Postoperative complications following TECA-LBO in the dog and cat.

The medical records for 133 total ear canal ablations combined with lateral bulla osteotomies (TECA-LBOs) performed on 82 dogs (121 ears) and 11 cats (12 ears) between 2004 and 2010 were reviewed to determine if the duration of preoperative clinical signs was associated with the incidence of postoperative facial nerve injury and Horner's syndrome. Other perioperative complications, such as a head tilt, nystagmus, incisional drainage, draining tracts, hearing loss, as well as bacterial culture results, were noted. Postoperative facial nerve paresis occurred in 36 of 133 ears (27.1%), and paralysis occurred in 29 of 133 ears (21.8%), with no significant difference between species. Thus, postoperative facial nerve deficits occurred in 48.9% of ears. The median duration of clinically evident temporary facial nerve deficits was 2 wk for dogs and 4 wk for cats. Dogs had a significantly longer duration of preoperative clinical signs and were less likely than cats to have a mass in the ear canal. Dogs were less likely to have residual (> 1 yr) postoperative facial nerve deficits. The incidence of postoperative Horner's syndrome was significantly higher in cats than dogs. The duration of preoperative clinical signs of ear disease was not associated with postoperative facial nerve deficits.

Unilateral facial paresis secondary to a suspected brainstem arachnoid cyst in a Maltese dog.

An 8-year-old, intact female Maltese dog was presented with decreased tear production and unilateral loss of eye blinking. Neuro-ophthalmic examination and brain magnetic resonance imaging were performed to determine the origin of facial paresis. A cystic lesion in the left pontomedullary region which displayed equal intensity to cerebrospinal fluid was revealed. Hyposignality was noted on fluid attenuated inversion recovery sequences, and the lesion was suggestive of an arachnoid cyst. This report described unilateral facial nerve dysfunction that resulted from a suspected brainstem arachnoid cyst in an unusual anatomic location.

Incidence, cause, outcome and possible risk factors associated with facial nerve paralysis in dogs in a Sydney population (2001-2016): a retrospective study.

OBJECTIVE: This study aims to assess the incidence and causes of facial nerve paralysis (FNP) in dogs in the Sydney region. Its outcome and possible risk factors are investigated to prognosticate and aid design of diagnostic and treatment plans. DESIGN: Retrospective case study. METHODS: Client-owned dogs presented to the University Veterinary Teaching Hospital, Sydney (UVTHS), between 2001 and 2016 with FNP were included (n = 122). The incidence of each cause of FNP was investigated. A reference population of noncases seen at the UVTHS during the same time period was used to study the association between idiopathic facial nerve paralysis (IFNP) and gender, age and breed. RESULTS: IFNP (29.5%) was the most common diagnosis. Male dogs (odds ratio [OR], 2.3) had increased odds of IFNP compared with female dogs. Age was a significant risk factor for both the occurrence of FNP and IFNP. There was higher occurrence of IFNP among middle-aged dogs (5-13 years) and reduced risk in juvenile dogs (less than 2 years). Cavalier King Charles Spaniels were over-represented for FNP (OR, 6.9) and IFNP (OR, 17.5). For IFNP, 6 of 16 dogs with known follow-up showed definitive resolution within 3 years of diagnosis. Concurrent vestibular signs were common in dogs with middle/inner ear abnormality and intracranial disease; and were also seen in 50% of dogs with IFNP. CONCLUSION: The results of this study demonstrate statistical predilections in age, gender and breed for IFNP. Guarded prognosis for recovery should be given to dogs diagnosed with IFNP and supportive management instigated.

Facial nerve paralysis in 64 equids: Clinical variables, diagnosis, and outcome.

BACKGROUND: Facial nerve paralysis (FNP) in equids is not well described in the veterinary literature. OBJECTIVE: To investigate the causes of FNP and associations among clinical variables, diagnosis, and outcome. ANIMALS: Sixty-four equids presenting with FNP between July 2000 and April 2019. Cases of postanesthetic FNP were excluded. METHODS: Medical records were retrospectively reviewed. Variables were evaluated for associations with outcomes (diagnosis and case outcome) using logistic regression. RESULTS: The most common cause of FNP was trauma (n = 20). Additional diagnoses included central nervous system (CNS) disease (n = 16), idiopathic (n = 12, 4 of which had adequate diagnostic investigation and were considered "true" idiopathic, and 8 of which were considered "not investigated" idiopathic), temporohyoid osteoarthropathy (n = 10), otitis media-interna (n = 3), lymphoma (n = 1), iatrogenic as a consequence of infiltration of local anesthetic (n = 1), and clostridial myositis (n = 1). Follow-up was available for 55 (86%) cases. Twenty-nine (53%) equids had full resolution of FNP, 14 (25%) were euthanized, 6 (11%) partially improved, and 6 (11%) were unchanged or worse. CONCLUSIONS AND CLINICAL IMPORTANCE: If FNP is the consequence of CNS disease, successful treatment of the primary disease likely leads to resolution of FNP. Most cases of FNP in equids are traumatic in origin. True idiopathic cases are uncommon.

