by R.M. Clemmons, DVM, PhD
Associate Professor of Neurology & Neurosurgery


All veterinary species suffer from various forms of vestibular disease. Many of which require only recognition, while others represent significant diagnostic challenges. Although there are a number of diseases which can affect the vestibular system, generally we can break them down anatomically into peripheral and central disorders. With certain exceptions, peripheral diseases bear a better prognosis in most species than central vestibular disease. Partially due to this concern, vestibular diseases represent a large number of neurologic referrals. Often, it is only reassurance that the problem will pass that is necessary. Recognition of when to intervene is as important as when not too.

The cardinal signs of unilateral vestibular disease are head tilt, nystagmus (spontaneous abnormal eye movements), circling (toward the lesion in "tight" circles), and incoordination. This is because the vestibular system is an important part of the CNS balance control system. In order for animals to know how they are oriented in space, three neural systems must be functioning. The vestibular system, through the stimulus-response of the hair cells in the semicircular canals, reacts to angular acceleration and deceleration. The visual system allows the animal to focus on the horizontal and vertical, orienting in space. Finally, gravity is detected by pressure receptors in the skin, orienting the animal on up and down. While the vestibular system is very important, it requires at least 2 of these orienting systems to function for the animal to negotiate within its environment. This can be important with vestibular disease, since, in acute disease, the nystagmus prevents the eyes from focusing on the horizon, effectively eliminating spacial orientation.

The anatomic structures involved in the vestibular system include the hair cells in the saccule and utricle (containing the semicircular canals), the vestibular portion of CN VIII, the vestibular nuclei in the brainstem and the flocculonodular lobe of the cerebellum. The vestibular nuclei send fibers forward in the medial longitudinal fasciculus (MLF) which coordinates ocular movements, projects fibers to the spinal cord as the vestibulospinal tract and descending MLF, projects fibers to the cerebellum, and sends fibers to various structures in the brainstem including the emetic center. Involvement of any of the portions of the vestibular system will result in signs of disfunction. Most lesions result in loss of function and, hence, are ablative in nature. The signs develop due to the imbalance existing between the normal and abnormal sides.

The nystagmus seen in vestibular disease can be helpful in localizing the disease process. While horizontal and rotatory nystagmus can be seen with disease anywhere within the vestibular system, vertical and positional nystagmus are almost exclusively seen with central vestibular diseases. Moreover, horizontal nystagmus from peripheral vestibular disease oscillates with the fast-phase away from the direction of the head tilt. With central vestibular disease (particularly of the cerebellum), however, the fast-phase is toward the lesion. So although horizontal and rotatory nystagmus are not specific for peripheral disease, they are compatible with it. Vertical and positional nystagmus suggest the lesion is within the CNS and indicate the need for a thorough neurologic work-up.

Vestibular diseases can be classified into three major disease processes: idiopathic vestibular disease, inner ear disease, or central vestibular disease. The former 2 represent common forms of peripheral vestibular disease which need to be separated from each other and from central vestibular disease.

Idiopathic Vestibular Disease:

All cranial nerves have the potential to develop specific syndromes which are clinically classified as idiopathic disorders. This is probably due to the fact that each cranial nerve represents a unique developmental anatomy from their respective brachial arches. This also gives them an unique antigenic signal allowing very specific immune attack upon them. Idiopathic vestibular disease represents one of these cranial nerve syndromes.

Clinically, idiopathic vestibular disease presents as an acute onset of vestibular signs with severe imbalance, due to its sudden onset and the severe nystagmus which is associated with the onset of the disorder. Since the eyes are unable to fix on the horizon and the vestibular mechanism is defective, there is severe vertigo. This often results in the rolling and rolling described by the owners. This can be mistaken for a seizure, which it is not. During the early phases of idiopathic vestibular disease, the patient often experiences nausea to the point of frequent vomiting and inappetence. The head tilt will be toward the side of dysfunction and the nystagmus will be horizontal or rotatory with the fast-phase away from the head tilt. If supported, there are no other neurologic deficits and proprioception is normal.

The diagnosis of idiopathic vestibular disease is tentatively made by the presence of acute clinical signs in the absence of other physical findings. The minimum data base include physical examination, otoscopic examination and neurologic examination. The lack of findings (other than the peripheral vestibular signs) supports the diagnosis. The signs of idiopathic vestibular disease are regressive, meaning that they disappear without treatment over time. As such, the fact that the disease is self-limiting is how the final diagnosis is achieved. The nystagmus will usually improve or disappear all together within 3-5 days of the onset. The patient will, then, improve in their imbalance and be more able to function normally. This improvement will continue until minimal deficits will remain. It is possible that there will be a residual head tilt. If the head tilt persists beyond 6 months following the onset of signs, it is likely to be permanent.

