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Compendium July 2012 (Vol 34, No 7)

Vestibular Disease: Anatomy, Physiology, and Clinical Signs

by Mark Lowrie, MA VetMB, MVM, DECVN, MRCVS

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    The vestibular system is responsible for keeping an animal oriented with respect to gravity. It is a sensory system that maintains the position of the eyes, body, and limbs in reference to the position of the head. Proper interpretation of neurologic deficits and precise neuroanatomic localization are essential to diagnose and prognosticate the underlying disorder. Neurologic examination can confirm whether the vestibular dysfunction is of peripheral or central nervous system origin. Idiopathic vestibular syndrome is the most common cause of peripheral vestibular disease in dogs and, despite its dramatic clinical presentation, can improve without intervention. Central vestibular diseases generally have a poorer prognosis.

    This article describes the clinically relevant anatomic components of the vestibular system and the clinical signs commonly seen in vestibular system dysfunction, with particular emphasis on the question of how to distinguish central from peripheral vestibular disease. A companion article describes some common specific vestibular diseases and their diagnostic differentials.

    Anatomy and Physiology

    For clinical purposes, the anatomic components of the vestibular system are divided into peripheral and central components. The peripheral components of the vestibular system are contained within the petrosal portion of the temporal bone (in what is known as the inner ear; FIGURE 1) and consist of the receptor organs (the saccule, utricle and semicircular canals, all housed within the semicircular ducts and the cochlear duct) and peripheral axons of the vestibular division of cranial nerve VIII.1,2 The central components (FIGURE 2) of the vestibular system consist of the vestibular nuclei in the medulla and the vestibular projections to the cerebellum (cerebellar nuclei), spinal cord (long tracts), and rostral brainstem.3

    The receptor organ consists of the saccule, utricule, and the crista ampullaris within the terminal portion of each semicircular canal and detects the position and movement of the head in space.1,2 This information is converted into electrical signals that travel along cranial nerve VIII to the brainstem. The vestibular nuclei receive the signals and send messages to various parts of the body to fulfill the following functions3:

    • To the spinal cord via the vestibulospinal tract to exert a facilitatory effect on the ipsilateral extensor muscles of the limb
    • To the eyes via the medial longitudinal fasciculus to control the muscles involved in eyeball movement (cranial nerves III, IV, and VI)
    • To the forebrain via the thalamus for conscious perception of position
    • To the cerebellum to maintain coordination of the eyes, neck, body, and limbs in relation to movements of the head
    • To the reticular formation in the brainstem, an area responsible for vomiting and motion sickness

    Clinical Signs

    It is important to recognize when an animal has vestibular disease (BOX 1). Once the presence of a vestibular disorder is confirmed, the next step is to determine whether the animal has central or peripheral disease (TABLE 1).

    Box 1. Clinical Signs Common to Central and Peripheral Vestibular Disease

    • Head tilt: The ventrally deviated ear is usually on the side of the lesion (except in cases of central vestibular disease with a paradoxical head tilt).
    • Nystagmus: Nystagmus has a fast phase and a slow phase. The slow phase is usually directed toward the side of the lesion (except in cases of central vestibular disease with a paradoxical head tilt). Horizontal, rotary, or vertical eye movements can be seen.
    • Strabismus: This refers to an abnormal position of the eyeballs and can be seen when the head is placed in an abnormal position (e.g., when extended dorsally) or when the animal is in dorsal recumbency.
    • Ataxia: Vestibular ataxia is differentiated from other forms of ataxia by its asymmetry. It is characterized by a broad-based stance, swaying of the trunk and head, and falling to one side. If bilateral vestibular disease is present, the animal may fall/roll to either side.

    A head tilt is one of the more common signs indicating a vestibular disorder (FIGURE 3). It is characterized by rotation of the median plane of the head, with one ear held more ventral than the other. This abnormal posture results from a loss of tone to the antigravity muscles of the neck, either ipsilaterally or contralaterally (depending on the site of the lesion). This is different from a head turn (torticollis) in which the median plane of the head remains perpendicular to the ground but the nose is turned toward the body. A head turn usually indicates an ipsilateral forebrain lesion and is not a sign of vestibular disease, although it can be seen with syringomyelia of the cervical spinal cord.

