key: cord-022243-lahg6xlm authors: Parent, Joane M title: The cat with a head tilt, vestibular ataxia or nystagmus date: 2009-05-15 journal: Problem-Based Feline Medicine DOI: 10.1016/b978-0-7020-2488-7.50043-0 sha: doc_id: 22243 cord_uid: lahg6xlm nan The presence of a head tilt, ipsilateral to the lesion, is the salient feature of vestibular disease. Nystagmus and/or vestibular ataxia may accompany the head tilt. The more acute the disease process, the more likely that nystagmus and ataxia are present. In vestibular ataxia, the animal leans, drifts, falls or rolls toward the side of the lesion. The nystagmus can be resting or positional (induced by holding the head in full extension), and, vertical, horizontal or rotatory in direction. The direction may change in time. Pendular nystagmus (oscillatory with rapid, short excursions) is not a sign of vestibular disease. Occasionally, there is bilateral vestibular disease. The animal may be reluctant to move because of severe disorientation. If able to walk, there are characteristic exaggerated motions of the head and neck and the cat moves in a crouched posture close to the ground. Physiological nystagmus is poor to absent. In these instances, a head tilt may not be present, or if present, is subtle on the most affected side. Circling is not a feature of vestibular disease but is frequent with thalamic and cerebral diseases. The most important diagnostic step is to differentiate if the disease involves the peripheral OR the central portion of the vestibular system. • The head tilt is toward the side of the lesion. The nystagmus is horizontal or rotatory but never vertical, and never changes in direction. The ataxia, if present, is on the side of the head tilt. • By close proximity, the neurological structures associated with the middle ear may be affected leading to facial nerve paresis/paralysis, dry eye from decreased to absent lacrimation, and/or Acute to peracute non-progressive onset of a head tilt with ipsilateral falling or rolling in an otherwise healthy cat. The disorientation may be severe. If the disease is bilateral, the head tilt is not evident, the physiological nystagmus is poor to absent, and the cat moves in a crouched posture, low to the ground. The head swings from side to side in exaggerated motions. • Aminoglycosides (p 849) Acute onset of peripheral vestibular signs uni-or bilaterally following systemic or topical therapy with aminoglycosides. Deafness may accompany the vestibular signs. • Ear flush (p 846) Peripheral vestibular signs that appear immediately or in the 72 hours following an ear flush. • Blue-tailed lizard ingestion (p 848) In southeastern United States, ingestion of a blue-tailed lizard is thought to be the cause of an acute unilateral peripheral vestibular syndrome. • Fracture of the petrous temporal bone or tympanic bulla, and ethmoid fracture (base of the skull) (p 848) Peripheral and central vestibular signs following a road accident. Horner's syndrome, partial or complete. The cochlear part of the vestibulo-cochlear nerve may be affected leading to ipsilateral deafness. • If the disease is bilateral, there is no head tilt or only a mild one on the side that is the most severely affected. The more acute the disease, the more severe the disorientation. The cat is reluctant to walk and has a crouched posture, low to the ground. The head characteristically moves from side to side in exaggerated motions and there is often ventroflexion of the head and neck. The physiological nystagmus (normal involuntary rhythmic typewriter-like movements of the eyes initiated by side-to-side movements of the head) is poor to absent. • The most consistent feature indicating central vestibular disease is the concomitant presence of somnolence, or quietness of the animal. This may or may not be obvious at time of examination, but will be evident with good history taking. • The head tilt is toward the side of the lesion. The nystagmus is horizontal, rotatory or vertical and may change in direction. • Due to their close proximity, other central nervous system structures may be involved ipsilaterally. These include the ascending reticular activating system or ARAS (somnolence) and the ipsilateral trigeminal nerve (loss of facial sensation and/or masticatory muscle atrophy), abducent nerve (strabismus), facial nerve (facial paresis/paralysis), cerebellum (tremors, hypermetria), ascending sensory pathways (proprioceptive deficits) and descending motor pathways (upper motor neuron weakness). • Bilateral involvement of the central vestibular system appears clinically similar to bilateral peripheral vestibular disorders in the early phase, except that the animal is more quiet or somnolent. If the cause is not corrected, involvement of other structures of the brainstem and/or cerebellum ensues. Paradoxical vestibular syndrome. • In this rare syndrome of central vestibular disease, the head tilt is contralateral to the lesion. The diagnosis is made on the presence of cerebellar signs or postural reaction deficits ipsilateral to the lesion but contralateral to the head tilt. Peripheral vestibular disease results from a problem in the petrosal bone or tympanic bulla. • The peripheral part of the vestibular apparatus (receptors and nerve) is situated in the inner ear, in close proximity to the middle ear. The inner and middle ear are located within the petrosal bone or tympanic bulla. The facial nerve, the parasympathetic innervation of the lacrimal glands and the sympathetic nerve for pupillary dilatation are the neurological structures associated with the middle