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Signs of neurologic dysfunction in dogs
SMALL ANIMALS/
with central versus peripheral vestibular disease
EXOTIC
Mark T. Troxel, DVM, DACVIM; Kenneth J. Drobatz, DVM, MSCE, DACVIM, DACVECC;
Charles H. Vite, DVM, PhD, DACVIM
Objective—To determine the frequency of specific
signs of neurologic dysfunction in dogs with central
vestibular disease (CVD) or peripheral vestibular dis-
ease (PVD) and whether the degree of head tilt, rate of
nystagmus, and number of beats of postrotatory nys-
tagmus can be used to help distinguish CVD from PVD.
Design—Prospective clinical study.
Animals—40 client-owned dogs with vestibular sys-
tem dysfunction.
Procedure—A standard neurologic examination was
performed, along with an expanded vestibular system
examination that assessed the degree of head tilt,
rate of nystagmus, and number of beats of postrota-
tory nystagmus.
Results—Dogs with CVD were significantly more
likely to be nonambulatory than were dogs with
PVD. Dogs with PVD were significantly more likely
to veer or lean in 1 direction and to have resting nys-
tagmus than were dogs with CVD. Median rate of
resting nystagmus was significantly higher for dogs
with PVD, but no significant differences between
groups were detected in regard to presence or
degree of head tilt, presence of positional ventral
strabismus, and number of beats of postrotatory
nystagmus.
Conclusions and Clinical Relevance—Results
suggest that nonambulatory tetraparesis is signifi-
cantly more common in dogs with CVD and veering
and leaning are significantly more common in dogs
with PVD. Although neither the degree of head tilt
nor the number of beats of postrotatory nystagmus
could be used to distinguish CVD from PVD, rate of
resting nystagmus may be useful in distinguishing
the 2 conditions. (J Am Vet Med Assoc 2005;227:
570–574)
T he vestibular system maintains the normal spatial
position of the eyes, head, trunk, and limbs relative
to the earth’s gravitational field despite changes in lin-
ear or rotatory acceleration or tilting.1-6 Diseases of the
vestibular system result in various degrees of balance
disturbance and abnormalities of head, neck, body, and
eye position. Common clinical signs of vestibular sys-
tem dysfunction include vestibular ataxia, falling, cir-
cling, rolling, head tilt, and nystagmus.1-6
From the Department of Clinical Studies, Matthew J. Ryan
Veterinary Hospital of the University of Pennsylvania, School of
Veterinary Medicine, University of Pennsylvania, Philadelphia, PA
19104. Dr. Troxel’s present address is Massachusetts Veterinary
Referral Hospital, 21 Cabot Rd, Woburn, MA 01801.
Presented as an abstract at the Annual Meeting of the European
Society of Veterinary Neurology, Philadelphia, September 2002.
Address correspondence to Dr. Troxel.
570 Scientific Reports: Original Study
The primary goal for a clinician examining a
patient with vestibular system dysfunction is to deter-
mine whether the patient has evidence of central
vestibular disease (CVD) or peripheral vestibular dis-
ease (PVD), as the differential diagnoses, diagnostic
and treatment considerations, and prognoses differ.2,3
Correctly identifying CVD requires identification of
clinical signs that cannot be attributed to diseases of
the peripheral vestibular system.1-6 Clinical signs that
are often cited as evidence of CVD include vertical nys-
tagmus, nystagmus that changes direction, multiple
cranial nerve deficits, cerebellar dysfunction, altered
consciousness, spinal ataxia, paresis, and postural reac-
tion deficits.1,6
To our knowledge, there are no prospective studies
in the veterinary literature that correlate clinical signs
of vestibular system dysfunction with lesion location.
The purposes of the study reported here, therefore,
were to determine the frequency of specific signs of
vestibular system dysfunction in dogs with CVD or
PVD and whether the degree of head tilt, rate of nys-
tagmus, and number of beats of postrotatory nystag-
mus could be used to distinguish CVD from PVD.
Materials and Methods
Patients—Forty client-owned dogs with signs of
vestibular system dysfunction were included in the study.
The first 20 dogs examined at the Matthew J. Ryan Veterinary
Hospital of the University of Pennsylvania during the study
period that were classified as having PVD and the first 20 that
were classified as having CVD were included.
