SMALL ANIMALS
CASE REPORT
Concurrent idiopathic vestibular syndrome and facial nerve paralysis
SMALL ANIMALS
in a cat
AR Fraser,* SN Long and MA le Chevoir
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.
Keywords cats; facial nerve paralysis; idiopathic vestibular syndrome
Abbreviations CSF, cerebrospinal fluid; MRI, magnetic resonance
imaging
Aust Vet J 2015;93;252–254 doi: 10.1111/avj.12338
V
estibular dysfunction with concurrent facial nerve paralysis
in the cat is typically a consequence of ear disease such as
neoplasia of the ear or surrounding soft tissues, peripheral
nerve tumours, otitis media/interna or nasopharyngeal polyps.1 Other
differential diagnoses to be considered are peripheral conditions,
including polyneuropathy or trauma, and intracranial causes such
as thiamine deficiency, neoplasia and feline infectious peritonitis,
and protozoal, bacterial or fungal meningoencephalomyelitis.1–4 For
dogs, an additional differential diagnosis of idiopathic vestibular syn-
drome with concurrent facial nerve paralysis is considered. Although
this condition has been reported in a number of dogs, to the authors
knowledge it has not been documented in cats.5–7 The purpose of this
report is to describe the occurrence of idiopathic vestibular syndrome
with concurrent facial nerve paralysis in a cat and the outcome.
Case report
A 4-year-old male neutered Domestic Medium-hair cat was presented
to the University of Melbourne Veterinary Hospital with a 2-week
*Corresponding author.
The University of Melbourne Veterinary Hospital, The University of Melbourne, 250
Princes Hwy, Werribee, Victoria 3030, Australia; anne.fraser@unimelb.edu.au
252 Australian Veterinary Journal Volume 93, No 7, July 2015
history of a right head tilt and falling to the right when jumping on
and off furniture.
The cat had failed to respond to a single injection of dexamethasone
and maropitant of unknown dose 10 days prior to referral. Computed
tomography of the head was performed prior to referral and was
reported as normal by the referring veterinarian.
The general physical examination was unremarkable. The cat was bright
and responsive. A right head tilt was noted, the right pinna was dropped
and the right palpebral fissure widened. The cat was leaning and inter-
mittently falling toward the right while ambulating. Postural reactions
were normal in all four limbs, as were the spinal reflexes. On cranial
nerve examination the right menace response was absent, but present
on the left. A direct and consensual pupillary light reflex was present
bilaterally. The right palpebral reflex was absent. Physiological nystag-
mus was slow. A spontaneous and positional nystagmus was not noted.
Otoscopic examination of the external ear canals and tympanic
membranes was performed and found to be unremarkable.
It was therefore established the cat had right facial nerve paralysis and right
peripheral vestibular syndrome. Differential diagnoses included peripheral
causes: neoplasia including peripheral nerve tumours, neoplasia of the ear
or surrounding soft tissues, idiopathic vestibular syndrome with concur-
rent facial nerve paralysis, otitis media/interna, nasopharyngeal polyp,
polyneuropathy or trauma. Intracranial causes were also considered but
as less likely: thiamine deficiency, neoplasia, feline infectious peritonitis
and protozoal, bacterial or fungal meningoencephalomyelitis.1–4
Haematology and serum biochemistry were performed. All serum
biochemistry parameters were within normal reference ranges. A
mild thrombocytopenia was reported; however, platelet clumping
was noted on the blood smear.
The cat was premedicated with butorphanol (Butomidor Injection,
Ausrichter Pty Ltd: 0.3 mg/kg IM) and anaesthesia was induced with
midazolam (HynovelW, Roche Products Pty Ltd: 0.3 mg/kg IV) and
propofol (Provive 1%, Claris Lifesciences (Aust) Pty Ltd: 5.0 mg/kg
IV) given to effect. Anaesthesia was maintained with a propofol contin-
uous rate of infusion 0.2–0.3 mg/kg/min intravenously and oxygen via a
4.5-mm endotracheal tube. Intravenous fluid administration included
compound sodium lactate (Hartmann’s Solution, Baxter Healthcare
Pty Ltd: 60 mL/h). Anaesthetic monitoring included pulse oximetry,
capnography, electrocardiography and non-invasive blood pressure.