ear. • Diseases of the inner ear can by extension reach the middle ear and vice versa. • The neurologic structures of the middle ear are more resilient to insult than the receptors in the inner ear (receptors vs axons). As a result, middle ear disease may be present without neurological deficits. With time, facial paresis/paralysis and/or Horner's syndrome may appear. • The auditory receptors are situated in the inner ear as well. Unilateral deafness goes unnoticed clinically but is diagnosed with electrodiagnostic testing (brain auditory-evoked potentials). Central vestibular disease results from an intracranial problem in the brainstem, at the level of the rostral medulla. This area is in close proximity to the cerebellum and pons. This anatomical location is called the cerebello-ponto-medullary angle. The most common causes of vestibular disease are peripheral and include: • Idiopathic vestibular disease. • Otitis media-interna. • Less common causes are the middle ear polyps and tumors. Central vestibular diseases are not as frequent as peripheral diseases. • Inflammatory diseases are the most common, with the clinical signs directly related to the location and severity of the inflammation. Although inflammatory diseases are multifocal or diffuse pathologically, this is often not the case clinically, where the neurological deficits in most cases can be assigned to one location. Diagnosis is based on careful history taking (to disclose if there is somnolence or quietness of the animal), physical, neurological, otoscopic and ophthalmoscopic (including Schirmer tear test) examinations, serum protein concentration, cerebrospinal fluid analysis (CSF), CSF anti-coronavirus IgG titer, electrodiagnostic testing (brain auditoryevoked responses), bullae radiography, computed tomography (CT) and magnetic resonance imaging (MRI) scan. Reference ranges for feline CSF. • RBC < 0.030 × 10 9 /L (30/μl) • WBC ≤ 0.002 × 10 9 /L (2/μl) • Cytology (%) -Monocytoid cells 69-100% -Lymphocytes 0-27% -Neutrophils 0-9% -Eosinophils 0 -Macrophages (large foamy mononuclear cells) 0-3% • Protein 0.036 g/L (36 mg/dl) It is good practice to request electrodiagnostic testing (BAER) to evaluate for deafness. If deafness is concomitantly present, it is an indication of a more aggressive disorder and a thorough diagnostic work up should be pursued. When a head tilt is present, or when there is facial paresis/paralysis or a Horner's syndrome, bulla radiography is recommended to evaluate the middle ear cavities. An open mouth view is best to compare the density between the bullae. Bulla radiography is not a sensitive tool. It may be normal despite the presence of disease. Computed tomography (CT) scan of the bullae is superior and should be done when available. Regardless of the cause of the vestibular signs, nystagmus and vestibular ataxia usually resolve, but the head tilt usually persists for the life of the animal. It may be barely noticeable but may be exacerbated after a general anesthetic or when the cat is ill. IDIOPATHIC VESTIBULAR SYNDROME*** Classical signs • Acute to subacute onset of a head tilt, falling, rolling and nystagmus. • Disorientation can be severe with the cat unwilling to move and crying out with anxiety. • Otherwise healthy cat. Unknown. Possibly higher incidence in July and August in northeast United States. Cats of any age or sex, median age is 4 years old. Acute, non-progressive, unilateral and occasionally bilateral, peripheral vestibular disturbance. The head tilt, ataxia and nystagmus (most often horizontal) can be severe with the animal crying out with anxiety, reluctant to walk, remaining in a crouched posture or with wide abduction of the limbs. Rarely, can be bilateral. Vomiting occasionally occurs, usually soon after onset of signs. Affected cats are otherwise healthy. History of an acute to subacute onset, in a previously healthy cat, of severe disorientation, falling and rolling, that improves rapidly (a few days to 2 weeks) and without treatment. The cat is otherwise healthy and has no other neurological signs. The otoscopic examination is unremarkable. Diagnosis is usually by exclusion of other diseases causing similar acute signs. With currently available diagnostic techniques it may not be possible initially to differentiate this syndrome from otitis media-interna, but the vestibular signs in otitis media-interna do not usually occur so acutely and severely. It is advisable to perform BAERs. If there is concomitant deafness, the idiopathic syndrome is ruled out as only the vestibular system should be affected. Otitis media-interna usually has a more progressive history. On otoscopic examination there may be otitis externa, mite infestation and/or a ruptured tympanic membrane. Signs of middle ear disease such as facial paresis/paralysis, decreased lacrimation and/or Horner's syndrome are often present. Radiographic changes in the tympanic bulla are rarely observed. Computed tomography and MRI scans are more sensitive for detecting changes. Middle ear polyps can cause peripheral vestibular disturbance uni-or bilaterally but since the polyps originate from the middle ear, facial and/or sympathetic nerve deficits are present. The onset is mild and progressive. Blue-tailed lizard ingestion is believed to cause similar signs in the southeastern United States. Vomiting, salivation, irritability and trembling are also observed. Signs may be indistinguishable from idiopathic vestibular syndrome. Aminoglycoside toxicity, especially topical streptomycin, can cause uni-or bilateral peripheral vestibular disturbance but the history reveals