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Paper 003 Disc
Veterinary Ophthalmology (1998) 1, 1, 17±20
Idiopathic Horner's syndrome in collie dogs
HeÂctor Daniel Herrera,*{ Adriana Patricia Suraniti* and Nuria Fernanda Kojusner{
*Veterinary Medicine Teaching Hospital. School of Veterinary Sciences, University of Buenos Aires, Argentina, {Private practice, Buenos Aires, Argentina
Address communications to:
H. D. Herrera
{ChorroarõÂn 280
1427 Buenos Aires
Argentina
Fax: +54 1 521 8316
e-mail: [email protected]
Abstract
Seven cases of idiopathic Horner's Syndrome in the Collie are described. Five males and
two females presented with unilateral miosis, ptosis of the upper eyelid, enophthalmos and
protrusion of the third eyelid. Thorough examination, pharmacological testing with
phenylephrine, complete blood counts and radiography of the tympanic bullae and thorax
were performed. The etiology was not identified in any of the cases. Clinical signs
improved with pharmacologic testing within 20±40 min. In five dogs, total resolution of
clinical signs was observed at 4 and 16 weeks after their initial appearance. Pharmacological
testing suggested that the deficit could be at the preganglionic neuron.
Ahed
Bhed
Ched
Dhed
Ref marKey Words: Horner's syndrome, dog, collie
ker
Fig marker
following road accidents, otitis media/interna, avulsion of T a b l e
INTRODUCTION
the roots of the brachial plexus, thoracic masses, central marker
Horner's syndrome (HS) is a group of clinical signs that result
nervous system infection or neoplasia, ischaemic myelo- Ref end
from loss or interruption of sympathetic innervation to the
pathy, intervertebral disc disease,1,3,4,5,6,8±10 and thyroid Ref start
globe and adnexa. These signs include miosis, ptosis of the
neoplasia.11 However, in approximately half of affected dogs
upper eyelid, enophthalmos and protrusion of the third eyelid.
the cause cannot be determined3,9,10 and these cases are
The sympathetic innervation of the eye and adnexa may
recognized as idiopathic HS. There are no reports of any
be divided into three neuroanatomic parts: central, preganbreed predisposition to the disease3,9 but a high incidence of
glionic and postganglionic. The central component consists
idiopathic HS has been described in the Golden Retriever.2
of fibers descending from the higher centers of the
The purpose of this paper is to describe the findings of seven
autonomic nervous system in the brain stem.1 They pass
cases of idiopathic HS in Collies in a total of eight dogs with
from the hypothalamus, tectum and tegmentum down the
HS presented to the authors between October 1994 and
tegmentospinal tract to synapse with preganglionic cell
December 1996.
bodies in the intermediate grey column of the cranial
thoracic segments of the spinal cord.2 Pain, fear or
emotional responses may cause pupillary dilatation by
MATERIALS AND METHODS
activating this pathway.3,4 The preganglionic cell bodies
Eight dogs (seven Collies and a Great Dane) with idiopathic
are located in the intermediate grey column of the first three
HS were studied between October 1994 and December
or four segments of the thoraxic spinal cord. The axons leave
1996. The medical records of the seven Collies were
the spinal cord with the ventral roots of the spinal nerves to
reviewed in the present study. Five males and two females
join the thoracic sympathetic trunk, and then pass through
aging from 5 to 11 years (mean 7 years) were included
the cervicothoraxic ganglion without synapsing, very close to
(Table 1). All of them presented with acute unilateral miosis,
the cranial lung lobe.1,4±6 These preganglionic axons travel
up the neck in the vagosympathetic trunk ending in the
ptosis of the upper eyelid, enophthalmos and protrusion of
cranial cervical ganglion, located caudomedial to the
the third eyelid. Clinical examination included a complete
tympanic bulla, where they synapse with the postganglionic
ophthalmic examination (seven cases), thorough ear examcell bodies.5,6 The postganglionic sympathetic axons travel
ination (seven cases), complete neurologic examination
forward, pass through the middle ear adjacent to the facial
(seven cases), pharmacological testing with topical 10%
nerve and join the ophthalmic branch of the trigeminal
phenylephrine (seven cases), complete blood counts and
nerve. The ophthalmic nerve enters the periorbita through
blood chemistry parameters (four cases), and radiographs of
the orbital fissure and distributes to the smooth muscles of
the thorax (three cases) and the tympanic bullae (two cases).
the periorbita, eyelids and the dilator muscle of the iris.3,4
In order to localize the site of the lesion, pharmacological
Several causes of HS have been proposed including
testing was performed through assessment of ocular
congenital anomalies,7 severe head, neck and chest trauma
response to the topical administration of 10% phenylephrine
# American College of Veterinary Ophthalmologists
Paper 003 Disc
18
HERRERA, SURANITI AND KOJUSNER
Table 1 Distribution by sex, age and affected eye, response to
pharmacologic testing and recovery times in the seven studied Collies
Case Sex
Age
(years)
Affected
eye
Pupillary response
with phenylephrine
Recovery time
(weeks)
1
2
3
4
5
6
7
9
6
5
8
11
5
5
OD
OS
OD
OS
OS
OS
OD
mydriasis
incomplete
incomplete
incomplete
mydriasis
mydriasis
incomplete
12
16
±
±
8
4
6
F
M
M
F
M
M
M
M, male; F, female; OD, right eye; OS, left eye.