Experimental design—Each dog underwent a standard
neurologic examination performed by a veterinary neurology
resident or a board-certified veterinary neurologist. The stan-
dard neurologic examination consisted of evaluation of men-
tal status (level of consciousness), gait and body posture,
postural reactions (conscious proprioception, hopping,
wheel barrowing, extensor postural thrust, hemistanding or
hemiwalking, and visual and tactile placing [small dogs]),
cranial nerve function, and segmental spinal reflexes (patel-
lar, cranial tibial, gastrocnemius, perineal, triceps brachii,
biceps brachii, and extensor carpi radialis). Other parameters
that were evaluated included degree of muscle tone, presence
of muscle atrophy, presence of signs of discomfort or pain
during vertebral palpation, cutaneous trunci reflex, and ocu-
lar fundic examination. Specific to the vestibular system, the
presence and direction of head tilt, strabismus, and nystag-
mus were documented.
The expanded vestibular system examination assessed
the degree of head tilt, the rate of nystagmus, and the number
of beats of postrotatory nystagmus. The degree of head tilt
was determined by taking a digital photograph of the patient
standing in front of a wall with a line drawn parallel to the
floor. The image was then imported into a commercial image-
editing program,a and a protractor was used to measure the
angle between a line drawn through the eyes at the level of the
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lateral canthi and the horizontal line on the wall. The rate of as stuporous. As expected, none of the dogs with PVD

SMALL ANIMALS/
nystagmus was calculated by counting the number of beats were characterized as depressed, stuporous, or
per minute (BPM) with the head in a neutral resting position comatose. Four dogs with CVD and 4 with PVD were

EXOTIC
as well as with the animal in dorsal recumbency and in right reported to be disoriented.
and left lateral recumbency. Postrotatory nystagmus was
assessed in patients that weighed < 20 kg (44 lb) that were Gait, body posture, and postural reactions—A
suspected to have vestibular system dysfunction but did not gait abnormality (Table 1) was identified in 37 of the
have resting nystagmus. The number of beats of postrotatory 40 (92.5%) dogs. Nine dogs were nonambulatory. A
nystagmus was counted following 5 complete revolutions in significant difference was detected between dogs with
each direction at a frequency of 34 rotations/min as counted
by a metronome. Postrotatory nystagmus was performed by CVD and dogs with PVD in regard to percentage that
holding the dog with the long axis of its head parallel to the were nonambulatory and percentage that had a gait
floor and its nose perpendicular to the direction of rotation. characterized by veering or leaning to 1 direction.
There were no significant differences between groups
Patient classification—Dogs were classified as having in regard to percentages of dogs falling, rolling, or cir-
CVD or PVD on the basis of clinical criteria adapted from the cling or dogs with a wide-based stance or gait.
method described by de Lahunta.1 Dogs (n = 20) were classi-
fied as having PVD if they had signs of dysfunction of the A head tilt was observed in 36 (90%) dogs. There
peripheral vestibular system, including loss of balance, was no significant difference in percentages of dogs
vestibular ataxia, head tilt, horizontal or rotary nystagmus, with a head tilt between dogs with CVD (n = 16) and
and positional strabismus. Dogs (n = 20) were classified as dogs with PVD (20).
having CVD if they had any of the following signs in addition Abnormal postural reactions aside from those that
to signs listed for dogs with PVD: consistent vertical nystag- could be attributed to concurrent conditions (eg, T3-
mus, nystagmus for which the fast phase changed direction L3 myelopathy) were detected in 19 (95%) dogs with
with a change in head position, and signs of dysfunction of CVD. One dog with CVD characterized by paresis of
brainstem or cerebellar structures adjacent to the vestibular multiple cranial nerves but no abnormal postural reac-
nuclei. These signs included altered mental status, spinal
ataxia, dysmetria, upper motor neuron paresis, postural reac-
tions had a mass consistent with meningioma en
tion deficits, intention tremors, and dysfunction of any cra- plaque evident on computed tomographs.
