Identifying and treating vestibular disease

Animals that present with neurological issues can make for puzzling cases. Often, the most challenging part of managing neurologically affected patients is successfully neurolocalizing the disease. Once this essential step is achieved, there are many resources to consult regarding possible diseases for a given patient. Like any other disease process, making your way through the case information systematically and in a logical order will make the process of reaching a diagnosis much easier. The remainder of this article is focused on guiding you through managing a patient with vestibular disease, starting with confirming the vestibular dysfunction, and concluding with what steps you can take in your practice to manage a patient with vestibular disease or set them up for a successful referral process. What are the signs of vestibular dysfunction? There are four hallmark signs of vestibular dysfunction. Some animals have all four; others may have some, but not all. These signs will allow you to confirm your patient has vestibular dysfunction. They will not, however, enable you to distinguish between the three vestibular localizations (peripheral vestibular disease, central vestibular disease, and paradoxical vestibular disease). 1. Head tilt: With a head tilt, the patient’s eyes are no longer parallel to the floor (Figure 1A). Figure 1A: Head tilt to the right. Photo by Marc Kent, courtesy Susan Arnold 2. Vestibular ataxia: The patient will fall to one side, and in severe cases, might walk in tight circles while tipping over. In the most severe cases, they may “gator roll” (Video 1). 3. Spontaneous nystagmus: Despite the head being stationary, the eyes spontaneously dart in one direction, called the fast phase, and move slowly in the opposite direction, called the slow phase. Nystagmus can be horizontal, rotary, or vertical (Video 2). 4. Positional strabismus: When the patient’s head is directed toward the ceiling, the eyes’ gaze will normally be directed toward the ceiling. If, instead, one of the eyes does not track toward the ceiling, revealing more of the dorsal sclera than the other eye, then this is a positional strabismus (Figure 1B). Figure 1B: Positional strabismus of the left eye. Photo by Juliet Armstrong, courtesy Susan Arnold How do we localize to peripheral, central, or paradoxical vestibular disease? The four hallmark signs offer little help in localizing your patient’s vestibular dysfunction. It is essential patients with suspected vestibular disease have complete neurological examinations performed. Abnormalities found on a complete neurological examination are what will help determine if your patient has peripheral, central, or paradoxical vestibular disease. Peripheral vestibular disease: This patient has a problem affecting the inner ear, which contains the receptors for the vestibular system (utricle, saccule, and three semicircular ducts) or in the vestibular branch of the vestibulocochlear nerve (cranial nerve VIII). As these patients do not have a problem in their brain, their mentation will be normal. Their only gait dysfunction will be vestibular ataxia. They will have normal postural reactions. Their spinal reflexes will be normal. Other than their spontaneous nystagmus, which will always be either horizontal or rotary, and their positional strabismus, their cranial nerve exam will be normal, with an important exception. Patients with structural diseases affecting the inner and middle ear may not only have signs referable to peripheral vestibular disease, but also referable to ipsilateral facial nerve dysfunction (cranial nerve VII; ipsilateral palpebral and menace deficits, drooped ear and lip, salivary pooling in the ipsilateral commissure, and possible neurogenic keratoconjunctivitis sicca), and the ipsilateral Horner pathway (ptosis, miosis, and enophthalmos). This is because these neurological structures all share a common location in the inner and middle ear regions. Video 3 shows the pertinent exam findings in a patient with peripheral vestibular disease. Video 3: Right-sided peripheral vestibular localization. Note the patient is showing right-sided vestibular ataxia and a right-sided head tilt. Postural reactions are normal. All cranial nerve testing is normal other than showing a horizontal nystagmus, fast phase to the left, and a positional ventral strabismus in the right eye (not shown). Central vestibular disease: This patient has a problem affecting the rostral medulla oblongata, which is where the vestibular nuclei are located in the brain. Given these patients have a problem in their brains, they will have other neurological deficits referable to the many other structures found in the medulla oblongata beside the vestibular nuclei. Their mentation may be decreased, ranging from obtundation to coma. In addition to vestibular ataxia, they may also have ipsilateral hemiparesis, characterized by a stiff gait, and ipsilateral general proprioceptive ataxia, characterized by crossing over midline as they are walking. They will likely have postural reaction deficits that are ipsilateral to their head tilt (to the eye that is closer to the ground). They may have ipsilateral cranial nerve deficits referable to cranial nerves V to XII, including decreased facial sensation from trigeminal nuclei involvement, a decreased palpebral reflex and menace response due to facial nuclei involvement, a decreased gag reflex from glossopharyngeal and vagal nuclei involvement, and decreased tongue movements from hypoglossal nuclei involvement. Patients with central vestibular disease can have horizontal, rotary, or