dysfunction,
ipsilateral facial paralysis, or ipsilateral Horner's syndrome.
The first step in evaluation is a thorough otoscopic examination,
which usually requires anesthesia and cleaning of the ears by gently
flushing with saline. 10 Standard otoscopic examination does not allow
visualization of the entire tympanic membrane, and visual inspection is
particularly difficult when there is inflammation and exudate in the
external ear canal. 42 A small (2-4 mm) endoscope allows a more complete
examination. 53 The tympanic membrane may be absent, disrupted, or
bulging. In many patients with otitis media, however, the tympanic
membrane appears intactY· 43 Tympanometry is also helpful in assessing
the tympanic membrane and middle ear. 42
Adequate radiography of the tympanic bullae requires general anes-
thesia to allow proper positioning of the patient's head. Useful views
include dorsoventral, oblique lateral, and rostroventral-caudodorsal
open-mouthed views. 32 Radiographic changes may include fluid density
within the tympanic cavity and sclerosis of the bulla, but radiographs
may be normal, especially early in the course of the disease. 49 CT and
MR imaging may be more sensitive in detecting small amounts of fluid
in the middle ear (Fig. 1). 45
Samples for cytology and culture and sensitivity testing should be
collected. Culturing of specimens from the middle ear obtained by
 VESTIBULAR DYSFUNCTION 237

Figure 1. CT of otitis media in a dog with ataxia and a head tilt to the right. On this
transverse image, there is increased density within the right tympanic bulla.

myringotomy may be preferable to that of samples from the external ear

canal, as results are often different in dogs with otitis media. 13 Myringo-
tomy can be performed with a 22-gauge spinal needle passed through
an otoscope. A 6-mL syringe is attached to the needle and used to gently
aspirate any fluid from the middle ear. The m yringotomy defect is small
and heals quickly. 10
Bacterial otitis media-interna should be treated with 4 to 6 weeks of
systemic antibiotics chosen on the basis of culture and sensitivity that
results. Topical antibiotics are insufficient for otitis media-interna. 10
Pending culture results, a first-generation cephalosporin (5-10 mg / kg of
cephalexin twice daily) should be used. Considering the insensitivity of
otoscopic examination and radiography, a course of antibiotic therapy is
indicated in suspected cases even if otitis media-interna cannot be identi-
fied conclusively. Surgery to provide drainage and remove infected
tissue may be necessary in patients refractory to medical therapy. A mild
head tilt, facial paralysis, or Horner's syndrome may persist, despite
effective therapy, because of permanent damage to neural structures.

Canine Idiopathic Vestibular Syndrome

This is the second most common cause of peripheral vestibular

disease in the dog. 55 Compared with dogs with otitis media-interna,
dogs with idiopathic vestibular disease tend to be older (mean age, 12.5
years). 55 There is a n acute onset of ataxia (which can be severe), head tilt,
rotational or horizontal nystagmus, and occasionally vomiting. Postural
reactions are normal, and dogs do not h ave facial paralysis or Horner's
238 THOMAS

syndrome. The cause of this syndrome is unknown. 9• 55 A similar disease,

vestibular neuronitis, occurs in people and may be caused by a virus. 6• 16
Affected dogs improve spontaneously within 2 weeks, although there
may be a mild persistent head tilt. Short-term administration of vestibu-
lar suppressants such as meclizine or diazepam may help, but as dis-
cussed previously, long-term therapy with these drugs may be counter-
productive.

