SHAKE, RATTLE, AND ROLL: TOP 10 THINGS YOU SHOULD KNOW ABOUT

VESTIBULAR DISEASE
Jared B. Galle, DVM, Diplomate ACVIM (Neurology)
Dogwood Veterinary Referral Center
4920 Ann Arbor-Saline Road
Ann Arbor, MI 48103
Introduction
The vestibular system is essential in maintaining balance and preventing an animal from falling
over. Head tilt, falling, rolling, leaning, circling, nystagmus, and ataxia are common signs of a
problem in the vestibular system. Clinical signs of vestibular disease may result from a lesion
involving the peripheral vestibular components (receptors in the inner ear or vestibular portion of
cranial nerve 8) or the central vestibular components (brainstem vestibular nuclei or vestibular
centers in the cerebellum). Knowing the neurologic signs that result from a lesion in each
component is important in determining potential causes and what diagnostics to perform. This
lecture will review the clinical approach to a patient with vestibular disease.
1. What are the most common signs of vestibular disease?
Vestibular diseases are common in dogs and cats and may result in any combination of the
following clinical signs: head tilt, falling, leaning, rolling, circling, nystagmus, strabismus, and
ataxia. Vomiting can also be seen with acute vestibular disorders.
Head Tilt: A head tilt commonly occurs with vestibular disease and is usually towards
the side of the problem. It is an abnormal head posture characterized by a rotation of
the head due to a loss of antigravity muscle tone on one side of the neck. A head tilt
must be differentiated from a head turn (torticollis) in where the median plane of the
head remains perpendicular to the ground, but the nose is turned to one side. A head
turn is not associated with a vestibular disorder but can occur with forebrain and
brainstem diseases.
Circling: Can occur with either a vestibular disease or with a focal forebrain disease.
Animals usually circle toward the side of the problem. Tight circles are usually seen
with vestibular diseases, while wide circles (almost pacing) are often associated with
forebrain diseases.
Nystagmus: This is involuntary, rhythmic oscillations of the eyeballs. There are two
types of nystagmus - physiologic and pathologic. Physiologic nystagmus occurs in
normal animals while pathologic nystagmus occurs with vestibular disease.
Physiologic nystagmus can be induced in a normal animal by turning the head side to
side (also know as the vestibulo-ocular reflex). It is characterized by a slow phase in
the opposite direction of the head movement and a fast phase (compensatory phase) in
the same direction of the head movement. The direction of the nystagmus is defined in
the direction of the fast phase which is typically away from the side of the problem.
Physiologic nystagmus can be decreased or absent in animals with vestibular disorders.
Pathologic nystagmus occurs with vestibular disease and can be either spontaneous or

positional. Spontaneous nystagmus is observed when the head is in a normal position

at rest. Positional nystagmus occurs when head position is altered; it can often be seen
by placing the animal upside down on its back. Nystagmus is classified by its direction
(horizontal, rotary, or vertical) and may change direction when head position is
changed.
Strabismus: This refers to an abnormal position of the globes. Strabismus is usually
detected when the head is placed in an abnormal position (dorsally extending the head
or placing the animal on its back) and is present on the side of the problem. Ventral or
ventrolateral strabismus is usually seen in the eye on the same side as the vestibular
disease.
Ataxia: This is defined as an uncoordinated gait and can be seen with vestibular
disease (vestibular ataxia), cerebellar disease (cerebellar ataxia), or a problem in the
spinal cord or brainstem (proprioceptive or sensory ataxia). Ataxia seen with vestibular
disease is characterized by swaying of the head and trunk, base-wide stance, leaning,
falling, and rolling to side of the lesion. Bilateral vestibular lesions usually cause wide
excursions of the head from side to side.
2. How do you determine if a patient has a peripheral or central vestibular disease?
The vestibular system consists of two components on each side of the body - the peripheral
component and the central component. Clinical signs of vestibular disease can result from a
lesion in one of the components. The peripheral component consists of receptor organs in each
inner ear and the vestibular portion of each cranial nerve eight which courses through the petrous
temporal bone. The central component consists of vestibular nuclei in the brainstem and parts of
the cerebellum. When assessing a patient with vestibular signs, the first step is to localize the
problem to the right or left side of the body, then localize it to the peripheral or central
component of the vestibular system. Localizing the vestibular signs is important because it will
help determine potential causes and the necessary diagnostics.
Peripheral and central vestibular diseases can cause a head tilt, horizontal or rotary nystagmus,
and ataxia. These signs are usually ipsilateral (same side) to the side of the lesion.
Peripheral Vestibular Disease (PVD)
Postural reaction deficits are not seen with PVD. Facial paralysis (cranial nerve 7) and Horners
syndrome (sympathetic innervation to the eye) may also be present on the same same as the PVD
because of the proximity of these nerves to the peripheral vestibular components in the inner ear.
A resting nystagmus rate 66 beats per is more likely to be seen with peripheral vestibular
disease. With bilateral PVD, nystagmus and head tilt will often not be present. Affected animals
will walk crouched and may have wide, side-to-side excursions of the head.
Central Vestibular Disease (CVD)
Postural reaction deficits are the the strongest indication of CVD. Postural reaction deficits
occur because the sensory and motor pathways that control these reactions are located in the
brainstem near the vestibular nuclei. The deficits are on the same side as the CVD. Other

