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Received: 30 June 2020 Revised: 4 November 2020 Accepted: 9 November 2020
DOI: 10.1002/vetr.61
ORIGINAL RESEARCH
Clinical reasoning in canine vestibular syndrome: Which
presenting factors are important?
Eleanor Harrison1Nick J. Grapes1Holger A. Volk2Steven De Decker1
1Clinical Science and Services, Royal
Veterinary College, University of London,
Hatfiel d, UK
2Department of Small Animal Medicine and
Surgery, University of Veterinary Medicine,
Hannover, Germany
Correspondence
Steven De Decker,Clinical Science and Ser-
vices, RoyalVeterinary College, University of
London, Hatfield, UnitedKingdom.
Email: sdedecker@rvc.ac.uk
Abstract
Background: Although the use of clinical reasoning has been evaluated for
several neurological presentations, this approach has not yet been investi-
gated for dogs with vestibular syndrome.
Methods: Two hundred and thirty-nine dogs presenting with vestibular syn-
drome were included in this retrospective study. Univariate analysis of vari-
ables (clinical history, signalment, clinical presentation and neurological
examination findings) was performed. Variables with p <0.3 were selected
for logistic regression.
Results: Ninety-five percent of dogs were represented by eight conditions:
idiopathic vestibular disease (n =78 dogs), otitis media interna (n =54),
meningoencephalitis of unknown origin (n =35), brain neoplasia (n =26),
ischaemic infarct (n =25), intracranial empyema (n =4), metronidazole toxic-
ity (n =3) and neoplasia affecting the middle ear (n =3). Idiopathic vestibular
disease was associated with higher age, higher bodyweight, improving clini-
cal signs, pathological nystagmus, facial nerve paresis, absence of Horner’s
syndrome and a peripheral localisation. Otitis media interna was associated
with younger age, male gender, Horner’s syndrome, a peripheral localisation
and a history of otitis externa. Ischaemic infarct was associated with older age,
peracute onset of signs, absence of strabismus and a central localisation.
Conclusions: Discrete clinical features can be used to identify the most likely
diagnosis in dogs with vestibular syndrome.
INTRODUCTION
Canine vestibular syndrome is a commonly encoun-
tered presentation in clinical practice. The term
encompasses over 20 different diagnoses, which
are associated with variable diagnostic approaches,
treatment recommendations and prognoses.1,2 Head
tilt, ataxia, nystagmus and positional strabismus
are common clinical signs in dogs with vestibular
syndrome.1–5 Although observation of these clinical
signs facilitates recognition of vestibular system dys-
function, they rarely assist in determining the under-
lying cause of disease.
The vestibular system is anatomically divided into
peripheral and central components.1,4 The periph-
eral vestibular system includes the receptors in the
membranous labyrinth in the inner ear and the
vestibulocochlear nerve, while the central vestibu-
lar system includes structures in the brainstem and
cerebellum.1,4 It is clear that obtaining a diagnosis
Abbreviations: CT, computed tomography; MRI, magnetic resonance
imaging; MUO, meningoencephalitis of unknown origin
of disorders affecting the central vestibular system
requires more advanced and expensive diagnos-
tics compared to disorders affecting the peripheral
vestibular components.6Although several neurolog-
ical examination findings, such as decreased menta-
tion, proprioceptive deficits and cranial nerve deficits
can help confirm the presence of central nervous
system involvement,3,7,8 the absence of these findings
does not exclude the presence of central disease.4,6,9
Recent studies have demonstrated the limitations
of using neurological examination findings to reli-
ably differentiate between central and peripheral
vestibular syndrome in dogs.6,9 It therefore remains
challenging for veterinary practitioners to correctly
identify those cases that will benefit from referral for
advanced diagnostic modalities, such as magnetic
resonance imaging (MRI), computed tomography
(CT), and cerebrospinal fluid (CSF) analysis.6It is
furthermore likely that not all owners will accept or
will be able to afford referral to specialist centres.
Due to the difficulties in determining aetiology
without further diagnostics, robust clinical reasoning
is paramount in order to recognise the most likely
Vet Rec. 2021;e61. © 2021 British Veterinary Association 1of10wileyonlinelibrary.com/journal/vetr
https://doi.org/10.1002/vetr.61
2of10 Veteri nary Record
differential diagnoses, suitably select cases for
advanced investigations and potential referral. Clini-
cal reasoning is the critical thinking process in which
cues of clinical information are used to influence clin-
ical decision-making.10 This decision-making process
directs the clinician towards taking the most suitable
action in a specific context and has been considered
’critical and central to veterinary practice’.11,12 Pre-
vious studies have demonstrated the usefulness of
clinical reasoning in a variety of common neurological
presentations, including spinal disease and epilepsy
in dogs and cats.13–16 Although a recent study has eval-
uated associations between the clinical presentation,
MRI findings and outcome in dogs with peripheral
vestibular syndrome,17 it is currently unclear if clinical
reasoning can reliably be used to identify the most
likely differential diagnoses in dogs with peripheral or
central vestibular syndrome.
