452 PART IX  •  NEUROLOGIC DISORDERS

CHAPTER 87 
VESTIBULAR DISEASE
Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN

KEY POINTS • Treatment of vestibular disease is determined by the underlying

etiology, but supportive care is extremely important, especially
• Patients with vestibular disease have dysfunction of the vestibular
during the initial stages of the disease.
system and often are presented for treatment on an emergent
basis.
• The vestibular system is comprised of a peripheral component
within the structures of the inner ear and central components in
the brainstem and cerebellum.
• The common clinical signs of vestibular disease include head tilt,
ataxia, and nystagmus.
• Peripheral vestibular disease can be accompanied by Horner’s Dogs and cats have the ability to control posture and movements of
syndrome and facial nerve paresis. the body and eyes relative to the external environment. The vestibular
• Central vestibular disease typically is accompanied by loss of system mediates these activities through a network of receptors and
proprioceptive and motor function, in addition to multiple cranial neural elements. Disease leading to dysfunction of the vestibular
nerve deficits and mentation changes.
system can lead to dramatic signs of disequilibrium. The investiga-
• The differential diagnosis for the cause of vestibular disease
depends on the localization of the lesion to the peripheral or tion, treatment, and prognosis of the cause of the disequilibrium can
central compartments. differ depending on whether the peripheral or central components
of the system are affected.