use of the drug. Supportive. In a few cats, fluid therapy, intravenously or subcutaneously, may be necessary initially. Sedation (acepromazine 0.05-0.10 mg/kg IM, SC, IV to a maximum of 1 mg) may occasionally be required if the rolling is severe. Antibiotics such as amoxicillin or cephalosporine for 10 days are indicated if otitis media-interna cannot be ruled out. Glucocorticoids are not indicated. Excellent. Rapid improvement of the clinical signs within the first 2 weeks in all cats. Most cats recover entirely but frequently have a mild residual head tilt. • Acute to chronic history. • Variable degree of peripheral vestibular disturbance. • Signs of otitis externa often present. • Facial paresis/paralysis, decreased lacrimation and/or Horner's syndrome often present. The infection extends from an otitis externa or from the oro-and nasopharynx by way of the eustachian tubes, or hematogenously. Most infections are caused by Staphylococcus spp., Streptococcus spp., Proteus spp., Pseudomonas spp. or Escherichia coli. Frequently, mites are the instigating factor for the otitis externa, which leads to secondary microbial infection with spread to the middle ear. The diagnosis of otitis media-interna is difficult as, except for surgical exploration of the tympanic bulla, the tests performed have a low diagnostic yield. The cat may have a history of chronic otitis externa. The ear may be sore to touch. There may be head shaking or scratching and frequent pawing at the ear. There may be difficulty in prehension or chewing food due to pressure on the petrosal bone region upon jaw opening as the temporo-mandibular joint is in the vicinity of the petrosal bone. The corner of the mouth may be wet with saliva. On otoscopic examination, the external ear canal may be red and inflamed with a brownish discharge. Mites may be present. The tympanic membrane may be red and bulging or perforated. The onset and the neurological deficits depend on the extension and severity of the infection. The onset of the vestibular signs may be acute with a marked head tilt, disorientation and nystagmus, or, chronic with nothing else other than a mild head tilt. The concomitant presence of facial nerve paresis/ paralysis, decreased lacrimation and/or Horner's syndrome confirms involvement of the middle ear. The facial weakness may be subtle. Look for a complete closure of the lids following a single stroke of the finger on both lids at once. Look for saliva-stained hair at the commissure of the lips or for a droop of the lips on the side affected. The symmetry of the pupils is best assessed in a dark room to evaluate for the presence of a partial Horner's syndrome. Facial nerve paralysis may be accompanied by keratoconjunctivitis sicca because innervation of the lacrimal glands is carried by the facial nerve. A Schirmer tear test should be routinely done in these cases to avoid the formation of corneal ulcer. Unilateral deafness is often present, but can be substantiated only with electrodiagnostic testing (BAER). Otoscopic examination may disclose an otitis externa, mite infestation or tympanic membrane bulging/perforation. If there is an otitis externa, cytology and culture with sensitivity testing should be done. The same organism may be causing the middle-inner ear infection. The presence of facial paresis/paralysis, decreased to absence of lacrimation or Horner's syndrome is a strong indicator of concomitant middle ear disease, but is not specific for infection. On physical examination, there may be pain on opening the mouth or pain upon manipulation of the head. • Concomitant deafness indicates a more significant disease process such as in middle-inner ear infection, but is not specific for the disease. It is an indi-cation that a more thorough diagnostic work up should be performed. • Normal hearing does not rule out middle-inner ear infection because the auditory receptors are in the inner ear. • It is important to obtain an open mouth view to visualize both bullae simultaneously for comparison. • A normal study does not rule out middle-inner ear disease. • The tympanic bulla may appear denser if there is an effusion. • Thickening of the bulla or bone lysis may be observed in more severe and chronic infections. Cytological examination and culture with sensitivity testing of the middle ear fluid is indicated when an effusion is suspected: • The myringotomy is done using an otoscope to guide a 2 1 ⁄2" spinal needle through the tympanic membrane. CT or MRI scans are superior to radiographs to confirm tympanic bulla disease, but the changes detected are not specific for infection. Surgical exploration of the middle ear with cytological examination and culture with sensitivity testing is the only definitive diagnostic tool in middle-inner ear disease. Idiopathic vestibular disease has an acute to per-acute onset in a cat that is otherwise healthy. There is no facial paresis/paralysis, decreased lacrimation, deafness or Horner's syndrome because the disease is limited to the vestibular part of the inner ear. Signs resolve over 1-2 weeks without treatment. Neoplasia and middle ear polyps can be difficult to differentiate from middle-inner ear infection without an exploratory bulla osteotomy. If a polyp is visible in the external ear canal or in the oro-nasopharynx, a diagnosis of middle ear polyp is likely. If a bacterial middle-inner infection is suspected, early and aggressive treatment with antibiotics is best. If cul-ture and sensitivity are not available, a broad-spectrum antibiotic is chosen such as trimethoprim-sulfa, cephalosporin or a