The aim of this study was therefore to evaluate if
discrete clinical characteristics, such as signalment,
clinical history, clinical signs and neurological exam-
ination findings, can be used to generate a prioritised
list of differential diagnoses in dogs with vestibular
syndrome. We hypothesised that statistical modelling
could be used to identify significant associations
between easy to identify clinical variables and the
most common causes of vestibular syndrome in dogs.
It is hoped that such information will provide veteri-
nary practitioners with clinically useful information
when assessing dogs with vestibular syndrome in first
opinion practice.
MATERIALS AND METHODS
Included animals
This study was approved by the Social Sciences Eth-
ical Review Board of the Royal Veterinary College,
University of London (RVC, URN SR2017-1342). The
digital medical database of the Small Animal Refer-
ral Hospital of the Royal Veterinary College was ret-
rospectively searched for dogs with vestibular syn-
drome between 25 June 2010 and 12 July 2018. Search
terms included ‘vestibular syndrome’, ‘vestibular dis-
ease’, ‘head tilt’, ‘nystagmus’ and ‘strabismus’. To be
included in this study, dogs had to have received a
full neurological examination performed by a board-
certified neurologist or neurology resident under the
direct supervision of a board-certified neurologist, full
blood work, including haematology and a biochem-
istry profile (including cholesterol and triglyceride
concentration), and additional appropriate diagnos-
tic investigations performed to obtain a reliable pre-
sumptive or definitive diagnosis. Dogs were excluded
if the medical records were incomplete, if none or
insufficient further diagnostic examinations were per-
formed, if the diagnostic studies were unavailable for
review or if no presumptive or definitive diagnosis was
reached.
Disease categories
All medical records and diagnostic studies were
reviewed by a board-certified neurologist (Steven De
Decker), and dogs were allocated to one of the follow-
ing eight disease categories: 1) idiopathic vestibular
disease, 2) otitis media interna, 3) meningoencephali-
tis of unknown origin (MUO), 4) brain neoplasia, 5)
ischaemicinfarct,6)intracranialempyema,7)metron-
idazole toxicity and 8) neoplasia affecting the middle
and/or inner ear structures.
For the purpose of this study, idiopathic vestibu-
lar disease was considered if no abnormalities were
observed on MRI or any other diagnostic tests.1–4
Dogs had to have MRI performed and total T4/TSH
evaluated with normal results to be considered for
this diagnostic category. Otitis media interna was
considered when MRI or CT demonstrated a fluid
accumulation in the middle ear.3In all dogs this diag-
nosis was further supported by cytological evaluation,
otoscopic examination, myringotomy or surgical
findings.1,5,18,19 A diagnosis of neoplasia affecting
the middle and inner ear was considered when MRI
or CT demonstrated an abnormal mass with soft
tissue intensity or density affecting the middle and
inner ear structures, which was further confirmed by
histopathology.3A diagnosis of ischaemic infarct was
considered when MRI of the brain revealed a sharply
demarcated homogenously T2W hyperintense lesion
in relation to a known arterial territory, which was not
associated with mass effect and did not enhance after
IV contrast administration.20 Intracranial empyema
was characterised by extension of otitis media interna
into the brainstem. This diagnosis was based on a
combination of compatible MRI and CSF findings.21
Metronidazole neurotoxicity was considered in dogs
receiving high doses (>65 mg/kg/day) of metronida-
zole, with compatible MRI findings, and in which
clinical signs improved after obtaining a diagnosis
and discontinuation of metronidazole.22,23 Diagnostic
criteria for MUO24,25 and brain neoplasia26 were based
on previously published literature.
Evaluated clinical variables
For all included cases, the following information was
retrieved from the medical records: signalment, body-
weight, clinical history of otitis externa, disease onset
and progression, mental status, gait and postural
abnormalities, proprioceptive deficits, unilateral or
bilateral vestibular signs, presence and type of nys-
tagmus, presence of a head tilt, positional strabismus,
Horner’s syndrome, facial nerve paresis, other cranial
nerve abnormalities and suspected neuro-anatomical
localisation. Onset (days to presentation) and progres-
sion were classified as categorical variables. Onset was
defined as peracute (<1day), acute (1–7days), sub-
acute (7–14 days) or chronic (>2 weeks). Progres-
sion was classified as static, progressive, improving or
Veteri nary Record 3of10
episodic, based upon the animal’s condition at the
time of admission compared to the history from the
referring veterinary surgeon and owner. An improved
clinical status was assumed when the dog’s clini-
cal signs had improved spontaneously without any
medical intervention from the referring or admitting
veterinary surgeon. Unilateral vestibular signs were
defined as one or a combination of the following:
vestibular ataxia, pathological nystagmus, unilateral
positional strabismus and head tilt. Vestibular ataxia
was characterised by leaning, falling, rolling or tight
circling to one side. Bilateral vestibular signs were
defined as one or a combination of the following:
absence of an oculovestibular response and absence of
a head tilt in combination with other signs of bilateral
vestibular syndrome, such as a crouched and wide-
based posture and pendular head movements.1,4 Sus-
pected neuro-anatomical localisation was categorised
into central or presumptive peripheral vestibular sys-
tem. Dogs that displayed vestibular ataxia, strabismus
or nystagmus and additionally one of the following:
decreased mentation, cranial nerve deficits other than
facial or vestibulocochlear nerve dysfunction, pro-
prioceptive deficits, hypermetria, intention tremor or
tetraparesis were considered to have central vestibu-
lar syndrome.6,8 Dogs without any of these additional
abnormalities were considered to have presumptive
peripheral vestibular syndrome.