Asymmetrical focal neurological deficits in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus): 27 cases (1999-2006).

OBJECTIVE: To describe basic epidemiological features, clinical characteristics and outcomes of asymmetrical focal neurological deficits identified in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus). DESIGN: A retrospective study. PROCEDURE: Computer records were reviewed for all dogs and cats treated for tick paralysis between July 1999 and June 2006 at a suburban veterinary hospital in Newcastle, New South Wales. RESULTS: Neurological deficits were identified in 17/197 dogs and 10/89 cats and included unilateral facial paralysis (14 dogs; 2 cats), anisocoria (4 dogs; 7 cats), unilateral loss of the cutaneous trunci reflex (1 dog; 1 cat) and Horner's syndrome in 2 cats with anisocoria. Occurrence of deficits was not linked to season, severity of tick paralysis, breed, age, sex or body weight. With facial paralysis and anisocoria, the site of tick attachment was invariably on the head or neck and always ipsilateral to the facial paralysis. By contrast, with anisocoria alone, no consistent relationship was noted between any one pupillary dimension and the side of tick attachment. With cutaneous trunci deficits the site of tick attachment was the ipsilateral caudal axilla. Compared with recovery times from generalised signs of tick paralysis, those for facial paralysis were significantly longer (days to weeks; P < 0.001), those for anisocoria showed no significant difference (P = 0.25) and those for cutaneous trunci deficits lagged by 6 and 7 days. CONCLUSIONS: Asymmetrical focal neurological deficits are a consistent finding in a proportion of dogs and cats with naturally occurring tick paralysis due to I. holocylcus.

Clinical presentations, treatments and risk factors for mortality in cats with tick paralysis caused by Ixodes holocyclus: 2077 cases (2008-2016).

Objectives The objective of this study was to describe seasonality, demographics, presentations, treatments, complications and outcomes for cats with Ixodes holocyclus causing tick paralysis, and to identify risk factors for mortality. Methods This was a retrospective single cohort study with 2077 cases occurring between 2008 and 2016, and presenting to one of four emergency clinics in south-eastern Queensland, Australia. Case mortality at 5 days post-presentation could be determined for 1742 cases, and potential risk factors for mortality were assessed using random-effects logistic regression. Results Cases occurred all year round, but there was a marked seasonal pattern with more cases presenting in spring than any other season. Overall, 54/1742 cases (3%) died by 5 days after presentation. Five day mortality incidence for cases that received polyclonal canine tick antitoxin serum (TAS) and recommended treatment was 28/1410 (2%) vs 4/52 (8%) for cases that did not receive TAS ( P <0.001). Mechanical ventilation was recommended for 131/2077 cases (6%). Where mechanical ventilation was recommended but not implemented, mortality incidence was 15/17 (88%), whereas 4/22 cases (18%) that received mechanical ventilation died by day 5. From multivariable analyses, initial gait score (overall P = 0.047) and body temperature on presentation (overall P <0.001) were independently associated with mortality; cases with higher gait scores and those with body temperatures <35°C were at greater risk of death. Cases that had an adverse reaction to TAS were also more likely to die ( P = 0.002). Additional ticks were detected at coat clipping for 80/872 (9%) the cases that were clipped, and coat clipping was associated with a reduced risk of mortality ( P = 0.020). Risk of mortality did not differ significantly by time of year, clinic location, breed, sex, neuter status, age, weight, coat length or number of ticks found. Conclusions and relevance The overall mortality risk for cats treated for tick paralysis caused by I holocyclus is low. Risk factors for mortality include advanced gait and respiratory scores, and hypothermia at presentation. Coat clipping and TAS reduce the risk of mortality, whereas the occurrence of a TAS reaction increases the risk. Mechanical ventilation reduces mortality risk in cats with respiratory failure due to tick paralysis.

