REVIEW ARTICLE
Horner Syndrome: A Practical Approach to
Investigation and Management
Zoe Gao, MBBS* and John L. Crompton, MBBS, FRANZCO, FRACS*
Abstract: Horner syndrome is typically described by the classic triad
of blepharoptosis, miosis, and anhydrosis resulting from disruption along
the oculosympathetic pathway. Because of the complex and extensive
course of this pathway, there are a large number of causes of Horner
syndrome ranging from benign to life-threatening diseases. This review
article aims to provide a practical approach to investigation and man-
agement, including evaluation of the more recent use of apraclonidine
for pharmacological testing.
Key Words: Horner syndrome, oculosympathetic pathway
(Asia-Pac J Ophthalmol 2012;1: 175Y179)
H orner syndrome is caused by disruption at some point along
the oculosympathethic pathway from the hypothalamus to
the eye, resulting in the clinical features of miosis, ptosis, and
anhydrosis.
It was rst described by Francois Pourfour du Petit1 in 1727
when he noted changes in the eyes and snout of dogs after
cutting the intercostal nerves in their necks. In 1852, Claude
Bernard,2 a French physiologist, described the syndrome in more
detail (and hence it is known as Bernard-Horner syndrome in
France), and in 1864, 3 American army physicians Silas Weir
Mitchell, William Keen, Jr, and George Read Morehouse pub-
lished a clinical report of the syndrome in a man shot through
the throat.3 However, it was only in 1869 that the Swiss oph-
thalmologist Johann Friedrich Horner described the classic triad
of ndings, and the syndrome subsequently bore his name.4
Because the oculosympathetic pathway has a long course,
there is the potential for involvement by many different dis-
ease processes. However, given that some are potentially life-
threatening such as internal carotid dissection and malignancies,
it is important to have a systematic approach to diagnosis and
management. This review discusses the important anatomic fea-
tures, clinical features, and investigations that should be ordered,
as well as experience from our center over the last 30 years.
CLINICAL ANATOMY
The oculosympathetic pathway consists of 3 orders of
neurons. The rst-order neuron, which if affected would result in
a central Horner syndrome, originates in the posterior lateral
aspect of the hypothalamus and descends uncrossed down the
brainstem and terminates in the ciliospinal center of Budge-
Waller. This spans the intermediolateral horn of the spinal cord
from C8 to T2.5,6
From the *South Australian Institute of Ophthalmology, Adelaide, c/o Royal
Adelaide Hospital; and Discipline of Ophthalmology & Visual Sci-
ences, University of Adelaide, North Terrace, South Australia, Australia.
Received for publication February 4, 2012; accepted March 16, 2012.
The authors have no funding or conicts of interest to declare.
Informed consent was obtained from all patients for use of images in this review.
Reprints: Zoe Gao, MBBS, Royal Victorian Eye and Ear Hospital,
32 Gisborne St, E Melbourne, Victoria 3002, Australia.
E-mail: zoegao@gmail.com.
Copyright * 2012 by Asia Pacific Academy of Ophthalmology
ISSN: 2162-0989
DOI: 10.1097/APO.0b013e318256009d
Asia-Pacific Journal of Ophthalmology & Volume 1, Number 3, May/June 2012
Copyright 2012 by Asia Pacific Academy of Ophthalmology. Unauthorized reproduction of this article is prohibited.
The second-order or preganglionic neuron leaves the
ciliospinal center of Budge-Waller via the ventral spinal roots of
C8-T2 and passes through the inferior and middle cervical
ganglia before synapsing at the superior cervical ganglion in the
neck. During its course, it is closely related to the apical pleura
and can therefore be damaged by lung cancer (Pancoast tumor:
Figure, Supplementary Digital Content 1; http://links.lww.com/
APJO/A12 and http://links.lww.com/APJO/A13). The superior
cervical ganglion is located at the level of C2-C3 posterior to
the carotid sheath at the level of the angle of the mandible. The
sympathetic sudomotor and vasoconstrictor bers to the face
leave prior to the superior cervical ganglion at the bifurcation of
the common carotid artery into the internal and external carotid
arteries. Therefore, a postganglionic lesion will not be associated
with signicant anhydrosis.5,6
The postganglionic neuron ascends along the internal ca-
rotid artery as a plexus before dividing into a medial and lateral
branch. The medial branch enters the cavernous sinus and joins
the oculomotor nerve before innervating Muller muscle in the
upper and lower lids. The lateral branch joins the abducens nerve
briey and then the ophthalmic division of the trigeminal nerve,
before reaching the dilator pupillae of the iris via the nasociliary
nerve and long ciliary nerves.5Y7
Given the long course of the oculosympathetic pathway, it
is not surprising that the causes of Horner syndrome are diverse,
and it may not be easy to determine the etiology (Table 1).
CLINICAL SIGNS
Horner syndrome results in miosis and mild ptosis as a
result of unopposed action of the sphincter pupillae and weak-
ness of Muller muscle, respectively. These 2 signs are the most
constant ndings in Horner syndrome. The anisocoria is accen-
tuated in dim light, and there is a dilation lag where the affected
pupil dilates slower compared with the healthy pupil because of
lack of pull from the dilator muscle.8
In addition, apparent enophthalmos due to ptosis (eleva-
tion) of the lower lid may be present. If the lesion is congenital
or longstanding, there may be hypochromic heterochromia of
the iris (Fig. 1). This sign is not, however, useful in the perinatal
period because iris color is not established until several months
of age (Supplementary Digital Content 2; http://links.lww.com/
APJO/A14). Anhydrosis is not always present and although
helpful is rarely elicited.7 Harlequin sign refers to unilateral
facial ushing that can occur in congenital Horner syndrome.
The areas that do not ush correspond with anhydrotic areas.
There is also a decrease in the skin temperature on the affected
side. These ndings are the result of impaired sympathetic
vasodilatation.9
Conjunctival hyperemia may be present as an early tran-
sient sign in response to loss of sympathetic innervation to the
conjunctival vessels resulting in vasodilation. This sign is rarely
present for more than a few weeks.5
Rarely, Horner syndrome may alternate between the 2 sides.
We have observed 2 such cases in quadriplegics with secondary
syringobulbia (Fig. 2). Both of these patients developed miosis in
the dependent eye, when changed from lying from one side to the
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Gao and Crompton Asia-Pacific Journal of Ophthalmology & Volume 1, Number 3, May/June 2012

