- Anomalous diseases
- Metabolic diseases
- Neoplastic diseases
- Inflammatory diseases
- Idiopathic diseases
- Toxic diseases
- Traumatic diseases
Congenital vestibular disease
Congenital vestibular diseases are seen infrequently in dogs and cats but have been reported in Siamese, Burmese and Tonkanese cats, and in Dobermann Pinschers, Cocker Spaniels, German Shepherd Dogs, Akitas, Smooth Fox Terriers and Beagles ().
Clinical signs. The onset is usually first noticed between 3 and 12 weeks of age. Head tilt, ataxia and circling may be seen, and the animal may be deaf. Nystagmus is not a characteristic feature.
Pafhogenesis. The pathogenesis is not known. One study of Dobermann Pinschers demonstrated noninflammatory cochlear degeneration in affected animals, with progressive loss of the auditory sensory hair cells (), whilst a separate study revealed the presence of lymphocytic labyrinthitis in affected Dobermann Pinscher puppies ().
Diagnosis. Diagnosis is by exclusion of other disorders and consideration of signalment and history.
Treatment and prognosis. No treatment is available. Vestibular signs may improve over time; this is most likely due to compensation for a static vestibular deficit rather than disease resolution. Deafness, if present, tends to be permanent. Affected animals should not be bred from as the condition is presumed to be inherited.
Peripheral vestibular disease has occasionally been reported in association with hypothyroidism.
Clinical signs. Clinical signs include head tilt, ataxia, circling and positional strabismus, unless the disease is bilateral, in which case wide excursions of the head and neck result. Facial nerve paresis has been reported in conjunction with the vestibular signs in some dogs. Signs commonly attributed to hypothyroidism, such as lethargy, weight gain and poor hair coat, are frequently absent in affected dogs. Onset of signs can be either acute or chronic, and the disease course may be either progressive or non-progressive.
Pathogenesis. The pathogenesis of peripheral nerve disease associated with the hypothyroid state is not completely understood, although it is believed to reflect a deficit in energy metabolism and resultant disturbance in axonal transpon.
Diagnosis. Diagnosis is based on laboratory evaluation of thyroid function and response to treatment.
Treatment and prognosis. Supplementation with levothyroxine is the standard therapy. Resolution of most neurological deficits are expected within 2 months, although a residual head tilt and positional strabismus may persist.
Tumours of the middle or inner ear
Clinical signs. Neoplastic conditions of the inner or middle ear can cause peripheral vestibular signs in dogs and cats. Tumours that have been reported to cause vestibular disease include: fibrosarcoma, chondrosarcoma and osteosarcomas of the osseous bulla; squamous cell carcinoma; adenocarcinoma; and lymphoma ().
Pathogenesis. Vestibular signs are caused by destruction or compression of cranial nerve VIII by the tumour.
Diagnosis. Radiographs of the skull often reveal destruction of the tympanic bulla; associated soft tissue swelling or periosteal reaction may also be evident. Advanced imaging via CT or MRI provides additional detail with respect to the origin and extent of the neoplastic process and determines whether the tumour has invaded the cranial vault ().
Treatment and prognosis.Complete surgical resection of tumours involving the middle or inner ear is difficult. Adjunctive radiation therapy is recommended when complete surgical resection is not possible. Prognosis depends on the tumour type and extent of disease, but overall tends to be poor.
Otitis media/interna (OM/OI)
Otitis media/interna is one of the more commonly recognized causes of peripheral vestibular disease in both dogs and cats.
Clinical signs. Evidence of otitis externa may be apparent on general physical examination. Facial nerve paralysis and/or Horner’s synd rome can be seen in association with the vestibular signs, due to the close association of cranial nerve VII and the sympathetic supply with the petrous temporal bone. Disease is most frequently unilateral, but bilateral disease can also occur.
Pathogenesis. OM/OI typically develops as an extension of otitis externa, with common bacterial isolates including Staphylococcus intermedius and Pseudomonas spp. (). OM/OI can occur in the absence of otitis externa, in which case it is believed to be due to ascent of bacteria from the oral cavity through the auditory tube or by haematogenous spread.
Diagnosis. Diagnosis is based on thorough otoscopic examination and imaging of the tympanic bullae. Radiographs of the tympanic bullae may reveal evidence of fluid density within, and sclerosis of, the bulla (). However, radiographs may be normal in some cases, particularly early in the course of disease, and thus additional imaging techniques such as CT or MRI, may be required to provide more sensitive imaging of the bone and soft tissue in the affected area ().
Any exudate noted in the external ear canal should be removed by gentle saline irrigation to visualize the tympanic membrane. The tympanic membrane is frequently ruptured; if it is intact, it may appear to be bulging into the external ear canal.
If fluid is visualized within the middle ear, an attempt should be made to obtain a sample via myringotomy. This can be performed by inserting a 22-gauge spinal needle or tomcat catheter through the ventral aspect of the tympanic membrane, using an otoscope for guidance. The fluid present can then be gently aspirated into a syringe and submitted for cytology and bacterial culture.
Treatment and prognosis. Treatment for bacterial OM/OI consists of a 4—6 week course of systemic antibiotics. The clinician’s choice of antibiotics should be based on the results of culture and sensitivity testing (if samples are successfu fly obtained via myringotomy). Otherwise, an antibiotic that is effective against the most common causative organisms and that will penetrate into the tympanic bullae should be chosen, e.g. amoxicillin/clavulanate, a cephalosporin or a fluoroquinolone.
