Vestibular dysfunction

Vestibular dysfunction is very common in veterinary neurology and clinical signs can be dramatic. The vestibular system maintains balance and coordination in the patient.

Basic neuroanatomy

The vestibular system can be divided into peripheral and central vestibular structures. The peripheral vestibular system consists of the 3 semicircular canals, utricle, and saccule of the inner ear, as well as the vestibulocochlear nerve (cranial nerve VIII). All of these structures are part of the inner ear located within the petrous temporal bone of the skull. The semicircular canals are responsible for detection of rotational movements of the head, while the utricle and saccule are responsible for static and kinetic movements. The central vestibular system consists of all of the vestibular structures located in the brain parenchyma. The vestibular portion of the vestibulocochlear nerve sends the majority of its axons to 4 vestibular nuclei located on each side of the dorsal aspect of the medulla just under the fourth ventricle and cerebellum, while some axons course through the caudal cerebellar peduncle and project to the fastigial nucleus, flocculus, or nodulus of the cerebellum. Axons from the vestibular nuclei pass caudally into the brainstem to form the lateral vestibulospinal tract, while other axons course both cranially as the medial longitudinal fasciculus (MLF) and caudally as the medial vestibulospinal tracts. The axons of the MLF project to the nuclei of cranial nerves III, IV, and VI and help coordinate ocular movements. Dysfunction of the MLF leads to clinical signs of nystagmus and positional ventral strabismus seen in vestibular disorders. The vestibulospinal tracts facilitate ipsilateral extensor muscles and contralateral flexor muscles. Normal function of both sides of the vestibular system balance each other out. Dysfunction of the vestibulospinal tract on one side of the body leads to decreased extensor muscle function ipsilateral to the lesion and increased flexor muscle function contralaterally. The vestibular system also sends axons to the vomiting center in the brainstem, which plays a role in nausea and vomiting with vestibular dysfunction, and sends axons rostrally to the cerebrum for conscious recognition of body location in space.

Common clinical signs of vestibular dysfunction

  • Head tilt
  • Vestibular ataxia – falling, rolling, leaning, veering, etc.
  • Nystagmus
  • Positional ventral strabismus
  • Other clinical signs are possible if the central vestibular system is affected (see below)

After performing a complete neurological exam, you should try to localize the lesion to either the central or peripheral vestibular system. Central vestibular dysfunction is likely present with identification of abnormalities that can only be associated with intracranial structures, such as altered mental status, cranial nerve deficits other than VII and VIII, true vertical nystagmus (see below), changing direction of the fast phase of nystagmus (e.g, right to left), postural reaction deficits, or cerebellar signs (e.g., dysmetria, hypermetria, intention tremors). The categories listed in red type in the chart are the neurological exam findings that distinguish peripheral from central vestibular dysfunction. NOTE: The presence of vertical nystagmus should not be the only finding found in a patient to push you toward central vestibular dysfunction. While it’s usually associated with central dysfunction, it will occasionally be observed in patients with peripheral vestibular dysfunction. In addition, there is sometimes a slight rotary component to the “vertical” nystagmus that can be easily missed if not examined carefully.

After deciding where the lesion is located, the next step is to determine the side of the lesion. With “classic” vestibular dysfunction, the head tilt and vestibular ataxia are usually toward the side of the lesion and the fast phase of nystagmuus is away from the side of the lesion (nystagmus “runs away” from the lesion). Postural reaction deficits are always ipsilateral to the lesion with vestibular dysfunction. As noted above, be careful during the early stage of severe, acute peripheral vestibular dysfunction because the nystagmus will occasionally look vertical, but it’s actually rotary. Postural reaction testing also may be difficult in moderately to severely affected patients. If the owner is leaning toward euthanasia, try to give the patient at least 24-72 hours before making a final decision. Many patients with severe vestibular dysfunction will eventually improve and even return to normal with appropriate treatment. Vestibular dysfunction is definitely a “don’t judge a book by its cover” situation.