Investigations
CT was performed with a 16-slice helical CT scan-
ner (PQ 500, Universal Systems, Solon; GE Health-
care), under sedation or general anaesthesia. MRI
was performed under general anaesthesia with a
high-field unit (1.5T, Intera; Philips Medical Systems,
Amsterdam, Netherlands). Imaging studies included
a minimum of T2- and T1-weighted sagittal and
transverse images and transverse fluid attenuation
inversion recovery and gradient echo images. T1-
weighted images were acquired before and after IV
administration of gadolinium-based contrast medium
(0.1 mmol/kg gadoterate meglumine, Dotarem; Guer-
bet, Milton Keynes, UK). CSF was collected via a cister-
nal puncture under general anaesthesia. A total nucle-
ated cell count (TNCC) below five cells/µLandatotal
protein concentration below 0.27 g/L were considered
normal.
Statistical analysis
Statistical analysis was performed using statistical
software (SPSS V.25.0.0.1; IBM). Univariate analy-
sis of the clinical variables was performed. Age and
bodyweight were included as continuous variables.
Sex, presence of a head tilt, nystagmus, positional
strabismus, abnormal mentation, ataxia, postural
reaction deficits, Horner’s syndrome, facial nerve
paresis, other cranial nerve deficits, cervical hyperaes-
thesia, clinical history of otitis externa and presumed
neuro-anatomical localisation (central or peripheral)
were included as binary categorical variables. Type
of nystagmus was categorised as horizontal, vertical
or rotary. Onset of clinical signs was categorised as
peracute (<1day), acute (1–7 days), subacute (7–14
days) or chronic (>2 weeks). Progression of signs
was categorised as improving, static or progressive.
Variables with p <0.30 were retained and a logistic
regression, using the forced entry method, performed
for each of the five most prevalent diseases. The vari-
ables retained for multivariable logistic regression
therefore varied between diagnoses. The small sample
size of the majority of breeds limited the performance
of logistic regression for this variable. Variables were
considered significant with a p <0.05. A false dis-
covery rate for multiple comparisons was performed
on the resultant p values.27,28 Results are presented
with odds ratios (OR) and 95% confidence intervals
for each condition compared to the rest of the popu-
lation. Non-normally distributed continuous data are
presented as median (range) while normal distributed
data are presented as mean (SD).
RESULTS
Three hundred and twenty-six dogs presented during
the study period for further evaluation of vestibular
syndrome. Seventy-six dogs were excluded because
insufficient diagnostic procedures were performed,
and a further 11 dogs were excluded because no
reliable presumptive or definitive diagnosis could
be reached. Two hundred and thirty-nine dogs were
therefore included in this study. This group included
105 females (73 neutered) and 134 males (84 neutered)
aged between 3 months and 14 years 10 months and
weighing between 1.6 kg and 63.9 kg. The Cavalier King
Charles spaniel was the most common breed (n =26
dogs), followed by the French bulldog (n =20), Boxer
(n =12), Staffordshire bull terrier, English springer
spaniel (n =11 for both), English cocker spaniel,
Shih-tzu, Golden retriever (n =10 for each), Labrador
retriever, Pug (n =8 for both), Border collie, Chihuahua
(n =6 for both), West Highland White Terrier, Bichon
Frise (n =5 for both) and Toy Poodle (n =4). Twenty-
six breeds were represented by three or fewer dogs,
and 22 dogs were cross breeds. In total, a presumptive
or confirmed diagnosis was made for fifteen disor-
ders in the study population. Idiopathic vestibular
disease was the most common diagnosis (n =78 dogs
or 34.2% of included dogs), followed by otitis media
interna (n =54; 23.7%), MUO (n =35; 15.4%), brain
neoplasia (n =26; 11.4%), ischaemic infarct (n =25;
11%), intracranial empyema (n =4; 1.8%), metronida-
zole toxicity (n =3; 1.3%) and neoplasia affecting the
middle ear (n =3; 1.3%). The remaining 11 dogs were
diagnosed with congenital cerebellar malformation,
corticosteroid responsive tremor syndrome, hypothy-
roidism, primary secretory otitis media (n =2 for each
disease), congenital vestibular syndrome, fucosidosis
and external trauma (n =1 for each disease). In all
dogs diagnosed with idiopathic vestibular syndrome,
total Thyroxine (T4) and Thyroid stimulating hormone
4of10 Veteri nary Record
(TSH) was evaluated, and in 47 of 78 dogs with this
diagnosis, a CSF sample was evaluated. No abnormal-
ities were detected on these examinations. In 11 of 54
dogs with otitis media interna, total T4/TSH was eval-
uated, and in 6 dogs with this diagnosis, a CSF sample
was evaluated. No abnormalities were detected on
these examinations. In 33 of the 35 dogs with MUO,
a CSF sample was evaluated, and 21 of these samples
were submitted for PCR evaluation for infectious
diseases (Toxoplasmosis, Neosporosis and Canine
Distemper). Thirty of the CSF samples demonstrated
an abnormally elevated TNCC and increased protein,
while all of the PCR samples returned negative. In one
dog with MUO, total T4/TSH was evaluated, which
returned within normal limits. In eight of the 26 dogs
with brain neoplasia, total T4/TSH was evaluated,
and in six dogs with this diagnosis, a CSF sample was
evaluated. No abnormalities were detected on these
examinations. In all dogs diagnosed with ischaemic
infarct, total T4/TSH was evaluated, and in 8 of 25
dogs with this diagnosis, a CSF sample was evaluated.