This chapter outlines the relevant anatomy of the vestibular
system and how this influences the clinical signs of its dysfunction,
in addition to the diseases that are most commonly responsible for
the acute onset of clinical signs.
NEUROANATOMY OF THE VESTIBULAR SYSTEM
The vestibular system can be divided into (1) peripheral components
located in the inner ear and (2) central nervous system (CNS) com-
ponents. Three major CNS areas receive projections from the periph-
eral sensory receptors of the vestibular system: the cerebral cortex,
the spinal cord, and the cerebellum. The projection to the cerebral
cortex incorporates extensions to the extraocular muscles.
Nerve Pathways to the Extraocular Muscles
Two neurons make up the pathway responsible for the sensory input
of the head to the cerebral cortex (Figure 87-1).
Neuron 1
The cell location for the first neuron is within the vestibular ganglion
of the eighth cranial or vestibulocochlear nerve, and the axon projects
into the ipsilateral vestibular nuclei. These neurons receive input
from the vestibular receptors in the membranous labyrinth con-
tained within a bony labyrinth in the petrous temporal bone. The
sensory neurons are incorporated into the vestibulocochlear nerve,
which leaves the petrous temporal bone via the internal acoustic
FIGURE 87-1  Diagrammatic overview of the neuroanatomy of the vestibu-
lar system. (From Platt S, Olby N, editors: Manual of canine and feline
neurology, ed 4, Gloucester, 2012, British Small Animal Veterinary
Association. A. Wright, illustrator.)
CHAPTER 87  •  Vestibular Disease 453
meatus, along with the facial nerve, and enters the medulla of the
brainstem.1
Neuron 2
The cell location for the second neuron is in the vestibular nuclei,
which are situated in the medulla oblongata. From these nuclei, axons
travel in the medial longitudinal fasciculus within the brainstem. The
ascending axons within the fasciculus give off numerous side branches
to the motor nuclei of cranial nerves III, IV, and VI, thereby providing
coordinated conjugated eyeball movements associated with changes
in position of the head. Some axons project from the nuclei into the
reticular formation and go on to provide afferents to the vomiting
center located there.1
Nerve Pathways to the Spinal Cord
The vestibulospinal tract descends from the vestibular nuclei and
projects mainly onto α-neurons or extensor motor neurons through-
out the length of the cord via interneurons in the ventral grey
column.1 This pathway is strongly facilitatory to the ipsilateral alpha
and gamma motor neurons to extensor muscles.
Nerve Pathways to the Cerebellum
The vestibular nuclei project directly to the cortex of the ipsilateral
flocculonodular lobe (the flocculus of the hemisphere and the
nodulus of the caudal vermis), as well as the fastigial nucleus of the
cerebellum.1 The return pathway from a cerebellar nucleus to the
vestibular nuclei is also ipsilateral; this is an extremely large projec-
tion, providing the cerebellum with a strong influence over the activ-
ity of the vestibular nuclei. These pathways between the cerebellum
and the vestibular nuclei travel in the caudal cerebellar peduncle.
CLINICAL SIGNS
Unilateral vestibular disease produces asymmetric signs, often on or
toward the side of the disease. The most common clinical signs of
vestibular disease are head tilt, nystagmus, and ataxia; these may be
single entities or a combination of signs.2 The primary aim of the
neurologic examination is to determine if these vestibular signs are
due to a peripheral vestibular system (inner ear) disease or a central
vestibular system (brainstem and cerebellum, or both) disease. Local-
ization of the disease determines the most appropriate diagnostic
tests, the differential diagnoses, and the prognosis.
The essential determination of whether these signs are due to a
peripheral or central disease may be possible by the identification of
associated neurologic signs that are present only with central disease.2
Signs of central vestibular syndrome suggest damage to the brainstem
and are not present in patients with inner ear disease unless there has
been extension of the inner ear disease into the brainstem, such as
can be seen with otitis media, otitis interna, and neoplasia.3
Specific Signs of Vestibular Dysfunction
Signs of vestibular dysfunction are outlined in Table 87-1.
Head tilt
Loss of equilibrium is most commonly represented clinically as a
head tilt that may be present with either central or peripheral ves-
tibular disease. The head tilt is always toward the side of the lesion
with peripheral disease but may be toward either side with central
disease. When the head tilt is opposite to the side of the lesion, it is
termed paradoxical.2 This can be seen with lesions of the flocculo-
nodular lobe of the cerebellum or the supramedullary part of the
caudal cerebellar peduncle, with sparing of the vestibular nuclei in
the rostral medulla; the head tilt often is accompanied by ipsilateral
cerebellar signs, paresis, and proprioceptive deficits.3
454 PART IX  •  NEUROLOGIC DISORDERS
Table 87-1  Neurologic Examination Findings in Animals with Peripheral and Central Vestibular Dysfunction
Clinical Signs Peripheral Vestibular Disease
Head tilt Toward the lesion
Spontaneous nystagmus Horizontal or rotatory with the fast phase
away from the side of the lesion
Rarely positional
Paresis and proprioceptive deficits None
Mentation Normal to disoriented
Cranial nerve deficits Ipsilateral CN VII deficit
Horner’s syndrome Common ipsilateral to the lesion
Head tremors None
Circling Infrequent but can be seen toward the
side of the lesion
CN, Cranial nerve.
Bilateral peripheral vestibular disease does not produce asym-
metric lesions such as a head tilt. A characteristic side-to-side head
movement is seen instead.
Nystagmus
Pathologic or spontaneous nystagmus is an involuntary rhythmic
oscillation of both eyes, occurs when the head is still, and is a sign of
altered vestibular input to the neurons that innervate the extraocular
eye muscles.2 This is in contrast to physiologic nystagmus, which can
be induced in normal animals. Pathologic nystagmus may be hori-
zontal, rotatory, or vertical. Vertical nystagmus implies a central ves-
tibular lesion but it is not a definitive localizing sign. If nystagmus of
any direction is induced only when the head is placed in an unusual
position, it is known as positional nystagmus, which may be more
common with, but not specific for, central disease; this term also may
refer to nystagmus that changes its predominant direction with
altered head positions.2
Nystagmus occurs with the fast phase away from the damaged
side; the slow phase commonly is directed toward the affected
side. In acute and or aggressive nystagmus, the eyelids may be seen
to contract at a rate corresponding to that of the nystagmus. Nystag-
mus may disappear with chronicity of the underlying lesion, particu-
larly with peripheral disease, but its presence usually indicates an
active disease process within the vestibular apparatus. Animals with
bilateral vestibular disease do not have pathologic or physiologic
nystagmus.4
Ataxia
Ataxia is a failure of muscular coordination or an irregularity of
muscle action. It generally is associated with a cerebellar, vestibular,
or proprioceptive pathway abnormality. Animals with vestibular dys-
function assume a wide-based stance and may lean or drift toward
the side of a lesion if the dysequilibrium is not too severe.4
Signs That May Be Associated
with Vestibular Dysfunction
Facial paresis, paralysis, and hemifacial spasm
Cranial nerve VII, the facial nerve, is involved commonly in the same
disease processes that cause peripheral vestibular disease.5 The result-
ing signs are those of facial paresis, paralysis or, more rarely, spasm.
Horner’s syndrome
Horner’s syndrome (miosis, ptosis, enophthalmos, and protrusion of
the third eyelid) of the ipsilateral eye may be present with either
Central Vestibular Disease
Toward the lesion, or away from the lesion with
paradoxical disease
Horizontal, rotatory, vertical, and/or positional
with the fast phase toward or away from the
lesion
Commonly ipsilateral to the lesion
Depressed, stuporous, obtunded, or comatose
Ipsilateral CN V, VII, IX, X, and XII
Uncommon
Can occur with concurrent cerebellar dysfunction
Usually toward the side of the lesion
middle or inner ear disease causing peripheral vestibular dysfunc-
tion.6 This association is seen because the vagosympathetic trunk
synapses in the cranial cervical ganglion deep to the tympanic bulla.
Horner’s syndrome rarely is associated with central vestibular
disease.1
Conscious proprioception deficits
Animals with central vestibular dysfunction often have ipsilateral
proprioceptive deficits manifested by abnormal postural reactions
such as hopping and proprioceptive placing. These deficits are due
to the concurrent disturbance of the ascending proprioceptive path-
ways located in the brainstem.
Hemiparesis or tetraparesis
Paresis suggests abnormal neurologic function (weakness) without
complete paralysis, which implies that some voluntary motion
remains. Locomotion is thought to be initiated in the brain stem of
animals, so paresis usually is seen with any lesion within the neuraxis
caudal to the level of the red nucleus in the midbrain.3 With unilateral
focal central vestibular diseases, paresis of the ipsilateral limbs (hemi-
paresis) may be seen if the motor pathways in the medulla oblongata
also are affected. A large lesion or multifocal lesions may cause an
asymmetric tetraparesis. Paresis does not occur with peripheral ves-
tibular disease.
Circling, leaning, and falling
With unilateral vestibular dysfunction, dogs or cats may exhibit an
ipsilateral reduction in extensor tone, and contralateral hypertonic-
ity, causing them to lean, fall, and circle toward the side of the lesion.2
Falling may occur when the animal shakes its head if there is aural
irritation.
Altered mental state
Disorders causing central vestibular dysfunction may be accompa-
nied by altered mentation. The reticular activating system of the
brainstem facilitates the alert and awake state in animals.1 Damage
to this area may cause the animal to become disoriented, stuporous,
or comatose.3 Although peripheral vestibular disease does not cause
stupor or coma, it may cause disorientation, which can make the
assessment of the animal’s mental status difficult.
Multiple cranial nerve dysfunction
Central vestibular syndrome may be accompanied by other cranial
nerve dysfunction as well. Clinical signs can include ipsilateral facial
 CHAPTER 87  •  Vestibular Disease 455