nial nerve other than cranial nerve VII.1-3 Cranial nerve examination—At least 1 cranial
Disease of the central vestibular system was confirmed nerve (Table 2) other than cranial nerve VIII was
by means of computed tomography (CT), magnetic reso-
nance imaging (MRI), or postmortem examination in 19 of affected in 12 of 20 dogs with CVD. Cranial nerves IX
the 20 dogs classified as having CVD. The only exception and X were each affected in 6 dogs with CVD, as deter-
was 1 dog in which metronidazole intoxication caused mined by decreased gag reflex and dysphagia.
vestibular system dysfunction.7,8 Disease of the peripheral Normal physiologic nystagmus was observed in all
vestibular system was confirmed by means of CT, MRI, or directions of head movement in 38 (95%) dogs. There
postmortem examination in 5 of the 20 dogs classified as was no significant difference between groups.
having PVD; these 5 dogs did not have any evidence of CNS Spontaneous resting nystagmus was observed in
disease. Since we did not image or histologically examine the 24 dogs. There was a significant (P < 0.001) difference
brains of all animals in the PVD group, the accuracy of our in percentage of dogs with spontaneous resting nystag-
clinical localization of PVD could not be definitively deter-
mined. For the remaining dogs classified as having PVD, dis-
mus between the CVD (n = 6) and PVD (18) groups.
ease of the vestibular receptors, vestibular ganglion, or No significant differences were observed between
vestibular nerve was inferred on the basis of results of oto-
scopic examination (n = 3), skull radiography (1), or thyroid Table 1—Gait abnormalities detected in 20 dogs with central
hormone analysis9 (1) or because clinical signs resolved with- vestibular disease (CVD) and 20 dogs with peripheral vestibular
disease (PVD).
out medical intervention within 14 days (suggestive of idio-
pathic vestibular disease; 10). Gait abnormality CVD PVD P value
Statistical analyses—Data for all continuous variables Veering or leaning 8 18 0.002
(eg, rate of nystagmus, duration of clinical signs, and age of Falling 15 15 0.999
animals) were not normally distributed; therefore, median Rolling 4 3 0.999
Circling 4 3 0.999
and range are reported. The Wilcoxon rank sum test was Nonambulatory tetraparesis 8 1 0.020
used to compare continuous variables between groups, and Hypermetria 4 0 0.106
the Spearman rank correlation method was used to assess the Wide-based stance or gait 1 4 0.342
relationship between rate of resting nystagmus and duration
of clinical signs. Receiver operating characteristic (ROC)
Table 2—Cranial nerve dysfunction detected in 20 dogs with
curve analysis and visual inspection of box plots were used CVD and 20 dogs with PVD.
to determine the rate of resting nystagmus that maximized
both sensitivity and specificity in diagnosing PVD. The area Cranial nerve CVD PVD P value
under the ROC curve was determined by use of the trapezoid
rule. Fisher exact tests were used to compare categorical vari- V (trigeminal) 4 0 0.106
VI (abducent) 0 0 NA
ables between groups. For all comparisons, a value of P VII (facial) 4 4 0.999
< 0.05 was considered significant. All data analyses were per- IX (glossopharyngeal) 6 0 0.020
formed with standard statistical software.b X (vagus) 6 0 0.020
XI (accessory) 0 0 NA
XII (hypoglossal) 0 0 NA
Results
Mental status—Eight dogs with CVD were char- NA = Not applicable.
acterized as dull or depressed, and 1 was characterized

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groups in regard to type of nystagmus (ie, horizontal,
SMALL ANIMALS/
rotary, or vertical nystagmus) or the change from rest-
ing to positional nystagmus (eg, resting rotary nystag-
EXOTIC
mus that changed to positional vertical nystagmus).
There were insufficient numbers of dogs to analyze
whether dogs with CVD that did not have resting nys-
tagmus (n = 14) were more likely than dogs with PVD
(2) to develop positional nystagmus.
Positional ventral strabismus was observed in 33
(82.5%) dogs. There was no significant difference
between groups in regard to prevalence of ventral stra-
bismus (CVD, n = 15; PVD, 18).
There were no significant differences between
groups in regard to prevalences of abnormalities of seg-
mental spinal reflexes, spinal hyperpathia, alterations
in muscle tone, muscle atrophy, alterations in the cuta-
neous trunci reflex, or ocular fundic abnormalities.