vertical nystagmus. Video 4 shows the pertinent exam findings in a patient with central vestibular disease. Video 4: Left-sided central vestibular lesion. This patient only has one of the hallmark signs of vestibular dysfunction: spontaneous nystagmus. Note that the nystagmus is vertical, which immediately localizes to the central vestibular system. This patient also has a delayed postural reaction in the left thoracic limb and an absent postural reaction in the left pelvic limb. This means that the affected side is the left central vestibular system. Paradoxical vestibular disease: This patient has a problem affecting the flocculonodular lobe of the cerebellum or the caudal cerebellar peduncle, which communicate with the vestibular nuclei. Patients with paradoxical vestibular disease have some or all of the hallmark signs of vestibular disease, but they also have gait abnormalities and postural reaction deficits on the opposite side of their head tilt. Their mentation will be normal. In addition to vestibular ataxia, they may also be hypermetric in the limbs contralateral to the head tilt. They may also have postural reaction deficits contralateral to the head tilt. Their spinal reflexes will be normal. Their only cranial nerve abnormalities will be their nystagmus and their positional strabismus. Video 5 shows the pertinent exam findings in a patient with paradoxical vestibular disease. Video 5: Left-sided paradoxical vestibular localization. Early in the video, a right-sided head tilt is observed. Additionally, truncal sway and an intention tremor are present, which point to a lesion in the cerebellum. Note the hypermetria of the left limbs, particularly the left thoracic limb, as well as the postural reaction deficits of the left limbs. The lesion is therefore in the left flocculonodular lobe of the cerebellum or the left caudal cerebellar peduncle. Which side do I localize to? Performing a complete neurological examination will allow you to not only determine if your patient has peripheral, central, or paradoxical vestibular disease, but it will also allow you to determine which side is affected. First, confirm the patient has vestibular disease by observing the hallmark signs previously mentioned.. Next, determine if the patient has postural reaction deficits. If the patient does not have postural reaction deficits, and the nystagmus is horizontal, then the patient most likely has peripheral vestibular disease. The lesion is, therefore, in the peripheral vestibular system on the side of the head tilt. The nystagmus fast phase will be away from the direction of the head tilt. If the patient has postural reaction deficits, determine if they are ipsilateral or contralateral to the head tilt. If they are ipsilateral to the head tilt, then the patient has central vestibular disease. The lesion is, therefore, in the central vestibular system on the side of the head tilt and postural reaction deficits. If the postural reaction deficits are contralateral to the head tilt, then the patient has paradoxical vestibular disease. The lesion is, therefore, in the cerebellum on the side of the postural reaction deficits, but opposite the side of the head tilt. What is causing the patient’s vestibular dysfunction? Each localization (peripheral, central, paradoxical) is associated with a different set of differential diagnoses. Differentials are prioritized based on their relevance compared to the patient’s signalment, acuity of signs, and degree of progression. This article uses the DAMNITV (degenerative, anomalous, metabolic, neoplastic, nutritional, inflammatory, idiopathic, toxic, traumatic, vascular) scheme for categorizing differential diagnoses. Extensive details regarding the various diseases is beyond the scope of this article. Peripheral vestibular disease These DAMNITV terms apply when looking at differentials for peripheral vestibular disease. Remember, patients with peripheral vestibular disease have an issue affecting their inner ear or the vestibulocochlear nerve. Degenerative: There are no degenerative causes of peripheral vestibular disease. Anomalous: Rarely, puppies and kittens can be born with incompletely formed components of the inner ear. Their vestibular dysfunction is evident from the time they start attempting to walk and does not worsen over time. In some cases, they may improve as the vestibular apparatus develops. Metabolic: Hypothyroidism can rarely cause peripheral vestibular disease. The signs are generally slowly progressive, but they can occur acutely. They may be the patient’s only sign of hypothyroidism. Neoplastic: Tumors of the ear canal and adjacent facial structures can lead to compression or destruction of the inner ear constituents. Such tumors include: cholesteatomas, squamous cell carcinomas, and fibrosarcomas. Additionally, nasopharyngeal polyps, particularly in cats, can lead to secondary otitis media-interna and resultant peripheral vestibular disease. Nutritional: There are no nutritional causes of peripheral vestibular disease in dogs and cats. Infectious: Otitis media-interna is the most common cause of peripheral vestibular disease in dogs and cats. Infections can directly extend from the external ear canal or the oropharynx via the auditory tube, or from hematogenous spread. The tympanic membrane may or may not be intact. Patients with otitis media-interna often also have ipsilateral facial paresis and Horner syndrome in addition to their vestibular dysfunction, as the facial nerve and the sympathetic pathway to the eye travel adjacent to the ear canal. Noninfectious inflammatory diseases: There are no noninfectious