Feline Idiopathic Vestibular Syndrome

Feline idiopathic vestibular syndrome is a common cause of periph-

eral vestibular dysfunction in cats.U This disease is most common in the
summer and fall months and can affect cats of any age, especially those
that spend time outdoors. It is characterized by a sudden onset of ataxia,
nystagmus, and head tilt consistent with a peripheral vestibular lesion.
Vomiting is uncommon. Rarely, signs of bilateral vestibular disease are
observed. Facial paralysis, Horner's syndrome, and proprioceptive posi-
tioning deficits are not features of this disease. Diagnosis is based on
clinical features and exclusion of other causes of peripheral vestibular
disease. The results of diagnostic tests such as otoscopic examination
and radiographs are normal. Neurologic deficits typically improve spon-
taneously within about 2 weeks. In some cats, there is a mild persistent
head tilt and ataxia. There is no firm evidence that corticosteroids,
antibiotics, antihistamines, or any other treatment influences the out-
come of this disease. Relapse has been reported but is rare. 11
The cause of this syndrome is unknown. A viral cause, as suspected
in people with vestibular neuronitis, is possible. Another theory is that
this syndrome is caused by aberrant migration of Cuterebra larvae. This
would explain the fact that affected cats usually have access to outdoors
and develop signs during the summer and fall months, coinciding with
the larval migration portion of the Cuterebra life cycle. 28

Nasopharyngeal Polyps

Inflammatory polyps arise from the lining of the tympanic cavity

or auditory tube in cats and, rarely, dogs. Affected cats are usually 1 to
5 years old. 35 Signs may reflect upper respiratory disease (sneezing,
respiratory stridor), pharyngeal disease (gagging, dysphagia), or inner
ear disease (peripheral vestibular dysfunction, Horner's syndrome, facial
paralysis). 35 Diagnosis is based on careful oropharyngeal and otoscopic
examination (Fig. 2). Radiographic abnormalities are similar to those
seen with otitis media. 35 Some polyps can be removed by simple traction,
but recurrence is possible. Definitive treatment may require bulla osteot-
omy to remove the portion of the polyp within the bulla cavity. The
prognosis is generally good. 35
 VESTIBULAR DYSFUNCTION 239

Figure 2. Nasopharyngeal polyp in a cat. A, There is a smooth, pale mass (arrow) in the
nasopharynx. B, The excised mass showing the stalk (arrow) that was attached to the
tympanic bulla. SP = soft palate; T = tongue.

Hypothyroidism
Hypothyroidism can cause peripheral vestibular dysfunction in
dogs. 33 The onset of signs may be acute or chronic. Affected dogs also
may have unilateral or bilateral facial paresis, lethargy, and generalized
weakness; however, vestibular dysfunction is often the only clinical sign,
and obvious signs of hypothyroidism may be absent. Diagnosis is based
on laboratory evaluation of thyroid function and response to thyroid
supplementation. Vestibular dysfunction typically resolves within 2
months of treatment. 33

Neoplasia
Neoplasia originating in the ear canal can cause peripheral vestibu-
lar dysfunction in dogs and cats. Examples include squamous cell card-
240 THOMAS

noma, ceruminous gland adenocarcinoma, and lymphoma. 36 Neoplasia

should be suspected in older animals and in animals with pain on
opening the mouth. 36• 55 Lysis or an active periosteal reaction involving
the bulla or temporal bone is almost always caused by neoplasia (Figs.
3 and 4). Complete surgical excision of tumors involving the middle or
inner ear is difficult. Radiotherapy may offer some benefit, but the
prognosis is generally poor.36

Ototoxicity

Although many drugs and chemicals are potentially toxic to the

inner ear, the prevalence of ototoxicity in dogs and cats appears to be
low. In this author's experience, topical application of chlorhexidine has
been associated with acute signs of peripheral vestibular disease and
occasionally deafness in dogs and cats. The potential contribution of any
underlying otitis and iatrogenic trauma in these patients is incompletely
understood. If vestibular dysfunction is evident immediately after instil-

Figure 3. Skull radiograph of squamous cell carcinoma of ear in a dog with ataxia, right
head tilt, and pain on opening the mouth. On this rostroventral-caudodorsal open-mouthed
view, there is lysis of the right tympanic bulla and petrous temporal bone. Compare to the
normal left tympanic bulla (arrows).
 VESTIBULAR DYSFUNCTION 241

Figure 4. CT of a ceruminous gland adenocarcinoma involving the ear. On this transverse

image there is lysis of the left tympanic bulla (arrows), which is filled with a soft-tissue den-
sity.

lation of a potentially ototoxic substance, the ear canal should be flushed

immediately with saline. Vestibular dysfunction tends to resolve in about
2 weeks, but any deafness may be permanent. 54

Central Vestibular Diseases

Inflammatory disorders of the brain (encephalitis) are common

causes of central vestibular lesions in dogs and cats. Other neurologic
deficits also can be seen depending on which areas of the nervous
system are involved.