penicillinase-resistant penicillin (enrofloxacin). Antibiotic treatment should be continued for 6-8 weeks. If otitis externa is present, the antibiotic is chosen based on the culture and sensitivity of the external ear canal. The otitis externa should be treated as well. Systemic treatment is preferable if the tympanic membrane is perforated or cannot be visualized. Avoid topical drugs that are toxic for the vestibular and/or auditory system (gentamycin, neomycin). Selamectin (Revolution®) or systemic ivermectin (200-300 μg/kg IM, SC, PO) is preferable as a miticide rather than topical treatment. Cats with radiographic changes in the bullae are treated with surgical curettage of the tympanic bulla to allow drainage, followed by long-term antibiotherapy based on the culture and sensitivity obtained from the sample collected at time of surgery. If the culture is negative, a broad-spectrum antibiotic as listed above is administered for 2-4 weeks. If there is chronic or recurrent otitis externa, ablation of the external ear canal is indicated. In the presence of paralysis of the eyelids, artificial tears are unnecessary if tear secretion is normal as the spread of the tear film is taken over by the third eyelid. Artificial tears should be administered 2-6 times daily in the affected eye, if the Schirmer tear test is abnormal (< 10 mm/minute), to avoid development of a corneal ulcer. Facial paralysis and partial Horner's syndrome often remain, although the severity is much improved. An ipsilateral mild deviation of the face occurs over time. The vestibular signs resolve in most cases, except for the head tilt, which frequently remains for the life of the animal. The cases managed medically may recur and require surgical curettage at later date. Treat otitis externa effectively when it occurs. Treat ear mites. • Mild and slowly progressive head tilt. • +/respiratory signs. • +/signs of otitis externa. • +/facial paresis/paralysis, +/-Horner's syndrome +/keratoconjunctivitis sicca, +/deafness. The pathogenesis is incompletely understood. The polyp originates from the middle ear cavity and is composed of inflammatory granulation tissue covered by respiratory epithelium. The instigating cause is not exactly known. Some believe that it is congenital, to explain its frequency in very young cats. Others postulate that it results from chronic inflammatory middle ear disease, secondary to upper respiratory infections. The respiratory infection would create abnormalities in the eustachian tube epithelium, resulting in poor middle ear ventilation and secondary inflammation. Most cats with middle ear polyps have a bacterial infection. The most common bacterial isolates are Pasteurella multocida, Streptococcus, Staphylococcus, Bacteroides and Pseudomonas. The polypoid growth has a tendency to exit the middle ear cavity. It can do so by rupturing the tympanic membrane and emerging into the external ear canal, causing characteristic signs of otitis externa, or it enters the eustachian tube to exit into the nasopharynx with subsequent upper respiratory signs. The frequency of each end location versus the other is unknown. The polypoid growth within the middle ear cavity may encroach on the inner ear leading to vestibular signs. Typically occurs in young cats, but any age can be affected (mean age 1-5 years; range 6 months to 15 years). The most common signs associated with a middle ear polyp, which extends into the nasopharynx, are upper respiratory signs including noisy breathing, dyspnea with or without nasal discharge, sneezing or coughing and gagging. Less often are signs characteristic of otitis externa. Rarely a head tilt may be present. The head tilt may occur without other signs, or with upper respiratory signs, or with a visible external ear canal polyp. Since the polyp originates within the middle ear cavity, the neurological structures of the middle ear may be affected causing facial paresis/paralysis, keratoconjunctivitis sicca and/or partial or complete Horner's syndrome. These can also occur without other signs. A mild and transient head tilt may be the only abnormality on neurological examination. The concomitant presence of a fibrous mass in the external ear canal, or upper respiratory signs, is pathognomonic for middle ear polyp. The concomitant presence of facial paresis/paralysis, decreased lacrimation and Horner's syndrome with a head tilt is indicative of middle and inner ear disease but is not diagnostic for the type of disease. If there are upper respiratory signs, visualization of the polyp in the nasopharynx under anesthesia is the most efficient way of reaching a diagnosis. • A glistening, red or pinkish mass filling the nasopharynx, or originating from the eustachian tube may be found. Otoscopic examination, which may necessitate sedation/anesthesia to evaluate both ear canals and tympanic membranes should be performed. • Aural inflammation may be present. • A pedunculated red, pink or grayish mass may be observed in the ear canal. The polyp may also affect hearing. Presence of deafness is evaluated by doing BAERs. When a head tilt is present and there is facial paresis/ paralysis, decreased lacrimation or a Horner's syndrome, bulla radiography is recommended to evaluate the middle ear cavities. An open mouth view is best to compare the density between the bullae. Bulla radiography is not a sensitive tool. It may be normal despite the presence of uni-or bilateral polyps. CT and MRI scans are superior in the diagnosis of middle ear cavities, and one of these scans should be performed if available. CT and MRI scans are the most