No abnormalities were detected on any of these exam-
inations. The clinical presentation and neurological
examination findings of these dogs are summarised in
Table 1.
Signalment
Higher age was significantly associated with diagnoses
of idiopathic vestibular disease (p <0.001), ischaemic
infarct (p =0.005) and brain neoplasia (p =0.02).
Younger age was significantly associated with diag-
noses of otitis media interna (p =0.015) and MUO
(p <0.001) (Table 2). Higher bodyweight was associ-
ated with a diagnosis of idiopathic vestibular disease
(p <0.001), and male gender was associated with a
diagnosis of otitis media interna (p =0.018) (Table 2).
Onset and progression of clinical signs
A peracute onset of clinical signs was associated with
a diagnosis of ischaemic infarct (p =0.025). Improving
clinical signs was associated with a diagnosis of idio-
pathic vestibular disease (p =0.025) (Table 2).
Head tilt, nystagmus and strabismus
Presence of a head tilt was significantly associated with
a diagnosis of brain neoplasia (p =0.034), the presence
of pathological nystagmus was associated with a diag-
nosis of idiopathic vestibular disease (p =0.04) and the
lack of strabismus was associated with a diagnosis of
ischaemic infarct (p =0.047) (Table 2).
Facial nerve dysfunction, Horner’s
syndrome and other cranial nerve deficits
Presence of facial nerve paresis was associated
with a diagnosis of idiopathic vestibular syndrome
(p =0.003). Presence of Horner’s syndrome was
associated with a diagnosis of otitis media interna
(p <0.001), while absence of Horner’s syndrome was
associated with a diagnosis of idiopathic vestibu-
lar syndrome (p =0.005). Presence of cranial nerve
deficits, other than facial nerve paresis and Horner’s
syndrome, was associated with a diagnosis of brain
neoplasia (p =0.018) (Table 2).
Neuro-anatomical localisation
A presumptive peripheral neuro-anatomical locali-
sation was associated with diagnoses of idiopathic
vestibular syndrome (p <0.001) and otitis media
interna (p =0.009). A central neuro-anatomical local-
isation was associated with diagnoses of ischaemic
infarct (p =0.012) and brain neoplasia (p =0.028)
(Table 2).
Clinical history of otitis externa
A clinical history of otitis externa was associated with
a diagnosis of otitis media interna (p <0.001). The
absence of a clinical history of otitis externa was asso-
ciated with diagnoses of idiopathic vestibular syn-
drome (p =0.007) or MUO (p =0.037) (Table 2).
DISCUSSION
This study evaluated if distinct clinical characteristics
can be used to identify the most likely underlying
diagnoses in dogs with vestibular syndrome. Our
results indicate that in our hospital, more than 95%
of dogs with vestibular syndrome are represented by
eight conditions and that four of the five most com-
mon causes of this clinical presentation (idiopathic
vestibular disease, otitis media interna, ischaemic
infarct and brain neoplasia) are statistically associ-
ated with multiple clinical variables derived from the
clinical history, signalment, clinical presentation and
neurological examination. Although it is clear that
clinical reasoning cannot replace specific diagnostic
tests, applying this methodology can assist veterinary
practitioners in creating a list of prioritised differ-
ential diagnoses in dogs with vestibular syndrome.