important features of CVD are vertical nystagmus and positional nystagmus (nystagmus that
changes direction on changing head position). The presence of cranial nerve deficits other than
facial (7) or vestibulocochlear (8) is suggestive of a central lesion. Alterations of consciousness
of mental status may also support a CVD.
The following table can be used to help differentiate a PVD versus CVD based on the clinical
signs.
PVD

CVD

Head tilt

Yes (ipsilateral)

Yes (ipsilateral; may be

contralateral with paradoxical
disease)

Ataxia

Yes (ipsilateral)

Yes (ipsilateral)

Nystagmus
Horizontal
Rotary
Vertical
Positional

Yes
Yes
NO
Rarely

Yes
Yes
YES
Yes

Postural reaction deficits

NO

YES (ipsilateral)

Circling

Yes (ipsilateral)

Yes (either way)

Facial paralysis

YES (ipsilateral)

Uncommon

Horners syndrome

YES (ipsilateral)

Uncommon

Once a lesion has been localized to the peripheral or central vestibular component on one side of
the body, a differential list and necessary diagnostics can be determined.
3. What is Paradoxical Vestibular Disease?
Paradoxical Vestibular Disease is a specific CVD that occurs with a lesion in the caudal
cerebellar peduncles or flocculonodular lobes of the cerebellum, which results in a head tilt that
is away from the side with the lesion. The patient may also circle away from the side with the
lesion. Another unique feature of this disease is the fast phase of the nystagmus will be towards
the side with the lesion. The key to localizing which side of the cerebellum has a lesion is to
determine which side has proprioceptive deficits. The postural reaction deficits will be on the
same side as the lesion, while the head tilt will be in the opposite direction. The most common
causes of Paradoxical Vestibular Disease include a tumor, an infarction, and an inflammatory
disease.

4. What are the most common peripheral vestibular diseases?

The most common PVDs include otitis media/interna, idiopathic vestibular syndrome, ototoxic
drugs, and hypothyroidism. Oropharyngeal polyps in cats can also cause peripheral vestibular
disease.
Otitis media/interna is the most common cause of PVD in both dogs and cats. This is usually
secondary to otitis externa that has progressed into the middle and inner ear. Otitis media/interna
can also be caused by a retrograde infection via the eustachian tube or by hematogenous spread.
The absence of otitis externa on otoscopic exam does not eliminate the presence of an otitis
media/interna. Facial paralysis and Horners syndrome may be seen. Diagnostics include an
otoscopic exam and imaging studies (bulla radiographs, CT, and MRI). If there is fluid in the
middle ear, a sample should be obtained via myringotomy for culture and cytology. Treatment
consists of systemic antibiotics for a minimum of 6-8 weeks. Surgical drainage via bulla
osteotomy should be considered if medical treatments fails. The prognosis for recovery is fair
because the head tilt and facial paralysis usually persist.
Idiopathic vestibular disease occurs in both dogs (usually geriatric) and cats (any age). The
clinical signs are typically peracute and most animals can be quite debilitated for the first 24-72
hours. Facial paralysis and Horners syndrome are not seen with this disease, so if present, other
differentials should be considered. The diagnosis is usually based on the signalment, history,
neurologic exam, and exclusion of other PVDs. Most affected animals will significantly
improve within 72 hours and will be back to normal in 2-4 weeks. The head tilt is typically the
last neurologic signs to improve and may be permanent. Treatment is supportive and
symptomatic. Meclizine may help decrease nausea. Recurrence is uncommon.
Ototoxic drugs administered orally or topically can cause PVD and deafness. These drugs
damage the vestibular receptors in the inner ear. Oral aminoglycoside antibiotics and earcleaning solutions are most frequently incriminated. Toxicity usually occurs when these drugs
are used at higher doses, when treatment is greater than 2 weeks, or the patient has impaired
renal function. Topical agents should never be introduced into the ear when the tympanic
membrane cannot be visualized or is ruptured because of the potential for ototoxicity. A
diagnosis is usually based on the development of vestibular signs with a recent history of
ototoxic drug administration. There is no definitive treatment. The ototoxic drug should be
stopped immediately. Vestibular signs usually improve over time but deafness may be
permanent.
Hypothyroidism has been associated with both PVD and CVD, but is more often associated with
PVD. The exact cause for the peripheral disease is unknown, but decreased axonal transport and
Schwann cell dysfunction have been implicated. The cause for central vestibular disease may be
related to ischemic infarction or hyperviscosity-associated hyperlipedemia. Diagnosis is based
on documentation of hypothyroidism and exclusion of other disease processes. Treatment
consists of thyroid hormone supplementation. Generally, dogs with PVD respond well to
treatment. Resolution of neurologic signs may take weeks or months with a head tilt often