sensitive imaging techniques to reach a diagnosis of middle ear disease, but are not specific for the type of disease. The final diagnosis is obtained at the time of surgery. Surgical exploration of the middle ear is the only reliable test to reach a diagnosis. Cytology and culture and sensitivity of the curetted tissue should always be done. If the disease process involves the middle ear, otitis media-interna, middle ear polyp and neoplasia of the middle ear cavity cannot be differentiated without biopsies taken at the time of surgical bulla exploration. Removal of the polyp from its origin through a ventral bulla osteotomy is the best therapeutic approach to avoid recurrence. Removal by grasping the polyp and cutting it at the base from the nasopharyngeal or aural location leads to a high recurrence rate. Horner's syndrome is a frequent complication of bulla osteotomy. It resolves in most cases in 1-3 weeks, but even if it remains, it does not alter the patient's quality of life. The head tilt, if present at onset, usually remains for the life of the patient. Occasional transient vestibular ataxia is rarely reported as a surgical sequella of polyp removal. The cat should be treated for 6-8 weeks with an antibiotherapy based on the culture and sensitivity done at the time of surgery. minimizes the risk of recurrence. Recurrence is frequent using oral or aural access to the polyp. The head tilt usually remains but the other vestibular signs (ataxia and nystagmus) usually resolve. If facial paralysis is present, ipsilateral deviation of the face ensues. If a Horner's syndrome is present, it usually improves and the residual deficit (aniscoria) is of no clinical significance. • Head tilt in a cat systemically ill for a few weeks. • Non-specific systemic signs such as fever, weight loss and lethargy. • Chronic progressive disease. • There may be neurological deficits other than a head tilt. See main references on page 372 for details (The Pyrexic Cat). The causative virus is a macrophage-tropic mutant of the ubiquitous feline enteric coronavirus. The clinical disease results from an immune-mediated response of the host to macrophage-infected feline infectious peritonitis virus (FIPV). The severity of the disease is based on host susceptibility and strain virulence. Affected cats are usually less than 3 years of age and from large multiple-cat households or breeders. The most common non-specific systemic signs are fever, weight loss and lethargy. Thirty-five percent of the cats with FIP have neurological signs. These vary with the lesion location. Behavioral changes, head tremor, seizures, depression, compulsive walking and decreased menace are some of the signs that may be observed. Clinically, the disease frequently appears to be focal, although this is not the case at postmortem. The head tilt is always associated with somnolence, with or without cerebellar signs, because the cerebellum is closely situated. Chorioretinitis may be present (see The Blind Cat or Cat with Retinal Lesions). The history of a young cat originating from a multicat household or breeder, with a protracted disease, vague systemic signs and neurological abnormalities raises the index of suspicion for FIP. The cerebrospinal fluid analysis on its own is not sensitive for a diagnosis of FIP. • Cell counts and protein concentration can be within reference range especially if the disease is focal. Typically, there is a moderate to severe pleocytosis, with mononuclear cells or neutrophils as the predominating cell type, and a marked increase in protein concentration. • Protein concentration > 2 g/L increases the likelihood of FIP. MRI scan of the brain is helpful, as frequently there is periventricular enhancement suggestive of ependymitis, and hydrocephalus with ventricular dilatation. The MRI findings are more representative of the neuropathological extent of the disease than is the clinical presentation, which is often focal in nature. Hematology and chemistry abnormalities are nonspecific except for a high serum total protein concentration, which is frequent. The anti-coronavirus IgG titer in CSF is consistently positive. The polymerase chain reaction (PCR) test detects the presence of feline coronaviruses but is not specific to FIP coronavirus. Immunohistochemistry and immunocytochemistry are techniques which appear promising for diagnosis of FIP. They use monoclonal antibody targeted against feline coronavirus to demonstrate coronavirus within macrophages in tissue or effusions. The concentration of infected monocytes in CSF fluid may make the test less sensitive for diagnosis of FIP than if used for tissue sections. At this point in time, no single test is diagnostic for the neurological form of FIP, but when the history, signalment, serum protein concentration, CSF results, CSF serology and MRI findings are combined, an antemortem diagnosis can be reached. Other inflammatory infectious diseases of the central nervous system may produce similar neurological abnormalities. However, no other central nervous system infections are typically presented with the gamut of abnormalities mentioned above. There is no effective treatment for FIP. Patients almost invariably die. Therapy is based on supportive care. Immunomodulating and antiviral agents seem promising in vitro but have not shown good results in cats. Poor. Most cats die of their disease from 6 weeks to 6 months after the onset of the neurological signs. Since most cats with FIP are from a multiple-cat household or breeder, adequate cleanliness is essential to prevent fecal-oral spread of virus. Vaccination