Canine Distemper Encephalomyelitis

Widespread use of effective vaccines has substantially reduced the
incidence of distemper in many regions, but outbreaks still occur among
unvaccinated dogs, and sporadic cases of distemper encephalomyelitis
in vaccinated dogs are by no means rare.69 The presence and pattern of
illness depend primarily on the viral strain and the age and immuno-
competence of the patienU· 40• 56• 62• 69 Dogs that develop an early effective
immunologic response recover with mild or no clinical signs.2• 40 Dogs
that are unable to mount an immunologic response suffer severe sys-
242 THOMAS

temic illness, including acute encephalitis, leading to death within about

3 weeks of exposure. 2, 40 Dogs with a delayed immunologic response do
not develop acute illness but may develop chronic encephalomyelitis. 69
Immature dogs with distemper encephalitis typically suffer a rapid
onset of systemic illness characterized by conjunctivitis, nasal discharge,
cough, vomiting, and diarrhea. Neurologic dysfunction can occur during
or after the systemic illness. Mature dogs are more likely to develop
chronic encephalomyelitis, which is most commonly manifested as
slowly progressive gait deficits or vestibular dysfunction, Many of these
dogs have an adequate vaccination history 65, 68 Signs of systemic illness
are often absent or transient. 65, 69
In puppies with acute distemper infection, a clinical diagnosis often
can be based on the typical systemic and neurologic signs. Diagnosis of
distemper encephalomyelitis in mature dogs is difficult, because concur-
rent systemic signs may be absent and laboratory tests are often nonspe-
cific. Active or inactive retinochoroiditis is evident on fundic examina-
tion in many patients but is not specific for distemper. 65 Lymphopenia
is the most consistent h~matologic abnormality, but this finding is not
specific and may be absent. 65' 69 Fluorescent staining of conjunctival
smears to detect distemper virus antigen is positive in about 50% of
patients. 65 Serology to detect antibodies to canine distemper virus is
often performed, but results can be difficult to interpret, because many
of these dogs have been vaccinated. 65 Analysis of CSF usually shows
moderate mononuclear pleocytosis with a moderate elevation in pro-
tein.57' 65' 69 The presence of antibody to canine distemper virus in the
CSF is probably the most reliable indicator of infection; however, false-
positive results can occur if there is damage to the blood-brain barrier
from some other cause that allows serum antibodies to leak into the
CSf.57
The prognosis is poor for puppies with severe systemic and neuro-
logic signs. Because there is no specific treatment, supportive care and
symptomatic treatment are important. Antibiotics are indicated because
of the immunosuppressive nature of the virus. Neurologic signs often
improve, at least temporarily, with corticosteroid administration (1 mg/
kg of prednisone daily for 7 to 10 days). Dogs with distemper encephalo-
myelitis occasionally recover; thus, treatment for at least 1 to 2 weeks
should be attempted. 69

Feline Infectious Peritonitis

Feline infectious peritonitis is caused by an immune-mediated re-
sponse to a coronavirus, Involvement of the nervous system is usually
associated with the parenchymatous (dry) form rather than with the
effusive (wet) form, Vestibular dysfunction is common. 25, 37 Affected
cats often have hyperglobulinemia and involvement of other organs,
especially the eyes, The serum antibody titers that are currently available
are nonspecific and may be negative in cats with neurologic signs. A
 VESTIBULAR DYSFUNCTION 243

mixed (neutrophilic and mononuclear) pleocytosis with elevated protein

concentration is the most common finding on CSF analysis. MR imaging
often shows T2-weighted hyperintensity and abnormal enhancement of
the ventricular lining, choroid plexus, and meninges in the brain
stem. 25, 64 There is no effective treatment, and the prognosis is poor. 25' 37