persisting. Dogs with CVD may not respond as well depending on the presence of a brain
infarction.
5. What are the most common central vestibular diseases?
The most common CVDs include encephalitis, brain tumors, vascular infarctions, and
metronidazole toxicity.
Encephalitis is probably the most common cause of CVD. Although encephalitis can occur in
any breed, it occurs most commonly in young to middle-aged, small breed dogs. Autoimmune
diseases (GME, necrotizing encephalitis) and infectious diseases (distemper, RMSF, E. canis,
FIP, Toxoplasmosis) are the main causes of encephalitis. A diagnosis is based on the history,
signalment, clinical signs, MRI findings (multifocal contrast enhancing lesions), cerebrospinal
fluid analysis, and infectious disease titers. Autoimmune encephalitis is treated with
immunomodulatory drugs. Corticosteroids are traditionally given as the primary treatment;
however, other immunomodulatory drugs (azathioprine, cytosine arabinoside, cyclosporine)
which have traditionally been used as an add-on therapy to corticosteroids are starting to be used
more often as the primary treatment. The prognosis for autoimmune encephalitis is guarded as
animals may live weeks to years. Treatment for infectious encephalitis is based on the cause and
the prognosis varies.
Brain tumors in the caudal fossa are a common cause of CVD in dogs older than 5 years of age.
Tumors in this location affect the vestibular nuclei in the brainstem and the vestibular portions of
the cerebellum. Meningiomas and choroid plexus tumors are the most common tumors that
occur in the caudal fossa. Clinical signs are often slowly progressive. A presumptive diagnosis
is made by advanced imaging (CT or MRI) and is confirmed with histopathology. Treatment and
prognosis depend on the location and tumor type. Surgical approaches to the caudal fossa can be
difficult and may limit surgery as a treatment option. Radiation therapy may be used to treat
primary intracranial tumors when surgery is not a treatment option. The median survival times
vary with treatment, tumor type and location.
Vascular infarctions can occur in the brainstem or cerebellum resulting in CVD, although they
are more likely to occur in the cerebellum. They are more common in dogs than cats.
Neurologic signs are acute and nonprogressive. MRI and spinal fluid analysis are needed to
exclude other CVDs and make a presumptive diagnosis. There is no definitive treatment;
however, animals usually improve within 5-7 days and may completely recover. Further
evaluation for renal disease, hyperadrenocorticism, hypothyroidism, hypertension,
pheochromocytoma, and diseases that may predispose for vasculitis and thrombosis should be
considered.
Metronidazole is commonly used to treat a variety of conditions in dogs and cats. CVD has been
reported to occur in animals taking dosages >60 mg/kg/day for 7-12 days but signs can occur in
animals taking lower dosages. A presumptive diagnosis is based upon neurologic signs and a
history of metronidazole administration. Clinical signs usually resolve 1-2 weeks after

discontinuing the drug. Diazepam administration in dogs can shorten the recovery time to 3 days
(0.43 mg/kg orally or IV every 8 hours for 3 days).
Vestibular Diseases
Disease

PVD

CVD

Degenerative

Uncommon

Uncommon

Anomalous

Congenital

Chiari-like malformation, Intracranial

cyst, Dandy-Walker syndrome

Metabolic

Hypothyroidism

Hypothyroidism (rare)

Neoplastic

Middle/inner ear tumor

Primary or metastatic tumor

Nutritional

Thiamine deficiency

Inflammatory/Infectious

Otitis media/interna
Nasopharyngeal polyp

Idiopathic

Idiopathic vestibular disease

Toxic

Aminoglycoside antibiotics
Chlorhexidene flush
Iodophors flush

Metronidazole

Trauma

Head trauma

Head trauma

Vascular

Autoimmnune encephalitis (GME,

necrotizing)
Infectious encephalitis (Distemper,
Toxoplasma, Neospora, FIP,
Fungal)