Left head tilt in a Springer Spaniel with peripheral vestibular dysfunction due to hypothyroidism.

Left head tilt in a Springer Spaniel with peripheral vestibular dysfunction due to hypothyroidism.

DIstinguishing peripheral from central vestibular dysfunction.
NOTE: Disorientation is possible for both PVD and CVD, but patients with PVD should remain responsive. Care should also be taken localizing the lesion in patients whose only sign of central vestibular dysfunction is vertical nystagmus. Some patients with PVD will appear to have a vertical nystagmus when it actually has a slight rotational component.

Exceptions to the “rules”

Paradoxical central vestibular dysfunction

At times, the abnormalities noted on neurologic exam are suggestive of central vestibular disorder (e.g., vertical nystagmus, postural reaction deficits), but they are conflicting with regard to the side affected. This is called paradoxical central vestibular dysfunction. It is due to disease in the cerebellum (flocculus, nodulus, fastigial nucleus) or the caudal cerebellar peduncle. The paradox occurs when the head signs suggest a lesion on one side, but the postural reaction deficits indicate the other side is affected. Believe the postural reaction deficits, since these are ipsilateral to the lesion in patients with vestibular dysfunction (see case example below). In some cases, patients with paradoxical vestibular dysfunction will have clear signs of cerebellar involvement, such as dysmetria, hypermetria, and intention tremors. Occasionally, animals with cerebellovestibular dysfunction will also have an absent menace response with intact vision (ruling out an optic nerve lesion) and intact palpebral reflex (ruling out a facial nerve lesion). As with postural reaction deficits, the absent menace response is always ipsilateral to the lesion in patients with cerebellovestibular dysfunction.

Case example: A 10-year-old MC Greyhound is presented to you with an acute onset of non-progressive clinical signs, including right head tilt, vestibular ataxia, resting and positional left rotary nystagmus, and left-sided general proprioception and hopping deficits. In this patient, the head tilt and nystgamus suggest a right-sided lesion, but the postural deficits suggest a left-sided lesion, hence the paradox. Since postural deficits are always ipsilateral with disease in the cerebellum or central vestibular structures in the medulla oblongata, the neurolocalization for this patient would be left paradoxical central vestibular.

Bilateral peripheral vestibular dysfunction

Patients with bilateral peripheral vestibular dysfunction often are presented with signs of vestibular dysfunction, including vestibular ataxia (often to both directions) and horizontal or rotary nystagmus, but lack of head tilt is fairly common or can be present and intermittently change sides. Some patients with bilateral peripheral vestibular dysfunction have no pathologic nystagmus. The patients often walk low to the ground or crouched and will have wide side-to-side lateral head excursions. Otitis interna is the most common cause of bilateral peripheral vestibular dysfunction, but bilateral signs can be observed in patients with other conditions (e.g., hypothyroidism).

Vestibular dysfunction due to thalamic disease

Just to confuse things even more, central vestibular signs occasionally occur secondary to a thalamic lesion, most often due to a thalamic infarct. This is not very common. It’s more important to remember the basic rules of localizing peripheral vs. central dysfunction.

Peripheral vestibular disorders

Otitis interna

MRI from a dog with an acute onset of peripheral vestibular signs with right otitis media-interna.

MRI from a dog with an acute onset of peripheral vestibular signs with right otitis media-interna.

Inner ear infection is the most common cause of peripheral vestibular dysfunction in dogs and cats, accounting for approximately 50% of cases. Otitis interna can occur secondary to direct extension of external ear infection across the tympanic membrane, via the eustachian tube or hematogenous spread. The most commonly isolated organisms are StaphylococcusStreptococcusPseudomonas, and Proteus species. Diagnosis is ideally made via otoscopy, advanced imaging (MRI or. CT) and bacterial culture of the middle ear. Empirical treatment can be started if the owner declines diagnostics. Oral cephalexin or amoxicillin-clavulanic acid (Clavamox) are generally effective. Treatment for at least 6 weeks is recommended as it can take this long to clear an inner/middle ear infection. Diagnostics and more invasive treatments (myringotomy/ear flush or bulla osteotomy) are recommended if the patient’s clinical signs do not resolve within 3 weeks or get worse at any time. A mild head tilt may persist long term.