A case of Murray Valley encephalitis in a 2-year-old Australian Stock Horse in south-east Queensland.

CASE REPORT: This report summarises the findings from a case of naturally-occurring Murray Valley encephalitis in a 2-year-old filly presenting with acute onset of depression and weakness. Serum samples tested at the onset of clinical signs were negative for Hendra and Kunjin virus antibodies, but positive for Murray Valley encephalitis virus (MVEV) using IgM-capture ELISA (1 : 300 dilution). A virus neutralisation assay performed 4 weeks later confirmed a titre of 1 : 160. Sera collected in the weeks preceding neurological signs returned a negative titre for MVEV 2 weeks prior followed by a titre of 1:80 in the week prior to illness. Serological surveillance conducted on 67 co-located horses returned a positive titre of 1 : 20 in one in-contact horse. There was no history of clinical disease in that horse. At 3 months after the onset of clinical signs in the index case, the filly continued to show mild facial paresis and hypermetria; the owners elected euthanasia and gave permission for necropsy. Histopathological analysis of the brain showed a mild meningoencephalitis. CONCLUSION: The progression of a naturally-occurring MVEV infection in a horse has been documented in this case.

Concurrent idiopathic vestibular syndrome and facial nerve paralysis in a cat.

CASE REPORT: A 4-year-old male neutered Domestic Medium-hair cat was referred for right head tilt and ataxia of 2 weeks duration. On examination it was determined that the cat had right facial nerve paralysis and peripheral vestibular signs. Haematology and serum biochemical testing were performed in addition to magnetic resonance imaging of the brain and ears, and cerebrospinal fluid analysis. An underlying condition was not identified. A diagnosis of idiopathic vestibular syndrome and concurrent idiopathic right facial nerve paralysis was consequently made. The cat was re-evaluated over the following weeks and was determined to have complete resolution of clinical signs within 7 weeks. CONCLUSION: Vestibular dysfunction and concurrent facial nerve paralysis have previously been reported in the cat, but not of an idiopathic nature.

Ultrastructural findings in idiopathic facial paralysis in the dog.

Unilateral facial paralysis of sudden onset is described in three dogs. Buccal nerve samples revealed widespread wallerian degeneration, and some attempts at regeneration. Regeneration was not sufficient to restore normal function.

Facial and vestibulocochlear nerve disease in six horses.

In 6 horses, clinical signs of illness implicated a lesion involving the facial and vestibulocochlear nerves. One horse had signs of otitis externa. Five horses had radiographic changes primarily involving periosteal bony proliferation of the stylohyoid bone at its articulation with the temporal bone. Five horses improved with antibiotic therapy. Otitis media-interna was found at necropsy of one horse.

Mycoplasma mycoides subspecies mycoides as the cause of a subauricular abscess and mastitis in a goat.

A 6-year-old female goat was admitted with right-sided subauricular swelling and facial nerve paralysis. Mastitis developed subsequently. The subauricular swelling localized to a mass and was excised. Mycoplasma mycoides subsp mycoides was cultured from samples obtained from the mass and mammary gland. After clinical improvement, the goat was discharged to the owner with instructions to isolate the goat and to submit milk samples from the rest of the herd for microbial culturing. Mycoplasma spp can spread to other tissues from an initial site of infection. In goats with clinical signs similar to those of the goat of this report, samples should be obtained for microbial culture on Mycoplasma medium. Goats infected with Mycoplasma spp should be isolated or culled because of the risk of transmission to uninfected animals.

Neurologic evaluation of the ear.

Diseases of the ear often cause signs of neurologic dysfunction because of damage of peripheral nervous system structures associated with the middle and inner ear. Vestibular dysfunction, facial paralysis, Horner's syndrome, and hearing deficits are the most common neurologic deficits that accompany middle and inner ear disease. Differentiating these signs from disease of the central nervous system is crucial for an accurate diagnosis and prognosis but can be difficult. Understanding the normal anatomy of the ear and its association with the brain is crucial to interpretation of the neurologic examination. This article reviews neurologic dysfunction commonly associated with diseases of the ear and differentiating these signs from central disease.

Idiopathic facial paralysis in the dog.

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.

Suspected protozoal myeloencephalitis in a two-month-old colt.