hypalgesia, atrophy of the masticatory muscles, reduced jaw tone,
facial paralysis, tongue weakness, and loss of the swallow or gag
reflex.
Decerebellate posturing
In severe forms of central vestibular dysfunction, the underlying
disease also may cause decerebellate posturing or rigidity; this is
characterized by opisthotonus with thoracic limb extension, normal
mentation, and flexion of the pelvic limbs.3 This posture can occur
intermittently and be accompanied by vertical nystagmus, the com-
bination being confused by owners as some type of seizure activity.
Dorsiflexion of the neck sometimes elicits this posture.
Vomiting
The vomiting center is located within the reticular substance of the
medulla, and there are direct connections to it from the vestibular
nuclei.1 Vomiting may be seen in animals affected acutely by vestibu-
lar disease.2
DIFFERENTIAL DIAGNOSIS OF ACUTE
VESTIBULAR DISEASE
Tables 87-2 and 87-3 outline the overall etiologies and infectious
causes of acute vestibular disease, respectively.
determine this, a complete history and a thorough physical and neu-
rologic examination are essential.
The following tests can be performed in sequence, advancing in
expense and invasive nature until satisfactory information is acquired.
All of the tests may be necessary if central disease is suspected,
whereas cerebrospinal fluid (CSF) analysis and advanced imaging
may not be necessary if peripheral disease is responsible for the
vestibular dysfunction.
Minimum Database
Hematology, a comprehensive serum biochemistry, thyroid function
analysis, urinalysis with culture and susceptibility, thoracic radio-
graphs, and abdominal ultrasonography or radiographs should be
analyzed in all cases of acute vestibular dysfunction to evaluate the
patient for multisystemic or concurrent disease.
Otoscopy and Pharyngeal Examination
General anesthesia is necessary to examine thoroughly the ears and
pharynx for abnormalities such as exudates and soft tissue masses.
Both ears should be examined with an otoscope. The tympanum
should be examined for color, texture, and integrity; it is usually dark
gray or brown in cases of otitis. An intact tympanum does not rule
out otitis media, and diagnosing otitis media on the sole basis of a
ruptured tympanum is also unreliable.5