    Nystagmus is a characteristic eye movement in animals with vestibular disease, specifically jerk nystagmus, in which there is a quick phase and a slow phase. There are two major categories of jerk nystagmus: physiologic and pathologic.

    Physiologic jerk nystagmus (or vestibular eye movements) can be induced in a normal animal by turning the head from side to side. Initially, a slow drift of the eye is seen away from the direction of travel, followed by a fast compensatory phase in the direction of movement of the head. A reduction or lack of vestibular eye movements is considered abnormal and can be seen with unilateral or bilateral vestibular disorders, respectively.

    Pathologic jerk nystagmusis seen when the vestibular system is dysfunctional. The eyes have a tendency to spontaneously drift in the direction of the lesion (slow phase) and, via a brainstem mechanism (involving the medial longitudinal fasciculus), quickly return to their initial location (fast phase). This type of abnormal nystagmus can be seen at rest (spontaneous nystagmus) or may only occur with abnormal head positions (positional nystagmus). Horizontal, vertical, and rotary nystagmus may be present. As a general rule, if vertical nystagmus is seen, a central vestibular lesion should be suspected. Horizontal and rotary nystagmus only signify vestibular disease and do not distinguish a central from a peripheral lesion.

    Strabismus results from a loss of vestibular control over maintenance of the normal eye position within the orbit. Vestibular information is projected through the medial longitudinal fasciculus to cranial nerves III, IV, and VI. If this input is abnormal, strabismus may be seen when the head position is perturbed and occasionally may be seen with the head in a normal position. Strabismus and nystagmus may be concurrent. Ventral or ventrolateral strabismus is most commonly observed ipsilateral to the lesion.

    Ataxia is defined as an uncoordinated gait and can be caused by a vestibular disorder (vestibular ataxia), a cerebellar disorder (cerebellar ataxia), or a spinal cord, brainstem, or peripheral nerve disorder (general proprioceptive ataxia).

    Circling is not pathognomonic for vestibular disease; it is also seen in patients with forebrain lesions. If the circles are small and poorly completed, then vestibular disease is most likely. However, if they are large and complete, a forebrain disorder should be considered.

    Central or Peripheral?

    In a 10-minute consultation, it can be difficult to prioritize which neurologic deficits should be evaluated. However, the decision of whether a lesion is central or peripheral has a significant impact on the likely prognosis and outcome for the patient. In a patient with vestibular disease, the lesion lies within the brain (central disease), cranial nerve VIII, or an ear (peripheral disease). Diagnosis and management of central lesions generally require more expensive diagnostics and therapies, and the common causes of central vestibular disease are often associated with a guarded prognosis. In contrast, peripheral vestibular lesions are broadly associated with a good prognosis (with some exceptions). The following clinical signs can be used to help determine whether vestibular disease is central or peripheral in origin. These signs are also listed in TABLE 1 and FIGURE 4 .4

    Horner syndrome (miosis, enophthalmos, protrusion of the third eyelid, ptosis of the upper eyelid) is usually seen only with peripheral vestibular disease.1,4 The sympathetic nerve supply to the eye is near the vestibular nerve between the petrous temporal bone and tympanic bulla (FIGURE 2). Facial paralysis may occur in either central or peripheral disease, as cranial nerve VII (the facial nerve) follows a similar course to the vestibular nerve as it runs through the petrous temporal bone (FIGURE 2).

    Lesions affecting the central vestibular system typically produce clinical signs suggestive of brainstem and/or cerebellar involvement in addition to the potential signs of peripheral disease.1,4 The reticular formation is integrally associated with the brainstem, as are the ascending and descending motor and sensory pathways (i.e., the long tracts) to the limbs. Therefore, abnormal mentation, hemiparesis, and postural reaction deficits are commonly associated with central vestibular disease (FIGURE 4). Note that when testing conscious proprioception in an animal with a vestibular disorder, it can be difficult to balance the patient’s weight evenly, so false-positive reactions may be seen. If the animal is small, then tactile placing responses are useful; however, in a larger animal, this is not practical, so hopping and paw placing should be evaluated by supporting the animal’s weight evenly.