This could potentially further facilitate selection of
diagnostic tests, formulation of treatment recom-
mendations, discussion of associated prognoses and
selection of cases for referral and advanced diag-
nostic procedures. Veterinary practitioners can feel
unconfident with neurological patients.29–32 This phe-
nomenon of ’neurophobia’29–32 is associated with a
reluctance of clinical practitioners to assess neurology
patients and perform a neurological examination.29,31
It is therefore important to emphasise that the results
of this study do not advise against the importance of
performing a neurological examination. Several of the
identified variables, such as presence of facial nerve
paresis, Horner’s syndrome, nystagmus and a central
Veteri nary Record 5of10
TABLE 1 Signalment, clinical presentation and neurological examination findings of 228 dogs with vestibular syndrome
Numbe r
of dogs
(%) Gender
Median
age in
months
(range)
Median
weight
(range) Onset Progression
History
of otitis
externa
(%)
Decreased
mentation
(%)
Ataxia
(%)
Head
tilt (%)
Postural
deficits
(%)
Nystagmus
(%)
Strabismus
(%)
Facial
nerve
paresis
(%)
Horner’s
syndrome
(%)
Other
cranial
nerve
deficits
(%)
Central
neuro-
anatomical
localisation
(%)
Idiopathic 78 M: 42 91 21.95 P: 7 Ep: 3 15 17 54 68 12 43 25 52 4 0 8
vestibular (34.2) F: 36 (21−165) (3.6−63.9) A: 58 Imp: 26 (19.2) (21.8) (69) (87.2) (15.4) (55.1) (32.1) (66.7) (5.1) (10.3)
disease S: 8 Prog: 17
C: 5 St: 32
Otitis 54 M: 38 72 12.4 P:2 Ep: 7 36 4 25 48 7 27 10 29 16 0 1
media/interna (23.7) F: 16 (7−128) (5.5−54.7) A: 29 Imp: 7 (66.7) (7.4) (46.3) (88.9) (13) (50) (18.5) (53.7) (29.6) (1.9)
S: 7 Prog: 17
C: 16 St: 22
Meningo- 35 M: 15 49.5 7 P: 2 Ep: 1 2 17 32 26 20 16 14 18 3 4 28
encephalitis of (15.4) F: 20 (6−125) (1.6−38) A: 29 Imp: 0 (5.7) (48.6) (91.4) (74.3) (57.1) (45.7) (40) (51.4) (8.6) (11.4) (80)
unknown S: 3 Prog: 32
origin C: 1 St: 2
Brain 26 M: 15 114 20.2 P: 0 Ep: 5 7 7 22 24 19 15 13 14 6 8 21
neoplasia (11.4) F: 11 (36−173) (7.2−38) A: 13 Imp: 0 (26.9) (26.9) (84.6) (92.3) (73.1) (57.7) (50) (53.8) (23.1) (30.8) (80.8)
S: 3 Prog: 16
C: 10 St: 5
Ischaemic 25 (11) M: 11 123 19.1 P: 9 EP: 2 2 5 19 17 16 15 5 10 3 2 18
infarct F: 14 (14−178) (2.2−36.7) A: 12 Imp: 7 (8) (20) (76) (68) (64) (60) (20) (40) (12) (8) (72)
S: 4 Prog: 8
C: 0 St: 8
Intracranial 4 (1.7) M: 3 71 11.55 A: 1 Prog: 4 2 1 3 3 3 1 2 2 0 0 4
empyema F: 1 (60-150) (8.7–16.7) S: 2 (50) (25) (75) (75) (75) (25) (50) (50) (100)
C: 1
Metronidazole 3 (1.3) M: 2 72 34.3 A: 3 Prog: 2 0 1 2 1 0 2 1 1 0 0 3
toxicity F: 1 (29–109) (9.5–60) St: 1 (33) (66) (33) (66) (33) (33) (100)
Middle ear 3 (1.3) M: 1 76 12.7 A: 1 Prog: 2 3 0 0 3 0 0 1 2 2 0 0
neoplasia F: 2 (65–115) (9.5–14.8) S: 1 St: 1 (100) (100) (33) (66) (66)
C: 1
Abbreviations: A, acute; C, chronic; Ep, episodic; F, female; Imp, improving; M, male; P, peracute; Prog, progressive; S, subacute; St, static.
6of10 Veteri nary Record
TABLE 2 Logistic regression analysis of signalment, clinical presentation and neurological examination characteristics of canine vestibular disorders with more than five cases
Gender Age Bodyweight Onset Progression
History of
otitis
externa Head tilt Nystagmus Strabismus
Facial nerve
paresis
Horner’s
syndrome
Other cranial
nerve deficits
Neuro-
anatomical
localisation
Idiopathic
vestibular
disease
Older p <0.001 Improving No Present Present Absent Peripheral
p<0.001 OR =1.09 p =0.025 p =0.007 p =0.04 p =0.003 p =0.005 p <0.001
OR =1.03 CI:
1.04–1.13
OR =14.38 OR =4.71 OR =5.09 OR =5.38 OR =9.26 OR =10.02
CI:1.01–1.04 CI:1.56–
132.21
CI:1.72–
12.91
CI:1.09–23.8 CI:1.99–14.5 CI:2.33–36.8 CI:2.98–33.7
Otitis media/
interna
Male Younger Yes Present Peripheral
p=0.018 p =0.015 p <0.001 p <0.001 p =0.009
OR =3.68 OR =0.98 OR =6.04 OR =17.12 OR =11.357
CI: 1.35–
10.03
CI:
0.97–0.99
CI: 2.31–
15.77
CI:
4.11–71.4
CI: 2.2–58.52
Meningo-
encephalitis
of unknown
origin
You n ger N o
p<0.001 p =0.037
OR =0.96 OR =9.27
CI:
0.93–0.98
CI:1.18–
72.73
Brain
neoplasia
Older Present Present Central
p=0.02 p =0.034 p =0.018 p =0.028
OR =1.02 OR =21.04 OR =14.96 OR =5.83
CI: 1.0–1.04 CI: 1.36–
325.17
CI:1.85–
120.89
CI:1.29–26.5
Ischaemic
infarct
Older Peracute Absent Central
p=0.005 p =0.025 p =0.047 p =0.012
OR =1.03 OR =148.9 OR =5.40 OR =7.91
CI:
1.01–1.04
CI:
2.29–9665.45
CI:
1.02–28.6
CI: 1.8–34.9
Presentation includes only statistically significant (p <0.05) variables, and data presented include odds ratio with 95% confidence intervals indicated in parentheses.