Magnetic resonance imaging (MRI) of the brain was performed using a
1.5-Tesla GE, Signa HDe. Sequences included sagittal T2-weighted fast
spin echo (TR/TE 5000/84 ms, 3.0 mm thick/0.5 mm gap), transverse
© 2015 Australian Veterinary Association

T2-weighted fast spin echo (TR/TE 5260/97 ms, 3.0 mm thick/0.5 mm gap),
transverse fluid attenuation inversion recovery (TR/TE 9502/119 ms,
TI 2375 ms, 3.0 mm thick/0.5 mm gap) and dorsal 3D T1-weighted
fast spoiled gradient echo with inversion preparation (TR/TE 12/5 ms,
TI 600 ms, 1.0 mm thick/0.5 mm overlap). The dorsal T1-weighted
sequence was repeated for administration of gadolinium (OmniscanTM,
GE Healthcare Australia Pty Ltd: 0.1 mmol/kg). The dorsal
T1-weighted pre- and post- contrast series were reformatted into sagit-
tal and transverse planes. The brain was normal and the inner ear,
tympanic bullae, external ear canals, other soft tissue and bone struc-
tures were also normal in appearance.
Cerebrospinal fluid (CSF) was collected from the cerebellomedullary
cistern. Grossly the fluid was transparent and colourless. The nucle-
ated cell count was 0 cells/μL (reference value: <10 cells/μL) and
total protein 0.04 g/L (reference value: <0.4 g/L). No infectious
agents or neoplastic cells were observed on microscopic examination.
Based on these findings a presumptive diagnosis of idiopathic
vestibular syndrome and concurrent idiopathic right facial nerve
paralysis was made. The cat was discharged with artificial tears
(Liquifilm TearsTM, Allergan Australia Pty Ltd) to be administered
to the right eye every 6 h for life or until resolution of the facial nerve
paralysis.
The referring veterinarian reported that the vestibular signs had
resolved by 17 days following presentation. However, the cat had
right facial nerve paresis rather than paralysis, with a dropped right
ear and reduced right menace response and palpebral reflex. By
35 days following presentation the veterinarian reported complete
resolution of neurological signs.
Discussion
To the authors knowledge this is the first report of idiopathic vestib-
ular syndrome occurring concurrently with idiopathic facial nerve
paralysis in a cat. Previously it has been reported that feline idiopathic
vestibular syndrome results in clinical signs attributable to peripheral
vestibular dysfunction only, with affected cats not having concurrent
facial nerve paralysis or Horner’s syndrome.2–4,8
Idiopathic vestibular syndrome and idiopathic facial nerve paralysis are
diagnoses of exclusion.1–4,8–10 MRI is considered the gold standard for
investigation of intracranial causes of vestibular dysfunction.11
Furthermore MRI provides soft tissue contrast that radiography and
computed tomography cannot, allowing better assessment of neoplas-
tic and inflammatory conditions of the ear.12
The normal MRI and CSF analysis in the reported case, in addition to
the resolution of clinical signs without medical therapy, supports the
diagnosis of idiopathic vestibular syndrome and concurrent idio-
pathic facial nerve paralysis. Although CSF was not submitted for
PCR analysis, bacterial or fungal culture, nor serum for toxoplasma
antibody or cryptococcus antigen assessment, resolution of clinical
signs without therapy suggests a bacterial, fungal or protozoal cause
was unlikely.
Smith et al. describe the use of post-contrast volumetric interpolated
breath-hold MRI with 1-mm slice thickness for investigating
© 2015 Australian Veterinary Association
SMALL ANIMALS
idiopathic facial nerve paralysis.7 That sequence was reported to be
more sensitive than conventional T1-weighted images for visualising
post-contrast enhancement of the facial nerve; 86–96% and 39–65%,
respectively.7 We did not use the sequence in this reported case, so
SMALL ANIMALS
it is possible that contrast enhancement existed but was not
visualised.
