Vestibular Disease
World Small Animal Veterinary Association World Congress Proceedings, 2015
A. Fauber, DVM, MS, DACVS, DACVIM (Neurology)
College of Veterinary Medicine, Purdue University, West Lafayette, IN, USA

The vestibular system is responsible for the maintenance of posture and balance. Damage to the vestibular system can cause loss of balance, vestibular ataxia, nystagmus and abnormalities in the positioning of the eyes, head, and neck. When examining a patient, it is important to determine whether peripheral or central vestibular disease is most likely to aid in forming a differential diagnosis list and determining prognosis.

Vestibular Anatomy and Function

The boney labyrinth is within the petrous bone and is made up of the semicircular canals, vestibule and cochlea. There are three semicircular canals arranged at right angles to each other to provide input in three planes of movement. In response to movement, hair cells within the cupula and macula move and cause stimulation of the sensory neurons of the vestibulocochlear nerve. Information on body position and movement is sent to the brainstem via the 8th cranial nerve (vestibulocochlear nerve) via the vestibular division. A majority of these axons synapse on the vestibular nuclei in the brainstem. Efferent tracts of the vestibular system send information to the eyes, head, vomiting center, and limbs to coordinate movement of the head and body and to maintain balance.

Peripheral Versus Central Vestibular Disease

Many of the clinical signs of vestibular disease are similar between peripheral and central vestibular disease. With unilateral peripheral vestibular disease, an asymmetric ataxia is seen. Patients will have normal limb strength but a loss of balance. A horizontal or rotary nystagmus can be seen with the fast phase of the nystagmus away from the side of the lesion. With bilateral peripheral vestibular disease, the patient may stay close to the ground when walking and standing. While an asymmetry in the gait may not be noted, the patient will stay in a crouched position and walk slowly.

For central vestibular disease, an asymmetric ataxia is seen. However, these patients may have vertical nystagmus or nystagmus that changes depending on the posture of the patient. While facial nerve (CN VII) deficits can be seen in patients with peripheral vestibular disease, patients with central vestibular disease can have deficits in cranial nerves other than the facial nerve. Also these patients can have postural reaction deficits on the side of the lesion. Paradoxical vestibular disease is caused by a lesion in the central vestibular system in the caudal cerebellar peduncle or flocculonodular lobe. In these cases the head tilt is away from the side of the lesion. Asymmetric deficits in conscious proprioception can help to localize the side of the lesion in paradoxical vestibular disease.





Horizontal, rotatory fast phase away from the lesion

Vertical most common, can change with changes in head position

Head tilt

Toward the side of the lesion

Typically toward side of lesion but can be paradoxical

Cranial nerve deficits

Only facial nerve (CN VII)

Other cranial nerves (V–XII) can be affected

Limb strength


Can be decreased

Postural reactions


Can be decreased

Level of consciousness


Can be decreased

Diseases Affecting the Vestibular System

One of the most commonly recognized peripheral vestibular diseases is canine geriatric vestibular disease. This disease typically presents in older dogs as an acute, unilateral peripheral vestibular disease, and patients are often severely affected. The cause of this disease has not been confirmed. A similar disease has been reported in cats. Treatment for this condition is supportive only and consists of fluid therapy for dehydrated patients who are vomiting, antinausea medication, and soft-padded bedding in a confined space so the patient doesn't injure themselves. Usually these patients show improvement within 3–4 days, but some can have a residual head tilt.

Otitis media/interna is commonly seen in pets and is the other main cause of peripheral vestibular disease. A complete physical examination with otoscopic evaluation should be performed in all patients with signs of vestibular disease. While extension of external ear disease is the most common cause of otitis media/interna, the latter cannot be ruled out without further examination and potential imaging of the medial ear. If otitis media/interna is diagnosed, treatment with systemic antibiotics based on culture results is recommended. Ear cleaning products should not be used in patients with a ruptured tympanic membrane or the vestibular signs could worsen.

Tumors of the middle or inner ear are reported to cause vestibular signs by disruption of the vestibulocochlear nerve. Benign nasopharyngeal polyps are seen in younger cats and are sometimes seen with concurrent respiratory signs or dysphagia. Some polyps can be removed with traction but there is a risk of regrowth. Other polyps may need to be removed surgically.

Inflammatory brain disease such as granulomatous meningoencephalitis can affect the central vestibular system. Advanced imaging and a spinal tap and cerebrospinal fluid analysis can help in diagnosing this disease. Immunosuppressive therapy is used in combination with immunomodulatory drugs.

Metronidazole toxicity can cause central vestibular disease signs in dogs. Doses as low as 30 mg/kg/day have been reported to cause vestibular signs in some animals, and the chronic use of lower dosages of metronidazole can also cause central vestibular signs. [AF1] Treatment for these patients includes discontinuation of the metronidazole and treatment with diazepam (one injection followed by oral diazepam for 3 days). The use of diazepam significantly shortens the recovery time following drug discontinuation.

Thiamine deficiency can cause bilateral central vestibular disease. These animals present a crouched posture with wide head excursions. Cats can have severe ventroflexion of the head and neck. Cats can develop thiamine deficiency from being fed raw fish diets, which are high in thiaminases. While this disease can be rapidly fatal, treatment with thiamin IM or SC injection followed by oral supplementation can reverse the clinical signs.


References are available upon request.


Speaker Information
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A. Fauber, DVM, MS, DACVS, DACVIM (Neurology)
College of Veterinary Medicine
Purdue University
West Lafayette, IN, USA

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