DIAGNOSTIC APPROACH TO THE ANIMAL Radiography

WITH ACUTE VESTIBULAR DISEASE Radiography is useful for evaluating the osseous tympanic bulla.
Skull radiographs should be performed under general anesthesia to
The approach to an animal with vestibular disease can depend on achieve adequate positioning. This may not be possible always, par-
whether a peripheral or central lesion is suspected (Figure 87-2). To ticularly in the trauma patient. Assessment of the tympanic bulla can

Table 87-2  Etiologies of Peripheral and Central Vestibular Diseases1,2,13

Specific Diseases

Disease Mechanism Peripheral Disease Central Disease

Degenerative — Cerebellar cortical abiotrophy

Lysosomal storage diseases
Anomalous Congenital vestibular disease Hydrocephalus
Intracranial intra-arachnoid cysts
Metabolic Hypothyroidism Hypothyroidism17
Nutritional — Thiamine deficiency
Neoplasia Squamous cell carcinoma Meningioma
Fibrosarcoma Oligodendroglioma
Osteosarcoma Medulloblastoma
Ceruminous gland or sebaceous gland adenocarcinoma Lymphoma
Extension of middle ear neoplasia
Metastasis
Inflammatory or infectious Bacterial otitis interna or labyrinthitis See Table 87-3
Cryptococcosis
Nasopharyngeal polyps
(Cuterebra larval migration)
Idiopathic Idiopathic vestibular syndrome —
Toxic Aminoglycosides Metronidazole
Furosemide Lead
Chlorhexidine
10% fipronil solution (aural administration)
Traumatic Iatrogenic: external middle ear flushing or bulla osteotomy Head trauma
Bulla fracture or hemorrhage
Vascular — Infarction or hemorrhage
Feline ischemic encephalopathy
Cuterebra larval migration
456 PART IX  •  NEUROLOGIC DISORDERS

Table 87-3  Infectious and Inflammatory Central Cerebrospinal Fluid Analysis

Nervous System Disorders That May Cause Vestibular CSF analysis is a useful adjunctive test for determining the cause
Dysfunction1,12,13 of central vestibular disease, although results are rarely specific.
Class of Although serum and CSF antibody titers have been used previously
Etiologic Agent Disease to diagnose infectious diseases, polymerase chain reaction analysis of
CSF can now be performed in specialized laboratories to evaluate for
Viral Feline infectious peritonitis the presence of infectious antigens (rather than antibody titers).10
Feline immunodeficiency virus
Feline leukemia virus The risk of iatrogenic CNS trauma or cerebellar herniation after
Rabies cisterna magna puncture in animals with space-occupying lesions
Pseudorabies should not be underestimated. It is preferable to obtain advanced
Borna disease virus imaging studies of the brain (see the following section) before per-
Distemper virus
forming CSF tap, especially if a caudal fossa lesion is suspected.
Protozoal Toxoplasmosis, neosporosis
Encephalitozoonosis Advanced Imaging
Bacterial Aerobes Computed tomography (CT) and magnetic resonance imaging
Anaerobes (MRI) have revolutionized the diagnosis of vestibular diseases. CT
Rickettsial Rickettsia rickettsii evaluation of the peripheral vestibular system is particularly useful if
Ehrlichia spp. radiographs have not determined an underlying cause, if nasopha-
Fungal Cryptococcosis ryngeal polyps and neoplasia are considerations and they cannot be
Blastomycosis visualized on physical examination, and if the extent of the lesion
Histoplasmosis needs accurate demarcating and the animal is a potential surgical
Coccidioidomycosis
candidate. CT evaluation for animals with central vestibular diseases
Aspergillosis
Phaeohyphomycosis may be less helpful because of the artifacts relating to the density of
the petrous temporal bones surrounding the medulla (e.g., beam
Parasitic Angiostrongylus vasorum
Cuterebra larval myiasis
hardening).11
Dirofilaria immitis MRI of the peripheral and central vestibular systems provides
excellent multiplanar soft tissue resolution when compared with
Agent Nonsuppurative meningoencephalomyelitis
unknown (presumed viral) CT.11 The improved soft tissue contrast provided by this modality
Eosinophilic meningoencephalitis allows better assessment of neoplastic and inflammatory conditions
Granulomatous meningoencephalitis that result in vestibular dysfunction (Figure 87-3). A typical MRI
Necrotizing meningoencephalitis (Pug, Maltese, study consists of T1-weighted, T2-weighted, and proton density–
Terrier, Chihuahua)
Necrotizing leukoencephalitis (Yorkshire Terrier)
weighted transverse images made before contrast medium adminis-
tration.11 Post-contrast sequences have been recommended if a mass
is present in the tympanic bulla or the external ear canal.