    Deficits of cranial nerves V to XII can also be associated with a central vestibular lesion due to the association of these nerves with the brainstem.1,4 A general rule to follow is that if two or more cranial nerves are affected (in addition to cranial nerve VIII), a central lesion should be suspected. However, an exception to this rule does exist (see below).

    The absence of specific central signs (TABLE 1) does not rule out a central vestibular lesion. However, their presence makes central disease far more likely.

    Occasionally, patients with peripheral vestibular disease have polyneuropathies.5 These animals have normal mentation with single or multiple cranial nerve deficits, such as dysphagia (cranial nerve IX and X), tongue weakness (cranial nerve XII), jaw weakness and masticatory muscle atrophy (cranial nerve V), and facial paralysis (cranial nerve VII). Paresis of the limbs is rarely present, although decreased tone and reduced segmental spinal reflexes may be observed.

    Central Vestibular Disease With a Paradoxical Head Tilt

    A head tilt and balance loss are occasionally appreciated in a patient that has proprioceptive deficits that are opposite to the direction of the head tilt6 (FIGURE 4). These specific clinical signs are seen when a lesion involves the vestibular apparatus of the cerebellum (i.e., the caudal cerebellar peduncle or flocculonodular lobe) on the side of the body opposite to that of the head tilt. The reason for this is that the cerebellar output is largely inhibitory, so it decreases activity within the ipsilateral vestibular nuclei (FIGURE 4). The head tilt in any vestibular syndrome is always to the side of least activity within the vestibular nuclei. If this inhibitory influence is lost (e.g., due to a severe cerebellar lesion), then activity in the ipsilateral vestibular nuclei is increased, causing the head to tilt to the side opposite the lesion. Clinically, the recognition of proprioceptive deficits on the opposite side to a head tilt should alert the observer to the possibility of a central vestibular lesion.

    Bilateral Vestibular Disease

    Bilateral vestibular disease (BVD) is rare and is most commonly peripheral in origin, although it can, theoretically, occur in very small focal and symmetric central lesions (e.g., due to metabolic, nutritional, or toxic causes such as thiamine deficiency).7 Diffuse, large central lesions are unlikely to cause BVD as they would severely disrupt the reticular formation, resulting in coma or death. Animals with BVD are reluctant to walk, exhibiting vestibular ataxia and wide head excursions, swinging their head from one side to the other. It is uncommon to see a head tilt or pathologic nystagmus in these patients, although normal physiologic nystagmus is absent.

    Downloadable PDF


    1. De Lahunta A, Glass E. Vestibular system: special proprioception. In: Veterinary Neuroanatomy and Clinical Neurology. 3rd ed. St. Louis, MO: Saunders Elsevier; 2009:319-347.

    2. LeCouteur RA, Vernau KM. Feline vestibular disorders. Part I: anatomy and clinical signs. J Feline Med Surg 1999;1:71-80.

    3. Kent M, Platt SR, Schatzberg SJ. The neurology of balance: function and dysfunction of the vestibular system in dogs and cats. Vet J 2010;185:247-258.

    4. Troxel MT, Drobatz KJ, Vite CH. Signs of neurologic dysfunction in dogs with central versus peripheral vestibular disease. J Am Vet Med Assoc 2005;227:570-574.

    5. Jaggy A, Oliver JE. Neurologic manifestations of thyroid disease. Vet Clin North Am Small Anim Pract 1994;24:487-494.

    6. Garosi LS, Dennis R, Penderis J, et al. Results of magnetic resonance imaging in dogs with vestibular disorders: 85 cases (1996-1999). J Am Vet Med Assoc 2001;218:385-391.

    7. Schunk KL. Diseases of the vestibular system. Prog Vet Neurol 1990;1:247-254.

    References »

    NEXT: Vestibular Disease: Diseases Causing Vestibular Signs

    CETEST This course is approved for 3.0 CE credits

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