Clinical signs in dogs with CVD and cerebellar
involvement—Cerebellar disease was definitively diag-
nosed in 8 dogs with CVD by means of MRI (n = 6) or
CT (2). Paradoxic vestibular signs (eg, head tilt con-
tralateral to postural reaction deficits) were observed
in 3 of these dogs. Mild or intermittent clinical signs
consistent with cerebellar dysfunction (eg, hyperme-
tria, intention tremor, and absent menace response
with intact vision and pupillary light responses) were
observed in 4 other dogs. The remaining dog did not
have any clinical signs suggestive of cerebellar disease,
but bilateral contrast-enhancing lesions in the cerebel-
lar nuclei and in the area of the right caudal cerebellar
peduncle were seen on computed tomographs.
Cerebellar lesions were intraparenchymal in 6 dogs,
with lesions located in the superficial grey matter (n
= 2), cerebellar nuclei (3), cerebellar peduncle (1), or
cerebellar white matter (3); 3 dogs had > 1 lesion. An
extra-axial (ie, outside the brain parenchyma) mass
caused compression of the cerebellum in 2 dogs, with
cerebellar herniation through the foramen magnum in
1 of these dogs. The lesion was ipsilateral to the clini-
cal signs in all 7 dogs with clinical signs suggestive of
cerebellar dysfunction.
Head tilt, rate of nystagmus, and postrotatory
nystagmus—During the expanded vestibular system
examination, the degree of head tilt, rate of nystagmus,
and number of beats of postrotatory nystagmus were
assessed. No significant differences were detected
between the 2 groups in regard to degree of head tilt.
Median degree of head tilt was 17.5o for dogs with CVD
(range, 0o to 90o) and 27.0o for dogs with PVD (range,
6o to 47o).
Significant differences were detected between
groups in regard to rate of resting nystagmus (P
< 0.001), rate of nystagmus in dorsal recumbency (P
< 0.001), and the change in rate of spontaneous nys-
tagmus when the dog was moved from a neutral rest-
ing position to either left lateral (P = 0.004) or right lat-
eral (P < 0.001) recumbency. Median rates of resting
nystagmus were 0 BPM (range, 0 to 150 BPM) for the
20 dogs with CVD and 90 BPM (range, 0 to 228 BPM)
for the 20 dogs with PVD. There was a significant (P
< 0.001) inverse correlation between duration of clini-
cal signs and rate of resting nystagmus. The longer the
572 Scientific Reports: Original Study
Figure 1—Box plots of rates of resting nystagmus (beats/min) in
20 dogs with central vestibular disease (CVD) and 20 dogs with
peripheral vestibular disease (PVD). Receiver operating charac-
teristic curve analysis and visual inspection of the box plots
were used to determine the rate of resting nystagmus that max-
imized sensitivity and specificity in diagnosing PVD (solid hori-
zontal line; sensitivity, 85%; specificity, 95%).
duration of clinical signs, the lower the rate of resting
nystagmus. A significant difference (P < 0.001) also
was detected between groups in regard to median rate
for positional nystagmus in dorsal recumbency. The
median rate for positional nystagmus in dorsal recum-
bency was 30 BPM (range, 0 to 258 BPM) for dogs with
CVD and 120 BPM (range, 0 to 294 BPM) for dogs with
PVD. However, there was no significant difference
between groups when comparing the difference in rate
of nystagmus with the head in a neutral position ver-
sus the rate of nystagmus with the head in dorsal
recumbency. As determined by ROC curve analysis and
visual inspection of box plots (Figure 1), a resting nys-
tagmus rate ≥ 66 BPM provided the highest combined
sensitivity (85%) and specificity (95%) in diagnosing
PVD (area under the ROC curve = 0.89).
Postrotatory nystagmus testing was performed in 5
dogs with CVD and 3 with PVD. There were no signif-
icant differences between groups regardless of direc-
tion of rotation. Median numbers of beats of postrota-
tory nystagmus were 8 (range, 3 to 18) for dogs with
CVD and 22 (range, 0 to 26) for dogs with PVD when
postrotatory nystagmus was tested by rotating to the
patient’s right and 6 (range, 4 to 11) for dogs with CVD
and 8 (range, 5 to 10) for dogs with PVD when postro-
tatory nystagmus was tested by rotating to the patient’s
left. There was no significant difference when compar-
ing number of beats of postrotatory nystagmus to the
side on which the lesion was located, as determined by
means of neurologic testing. Testing was performed on
an insufficient number of patients to analyze the num-
ber of beats of postrotatory nystagmus between groups
in relation to the side on which the lesion was located
as determined by means of MRI, CT, or postmortem
examination.