Veteri nary Record 7of10
or suspected peripheral neuro-anatomical localisation
are derived from the neurological examination.
Idiopathic vestibular disease was the most common
condition in our study population. Although this is in
agreement with previous reports,9,17 it has also been
suggested that otitis media interna should be consid-
ered the most common cause of peripheral vestibu-
lar disease in dogs.1,5 Our study included exclusively
cases referred to a specialist hospital, which could
have favoured emergency presentations. It is there-
fore likely that the prevalence of specific diagnoses in
our study does not reflect the prevalence of diagnoses
in first opinion practice. Idiopathic vestibular disease
is indeed a common cause of acute onset intracra-
nial signs in dogs,33 and veterinary surgeons might
prefer to refer dogs with this clinical presentation for
advanced veterinary care. Despite the acute onset of
often severe, vestibular signs, idiopathic vestibular dis-
ease has a good prognosis with spontaneous improve-
ment typically seen after several days.1,4,17 This was
also illustrated in this study in which an improving
clinical course was associated with this condition.
Idiopathic vestibular disease was further associated
with a higher age, higher bodyweight, the absence of a
clinical history of previous otitis externa, the presence
of pathological nystagmus, presence of concurrent
facial nerve paresis, absence of Horner’s syndrome
and a presumptive peripheral localisation of vestibular
signs. It is well known that this condition occurs com-
monly in older17 large breed dogs and has therefore
also been referred to as ‘idiopathic geriatric vestibu-
lar disease’.1,4 The high prevalence of pathological jerk
nystagmus in dogs with idiopathic vestibular disease
is in agreement with previous findings.34,35 Pathologi-
cal nystagmus is most often seen in the acute stages of
vestibular disease and is rapidly compensated for by
conscious visual fixation.1,34 It is therefore not surpris-
ing that this neurological abnormality is statistically
associated with a disorder characterised by an acute
onset of clinical signs. Although idiopathic vestibular
disease is characterised by acute onset vestibular signs
without other neurological deficits, concurrent facial
and vestibular neuropathy of unknown origin has
been reported previously.3,17,35–37 In one study, evalu-
ating the MRI characteristics of dogs with idiopathic
facial nerve paresis, 70% also had idiopathic vestibu-
lar disease.36 The common observation of concurrent
facial and vestibular neuropathy can be explained by
the close anatomical proximity of both cranial nerves.
The facial and vestibulocochlear nerves enter the
petrous part of the temporal bone through the internal
acoustic meatus and are enclosed in a common dural
sheath and have the same blood supply.38 The patho-
physiology of idiopathic facial nerve paresis and idio-
pathic vestibular disease is unclear.17,36 It is further
unclear if idiopathic vestibular disease without facial
nerve involvement should be considered a different
disease entity compared to acute vestibular disease of
unknown cause with concurrent facial nerve paresis.35
Although our results are largely in agreement with pre-
viously published reports, a proportion of dogs with
idiopathic vestibular disease demonstrated less typical
clinical characteristics, such as a perceived progres-
sion of clinical signs. This finding highlights a poten-
tial limitation of clinical reasoning in which subjec-
tive clinical information, provided by pet owners, is
relied on to identify the most likely differential diagno-
sis. It is possible that the multifactorial nature of clini-
cal signs in dogs with acute vestibular syndromes (i.e.