Primary Secretory Otitis Media (PSOM; “glue ear”), an apparently non-infectious form of otitis media, occurs in the Cavalier King Charles Spaniel. This disease is characterized by an accumulation of thick mucus exudate in the tympanic bulla with associated clinical signs of middle ear disease and occasionally vestibular signs. Some speculate that this disease is due to excessive secretion of mucus, decreased drainage through an abnormal eustachian tube, or both. Surgical removal via myringotomy or ventral bulla osteotomy is recommended.

Idiopathic Vestibular Disease (a.k.a., “old dog” vestibular)

This condition is seen in geriatric dogs (average, 12 yrs) and at any age in cats. Patients are typically presented with a peracute to acute onset of peripheral vestibular signs. The clinical signs may worsen for 12-24 hours, but continued progression after 24 hours is suggestive of another cause for the vestibular signs. The cause of this condition is unknown and there is no known medication that will improve the degree or speed of recovery. Maropitant citrate (Cerenia) or meclizine may be helpful in controlling nausea, vomiting, and motion sickness in these patients.  The clinical signs typically resolve within 1-2 weeks. Recurrence is uncommon but can occur.


Unilateral peripheral vestibular signs may be observed in some dogs with hypothyroidism. Acute onset of clinical signs is possible. Diagnosis is made by finding a low total T4 and free T4 with a concurrent elevated TSH level. The condition is usually reversal with supplementation but may take 4 weeks for clinical signs to resolve.

Video otoscopy showing a nasopharyngeal polyp extending into the horizontal ear canal.

Video otoscopy showing a nasopharyngeal polyp extending into the horizontal ear canal.

Nasopharyngeal polyp

Nasopharyngeal polyps are benign inflammatory masses that arise from the epithelial lining of the eustachian tube or tympanic bulla. Clinical signs of middle ear disease (e.g. shaking head, scratching ears/face) will occur if the polyp arises from or extends into the tympanic bulla. Peripheral vestibular signs may be observed if the inner ear is affected. Oropharyngeal signs (e.g., gagging, retching) and upper respiratory signs may be seen if the polyp extends into nasopharynx. Diagnosis can often be made via otoscopy and/or oropharyngeal exam, but advanced imaging (MRI or CT) may be needed. Surgical excision is usually curative if the entire mass is removed. A ventral bulla osteotomy is strongly recommended for these patients. Simply pulling on the mass often does not remove the entire polyp and it will regrow leading to a recurrence of clinical signs.


Tumors may arise from any cell type in the region. The most common ear tumors, ceruminous gland adenocarcinoma and squamous cell carcinoma, can invade into the middle & inner ears. Other tumors include osteosarcoma, salivary gland carcinoma, chondrosarcoma, and fibrosarcoma. Treatment options include surgical debulking, radiation therapy, chemotherapy, and palliative control of clinical signs. Unfortunately, the prognosis is generally guarded to poor.

Other peripheral vestibular disorders

  • Congenital peripheral vestibular disease – This is thought to be due to congenital malformation or degeneration of the inner ear structures. It has been reported in German Shepherds, English Cocker Spaniels, Doberman Pinschers, Siamese cats, and Burmese cats.
  • Head trauma
  • Toxicity – Vestibular signs and/or hearing loss can occur in some patients given aminoglycosides, loop diuretics (e.g., furosemide), or platinum-containing chemotherapeutics (e.g., cisplatin, carboplatin).  Ear cleaning products can also cause peripheral vestibular signs if the tympanic membrane is ruptured allowing the product to enter the middle & inner ears. The ears should be cleaned with saline only until the tympanic membrane can be seen and confirmed to be intact.