inflammatory diseases (immune-mediated/autoimmune) that affect the peripheral vestibular system. Idiopathic: Idiopathic peripheral vestibular disease is the second most common cause of peripheral vestibular disease in dogs and cats. Dogs tend to be of advanced age. Cats of any age can develop idiopathic vestibular disease. Vestibular signs develop peracutely and are often severe. In general, the nystagmus improves/resolves within three days. The vestibular ataxia improves/resolves within three weeks. The head tilt may resolve within three months, but some degree of head tilt may persist. Trauma: Extreme head trauma can lead to peripheral vestibular disease. However, this is uncommon, as the vestibular system is housed within the petrous portion of the temporal bone and is therefore highly protected. Toxins: Topical ototoxic medications, including aminglycoside-based medications and chlorhexidine-based cleaning solutions, can lead to a combination of deafness and peripheral vestibular dysfunction. The deafness is usually permanent, but the vestibular dysfunction can resolve. Systemic aminoglycosides can also lead to ototoxicity, as can several chemotherapeutic medications. Vascular: There are no vascular causes of peripheral vestibular disease in small animals. Central vestibular disease These DAMNITV terms apply when looking at differentials for central vestibular disease. Remember, patients with central vestibular disease have an issue affecting their rostral medulla oblongata. Degenerative: Although there are degenerative diseases of the brain, they generally do not cause signs referable to the rostral medulla. Anomalous: Congenital hydrocephalus can cause compression on the rostral medulla and higher centers of the brain involved in the vestibular system. Affected puppies and kittens with congenital hydrocephalus have other neurological signs referable to their prosencephalon, and their condition remains static or may be slowly progressive. Another congenital anomaly called a supracollicular collection of fluid, can also result in central vestibular disease in young animals. Metabolic: Hypothyroidism can rarely cause central vestibular disease. Neoplastic: Tumors of the rostral medulla can lead to central vestibular disease. Primary brain tumors in dogs and cats include: meningiomas, gliomas (subdivided into astrocytomas and oligodendrogliomas), ventricular tumors (subdivided into ependymomas, choroid plexus papillomas, and choroid plexus carcinomas), and other rare tumors that include primitive neuroectodermal tumors, granular cell tumors, and germ cell tumors. Ventricular tumors, particularly choroid plexus tumors, can cause obstructive hydrocephalus, which can also lead to central vestibular disease. Metastatic brain tumors in dogs and cats include: hemangiosarcoma (most common metastatic brain tumor in dogs), lymphoma (most common metastatic brain tumor in cats), and a variety of other carcinomas, sarcomas, and round cell neoplasms. Intracranial neoplasia usually leads to gradually progressive dysfunction, but signs may be acute in up to 50 percent of cases. Nutritional: Thiamine (vitamin B1) deficiency can lead to central vestibular disease. Patients with thiamine deficiency can also develop ataxia, mydriasis and absent pupillary light reflexes, blindness, and seizures. Infectious: Viral diseases, including rabies in both dogs and cats, canine distemper virus, and feline coronavirus can all lead to central vestibular disease. Bacterial causes of central vestibular disease are generally in the form of otogenic meningoencephalitis, in which otitis media-interna breaks through the petrous temporal bone and results in an intracranial abscess adjacent to the brainstem. Protozoal diseases, including Toxoplasma gondii in both dogs and cats and Neospora caninum in dogs only can occasionally cause central vestibular disease but are more likely to cause paradoxical vestibular disease. Fungal diseases such as Blastomyces dermatitidis, Histoplasma capsulatum, and Coccidioides immitis, can occasionally cause central vestibular disease. Parasitic diseases such as Cuterebra species and Baylisascaris procyonis can occasionally cause central vestibular disease. Noninfectious inflammatory diseases: Meningoencephalitis of unknown etiology (MUE) conditions are a group of immune-mediated causes of meningitis and encephalitis in dogs. Based on histopathologic diagnosis, the disease subsets include: granulomatous meningoencephalitis (GME), necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and eosinophilic meningoencephalitis. Onset and progression of signs can range from peracute and progressive to chronic and slowly progressive. Multifocal disease affecting multiple regions of the brain may be evident. Between infectious and non-infectious inflammatory causes of central vestibular disease in dogs, noninfectious inflammatory causes are more common. Idiopathic: There are no idiopathic causes of central vestibular disease. Trauma: Head trauma can result in central vestibular disease. Toxins: Metronidazole toxicity can lead to central vestibular disease. Vascular: It is uncommon for dogs (and even more rare for cats) to develop strokes in the region of their rostral medulla. However, the thalamus plays a role in the central vestibular system, so strokes to the thalamus can lead to central vestibular disease. Signs are peracute, nonprogressive, and generally improve over time. Paradoxical vestibular disease These DAMNITV terms apply when looking at differentials for paradoxical vestibular disease. Remember, patients with paradoxical vestibular disease have an issue affecting