In a retrospective case series reporting 16 cats with facial neuropathy,
8 had facial neuropathy alone without other clinical signs and 7 had
concurrent vestibular signs.13 The authors of that paper reported that
the facial neuropathy was idiopathic in 4 cats. It cannot be deter-
mined from the paper, however, if any of the cats with idiopathic
facial neuropathy had concurrent vestibular signs, and advanced
imaging was not performed, so intracranial causes were not ruled
out. Furthermore, although information was provided on recovery,
it was not stipulated if the cats that recovered had idiopathic facial
paralysis or an alternative syndrome.13
It has been reported that canine idiopathic vestibular dysfunction
does not occur concurrently with facial nerve paralysis.3,4,14 However,
in a case series of 7 dogs with idiopathic facial nerve paralysis, it was
reported that 5 dogs had clinical signs consistent with vestibular
disease (head tilt and/or disorientation with occasional falling) that
were of short duration and not observed at the time of presentation,
2 weeks to 4 months after onset.5
Furthermore, in a retrospective review of 85 dogs with vestibular
disorders, 2 dogs with idiopathic vestibular syndrome based on
normal MRI, CSF and thyroid stimulating hormone results had con-
current facial nerve paralysis.6 Those authors, however, suggested
that the sensitivity of the MRI was not adequate to observe potential
middle and inner ear pathology in the dogs.6 In a more recent report
of 20 dogs with idiopathic facial nerve paralysis, 14 were reported to
have concurrent idiopathic vestibular dysfunction.7
Given the previous reports of idiopathic vestibular syndrome with
concurrent facial nerve paralysis in dogs, it appears that these two
neuropathies can occur simultaneously without the presence of ear
disease in dogs. Certainly, the aetiology of idiopathic vestibular syn-
drome is currently unknown in both dogs and cats, as is the aetiology
of idiopathic facial nerve paralysis.2,3,5,9–11,15
In humans, herpes simplex virus type 1 latency-associated transcripts
have been demonstrated in the vestibular ganglia, geniculate ganglia
and trigeminal ganglia.16 Therefore, it has been proposed that reactiva-
tion of the virus may be the cause of acute vestibular neuritis, an idio-
pathic condition in humans.16
Little information regarding feline idiopathic facial nerve paralysis
and potential aetiologies exists. Canine idiopathic facial nerve
paralysis has been reported to resemble Bell’s palsy in humans.5,10
The aetiology of Bell’s palsy is unknown; however, herpes viruses,
including herpes simplex type 1 virus, and varicella zoster virus are
thought to be the most probable cause.17 It is therefore possible that
idiopathic vestibular syndrome and idiopathic facial nerve paralysis
in dogs and cats has a viral origin, but further investigation is
required.
A review of 75 cats with idiopathic vestibular syndrome in northern
America revealed that significantly more cats (60/75) present with the
Australian Veterinary Journal Volume 93, No 7, July 2015 253
 SMALL ANIMALS
syndrome during summer.15 The reason for this increased case num-
ber during the summer months is unknown, but the authors suggest
the effect of environmental factors such as temperature, humidity
SMALL ANIMALS
and seasonal toxins on perilymph and endolymph composition, pro-
duction and absorption.15 The cat reported in our study presented
during winter.
The migration of Cuterebra lavae within the inner ear has also been
proposed as a possible cause of feline idiopathic vestibular syn-
drome.18 This hypothesis has not yet been proven and it is unlikely
that the cat in the present report had cuterebriasis because Cuterebra
spp. are not present in Australia.18
In a MRI study of 6 dogs with idiopathic facial nerve paralysis,10 con-
trast enhancement of the facial nerve was observed in 4 dogs; images
were acquired with a 0.5 Tesla MRI. The 2 dogs without contrast
enhancement of the facial nerve had resolution of clinical signs within
4 weeks, while those with enhancement either failed to improve over
6 months or had a prolonged recovery.10 In the cat reported here,
contrast enhancement of the facial nerve was not noted and the cat went
on to make a full recovery.
In this report the cat had resolution of vestibular dysfunction approxi-
mately 4 weeks after onset and resolution of facial nerve paralysis within
7 weeks. In a retrospective study, 8/20 cats with idiopathic vestibular
syndrome had complete resolution of clinical signs within 4–6 weeks
of onset, while 5/20 cats continued to have ataxia and a head tilt for sev-
eral months.15 Overall, it is well documented for idiopathic vestibular
syndrome that clinical signs stabilise within 3–5 days of onset and
recovery occurs within 2–4 weeks, although a residual head tilt may
persist.2–4,9,19 Furthermore, the prognosis for idiopathic vestibular
syndrome in cats is considered good to excellent.2,11,19
In contrast, the clinical signs of idiopathic facial nerve paralysis are typically
of longer duration.5,10 In one report, 3/6 dogs failed to show resolution of
clinical signs by 6 months.10 In a second report, 3/3 dogs had return of
blinking within several months, but lip paralysis persisted.5
Conclusion
Concomitant vestibular dysfunction and facial nerve paralysis in the
cat has been thought to be an indication of a structural lesion within
the brainstem (causing central vestibular syndrome) or ear (causing
peripheral vestibular syndrome). In the case reported here, MRI and
CSF analysis did not reveal an underlying condition and the cat
made a full recovery without medical treatment, thus supporting
the diagnosis of idiopathic vestibular syndrome and concurrent
right facial nerve paralysis. Given this report, idiopathic vestibular
syndrome and concurrent idiopathic facial nerve paralysis should
be considered as a differential diagnosis in cats presenting with the
254 Australian Veterinary Journal Volume 93, No 7, July 2015
appropriate clinical signs. Furthermore, in situations where ad-
vanced imaging is not available it would not be unreasonable to
monitor the cat.
Acknowledgment
The authors acknowledge Kane Wilson for providing MRI-related
technical skills and knowledge.
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(Accepted for publication 16 December 2014)
© 2015 Australian Veterinary Association