There is no treatment which will hasten the recovery from idiopathic vestibular disease. Corticosteroids probably do not offer an effective treatment. On the other hand, since idiopathic vestibular disease may represent an immune disease, anti-oxidant steroids (such as Solu Medral) may decrease severe symptoms. During the early phases, anti-vertigo drugs might make the patient more comfortable. Generally, I use diphenhydramine at 2-4 mg/kg every 8 hours as needed. Diphenhydramine is a centrally active anticholinergic, antihistamine which helps reduce vertigo and nausea. Assuming that the regressive course becomes evident, then I monitor the patient periodically for the signs of continued improvement.

Antidotal evidence suggests that idiopathic vestibular disease may represent toxicity to eating certain strains of lizards. Owners often notice the cat with a lizard in its mouth just prior to the onset of clinical signs. However, experimental feeding of the suggested lizard species to cats does not lead to the disease. It is still possible that laboratory conditions do not mimic field conditions. On the other hand, idiopathic vestibular disease occurs in many animals and in animal species where exposure to lizards plays no role in the condition. It is most likely that idiopathic vestibular disease is an immune-related condition affecting the unique antigens presented by the vestibular nerve. It can recur and is often more severe on recurrence.

Inner Ear Disease:

Many different problems result in inner ear disease; however, the clinical signs caused by these diseases are similar, indicating the location of the disease rather than the specific cause. These signs are those of peripheral vestibular dysfunction, including head tilt, nystagmus, circling and imbalance. On the other hand, since the diseases which cause inner ear disease are usually slower in evolution, these signs are generally less severe than with idiopathic vestibular disease. In addition to the vestibular signs, there are also varying degrees of facial nerve dysfunction and often Horner's syndrome. Anatomically, the facial nerve and the sympathetic fibers heading to the eye pass near the inner ear in the osseous petrous temporal bone. Damage of these neural structure, in addition to the damage of the vestibular nerve is a hallmark for inner ear disease. It is possible to affect both the facial and vestibular nerves together in the calivarium, but it is rare to see Horner's syndrome from central nervous system disease. As such, Horner's syndrome suggests that the disease in process is in the peripheral C8-T2 nerve roots, the vagosympathetic trunk, the inner ear or within the orbit. When Horner's syndrome is seen in combination with vestibular disease and facial nerve disease, the location must be in the peripheral vestibular system in the region of the osseous petrous temporal bone.

The signs of facial nerve dysfunction include paresis or paralysis of the muscles of facial expressions (lack of ear movement, lack of blink and lack of buccal muscle reaction on palpation). This leads to deficiency of the vibrissa reaction, decreased to absent menace response and diminished to absent palpebral response. In addition, the facial nerve supplies parasympathetic innervation to the lacrimal gland of the eye. As such, peripheral facial nerve disease can lead to diminished tear production in the eye on the affected side. This can be rather catastrophic in inner ear disease where the facial nerve dysfunction results in the inability to close the eye, while also decreasing tear production. As such, every dog with inner ear disease should have a Schirmer's tear test run on the eyes and appropriate treatment instituted if tear production is deficient.

Horner's syndrome varies among species. In small animals the ocular signs predominate, including myosis, ptosis and enophthalmos. In horses, the signs of Horner's syndrome are expressed primarily as excessive sweating on the affected side of the face. In cattle, there is a lack of sweating on the muzzle of the affected side.

The most common cause of inner ear disease in all species is secondary in inner ear infection. Most of these represent bacterial extension from otitis media which can arise from hematogenous spread from bacteremia or from spread up the eustachian tube to the middle ear. Luckily, these infections, once recognized, can often be successfully treated. Other causes of inner ear disease may not be treatable, including fungal infections and neoplasia. Therefore, it is generally best to "treat-for-the-treatable" when dealing with inner ear disease, using appropriate antibiotic therapy.

The minimum data base for diagnosis of inner ear disease includes physical and neurologic examination, Schirmer's tear test, otoscopic examination (with culture of the external ear canal, if indicated), pharyngeal examination, CBC and urinalysis. If there is evidence of cardiac murmur, then cardiac ultrasound should be performed. Skull radiographs are then necessary to evaluate the degree of change in the osseous structures of the inner ear. This will be helpful in making the diagnosis and in monitoring the response to treatment.

The treatment of bacterial inner ear infection must consider the fact that the disease represents bone infection. As such, the antibiotic must be able to penetrate bone, develop good tissue concentrations (including the blood-ear barrier) and, preferably, be bactericidal in action. Many veterinarians use enrofloxacin as their antibiotic of choice. I find that enrofloxacin is great for treating gram negative infections in the lung, but it may not reach tissue concentrations within neural structures like the inner ear. It needs additional help to do this. Therefore, if I do not use my treatment of choice, I will add a sulfa drug to enrofloxacin to take advantage of the synergistic effect of sulfa drugs. My antibiotic regime of choice is cephalosporins and sulfa drugs (sulfadimethozine) in combination. This meets the criteria for the ideal therapy for inner ear disease. It is excellent in treating gram positive bacteria, which are the most common organisms infecting the inner ear. Since this is a bone infection, the treatment must be continued for 6-8 weeks, minimum. The most common cause of treatment failure is not treating long enough.