may be preventive. • Otitis externa initially. • Subsequent development of peripheral vestibular signs. • Swollen face. • Facial nerve paresis/paralysis and Horner's syndrome are frequent. The most common tumor affecting the middle-inner ear is the squamous cell carcinoma. The tumor arises from the epithelial lining of the ear canal and is usually aggressive, invading the adjacent tissue (middle and inner ears) then the skull. Squamous cell carcinomas of the ear canal are most commonly presented with neurological signs. Ceruminous gland adenocarcinomas are also reported with some frequency in the middle-inner ear. Middle-aged to older cats. Initially, the signs relate to otitis externa. There is a more or less rapid progression depending on the tumor type, to cause peripheral vestibular signs, i.e., a head tilt, with or without nystagmus or vestibular ataxia. Due to the invading nature of the squamous cell carcinoma and the ceruminous gland adenocarcinoma, the facial nerve and the sympathetic chain in the middle ear are involved leading to facial paralysis, decreased lacrimation and Horner's syndrome. There is pain when the mouth is open, which may result from involvement of the temporo-mandibular joint, soft tissue pain, microfractures (pathological), bone pain from lysis or involvement of the bulla structures. The face may be swollen and firm on palpation. The history of an older cat presented with a rapid onset of neurological signs relating to the inner (vestibular signs and deafness) and middle ear (facial paralysis, decreased lacrimation and Horner's syndrome) with pain upon jaw opening and a swollen face increases the index of suspicion. In most cases, bulla radiography is diagnostic for the presence of a destructive process. There is opacity in the tympanic bulla with sclerosis and lysis of the bone. Depending on the tumor and how invasive it is, adjacent bony tissue such as the temporo-mandibular joint and the zygomatic arch may also be affected. As in most cases of middle-inner ear disease, if there is no swelling of the face, surgical exploration of the bulla is the only reliable approach to reach a definitive diagnosis. Middle ear polyp is usually in young cats, but can be in older cats. Typically, the progression is slower. The polyp may be visible in the ear canal or oro-nasopharynx. There is no pain, and no swelling of the face. Aggressive excision including ear canal ablation and lateral bulla osteotomy is the treatment of choice for malignant ear canal tumors. If excision is incomplete, radiation therapy can be a useful adjunct to surgery. Prognosis is guarded because of the invasive nature of the tumor and advanced stage of the disease by the time neurologic signs are present. Cats with ceruminous adenocarcinoma have a 75% 1-year survival rate following aggressive ear ablation and bulla osteotomy compared to a 33% 1-year survival after conservative surgical resection. The prognosis is more guarded for squamous cell carcinoma. • Acute onset of peripheral vestibular signs that develop immediately or in the 72 hours following an ear flush. The exact pathogenesis is unknown, but several mechanisms have been postulated to be involved. An ear flush that leads to such consequences is usually done under anesthesia or heavy sedation. If the signs develop immediately after the flush, it is possibly due to: (1) a change in the temperature of the endolymph; (2) flooding of the inner ear through a perforated tympanic membrane; or (3) a toxic effect on the vestibu-lar receptors by the product used to flush the ear (e.g. chlorhexidine, quaternary ammonium compounds). hours following an ear flush, an inner ear infection is suspected. Bacteria may have been introduced through a perforated tympanic membrane at the time of the flush. The ear flush may not be vigorous for this to occur because the tympanic membrane may have already been ruptured secondary to an otitis externa. Alternatively, topical (e.g. gentamycin-containing ear drops) or systemic treatment administered after the ear flush may be toxic to the vestibular receptors. Acute onset of peripheral vestibular signs in the 72 hours following an ear flush. The flush may have been an elective procedure or therapeutic for a severe otitis externa. Diagnosis is based on the history of acute vestibular signs following a recent ear flush. Idiopathic vestibular syndrome cannot be differentiated from the iatrogenic cause if the signs appear 2-3 days following the flush. Whenever acute vestibular signs appear to be associated with an ear flush, a broad-spectrum antibiotic such as trimethoprim-sulfa, a cephalosporine or amoxicillin should be administered for 2-6 weeks. If the onset was immediate and due to a change in the temperature or flooding of the inner ear, then the signs may disappear within a few hours. If the signs are the result of toxicity, the head tilt may remain. If the signs appeared 2-3 days later, most vestibular signs resolve except for the head tilt, which usually persists for the life of the animal. If an elective ear flush is to be performed under anesthesia or with heavy sedation, ensure the tympanic membrane is intact prior to the procedure. If the tympanic membrane cannot be visualized, use only sterile normal saline, as most ear-cleaning solutions contain components that are potentially ototoxic, such as propylene glycol, salicylic acid, malic acid, lactic acid detergents and dioctols. Perform ear flush with extreme care. Cleansing the ear with rubber bulb syringes, plastic syringes or waterjet appliances may rupture the tympanic membrane. If the ear needs