Rickettsial Encephalitis
Neurologic abnormalities are seen in about 40% of dogs with Rocky
Mountain spotted fever (RMSF) and 20% of dogs with ehrlichiosis. 29
Many affected dogs also have lethargy, fever, and thrombocytopenia.
Leukocytosis is more common with RMSF, and ehrlichiosis is more likely
to cause leukopenia and anemia. On CSF analysis, RMSF may cause
a neutrophilic pleocytosis and mildly elevated protein concentration,
although ehrlichiosis is more likely to cause a mononuclear pleocytosis
and markedly elevated protein concentration. Diagnosis of RMSF is
based on a rise in serum antibody concentration in acute and convales-
cent samples. A single positive IgG titer is usually sufficient to diagnose
ehrlichiosis. Treatment of either disease consists of administering doxy-
cycline (5 mg/kg orally twice daily) or chloramphenicol (50 mg/kg
orally every 8 hours) for 2 to 3 weeks. The prognosis is generally good
with prompt treatment, although neurologic deficits may progress or
persist, despite treatment.l 4

Fungal Encephalitis
Cryptococcosis is the most common fungus to involve the nervous
system of dogs and cats. Affected animals may have involvement of
other organ systems such as the eyes, nose, or skin. Results of CSF
analysis are variable, but organisms may be identified on cytology.
Detection of cryptococcal capsular antigen in serum or CSF is also
helpful in the diagnosis. The recommended treatment is fluconazole (5
mg/kg orally twice daily). Therapy should be continued for at least 6
months to prevent relapse?, s, 26,6 7
Blastomycosis occasionally involves the central nervous system. Af-
fected animals usually have evidence of involvement of other organs
such as the lungs, eyes, skin, or lymph nodes. There may be a neutro-
philic pleocytosis on CSF analysis. Definitive diagnosis is best made by
identifying organisms in extraneural tissue such as lymph nodes. Serum
antibody titers are also helpful. Treatment with itraconazole or ampho-
tericin B can be attempted, but the prognosis for blastomycosis that
involves the nervous system is poor. 3' 41
Coccidiomycosis should be considered in animals with a history of
being in the southwestern United States. Most affected dogs do not have
obvious signs of extraneural involvement. On CSF analysis, there may be
a neutrophilic or mixed (mononuclear cells and neutrophils) pleocytosis.
Serology is also helpful in the diagnosis of coccidiomycosis. Treatment
consists of long-term administration of fluconazole (5 mg/kg orally
244 THOMAS

twice daily). Many dogs with relatively mild signs recover if treated
early. The presence of severe neurologic deficits warrants a guarded
prognosis. 4' 12

Granulomatous Meningoencephalomyelitis
Granulomatous meningoencephalomyelitis is an idiopathic disease
that results in inflammation of the central nervous system and occasion-
ally the eyes. Adult dogs are affected, and small breeds (terriers and
poodles) may be predisposed. Signs consist of an acute or chronic onset
of focal or multifocal neurologic deficits or signs of meningitis. 1' 15, 51, 59, 63
A tentative diagnosis is based on CSF findings and exclusion of infec-
tious causes of meningoencephalitis, but definitive antemortem diagno-
sis is difficult. A mononuclear pleocytosis with an increased protein
concentration is the most common CSF finding, but a predominantly
neutrophilic response also can occur. 5' 59, 6°CT or MR imaging may show
one or more contrast-enhancing masses.23, 44' 61 A definitive diagnosis
usually requires histopathologic examination of nervous tissue obtained
by biopsy or necropsy.
Signs often improve with 1 to 2 mg/kg of prednisone daily. The
dose is tapered gradually to establish the minimal effective dose. Radia-
tion therapy is successful in some patients and should be considered in
dogs refractory to corticosteroids. 47 Most patients improve with therapy,
but relapse is common, and many dogs are eventually euthanized be-
cause of neurologic disability. Some dogs do recover with therapy,
however. 47' 61