affected dogs often demonstrate multiple concurrent
neurological abnormalities) complicates assessment
of onset and progression for pet owners. It should
further be highlighted that the underlying aetiology
and pathogenesis of canine idiopathic vestibular syn-
drome are currently unknown. It remains unclear if
this condition represents a single disease entity or
should be considered an umbrella term for different
causes of acute onset of vestibular signs.17 A more
insidious and progressive course of clinical signs has
also been reported in a proportion of cats with idio-
pathic vestibular syndrome.39
Otitis media interna was associated with a lower
bodyweight, younger age, male gender, a clinical his-
tory of previous otitis externa, concurrent Horner’s
syndrome and a presumptive peripheral localisation
of vestibular signs. The association between a previous
clinical history of otitis externa and a diagnosis of oti-
tis media is not surprising. There is a close anatomical
relationship between the external, middle and inner
ear structures and otitis media and interna occurs
most commonly as a complication from chronic oti-
tis externa.17,40,41 It is therefore possible that dogs
with vestibular signs caused by otitis media interna
will also display non-neurological signs, such as head
shaking, ear discharge and pain on opening of the
mouth or palpation of the bullae.1It should how-
ever be noted that otitis media interna is not always
caused by extension of otitis externa, and chronic oti-
tis externa will not necessarily result in otitis media
and interna.17,41 This is in agreement with the find-
ings of this study in which only two thirds of dogs
with otitis media interna had a clinical history of pre-
viously diagnosed otitis externa, and otitis externa was
also commonly observed in dogs suffering from other
causes of vestibular syndrome (Table 1). The recep-
tors of the vestibular system are located in the mem-
branous portion of the inner ear, and vestibular signs
will therefore only occur if structures in the inner ear
(i.e. otitis interna) are affected.1,4,5 In this study, the
presence of Horner’s syndrome was associated with
the highest OR to predict a diagnosis of otitis media
interna (Table 2). The middle ear structures have
a close anatomic relationship with the sympathetic
innervation of the eye.5The three-neuron anatomi-
cal pathway of the sympathetic innervation to the eye
is complex and involves axons that course between
the temporal bone and the tympanic bulla.42 Animals
with disorders affecting the tympanic bulla can there-
fore also display signs of Horner’s syndrome, includ-
ing miosis, ptosis, enophthalmos and protrusion of the
third eyelid.4,5 Dogs with otitis media interna as the
cause of their vestibular signs were younger than dogs
8of10 Veteri nary Record
with other causes of vestibular syndrome. Previous
studies have reported that dogs with ear disorders are
typically between 1 and 5 years old and will only rarely
be very young or elderly patients.19,43–45 Although oti-
tis media and interna was associated with lower body-
weight, this finding is likely influenced by geographical
breed distributions and hence the overrepresentation
of specific small breed dogs in our study population.
Cavalier King Charles Spaniels and French bulldogs,
two breeds predisposed for otitis externa and otitis
media,19,46 were the most commonly included breeds
in this study. The association with male gender is diffi-
cult to explain. Although most studies do not report an
association with gender and otitis externa,44,47 some
studies have suggested a male45,48,49 or female43 pre-
dominance.
MUO was not associated with multiple specific clin-
ical characteristics, complicating the use of clinical
reasoning to recognise vestibular syndrome caused by
this disorder. This diagnosis was only associated with
younger age and the absence of a clinical history of
previous otitis externa. This finding illustrates the dif-
ficulty of making a presumptive diagnosis of vestibu-
lar syndrome caused by MUO in clinical practice and
also demonstrates the limitations of clinical reason-
ing. MUO is associated with a wide variation in clinical
presentations and signalment of affected animals.24,25
Although MUO was the most common cause of central
vestibular syndrome in this study, the nature of clini-
cal signs in affected dogs is variable and reflected by
the location of lesions in the central nervous system.
Meningoencephalitis has been associated with young
animals and small breed dogs.24 It should however be
noted that every dog breed can be affected, and that up
to 25% of dogs with MUO are large breed dogs.50 The
difficulty of making a reliable presumptive diagno-
sis of vestibular syndrome caused by MUO in clinical
practice is however concerning. This condition has a
potentially guarded prognosis. Approximately 26–33%
of dogs with MUO die within the first week of mak-
ing a diagnosis, and the remaining dogs often require
lifelong immunosuppressive treatment.51,52 It is there-
fore clear that making an early diagnosis and initiat-
ing prompt and appropriate treatment are of major
importance in dogs with MUO.
Ischaemic infarct was associated with a higher
age, a peracute or acute onset of clinical signs, the
absence of positional strabismus and a central neuro-
anatomical localisation. Previous studies have indeed
reported that ischaemic infarcts occur most com-
monly in older animals and that the clinical presen-
tation is typically characterised by a peracute onset
of severe neurological signs.53–56 Dogs with ischaemic
infarct and idiopathic vestibular syndrome have a
similar onset and progression of clinical signs and
can therefore be difficult to differentiate in veterinary
practice.33 The results of this study indicate that obser-
vation of neurological deficits suggestive for a central
neuro-anatomical localization could potentially help
to differentiate dogs with an ischaemic infarct from
those with idiopathic vestibular disease. The results
of this study further suggest that positional strabis-
mus is not commonly seen in dogs with ischaemic
infarcts. Previous studies reporting the clinical signs
and neurological deficits in dogs with suspected ros-
tral cerebellar56 and thalamic ischaemic infarcts54
reported that vestibular signs, consisting of ataxia,
head tilt and nystagmus were commonly observed.
In agreement with the results of our study, positional
strabismus has only rarely been reported in dogs
with cerebellar and thalamic ischaemic infarcts.54,56
Although positional strabismus can occur with lesions
in any component of the vestibular system,57 it is
possible that lesions in the rostral cerebellum and
paramedian thalamic region will only have a mini-
mal influence on the development of this neurological
deficit.