cleaning in the consultation room, avoid using solutions that are acidic or potentially ototoxic. Instead of removing the debris manually, let the animal shake its head and dislodge the debris itself after the medication had been put and massaged into the external ear canal. • Lethargic cat with a head tilt, +/ataxia, +/nystagmus. Typically, the cat has usually been ill for a few weeks prior to the development of the neurological signs. The systemic signs may have been vague such as decreased appetite, weight loss, lethargy, or signs may relate to a specific system such as the upper respiratory tract, the skin or a combination of both. Chorioretinitis may be present (see The Blind Cat or Cat With Retinal Lesions). The development of central nervous system signs in a cat systemically ill for a few weeks or having upper respiratory tract signs and/or draining skin lesions should raise the index of suspicion for this infection. A latex agglutination test measuring the cryptococcal polysaccharide capsular antigen can be performed on the serum, cerebrospinal fluid or urine. However, negative results do not exclude the possibility of disease. The CSF analysis is often diagnostic because the characteristic budding yeast forms are visible. This is best seen using India ink, but new methylene blue, Diff Quick, and Gram's stain preparation are adequate. Sometimes organisms are not evident, but grow when the CSF is cultured. • The CSF inflammatory response associated with Cryptococcus neoformans varies greatly. The CSF may be normal to grossly abnormal with WBC counts ranging from 0 to > 500 cells × 10 6 /L (0-0.5 × 10 9 /L). • In mild inflammation, lymphocytes and monocytes predominate. In severe inflammatory responses, neutrophils and occasionally eosinophils are present. • The protein concentration varies from mildly to markedly increased (> 2 g/L). If the disease is suspected, but the organism is not visible in the CSF, CSF culture and/or serology may provide a definitive diagnosis. Cats may be simultaneously positive for feline leukemia virus (FeLV) and/or feline immunodeficiency virus (FIV), increasing their susceptibility to infection. Cryptococcosis cannot be differentiated from feline infectious peritonitis in cats presented with a protracted illness and vague systemic signs on history, physical and neurological examination alone. If Cryptococcus organisms are not visible, culture or serology may be necessary to establish the diagnosis. Fluconazole is the drug of choice because of its broad antifungal spectrum, its meningeal penetration even in the absence of inflammation, and the fact that serious side effects are uncommon. The recommended dose is 10 mg/kg/day divided twice daily for a period that extends beyond the resolution of all signs by 2-3 months. The drug should be given with food. Ketoconazole should not be used. It does not penetrate the blood-brain barrier effectively and is hepatotoxic. See page 26 (The Cat With Signs of Chronic Nasal Disease) for further details on treatment of cryptococcosis. • Bilateral vestibular signs, i.e., a characteristic ventro-flexion of the neck associated with a crouched body posture and reluctance to move. • Bilateral pupillary dilatation with poor light reflexes. Thiamine is a co-enzyme in the oxidative metabolism for energy production in the central nervous system. Thiamine deficiency typically produces lesions (polioencephalomalacia) in the brainstem gray matter and more specifically in the vestibular, oculomotor and lateral geniculate nuclei. Focal, bilaterally symmetric hemorrhages are present in affected areas. The deficiency occurs in cats that are fed an uncooked all-fish diet (due to the thiaminase content of the viscera), diets entirely made of cooked meat (where the thiamine is destroyed by heating), poor-quality thiamine-deficient commercial diets, or commercial food stored for long periods of time or in excessively hot conditions. In addition, the meat preserver sodium metabisulfite releases sulfur dioxide, which destroys thiamine. Pet mince meat containing this preserver is thiamine-deficient, and even when mixed with other food may have sufficient preserver to destroy all dietary thiamine. Anorexia in a sick cat especially associated with polydipsia and polyuria or fluid diuresis may precipitate thiamine deficiency and complicate the primary illness. Lethargy and decreased appetite, sometimes with increased salivation, occur after 2-4 weeks on a deficient diet. The cat has an inability or a reluctance to walk and therefore may appear weak. This is associated with a characteristic rigid ventro-flexion of the neck, a crouched body posture and loss of righting responses. There is bilateral mydriasis with poor light reflexes from the involvement of the oculomotor and geniculate lateral nuclei. Physiologic nystagmus is poor to absent. Brief episodes of opisthotonus or neck ventroflexing and muscle rigidity may appear like seizures. Bradycardia, and marked sinus arrhythmia may also occur. If untreated, the cat becomes comatose and dies. The time of death varies from 1 week to a few weeks to months depending on the health status of the animal and the amount of thiamine in the diet. Diagnosis is based on a combination of a history that the cat has been quiet and anorexic, signs of a characteristic posture with poor to absent physiologic nystagmus indicative of bilateral vestibular disease and documentation of a thiamine-deficient diet (usually large quantities of uncooked fish). Rapid response (within 24 hours) to treatment confirms the diagnosis. In bilateral idiopathic