A two-month-old Appaloosa colt developed neurological signs shortly after birth involving deficits affecting cranial nerves IV, VII, VIII, IX, X and XII, and possibly nerve VI. The most likely differential diagnoses were congenital anomalies, meningoencephalitides, trauma or nutritional causes. The foal was investigated by the analysis of cerebrospinal fluid (CSF), electromyelography (EMG), brain auditory evoked responses, magnetic resonance imaging (MRI), peripheral nerve biopsy, and Western blot analysis for the presence of intrathecal antibodies to Sarcocystis neurona, the causative agent of equine protozoal myeloencephalitis. Significantly abnormal EMG findings included spontaneous electrical activity of the tongue, suggesting denervation. The MRI was useful in ruling out masses, congenital anomalies and focal abscessation. The cytology of CSF revealed mild mononuclear reactivity. Western blot testing of CSF was positive, indicating the intrathecal presence of antibodies to S neurona. The foal was treated with pyrimethamine and trimethoprim-sulphadiazine for two months and returned to nearly normal neurologic status.

Space occupying lesions of cranial nerves in calves with facial paralysis.

Clinical and pathological data of a recently discovered neurological disorder in young calves were studied. The symptoms were those of a paralysis of the nervus facialis and a dysfunction of the nervus vestibulocochlearis. Macroscopically, space occupying lesions were found at the roots of these two cranial nerves and in some cases further on their course into the os petrosum. On histological examination, these legions contained multiple nodules with mainly histiocytic cells, some plasma cells and multinucleated giant cells. Around these nodules, dense bands of connective tissue with fusocellular fibroblasts, some plasma cells and small blood capillaries were present. The nodular lesions were usually in close contact with the nerve. Ultrastructurally, a variety of cells, predominantly histiocytes and some plasma cells, were seen next to Schwann cells which contained degenerating axons.

Vestibular disease, and its relationship to facial paralysis in the horse: a clinical study of 7 cases.

The signs observed in 6 cases of peripheral vestibular disease included incoordination, head tilt and nystagmus. The intensity of the signs varied greatly with duration of the disease, and in 3 cases facial paralysis was also present. Tympanosclerosis was demonstrable in all cases subject to radiology. Trauma was the causative factor in most cases. The causes of, and relationships between, vestibular dysfunction and concomitant facial paralysis are discussed. The exact etiology of the tympanosclerosis is unknown.

Lateral canthoplasty for facial nerve paralysis and exposure keratitis in a mouse.

An 11-month old entire male mouse was presented with mucopurulent discharge and corneal scarring of the left eye. This mouse previously had a history of ear mites that responded to therapy, and had undergone surgery to remove a large discharging mass from the left side of the neck. The eye problem was noted prior to surgery, but after the ear mite infection. Examination revealed absence of a palpebral reflex in the left eye, and no spontaneous movements of the left ear or lip and whiskers. Examination of the left eye revealed extensive corneal vascularisation and pigmentation. Intraocular structures were not visible. A diagnosis of facial nerve paralysis and secondary exposure keratitis was made. Surgery was performed to close the lateral canthus and reduce corneal exposure. Following surgery the eye discharge ceased and corneal vascularisation resolved, however corneal pigmentation persisted.

Temporohyoid osteoarthropathy and unilateral facial nerve paralysis in a horse.

A 13-year-old broodmare was referred for weight loss and left facial nerve paralysis. Bilateral temporohyoid osteoarthropathy was diagnosed based on proliferation of the temporohyoid joints and stylohyoid bones on radiographs and guttural pouch endoscopy. The left side was more severely affected. Treatment resulted in little or no improvement.

Total ear canal ablation in the cat: indications, morbidity and long-term survival.

Fifty-two total ear canal ablation (TECA) procedures in 44 cats were reviewed. The indication for surgery was neoplasia in 41 per cent of the cats, 86 per cent of which had ceruminous gland adenocarcinoma. Chronic inflammatory or polypoid disease accounted for 50 per cent of surgical procedures. Postoperative complications included Horner's syndrome (42 per cent) and facial paralysis (56 per cent) and these were permanent in 14 per cent and 28 per cent of cases, respectively, with the rest resolving in the ensuing weeks or months. The higher incidence of Horner's syndrome and facial paralysis in the cat, compared to the dog, was attributed to greater fragility of the feline tympanic plexus and facial nerve. The median survival time of cats with ceruminous gland adenocarcinoma was 50-3 months, and did not differ significantly from that for inflammatory or polypoid disease. A potential prognostic indicator for this tumour was the mitotic index (MI): cases with MI < or = 2 survived significantly longer than those with MI > or = 3.