their flocculonodular lobe of their cerebellum or their caudal cerebellar peduncle. Although there are likely some exceptions, cats do not appear to develop paradoxical vestibular disease. Degenerative: Storage diseases generally lead to progressive, diffuse cerebellar dysfunction. Therefore, patients with storage diseases may have a vestibular component to their disease, but rarely do they exclusively show vestibular dysfunction. Anomalous: Although there are anomalous diseases that affect the cerebellum, they generally do not cause paradoxical vestibular dysfunction. Metabolic: There are no metabolic causes of paradoxical vestibular dysfunction. Neoplasia: The same tumors as detailed in the section on central vestibular disease can lead to paradoxical vestibular disease if the tumor is located in or compressing the flocculonodular lobe of the cerebellum or the caudal cerebellar peduncle. Nutritional: There are no nutritional diseases that lead to paradoxical vestibular dysfunction. Infectious: The same infectious diseases as detailed in the central vestibular disease section can lead to paradoxical vestibular disease if the infection is affecting the flocculonodular lobe of the cerebellum or the caudal cerebellar peduncle. Noninfectious inflammatory: Meningoencephalitis of unknown etiology (MUE) can cause paradoxical vestibular disease in dogs. Idiopathic: There are no idiopathic causes of paradoxical vestibular disease. Trauma: Head trauma could theoretically lead to paradoxical vestibular disease, although this is less likely than central vestibular disease. Toxin: There are no toxins that cause paradoxical vestibular disease. Vascular: An ischemic stroke to the rostral cerebellar artery is the most common cause of acute, nonprogressive paradoxical vestibular disease in dogs. What should I do in my clinic to work up a patient with vestibular disease? Once you have observed the hallmark signs of vestibular disease (at least one, but potentially all four), the next step is to localize the patient’s dysfunction as either peripheral, central, or paradoxical. Beware that approximately 10 percent of patients whose examinations are suggestive of peripheral vestibular disease actually have central or paradoxical vestibular disease. All patients with vestibular disease should have an otoscopic examination performed. All cats should have an oral exam for a nasopharyngeal polyp. Myringotomy using a spinal needle through an otoscope is a simple procedure that can be performed under general anesthesia to obtain a sample of tympanic bulla effusion, which can then be cultured for organisms. Adult dogs may be tested for hypothyroidism with a panel containing T4 AND TSH. All patients, especially those with central and paradoxical vestibular disease, should be offered referral to a neurologist for imaging. In general, magnetic resonance imaging is preferred because it provides a view of the inner ear and the brain parenchyma, but in some cases, computed tomography may be performed. Radiographs are unhelpful in vestibular disease. If otitis media-interna is suspected or confirmed, treatment consists of systemic antibiotics and, in some cases, a low dose of steroids (less than 0.5mg/kg/day prednisone/prednisolone) for at least four weeks. If vestibular dysfunction does not resolve, more aggressive management, including flushing and surgical treatment may be necessary, requiring referral. If idiopathic vestibular disease is suspected, recommend supportive care and anti-nausea medications. For all other diseases, and for patients with central or paradoxical vestibular disease, referral is recommended. In cases in which referral is not possible or is declined, differentials should be prioritized based on likelihood in the individual patient. Dogs with peracute paradoxical vestibular dysfunction should be considered to have a stroke to the rostral cerebellar artery, in which case they will improve, or neoplasia, in which case their signs will progressively worsen. Infectious diseases, including toxoplasmosis, neosporosis, and cryptococcosis should be tested for using serologic testing. If these are negative and the patient has progressive central or vestibular signs, then meningoencephalitis of unknown etiology can be considered in young- to middle-aged dogs, and neoplasia can be considered in middle-aged to older animals. Steroids can then be started at an anti-inflammatory dose of 0.5mg/kg/day. If no improvement is observed, it can be increased to 1mg/kg/day. Caution owners that it is possible steroid administration without a confirmed disease may result in deterioration if an infectious disease is the underlying cause of the patient’s dysfunction. Summary Vestibular disease is common in dogs and cats. The most common cause in both species is otitis media-interna, which leads to peripheral vestibular disease. Localization to one of the three possible vestibular localizations is critical in forming differential diagnoses lists and guiding treatment and prognosis. Susan A. Arnold, DVM, DACVIM (neurology) is an assistant professor of neurology and neurosurgery at the University of Minnesota College of Veterinary Medicine. She is boarded within the American College of Veterinary Internal Medicine (neurology). In her role, Dr. Arnold practices neurology and neurosurgery, trains interns and residents, and teaches veterinary medical students in both didactic and clinical settings.

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Identifying and treating vestibular disease

A detailed look — including videos — of this condition

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