Toxoplasmosis and Neosporosis

Toxoplasma gondii occasionally can cause a nonsuppurative encepha-
litis in dogs and cats. Infected cats often have evidence of disease in
other organs such as uveitis, pancreatitis, and respiratory disease. Dogs
with toxoplasmosis also often have other diseases such as canine distem-
per.20 Neospora caninum also can infect the nervous system of dogsP, 22
Toxoplasmosis and neosporosis are clinically similar. Affected ani-
mals may develop a range of clinical manifestations, including encepha-
lomyelitis, myositis, dermatitis, or multifocal dissemination. 1B--2o, zz, 30
Paraparesis is the most common neurologic sign, but seizures, abnormal
behavior, and vestibular dysfunction also can occur. 22
The diagnosis of toxoplasmosis is based on identifying the organism
in tissue or on a four-fold increase in IgG antibody in paired sera. In
cats, a high concentration of IgM antibody in serum or CSF is supportive.
An indirect fluorescent antibody test is available to detect serum antibod-
ies to N. caninum. A high titer with appropriate clinical signs is sufficient
for a diagnosis of neosporosis. 18
Clindamycin administered at an oral dose of 10 mg/kg three times
daily for a minimum of 4 weeks has been recommended to treat neo-
sporosis and toxoplasmosis. 38 Another protocol is a combination of tri-
 VESTIBULAR DYSFUNCfiON 245

methoprim and sulfadiazine (15 mg/kg twice daily) with pyrimeth-

amine (1 mg/ kg daily). 38 Supplementation with folinic acid (5 mg/ d)
may help to prevent the bone marrow toxicity associated with pyrimeth-
amine.19 With early treatment, clinical signs may resolve within 1 to 2
weeks.19, 3s

Neoplasia

In dogs, the most common tumors to cause central vestibular dys-

function are meningiomas and choroid plexus papillomas located in the
brain stem. In cats, meningioma and lymphoma are the most common
brain tumors. Central vestibular dysfunction also can occur with tumors
of the forebrain, which cause caudal transtentorial herniation with sec-
ondary compression of the brain stem. Neurologic dysfunction often
progresses over a period of weeks to months. Hemiparesis with asym-
metric postural reaction deficits is common. Deficits of cranial nerves V,
VI, VII, IX, and X can occur. Altered levels of consciousness are common
late in the course of the disease.
CT and MR imaging are the most helpful diagnostic procedures
(Fig. 5). Skull radiography identifies tumors involving the skull but is

Figure 5. MR imaging of a choroid plexus papilloma in a dog with ataxia, head tilt to the
left, and right hemiparesis (paradoxical vestibular syndrome). On this transverse plane, T1-
weighted image obtained after contrast administration, there is a homogeneously enhancing
mass (arrow) in the region of the right lateral aperture of the fourth ventricle (0.5 Tesla; TR
450 msec; TE 20 msec).
246 THOMAS

usually normal in patients with primary brain tumors. Analysis of CSF

is seldom diagnostic for brain tumors but is indicated if inflammatory
disease is suspected. Ideally, MR imaging or CT should be performed
first to rule out an intracranial mass, because the collection of CSF
may be detrimental in patients with increased intracranial pressure. 46
Although the CT and MR imaging features of the common types of brain
tumors have been described, nonneoplastic lesions such as vascular and
inflammatory disorders may appear identical.39• 66• 70
Supportive therapy with corticosteroids (1 mg/kg of prednisone
daily) is often helpful in temporarily alleviating peritumoral edema.
Definitive therapy consists of surgery or radiation therapy. 46 In general,
the long-term prognosis for tumors affecting the brain stem is poor.

Metronidazole Toxicity

Signs of metronidazole toxicity in dogs consist of vertical nystag-

mus, generalized ataxia, anorexia, and vomiting. 17• 24 Seizures and head
tilt also have been seen. Acute development of neurologic dysfunction
may occur 3 to 14 days after starting administration of metronidazole at
doses greater than 60 mg/kg/ d. There appears to be much individual
variation in the susceptibility of dogs to the adverse effects of this drug.
Treatment consists of stopping medication and supportive care. Dogs
typically recover within 1 to 2 weeks. In cats, metronidazole toxicity
typically causes signs of forebrain involvement (disorientation, seizures,
ataxia, blindness) rather than vestibular dysfunctionP

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Address reprint requests to

William B. Thomas, DVM, MS
Department of Small Animal Clinical Sciences
University of Tennessee
PO Box 1071
Knoxville, TN 37901-1071

e-mail: wthomas@utk.edu