Central vestibular disorders

Meningioma in a dog with central vestibular signs.

Meningioma in a dog with central vestibular signs.


Both primary and secondary brain tumors occurring in the region of the central vestibular structures can cause central vestibular dysfunction. The most common primary brain tumors that occur in this region include meningiomas, gliomas, and choroid plexus tumors. Other primary brain tumors include medulloblastoma, ependymoma, epidermoid or dermoid cysts, and other rare tumors. Secondary brain tumors (e.g., multilobular tumor of bone, osteostarcoma, metastatic hemangiosarcoma) can also occur in this area. Treatment options include surgery if accessible, radiation therapy, chemotherapy, and palliative control of cerebral edema with corticosteroids. See the neoplasia disease pages under the intracranial menu above for additional information.


Central vestibular dysfunction is relatively common in dogs with immune-mediated (presumably non-infectoius) inflammatory brain diseases. Granulomatous Meningoencephalomyelitis (GME) and Necrotizing Leukoencephalitis are the most common disorders.

The most common infectious causes of central vestibular dysfunction are canine distemper virus and feline infectious peritonitis (FIP) in dogs and cats, respectively. Other infectious organisms that cause central vestibular dysfunction include rickettsial organisms (Rocky Mountain Spotted Fever, Ehrlichia species, Anaplasma phagocytophilum), fungal organisms (Cryptococcus neoformans, others based on regional exposure risks), protozoa (Toxoplasma gondiiNeospora caninum), other viral diseases (FeLV, FIV), bacterial infection, and rare algal infection (e.g., Prototheca species).

See the encephalitis pages under the intracranial menu above for additional information.


Cerebellar infarcts are a relatively common cause of paradoxical central vestibular signs in dogs. Brainstem infarction is possible, but less common. The classic MRI appearance of cerebellar infarction is an intra-axial wedge-shaped hyperintense lesion on T2-weighted images that is iso- to hypointense on T1-weighted images and does not contrast enhance (“blushing” contrast enhancement is occasionally observed). A search for an underlying medical condition should be performed, but cerebellar infarcts are often idiopathic in nature. Conditions that predispose to infarction include hyperadrenocorticism, protein-losing nephropathy, hypothyroidism, systemic hypertension, coagulopathy, and others.

Metronidazole toxicity

Metronidazole can cause central vestibular signs in both dogs and cats. Vestibular signs are more common in dogs, while forebrain signs (e.g., seizures, mental dullness, blindness) are more common in cats. Patients with metronidazole toxicity frequently present with symmetrical signs of vestibular ataxia, nystagmus, postural reaction deficits, and non-specific signs of nausea and vomiting. Head tilt is frequently absent in these patients. Toxicity can occur acutely within 7-12 days in patients given greater than 60 mg/kg/day. It has also been reported in patients given “chronic” doses in the 30-60 mg/kg/day range. As a result, it is recommended that the dose be kept below 30 mg/kg/day. Most patients do not need doses higher than this.

Thiamine deficiency

Central vestibular dysfunction is occasionally observed in patients with thiamine deficiency. This occurs most commonly in patients fed a diet that is thiamine deficient, an all-cooked diet (thiamine is heat-labile) or diets high in thiaminase (e.g., fish viscera) which breaks down thiamine in the food. Thiamine deficiency causes bilaterally symmetrical necrosis and hemorrhage in the lateral geniculate nuclei of the thalamus, the caudal colliculi of the midbrain, the vestibular nuclei, and the nodulus of the cerebellum. Complete resolution of clinical signs is possible if treated early with change to a high-quality diet and thiamine (vitamin B1) supplementation.

Other possible causes of central vestibular dysfunction

  • Degenerative diseases, such as lysosomal storage diseases
  • Anomalies – occasional intracranial intra-arachnoid cysts
  • Metabolic – hypothyroidism occasionally causes central vestibular dysfunction
  • Head trauma
Last updated by NeuroPetVet on January 21, 2018.