Brain neoplasia was associated with higher age,
the presence of a head tilt, multiple cranial nerve
abnormalities and a central neuro-anatomical local-
isation. Intracranial neoplasia, such as meningioma,
choroid plexus tumors, and gliomas commonly occur
in the cerebellopontomedullary region or brainstem
parenchyma.1,26 It is therefore not surprising that
affected animals demonstrate neurological deficits
suggestive for brainstem involvement, such as multi-
ple cranial nerve deficits. Although a head tilt was also
commonly present in dogs with other vestibular disor-
ders, this clinical sign was only significantly associated
with a diagnosis of brain neoplasia. This result sug-
gests that a head tilt is commonly observed as the only
sign of vestibular dysfunction in dogs with brain neo-
plasia without other vestibular signs.
This study was limited by its retrospective
study design and the inclusion of cases without a
histopathologically confirmed diagnosis. Although
classification into specific disease categories was
based on advanced diagnostic investigations, specific
disease categories, such as gliomas and ischaemic
cerebrovascular accidents can be difficult to differ-
entiate based on MRI alone.58 It should further be
emphasised that all included dogs were referred to a
specialist referral hospital, which might have favoured
emergency and more complex clinical presentations.
It is therefore likely that the distribution of diagnoses
in this study does not represent the distribution
of canine vestibular disorders in general practice.
Included dogs did not undergo a standardised diag-
nostic approach, and the selection of diagnostic tests
was based on a combination of presenting clinical
characteristics, owner’s and clinician’s preference. The
clinical characteristics of some of the most common
conditions, such as idiopathic vestibular disease and
ischaemic infarct have been well reported, and both
conditions are typically associated with a peracute to
acute onset of non-progressive clinical signs.1–4 Sev-
eral dogs in this study were however reported to have
atypical clinical characteristics, such as progressive
clinical signs. This finding illustrates that applying the
principles of clinical reasoning might be limited in
animals that present with atypical signs of a common
neurological disorder.
Veteri nary Record 9of10
Although this study aimed to identify easy-to-
recognise clinical characteristics associated with the
most common causes of canine vestibular syndrome,
this study failed to identify discrete clinical features
that would be predictive for one of the most com-
monly identified causes of vestibular syndrome, MUO.
This study has therefore not only identified the clin-
ical potential, but also the limitations of using clin-
ical reasoning in dogs with vestibular syndrome. It
should further be noted that only the most common
causes of vestibular syndrome could be taken forward
for statistical analysis. The results of this study can
therefore not be extrapolated to less common and rare
causes of canine vestibular syndrome. Because of the
uneven prevalence of specific diagnoses, some condi-
tions were overrepresented compared to others. Diag-
noses represented by larger case numbers, such as
idiopathic vestibular disease, were associated with a
higher statistical power, which could have resulted in a
larger number of significantly predictive clinical vari-
ables associated with this condition. A large number
of dogs were excluded because insufficient diagnostic
tests were performed to reach a definitive or presump-
tive diagnosis. The efficiency of clinical reasoning is
improved by increased knowledge and experience.10
It is therefore likely that veterinary specialists more
naturally use the process of clinical reasoning in daily
clinical-decision making. The lack of further diagnos-
tics in a large proportion of dogs with vestibular dis-
ease could therefore represent the ability of veteri-
nary specialists to recognise the most likely differential
diagnosis without the need to perform advanced diag-
nostics.
Despite these limitations, this study demonstrated
that variables from the signalment, clinical history,
general and neurological examinations can be used
to create a list of prioritised differential diagnoses
in dogs with vestibular syndrome. This information
can help veterinary practitioners to select more con-
fidently appropriate diagnostic test, formulate treat-
ment recommendations and select those cases that
will benefit from referral to specialist centres. This
study further highlighted the limitations of clinical
reasoning, which emphasises the importance of reflec-
tion and the fact that this thought process ultimately
cannot replace specific diagnostic tests.
AUTHOR CONTRIBUTIONS
Eleanor Harrison, Nick J. Grapes, Holger A. Volk and
Steven De Decker conceived the study and partici-
pated in its design and coordination. Eleanor Harri-
son and Steven De Decker wrote the final version of
the manuscript. Eleanor Harrison, Nick J. Grapes, and
Steven De Decker collected the data. Nick J. Grapes
performed statistical analysis. Eleanor Harrison, Nick
J. Grapes, Holger A. Volk and Steven De Decker inter-
preted the data. All authors have read and approved
the final manuscript. Steven De Decker is responsible
for the overall content as guarantor.
ORCID
Nick J. Grapes https://orcid.org/0000-0002-8849-
5508
Steven De Decker https://orcid.org/0000-0002-
2505-2152
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How to cite this article: Harrison E, Grapes NJ,
Volk HA, De Decker S. Clinical reasoning in
canine vestibular syndrome: Which presenting
factors are important?. Vet Rec. 2021;e61.
https://doi.org/10.1002/vetr.61