Discussion
Results of the present study suggest that preva-
lences of certain specific signs of vestibular system dys-
function differ between dogs with CVD and dogs with
PVD. In particular, nonambulatory tetraparesis was
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significantly more common in dogs with CVD, and
veering and leaning were significantly more common
in dogs with PVD. However, neither the degree of head
tilt nor the number of beats of postrotatory nystagmus
could be used to distinguish CVD from PVD. On the
other hand, the rate of resting nystagmus was signifi-
cantly higher in dogs with PVD, and resting nystagmus
> 66 BPM was a sensitive (85%) and specific (95%) test
for PVD in these dogs.
In the present study, the diagnosis was confirmed
in 19 of the 20 dogs classified as having CVD and the
remaining dog was suspected to have CVD secondary
to metronidazole toxicosis. The diagnosis of an inner
ear or cranial nerve VIII lesion could not be confirmed
in all dogs classified as having PVD in the present
study because advanced imaging or postmortem exam-
ination was not performed on all dogs in this group.
Most dogs classified as having PVD recovered, meaning
that they were not available for postmortem examina-
tion, and the expense of advanced imaging could not
be justified. In addition, because it is technically diffi-
cult to properly fix and histologically examine the
inner ear at the time of postmortem examination, this
procedure often is not done. Thus, it is important to
acknowledge that some dogs in the present study that
were classified as having PVD may in fact have had
small, nonprogressive CNS lesions (eg, cerebrovascular
infarct) that failed to cause clinical signs suggestive of
CVD and were improperly classified.
Level of consciousness is controlled by the ascend-
ing reticular activating system located in the brain-
stem.1 Thus, dogs with CVD may have altered con-
sciousness (ie, stupor, coma, or signs of depression),
whereas dogs with PVD should be alert and appropri-
ate to their surroundings.1,3,5,6 In the present study, stu-
por, coma, or signs of depression were observed in 9
(45%) dogs with CVD.
Asymmetric ataxia is commonly reported1-6 in ani-
mals with vestibular dysfunction, and 37 (92.5%) dogs
in the present study had a gait abnormality. Previous
reports1-6 have suggested that there is little difference in
gait between dogs with CVD and dogs with PVD, with
the exception that dogs with CVD may have cerebellar
ataxia (eg, hypermetria), upper motor neuron paresis,
or proprioceptive ataxia. In the present study, preva-
lence of nonambulatory tetraparesis was significantly
higher in dogs with CVD, whereas veering or leaning
was significantly more common in dogs with PVD.
Hypermetria is observed most often in animals with
cerebellar disease,1 and we expected there to be a sig-
nificantly greater prevalence of hypermetria among
dogs with CVD. The lack of a significant difference
between groups was likely a result of the small patient
population in the study.
Dysfunction of cranial nerves other than cranial
nerves VII and VIII has been cited1-6 as an indication
that an animal has CVD. This would be expected on
the basis of the neuroanatomic relationship between
central vestibular structures and the origin of cranial
nerves V through XII. In the present study, 6 (30%)
dogs with CVD had a diminished gag reflex or dyspha-
gia indicative of cranial nerve IX or X involvement.
However, there was no significant difference between
JAVMA, Vol 227, No. 4, August 15, 2005
groups in regard to prevalence of dysfunction of cranial
SMALL ANIMALS/
nerves V and VII, and none of the dogs in either group
had evidence of dysfunction of cranial nerves VI, XI,
EXOTIC
and XII. The lack of a significant difference between
groups was likely a result of the small patient popula-
tion in the study.