(Poenefrina: Poen Lab., Buenos Aires). Two drops were
placed in each eye using the control eye for comparison.
Ocular examination was repeated every 10 min for 50 min;
the time when the affected eye resumed to normality and
mydriasis occurred in both the control and affected eye was
noted. Two cases had a history of otitis externa; radiographs
of the tympanic bullae were performed in these two patients,
in addition to the otoscopic examination. Follow-up could be
carried out by telephone contact with the owners in five of
the cases.
RESULTS
Four dogs were affected on the left side and three dogs were
affected on the right side. The cause could not be
determined in any of the cases. There was no history of
trauma, infectious or non infectious disease of the central
nervous system, or ear disease except in two cases with
previous mild otitis externa. Ophthalmic and otoscopic
examination, and hematological and serum biochemical
analysis were normal as well as radiographic examination,
except in one case which showed spondylosis deformans
from C6 to T2 with no peripheral neurologic signs. All the
dogs responded to the pharmacological testing (Figs 1 and 2).
All the clinical signs showed a complete improvement within
20±40 min after application of the topical phenylephrine,
except the pupil, which had an incomplete response in four
of the affected eyes (Table 1). Mydriasis occurred in all the
control eyes at the same time as the affected eyes. In the five
dogs that could be followed up, total resolution of clinical
signs was observed between 4 and 16 weeks (mean 9.2 weeks)
after its appearance.
DISCUSSION
The sympathetic supply of the eye is responsible for
maintaining normal tone of the smooth muscles of the
periorbita, eyelids and dilator muscle of the iris. It keeps the
globe positioned normally, the third eyelid retracted, the
pupil partially dilated, and modulates palpebral fissure
width.1,4 Horner's syndrome (HS) is the name given to the
group of clinical signs which results from interruption or loss
of sympathetic innervation. These signs include miosis
(actually the affected pupil dilating incompletely in low light
conditions2), ptosis of the upper eyelid, enophthalmos, and
protrusion of the third eyelid.
HS is not an uncommon finding in dogs. Previous reviews
of cases of HS have shown a relatively high incidence of the
condition. One author diagnosed 74 cases in 10 years.9 In
another report, 33 dogs with HS were diagnosed over a
period of six years,3 while only two cases were diagnosed in 4
years by another author.8 In our series, eight cases of
idiopathic HS were diagnosed in the last two years and seven
of these cases were in Collies.
Collies are not a common breed in the Argentinian dog
population. In fact, only 12 Collies with ophthalmic disease
were presented to one of the authors (H.D.H.) in the review
period and seven of them had HS. Thorough examination
and pharmacological testing with phenylephrine were
performed in these seven Collies; complete blood counts
and radiographs of the tympanic bullae and thorax were
performed in some of them but the cause could not be
determined in any case. Boydell has reported a high
incidence of idiopathic HS in Golden Retrievers;2 however,
there are no reports of any breed predisposition in other
studies.3,4,8±10
There is no general agreement about the utility of
pharmacologic testing for HS. Use of 0.001% epinephrine
and 2 or 4% cocaine,12,13 hydroxyamphetamine,14 hydroxyamphetamine and 10% phenylephrine,4±6 epinephrine,3,9
and phenylephrine2 have been utilized in both humans and
dogs in order to localize the site of the lesion. The combined
use of an indirect and a direct-acting sympathomimetic
agent appears to be the most useful method. Instillation of
an indirect-acting sympathomimetic such as 1% hydroxyamphetamine results in normal mydriasis of the miotic
pupil if the lesion is preganglionic. This drug acts by
releasing endogenous norepinephrine from adrenergic nerve
endings. When the lesion is postganglionic, the stores of
norepinephrine contained in the nerve terminals are
depleted and the pupil remains miotic.4±6 A direct-acting
sympathomimetic such as 10% phenylephrine or 0.001%
epinephrine can be used to confirm a postganglionic lesion
in cases of incomplete or absent mydriasis after instillation of
hydroxyamphetamine. In these cases of sympathetic denervation, adrenergic nerve endings become supersensitive to
direct-acting sympathomimetics and mydriasis quickly occurs in postganglionic lesions.4±6,12
Boydell refers to the criteria developed by Kay (1981)15 of
noting the time when mydriasis occurs after instillation of
10% phenylephrine.2 If mydriasis occurs within 20 min of the
instillation, a postganglionic lesion is suggested. If dilatation
occurs between 20 and 45 min, a preganglionic lesion is
diagnosed. Finally, if mydriasis takes longer than 45 min, a
central lesion may exist. Different authors have reported,
however, that 10% phenylephrine does not consistently
produce mydriasis in preganglionic lesions.4±6 In our cases
all pharmacological testing was performed with 10%
phenylephrine. Clinical signs improved within 20 and 40 min
# American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20
Paper 003 Disc
IDIOPATHIC HORNER'S SYNDROME
19
Figure 1. Case no. 6. Protrusion of the third eyelid;
enophthalmos and ptosis of the upper eyelid are
present on the left eye.
