My Dog Is Drunk: The Patient with Vestibular Ataxia
World Small Animal Veterinary Association Congress Proceedings, 2017
M. Berendt
Department of Veterinary Clinical Sciences, Dyrlaegevej, Denmark

Maintaining balance is a complex process which involves vision, a sense of gravity, the ability to direct movement and adjust the speed of movement, and the ability to maintain body posture. Sensory input from vision, the vestibular apparatus (special proprioception) and general proprioception is used to regulate the muscles of the eyes, head and body in order to secure posture and coordinated interaction of the position of the eyes and different body parts during all kind of activities.

Vestibular Anatomy

The vestibulocochlear nerve (CN VII) contains a cochlear division and a vestibular division which is concerned with hearing and balance respectively. This text will focus on the vestibular component which is concerned with the sense of balance and spatial orientation (special proprioception).

Peripheral and Central Vestibular System

The vestibular system can be divided into a peripheral vestibular component including receptors for special proprioception located in the membranous labyrinth (continuous with the cochlea). The membranous labyrinth consists of two otolith organs (the utricle and the saccule with its macula) which observe orientation in a vertical orientation and linear movement (gravity), and the three endolymph filled semicircular canals located at right angles to each other and their connected ampullae (the site for the cristae ampullaris), which detect movements of the head in any plane including rotational. The dendritic parts of the bipolar sensory neurons forming the vestibular nerve fibers are connected with the peripheral receptors (hair cells of crista ampullaris, macula utriculi and macula sacculi). From here axons travels through the internal acoustic meatus close to the cochlear component of CN VIII to the petrosa l bone where the vestibular fibers form the vestibular ganglion. The vestibular nerve continues to enter the rostral part of the brain stem at the cerebellomedullary angle. Most axons terminate in the four vestibular nuclei (representing the central vestibular component of the vestibular system), whereas a minor portion of axons continue directly to the cerebellar peduncle to enter the cerebellum in the fastigial nucleus and flocculonodular lobe (the direct vestibulocerebellar tract). The vestibular nuclei receives information from formatio reticularis, mesencephalon & cerebellum and send information to spinal cord motor neurons, nuclei for extraocular muscles & cerebellum. Together these integrated structures are orchestrating that the position and activity of the head and body, and movements of the eyes, are at all times coordinated. Communication between the vestibular system and the cranial nerve nuclei of the cranial nerves associated with eye movements, CN Ill: oculomotor nerve, CN IV: trochlea r nerve and CN VI: abducent nerve, is conducted through the fasciculus longitudinalis medialis situated in the core of the brainstem. Physiological nystagmus will only be present if these structures are intact and functional.

Structures that are anatomically closely related to the peripheral vestibular system are the facial nerve which travels very close to the vestibular nerve in the petrosal bone and postganglionic sympathetic nerve fibers which travels from the internal carotid sympathetic plexus close to the tympanic bulla.

Structures anatomically closely related to the central vestibular system in the brain stem are the ascending reticular activating system (ARAS) which is responsible for maintaining arousal, neighboring cranial nerve nuclei and roots (CN V: trigeminal nerve, CN VI: abducens nerve, CN VII: facial nerve and CN IX: glossopharyngeal nerve), ascending proprioceptive pathways and descending UMN pathways.

Clinical Signs of Vestibular System Dysfunction

Dysfunction of the vestibular system is characterised by problems with keeping balance and associated ataxia. The animal will have a wide-based stance. The most significant and consistent clinical sign of vestibular dysfunction is head tilt. Other clinical signs such as circling, leaning, falling, rolling, pathological nystagmus (involuntary repetitive eye movements expressing a slow and a fast phase) and vestibular strabismus (ipsi-lateral ventral deviation of the eye ball) may also be present. In the majority of cases, vestibular dysfunction is caused by unilateral lesions, and in those cases head tilt, circling, leaning, falling and rolling will with few exceptions be directed towards the lesion. With nystagmus, the slow eye movement phase is towards the lesion (the pathological phase), whereas the fast eye movement phase is away from the lesion (the compensatory phase). Nystagmus may be horizontal, vertical, rotatory or of changing direction.

In rare cases of bilateral vestibular disease, the animal will not display asymmetrical signs but is characterized by abnormal head movements where the head is swinging from one side to the other.

Please note that middle-aged to older individuals may experience transient vestibular signs with no indication of centra l involvement (so-called idiopathic vestibular syndrome which is of unknown aetiology). In this case the vestibular signs may initially be dramatic, but will resolve within days to weeks with no treatment.