Central Vestibular Disease:

Whenever anything else is seen other than the signs above, one must consider the likelihood that the problem is due to central vestibular disease. Additional cranial nerve deficits, proprioceptive deficits and motor deficits indicate brainstem damage affecting the vestibular nuclei and sensor and motor pathways which course through the vestibular region of the brainstem. In addition, the nystagmus seen in central vestibular disease will often be vertical or positional in nature, supporting the location of the disease process within the brainstem or cerebellum. If there is whole body and head tremors, the lesion is likely to be within the flocculonodular lobe of the cerebellum. While diseases which affect the peripheral vestibular system are usually good diseases; that is, diseases which regress without treatment or which respond to appropriate antibiotic therapy, most central vestibular diseases carry a less optimistic prognosis.

The major causes of central vestibular disease are inflammatory/infectious diseases or neoplasia. Organophosphate intoxication, liver disease (with metabolic brainstem degeneration) and thiamine deficiency can occasionally result in central vestibular disease (depending upon the species of animal), but these causes are far less than the inflammatory or neoplastic causes. In dogs, canine distemper virus, granulomatous meningoencephalitis, toxoplasmosis, neosporidiosis, aspergillosis, cryptococcosis, steroid-responsive meningoencephalitis, Lyme's disease, Rocky Mountain spotted fever and ehrlichiosis are the most common inflammatory and infectious diseases recognized. In the cat, FeLV, FIP, and cryptococcosis are the most common infectious diseases. Any of the primary brain tumors can occur in dogs, while only meningiomas are common in cats. Cats who are not eating and stressed can easily develop thiamine deficiency and this should not be overlooked in treating sick cats with vestibular signs.

Diagnosis of central vestibular disease involves the minimal data based for inner ear disease, but must be expanded to include a chemistry profile, a CSF tap and analysis (including species specific titers) and, often, advanced brain-imaging techniques, such as MRI examination. Since CSF cytology is important in assessing central vestibular disease and advanced imaging techniques are needed, central vestibular disease crosses "the referral line", the point in assessing disease which may require the interaction or interpretation of a neurologist.

The treatment and prognosis for central vestibular disease depends upon the cause. In neoplasia, biopsy may help determine whether radioablative surgery might be useful. Unfortunately, the brainstem is not an area amenable to conventional neurosurgery. In small animals, bacterial infections causing central vestibular disease is uncommon. Rickettsial infection is also rare. In cats, cryptococcosis may respond to therapy whether with remission or control of the neurologic signs. In dogs, fungal diseases usually progress in spite of vigorous treatment. Toxoplasmosis may be controllable for a period in the dog and treatable in the cat. Canine distemper virus infection may run its course and stop or be chronic and progressive. FeLV and FIP infections are generally, rapidly progressive. Granulomatous meningoencephalitis (GME) will respond temporarily to corticosteroid therapy, but ultimately progress. Steroid-responsive meningoencephalitis can be controlled with medication for long periods in the dog. Finally, organophosphate intoxication and thiamine deficiency may respond to appropriate therapy.

So, while central vestibular disease has many causes, in the absence of specific disease processes, there is limited hope for successful treatment and that hope is often based upon the response of the animal to medical management. The medical management is largely based upon the responsiveness of the disease process to corticosteroids. In other words, there are many causes of central vestibular disease, but often only one treatment approach. If the client understands this, it is possible to treat central vestibular disease without a specific diagnosis, realizing that the response to therapy can suggest whether the disease was "good" or "bad". The treatment approach that I use when a specific diagnosis cannot be made (either because the patient is too ill to undergo the diagnostic test or the client cannot afford them) is to treat with corticosteroids (usually oral prednisolone) and antibiotics (doxycycline and sulfadimethozine). The prednisolone will reduce inflammation while the doxycycline can help control bacterial and rickettsial disease while the sulfadimethozine may help control protozoal infection. I take a more pro-active approach in cats, since toxoplasmosis and cryptococcosis might be treatable. Therefore, I prefer to always perform CSF tap and analysis in cats with central vestibular disease, particularly when they also exhibit active chorioretinitis. I also add parenteral thiamine therapy when treating cats.

We have made important strides in understanding the breadth of central vestibular diseases. There are new promising approaches which may help treat more of the diseases than we have previously been able to treat. New antifungal drugs offer hope in controlling CNS fungal infections. More potent cytotoxic drugs may help diminish the effects of GME in the dog. Computer-Assisted Radioablative surgery offers hope in treating brainstem tumors. On the other hand, we have a long way to go. These new methods are expensive and not always available to every pet owner. We are, however, investigating whether natural medicine might be useful adjunctive therapies in many vestibular diseases. These approaches might reduce the cost and improve the outcome and prognosis for many patients.

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Last updated 27 August 2002