Otic cleansing products should not be used, particularly if the tympanic membrane cannot be initially visualized. If cleansing products escape into the middle ear, they can worsen the vestibular signs and cause deafness.
Prognosis is good for resolution of the infection, although neurological deficits may persist after effective medical therapy due to irreversible damage to the neural structures. Cases that are unresponsive to medical therapy may require surgical drainage and debridement via bulla osteotomy. Occasionally, an infection can extend into the cranial vault causing central rather than peripheral vestibular signs to predominate (). This may be more common in animals with OM/OI that have been treated with corticosteroids.
Nasopharyngeal (inflammatory) polyps are comprised of well vascularized fibrous tissue lined by epithelium.
Clinical signs. Disease is identified most frequently in cats from 1 to 5 years of age. Polyps may cause signs of upper respiratory disease and dysphagia in addition to peripheral vestibular dysfunction. Evidence of otitis externa is often present.
Pathogenesis. Nasopharyngeal polyps originate in the auditory tube or the lining of the tympanic cavity, and grow passively into the nasopharynx or middle ear of cats, and very rarely dogs. Otitis media/interna can be a complication of auditory tube obstruction by the polyp.
Diagnosis. Diagnosis is based on visualizing the polyp in the nasopharynx or external ear canal during a thorough pharyngeal and otoscopic examination performed under anaesthesia. Radiographs may reveal occlusion of the nasopharynx or sclerosis and soft tissue opacity within the tympanic bulla. Advanced imaging can provide additional information on the extent of soft tissue involvement associated with the polyp ().
Treatment and prognosis. Treatment involves removal of the polyp. Many polyps are attached to the auditory tube by a narrow stalk of tissue and this can be successfully removed with simple traction. More extensive polyps may require surgical removal via ventral bulla osteotomy. Horner’s syndrome is a common postoperative complication following ventral bulla osteotomy, but tends to be transient.
Overall prognosis is good. However, recurrence is possible , especially for polyps removed non-surgically.
Idiopathic vestibular disease
Idiopathic vestibular disease is a common cause of vestibular disturbance in both dogs and cats.
Clinical signs. These most commonly reflect unilateral involvement of the peripheral vestibular system and can be quite severe and acute at onset. Occasionally, bilateral disease is seen, especially in cats. In contrast with many of the other diseases affecting the peripheral vestibular system, facial paresis and Horner’s syndrome are not features of idiopathic vestibular disease ().
Pathogenesis. Idiopathic vestibular disease is characterized by the acute or even peracute onset of non-progressive peripheral vestibular signs.
The canine form typically, but not exclusively, affects older dogs and is also known as canine geriatric vestibular disease.
The feline disease is seen in cats of all ages and is documented to be most common in spring to autumn months, especially in the north-eastern states of the USA (no such temporal association has been made in Europe).
The aetiology of these disorders has not been determined. However, it has recently been hypothesized that the feline disease in the USA may be caused by Cuterebra larval migration ().
Diagnosis. Diagnosis is based on the presence of compatible history and physical examination findings, and by exclusion of other causes of peripheral vestibular disease. Typically, improvement in clinical signs is seen within 2-3 days.
Treatment and prognosis. No treatment is recommended aside from supportive care, which consists of administering intravenous fluids to animals that are vomiting, and confining the animal to a well padded area in order to minimize self-trauma secondary to disorientation. Meclozine can be given to treat nausea.
Prognosis is good, as the condition resolves on its own within 2-4 weeks. A mild residual head tilt or ataxia may persist in some animals.
Clinical signs. Ototoxic agents can affect vestibular function, hearing or both.
Pathogenesis. The systemic administration of aminoglycoside antibiotics is most commonly associated with ototoxicity. Prolonged therapy for more than 2 weeks with high doses of drug are necessary to induce the changes in normal animals; however, animals with renal impairment are more susceptible to developing toxicity.
Of the aminoglycoside antibiotics, streptomycin is most often associated with damage to the vestibular system. Other agents can induce ototoxicity when used topically, the most notable of which are the iodophors and chlorhexidine. Due to the potential for ototoxicity, topical otic preparations should never be introduced into the ear when the tympanic membrane cannot be visualized or is determined to be ruptured.
Diagnosis. Diagnosis is based on the acute onset of compatible clinical signs in an animal that has recently been administered an ototoxic agent, in addition to exclusion of other causes. Deafness can be confirmed with BAER testing.
Treatment and prognosis. No definitive treatment is possible. Vestibular signs usually improve over time, due to resolution of the damage or compensatory mechanisms, but deafness tends to: be permanent.
Trauma to the middle or inner ear
Clinical signs. Traumatic injuries to the middle and inner ear may result .in peripheral vestibular signs. Horner’s syndrome and facial nerve involvement may also. be seen , due to the close association of these nerves to cranial nerve VIII in the area of the petrous temporal bone.
Facial abrasions and swelling may be apparent in some animals, and haemorrhage may be present in the external ear canal on the affected side.
Pathogenesis. Vestibular signs are caused by direct damage to cranial nerve VIII, or compression by bone fragments or haemorrhage.
Diagnosis. In addition to a suggested or confirmed history of trauma, radiographs may reveal fractures of the tympanic bulla. CT or MRI () can be helpful in showing fractures not identified on skull radiographs, as well as determining the extent of soft tissue involvement, respectively.
Treatment and prognosis. No specific treatment is typically recommended other than that required for the head trauma itself ().
Prognosis depends on the severity of the injury. In general, vestibular signs tend to improve over time, but residual deficits may persist.