Figure 2. Same dog as in Fig. 1, 30 min after
instillation of 10% phenylephrine. The clinical signs
including miosis show complete recovery.
after application in all cases except for the pupils demonstrating incomplete recovery in four of the affected eyes.
Control eyes dilated at the same time as the affected eyes.
Regarding recovery times, Morgan mentioned that 25 out
of 33 dogs showed complete reversal of clinical signs in a
time ranging from 24 h to 30 weeks.3 In our study, five out
of seven patients demonstrated total spontaneous resolution
between 4 and 16 weeks.
According to our results, Collies may have a breed
predisposition to idiopathic Horner's syndrome. Pharmacological testing performed in these cases suggested that the lesion
could be affecting the preganglionic neuron, but the correct site
is not able to be confirmed using only phenylephrine.
ACKNOWLEDGEMENTS
The authors wish to thank Dr Dennis Brooks of
the Department of Small Animal Clinical Sciences, Uni-
versity of Florida, Gainesville, for the correction of
the manuscript.
REFERENCES
1 DeLahunta A. Veterinary Neuroanatomy and Clinical Neurology. 2nd
edn. WB Saunders Co.: Philadelphia, 1983; 116±120.
2 Boydell P. Idiopathic Horner's syndrome in the Golden Retriever.
Journal of Small Animal Practice 1995; 36(9): 382±384.
3 Morgan RV, Zanotti SW. Horner's syndrome in dogs and cats: 49
cases Journal of the American Veterinary Medical Association 1989;
194(8): 1096±1099.
4 Neer TM. Horner's syndrome: anatomy, diagnosis and causes.
Compendium of Continuing Education for Practicing Veterinarians 1984;
6(8): 740±746.
5 Scagliotti RH. Current concepts in veterinary neuro-ophthalmology. Veterinary Clinics of North America (Small Animal Pract) 1980;
10(2): 431±434.
6 Scagliotti RH. Neuro-ophthalmology. In: Veterinary Ophthalmology,
2nd edn. (ed. Gelatt KN). Lea & Febiger: Philadelphia, 1991; 706±743.
# American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20
Paper 003 Disc
20
HERRERA, SURANITI AND KOJUSNER
7 Brightman AH, Helper LC, Parker AJ. Congenital Horner's
syndrome. Canine Practice 1977; 4: 19±23.
8 Jones BR, Studdert VP. Horner's syndrome in the dog and cat as an
aid to diagnosis. Australian Veterinary Journal 1975; 51: 329±332.
9 Kern TJ, Aromando MC, Erb HN. Horner's syndrome in dogs and
cats: 100 cases. Journal of the American Veterinary Medical Association
1989; 195(3): 369±373.
10 Van Den Broek AHM. Horner's syndrome in cats and dogs: a
review. Journal of Small Animal Practice 1987; 28(10): 929±940.
11 Melian C, Morales M, Espinosa de los Monteros A, Peterson ME.
Horner's syndrome associated with a functional thyroid carcinoma
in a dog. Journal of Small Animal Practice 1996; 37(12): 591±593.
12 Bistner S, Rubin L, Cox TA, Condon WE. Pharmacologic diagnosis
of Horner's syndrome in the dog. Journal of the American Veterinary
Medical Association 1970; 157(9): 1220±1224.
13 Maloney WF, Younge BR, Moyer NJ. Evaluation of the causes and
accuracy of pharmacologic localization in Horner's syndrome.
American Journal of Ophthalmology 1980; 90(3): 394±402.
14 Skarf B, Czarnecki JS. Distinguishing postganglionic from preganglionic lesions. Studies in rabbits with surgically produced Horner's
syndrome. Archives of Ophthalmology 1982; 100(8): 1319±1322.
15 Kay WJ. Neuro-ophthalmology. In: Veterinary Ophthalmology, 1st
edn. (ed. Gelatt KN) Lea & Febiger: Philadelphia, 1981; 672±698.
# American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 1, 17±20