Infarction
Hemorrhage

6. What tests can be done in a general practice for a patient that has vestibular disease?
The minimum data base for all patients with vestibular signs should include a complete blood
count, biochemistry profile, thyroid testing, urinalysis, otoscopic exam, and pharyngeal exam.
Peripheral Vestibular Disease
The diagnostic plan for patients with PVD includes a thorough otoscopic exam and imaging of
the tympanic bulla radiographs. These tests should be done under sedation or general anesthesia.
A thorough examination of the external ear canal can be performed with a hand-held otoscope or
video-otoscopy. Middle ear pathology should be suspected if the tympanic membrane is
ruptured, bulging, or cloudy. While diseases affecting the external canal may be visualized, the
presence of an intact tympanic membrane does not eliminate the possibility of a middle ear
disease. If the tympanic membrane is ruptured, a culture can be taken from the middle ear
cavity. If the tympanic membrane is intact, a myringotomy can be performed to obtain a culture.

Radiographs of the tympanic bulla require general anesthesia to allow for adequate positioning.
Five conventional radiographic views are needed to investigate the osseous bulla: dorsoventral,
lateral, open-mouth, and a right and left 20 lateral oblique views. Although positive radiographs
can diagnose middle ear disease, negative radiographs do not rule out the presence of middle ear
disease. Radiographic evaluation of animals with vestibular disease is not typically performed
because of the complexity of the anatomy of the head, superimposition of structures, and the lack
of specificity associated with radiographic findings. Computed tomography and MRI are more
sensitive than radiographs in diagnosing middle ear disease.
Thoracic radiographic should be obtained in older animals to exclude systemic diseases that may
have spread to the nervous system (i.e. fungal disease or metastatic neoplasia). Similarly, in
animals exhibiting clinical signs referable to the abdominal cavity, radiographic or
ultrasonographic examination of the abdomen should be performed. Identifying an underlying
systemic disease through noninvasive imaging technique may provide a presumptive diagnosis
for vestibular dysfunction, thereby eliminating unnecessary risk to the animal and expense to
owners.
Central Vestibular Disease
In addition to the minimum database, the diagnostic workup for patients suspected of having
CVD includes advanced imaging (computed tomography or MRI), cerebrospinal fluid analysis
(CSF), and serum/CSF titers for various organisms.
Additional testing would be based on the presumptive diagnosis.
Brain tumor (biopsy, investigate for metastatic disease)
Cerebrovascular accident (clotting profile, blood pressure, cardiac evaluation, adrenal
testing)
7. When should I refer a patient with vestibular disease to a neurologist?
Any patient that has neurologic deficits consistent with CVD should be referred to a neurologist
for further evaluation. These include postural reaction deficits and vertical nystagmus. If either
of these are present, the patient should be referred. Patients with otitis media/interna that are not
responding to therapy should also be referred for further evaluation. Patients suspected of
having idiopathic disease that do not improve or develop other neurologic deficits should be
referred. Referral should also be recommended for any patient that has intermittent vestibular
signs.
8. What is the prognosis for vestibular disease?
The prognosis for vestibular disease depends on the cause. The one thing to stress to clients
when discussing prognosis is that regardless of the cause, the head tilt is often the last neurologic
sign to improve and is often permanent. This does not interfere with the animals quality of life
and is not debilitating.

9. I have a patient with CVD. The client doesnt have money for an MRI. What can I do?
When a client does not have money for diagnostics, empirical treatment for the most common
CVDs can be initiated. The minimum diagnostic database (bloodwork, thoracic radiographs,
urinalysis, complete thyroid panel) should be done prior to starting empirical treatment.
Empirical Treatment

Dose

Rationale

Prednisone

1 mg/kg PO BID tapering dose

Inflammatory disease
Peritumoral edema

Clindamycin

10 mg/kg PO TID x 28 days

Toxoplasmosis infection
Neosporosis infection

Doxycycline or
Minocycline

10 mg/kg PO BID x 28 days

E. canis
RMSF

Meclizine

25 mg PO SID (dogs)
12.5 mg PO SID (cats)

Reduce nausea

Cerenia

1mg/kg SC q 24hrs up to five days

8 mg/kg PO q 24hrs x 2 consecutive days

Stop vomiting

10. Are there any drugs other than Meclizine (Antivert) that treat nausea?
Diphenhydramine (Benadryl) or Dimenhydrinate (Dramamine) can be used to help treat motion
sickness and nausea that can occur with vestibular disease. The exact mechanism of how these
drugs interact with the vestibular system and vomiting center is not known.
Drug

Dose

Diphenhydramine (Benadryl)

2-4 mg/kg PO TID

Dimenhydrinate (Dramamine)

4-8 mg/kg PO TID