vestibular syndrome, the cat is healthy just prior to the development of the clinical signs. Thiamine-deficient cats are typically lethargic and anorexic. Injectable thiamine at 10-20 mg intramuscularly. For supplementation, give 5-30 mg/cat/day PO to a maximum of 50 mg/cat/day. Prognosis is good if treatment is given early when the only clinical signs are bilateral vestibular signs. Prognosis is poor in the late stage of the disease when the animal's consciousness is significantly altered. • Siamese, Himalayan and white tiger cats. • Pendular nystagmus, i.e., the phase of the nystagmus is equal on both sides. • Present from birth. Typically, the nystagmus has a rapid, short and oscillatory motion that is equal bilaterally. It is observed especially when the cat is fixing its gaze. The defect is within the visual pathways and not the vestibular pathways. No obvious visual impairment is present. The nystagmus is always congenital and is evident in the first few weeks of life. It occurs primarily in Siamese, Himalayan and white tiger cats. Medial strabismus is usually simultaneously present. Diagnosis is based on the characteristic oscillatory nystagmus. • Altered consciousness and head tilt after a recent accident. • +/-Facial nerve paresis/paralysis and Horner's syndrome. • +/-Signs of brainstem involvement such as proprioceptive deficits. Sudden onset of head tilt associated with somnolence or stupor following a road accident or other trauma that caused a fracture at the base of the skull affecting the petrosal and ethmoid bones. Facial paresis/paralysis and/or Horner's syndrome may be present if there is hemorrhage in the middle ear. If the injury is primarily intracranial, facial paresis/paralysis and/or ipsilateral proprioceptive deficits may be present. On otoscopic examination, blood may be observed in the ear canal. History of a road accident. Brain auditory-evoked responses (BAER) may be helpful in localizing the lesion to mainly a peripheral or central location. Survey radiographs of the skull are difficult to interpret because of the juxtaposition of multiple structures. • Unilateral or bilateral peripheral vestibular signs, following the use of drugs that are toxic for the vestibular receptors. • Concomitant deafness is frequent. Multiple drugs cause damage to the vestibular and/or auditory receptors separately or simultaneously. Aminoglycosides especially streptomycin, chloramphenicol, chlorhexidine, cisplatin, furosemide, salicylates and ceruminolytic agents are a few of a long list of agents that may cause damage to these receptors. Toxicity occurs following systemic or topical administration. The vestibular signs are peripheral and can be unilateral, or bilateral. The signs may develop acutely following exposure to a high dose or after prolonged administration (> 14 days). Cats with renal dysfunction are at risk because decreased renal excretion of many drugs results in higher plasma concentrations. The vestibular signs may disappear following discontinuation of the drug. The history of use of a drug potentially toxic for the vestibular receptors, topically or systemically. The vestibular signs may appear immediately following an ear flush, or following topical treatment with a toxic medication, in a cat that has a perforated tympanic membrane. Avoid using any medication in the external ear canal if the tympanic membrane is perforated or cannot be visualized. This includes ceruminolytic agents and detergents. • Unilateral or bilateral vestibular signs present at birth or developing in the first 12 weeks of life. • Siamese, Burmese and Tonkinese cats. • Head tilt and tipping or rolling. Reported in Siamese, Burmese and Tonkinese cats. Usually unilateral vestibular signs, but can be bilateral. Head tilt with tipping, rolling or falling developing at birth or in the first 12 weeks of life. The head tilt can be marked and may vary with time. The clinical signs are non-progressive and decrease in severity with time, but usually persist for life. Diagnosis is based on characteristic signs in a kitten from a susceptible breed. • Southeastern United States. • Unilateral peripheral vestibular signs following the ingestion of a blue-tailed lizard. • The cat also salivates, vomits, trembles and is irritable. Acute onset of unilateral peripheral vestibular disturbance following ingestion of the blue-tailed lizard. The syndrome has not been well substantiated. Varying degrees of vestibular signs associated with salivation, vomiting, trembling and irritability. Death may occur. Acute onset of unilateral peripheral vestibular signs in a cat living in southeastern United States with access to lizards. Signs are indistinguishable from the idiopathic vestibular syndrome although salivation, vomiting and trembling are less common with the idiopathic disease. Review of idiopathic feline vestibular syndrome in 75 cats Results of ventral bulla osteotomy for treatment of middle ear polyps in cats Diagnostic features of clinical neurologic feline infectious peritonitis A comparison of the rostrocaudal open mouth and rostro 10v entro-caudodorsal oblique radiographic views for imaging fluid in the feline tympanic bulla JR (ed) Consultations in Feline Medicine, 3 rd edn Evaluation of dogs and cats with tumors of the ear canal: 145 cases (1978-1992) Reference intervals for feline cerebrospinal fluid: Cell counts and cytologic features Reference intervals for feline cerebrospinal fluid: Biochemical and serologic variables, IgG concentration, and electrophoretic fractionation A comparison of radiographic versus surgical diagnosis of otitis media