Please note that acute cerebellar disease may be confused with vestibular disease. In cases of rostral cerebellar ischemic stroke, signs such as head tilt and nystagmus are very common.

Please note that congenital vestibular disease occur in both cats (e.g., Siamese and Burmese) and dogs (e.g., Dobermann and English cocker spaniel). Congenital nystagmus has been reported in Siamese cats and congenital strabismus have been reported in Siamese and Himalayan cats.

Differentiating Central Vestibular Syndrome from Peripheral Vestibular Syndrome

Lesions of the vestibular system affecting the vestibular nuclei situated in the brainstem can cause a so-called central vestibular syndrome, whereas lesions of the vestibular system affecting the middle and inner ear or the vestibular nerve can cause a so-called peripheral vestibular syndrome. When trying to discriminate between peripheral and central vestibular syndrome, it is of great importance to understand the anatomy of the vestibular system and its adjacent structures.

Peripheral Vestibular Lesion

With lesions solely affecting the peripheral vestibular system no brain stem signs are present. Note, however, that signs of facial nerve (CN VII) dysfunction and Homer’s syndrome (caused by sympathetic nerve fiber deficiency) may be present with lesions of the peripheral vestibular system, as these are travelling in relation to the petrosal portion of the temporal bone and the tympanic cavity. They may therefore be affected with e.g. inflammatory or infectious disease or neoplasms related to these structures. See Table 1.

Table 1. Clinical signs related to central and peripheral vestibular syndrome

Clinical signs

Central vestibular

Peripheral vestibular

Head tilt



Circling (in small circles), rolling






Postural reactions




Decreased arousal

Alert (may however appear confused
because of balance problems)

Cranial nerve deficits

CN V (trigeminal)
CN VII (facial)
CN XI (glossopharyngeal)

CN VII (facial)

Horner’s syndrome



Central Vestibular Lesion

A central vestibular lesion should be suspected if clinical signs of vestibular dysfunction are accompanied by additional signs indicating brain stem involvement. This could be ipsilateral deficits of proprioception, decreased arousal indicating ARAS malfunction, or lesions affecting or compressing adjacent cranial nerve nuclei or the cranial nerves where they exit the brain stem (such as the trigeminal, facial and glossopharyngeal nerves). Please note that involvement of the facial nerve can arise from lesions affecting the central as well as the peripheral vestibular system. See Table 1.

Diagnostic and Therapeutic Approach to the Vestibular System

Lesions of the vestibular system may be of degenerative, anomalous, metabolic, neoplastic, inflammatory infectious, traumatic or vascular origin, and should be addressed accordingly with respect to the diagnostic approach and therapeutic interventions (Table 2). A standard work­up includes a clinical inspection of the ear, otoscopy, a full neurological examination and standard blood work including haematology and blood biochemistry. For visualization of the middle and inner ear, standard radiographs with lateral, dorso-ventral and open mouth view may be helpful. Computerized tomography (CT) is, however, superior as CT can visualize subtle changes which are often not detectable on radiographs. For visualization of the brainstem and soft tissue structures adjacent to the central vestibular nuclei, a magnetic resonance imaging (MRI) scan is the diagnostic procedure of choice. If inflammatory or infectious disease of the CNS is suspected, cerebrospinal fluid (CSF) examination should also be performed.

Table 2. Common examples of vestibular disease







(Otitis media)

Antibiotics (universal)

Nasopharyngeal polyps


(Often young cats)

Surgical extirpation


Affecting brain stem

Affecting middle or inner ear

Surgical extirpation of peripheral neoplasms may be possible

Inflammatory CNS disease (non-infectious meningoencephalitis)



Long-term steroid therapy

Aminoglycoside antibiotics
Metronidazole overdose


Toxicity to inner ear tissue

Stop treatment



associated polyneuropathy involving vestibular nerve

Treatment directed against hypothyroidism


Unknown cause

Unknown cause

None - will resolve spontaneously

Animals suffering from acute vestibular disease often experience nausea and loss of appetite and may therefore need acute supportive care with fluids and antiemetic’s as well as assisted feeding. If the animal is non-ambulatory it should be held in a protected environment until able to coordinate and ambulate normally.


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Speaker Information
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M. Berendt
Department of Veterinary Clinical Sciences
Dyrlaegevej, Denmark

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