TREATMENT AND PROGNOSIS

be made using lateral, dorsoventral, or ventrodorsal, lateral-20
degree ventral-laterodorsal oblique, and rostral-30 degree ventral-
caudodorsal open-mouth oblique radiographic images.7
Myringotomy
Myringotomy is the deliberate puncture or incision of an intact,
although not necessarily healthy, tympanic membrane.8 Needle
puncture and subsequent aspiration through the ventrocaudal part
of the tympanic membrane allows for collection of fluid from the
tympanic cavity for cytologic examination and microbial culture and
susceptibility testing.
Brainstem Auditory Evoked Potentials
Brainstem auditory evoked potentials testing, also known as brain-
stem auditory evoked response testing, can be used to assess the integ-
rity and function of the peripheral and central auditory pathways,
which allows for indirect evaluation of the vestibular pathways
because of their close association.9 Brainstem auditory evoked poten-
tials are recordings of sound-evoked electrical changes in portions of
the auditory pathway between the cochlea and the auditory cortex.
Because of the level of patient cooperation required, sedation or a
light plane of general anesthesia often is needed to perform and
interpret this test properly.9
The damaged vestibular system can compensate over time with
central reprogramming of eye movements and postural responses, as
well as reliance on visual and other sensory input that replaces lost
vestibular input.2,14 If the underlying disease process can be deter-
mined, the prognosis for a functional recovery can be good. Residual
signs, such as a head tilt, are always possible. Recurrences can occur
at times of stress, recurrent disease, or after anesthesia.
Supportive care is essential, especially because these animals are
frequently anorexic; feeding tubes and fluid therapy can be vital
initially until the patient can self-maintain. Vomiting, salivation, and
nausea associated with vestibular disease can be treated with anti-
emetic medications. Drugs commonly used include the phenothi-
azine derivative chlorpromazine (0.5 mg/kg IV, IM, SC q-6-8h in
dogs, 0.2 to 0.4 mg/kg IM, SC q6-8h in cats), serotonin receptor
antagonists dolasetron (0.6 to1 mg/kg IV, SC, or PO q12-24h) and
ondansetron (0.1 to 1 mg/kg IV, PO q8-12h), metoclopramide, an
antidopaminergic serotonin receptor antagonist and chemoreceptor
trigger zone inhibitor (0.1 to 0.5 mg/kg IV, IM, SC, or PO q6-12h or
as an IV infusion of 1 to 2 mg/kg q24h), or the antihistamines
diphenhydramine (2 to 4 mg/kg PO or IM q8h) and meclizine
(12.5 mg PO q24h; see Chapter 162).2 Recently, maropitant, a novel
neurokinin type-1 receptor antagonist, has been described as a good
choice to prevent vomiting in dogs and cats (1 mg/kg SC q24h or
2 mg/kg PO q24h),15,16 and anecdotally has been effective as an
adjunctive treatment in animals affected by vestibular disease.
 CHAPTER 87  •  Vestibular Disease 457

Stupor or paresis and or

proprioceptive deficits?

No Yes

No Vertical nystagmus? Yes Central vestibular disease

Peracute onset/
Likely peripheral
asymmetric deficits/
vestibular disease
no progression?

Peracute onset/no other deficits No Yes

(e.g., Horner’s)/no progression?

Yes No CT or MRI/
Otoscopy/
 CSF tap
myringotomy/
culture and
susceptibility testing

CNS Consider
inflammatory vascular
Positive Negative disease or disease
findings findings neoplasia

Treat for
otitis media/interna

Radiographs/
CT or MRI
No response/
rapid recurrence
Negative Positive
findings findings

Polyp/
neoplasia/
abscess
Treat for
Idiopathic vestibular otitis media/interna; Surgical
syndrome consider toxicity treatment

FIGURE 87-2  Algorithm detailing the approach to the patient with acute vestibular disease. CNS, Central
nervous system; CSF, cerebrospinal fluid; CT, computed tomography; MRI, magnetic resonance imaging.

FIGURE 87-3  Transverse T2-weighted fluid-attenuated inversion recov-
ery magnetic resonance study of a 4-year-old mixed breed dog with
central vestibular disease and multiple cranial nerve involvement. A
large irregular lesion hyperintense to the surrounding brainstem is
identified (arrows). Pathologic examination confirmed granulomatous
meningoencephalomyelitis.
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