Previous reports1-6 have suggested that horizontal
or rotary nystagmus can be observed in dogs with
either CVD or PVD, but that vertical nystagmus is
observed only in dogs with CVD. In the present study,
there was no significant difference between groups in
regard to prevalence of vertical nystagmus, but most
dogs had rotary nystagmus, and only a few had vertical
nystagmus, which may explain the lack of a significant
difference. Our clinical experience is that vertical nys-
tagmus occurs more frequently in dogs with CVD. In
rare instances, we have observed dogs that did not have
any magnetic resonance or computed tomographic evi-
dence of a CNS lesion that had vertical nystagmus at
the time of initial examination following an acute onset
of signs of severe vestibular dysfunction that later con-
verted to rotary nystagmus. The vertical nystagmus in
these dogs has most often been a positional vertical
nystagmus.
Positional ventral strabismus refers to strabismus
seen in dogs with vestibular dysfunction when the
head is straightened and the neck is extended and has
been reported to occur most often on the side of the
lesion.1-6 Previous reports1-6 state that this strabismus is
frequently observed in dogs with CVD or PVD, and
positional ventral strabismus was seen in 33 (82.5%)
dogs in the present study. There was no significant dif-
ference between groups in regard to prevalence of posi-
tional ventral strabismus nor was there any association
between the eye demonstrating positional ventral stra-
bismus and definitive location of the lesion, as deter-
mined by means of advanced imaging or postmortem
examination. This may be attributable to the fact that
several dogs had bilateral disease in the present study;
as a result, there was an insufficient number of dogs
with unilateral disease to compare the eye demonstrat-
ing positional ventral strabismus and lesion location.
Abnormal postural reactions have been cited1-6 as
being suggestive of brainstem disease consistent with
CVD, whereas postural reactions should be normal in
dogs with PVD. Postural reaction deficits are seen
because of direct or indirect involvement of proprio-
ceptive or upper motor neuron pathways traversing the
brainstem.1,3-6 In the present study, postural reaction
deficits were detected in 19 (95%) dogs with CVD.
As part of an expanded neurologic examination for
dogs in the present study, we analyzed the degree of
head tilt, rate of nystagmus, and number of beats of
postrotatory nystagmus to determine whether these
tests could be used to help differentiate CVD from
PVD. There was no significant difference in median
degree of head tilt between dogs with CVD (17.5o) and
dogs with PVD (27.0o); however, no dog with PVD had
a head tilt > 47o, whereas 4 dogs with CVD had head
tilts > 47o. The direction of head tilt was associated
with side on which the lesion was suspected to be
located at the time of initial examination. This was not
unexpected because it has previously been reported
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that the head tilt should be toward the side of the
SMALL ANIMALS/
lesion, with the exception of dogs with paradoxic
vestibular signs. In the present study, the direction of
EXOTIC
head tilt was not associated with side on which the
lesion was located, as determined by means of
advanced imaging or postmortem examination. This is
likely explained by the presence of bilateral or multifo-
cal disease in many dogs. There was an insufficient
number of cases to allow statistical analysis of dogs
with unilateral disease.
To our knowledge, there are no reports of whether
the rate of nystagmus in a neutral head position or in
various other positions can be used to differentiate
CVD from PVD. Our data suggest that rate of nystag-
mus can assist with differentiation of CVD from PVD.
Median rates of resting and positional nystagmus were
significantly faster for dogs with PVD than for dogs
with CVD, and a rate of resting nystagmus > 66 BPM
was associated with high sensitivity (85%) and speci-
ficity (95%) for diagnosis of PVD.
Postrotatory nystagmus testing was performed in
8 dogs in the present study. Postrotatory nystagmus
can be induced in normal animals by spinning them
in a circle and then stopping suddenly.1 In patients
with PVD, postrotatory nystagmus is typically
depressed when the patient is spun in the direction
opposite to the side of the lesion.1 In the present
study, however, there were no significant differences
between groups in regard to median number of beats
of postrotatory nystagmus after spinning in either
direction. There also was no significant difference
between median numbers of beats of postrotatory
574 Scientific Reports: Original Study
nystagmus after spinning in the direction of the sus-
pected lesion, as determined by means of neurologic
examination. Thus, postrotatory nystagmus testing
could not be used to differentiate CVD from PVD in
this population of dogs.
a. Adobe Photoshop, version 5.0, Adobe Systems Inc, San Jose,
Calif.
b. Intercooled Stata for Windows, version 8.0, Stata Corp, College
Station, Tex.
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