TABLE 1. Breakdown of Causes of Horner Syndrome

Based on Anatomic Location

Anatomic Site Etiologies

Central Hypothalamus
Stroke
Tumor
Brainstem disease
StrokeVPICA/vertebral artery
) Lateral medullary syndrome
Demyelination
Tumor
Syringomyelia FIGURE 1. Congenital right Horner syndrome from right
Cervical/thoracic myelitis brachial plexus birth trauma. Her right iris never developed
Spinal cord tumor pigmentation.
Diabetic autonomic neuropathy
swallowing difculties, or unilateral facial numbness. The cau-
AVM ses of a preganglionic Horner are often trauma (Fig. 3) or iat-
Preganglionic Tumor rogenic (Fig. 4), which should be elicited from a thorough
Thyroid/mediastinal history.11Y13 Postganglionic Horner syndrome may have local-
Neuroblastoma izing signs such as involvement of other cranial nerves secondary
Sympathetic schwannoma to cavernous sinus pathology. For example, cavernous sinus
Pancoast masses from metastases, pituitary tumor invasion, or aneurysms
Trauma, including birth trauma can cause Horner syndrome and isolated abducens nerve palsy.
Brachial plexus injury A Horner syndrome associated with pain in the face and neckV
Postsurgical/iatrogenic Raeder paratrigeminal syndromeVcan be associated with the
serious diagnosis of a carotid artery dissection. Although there
Sympathectomy for peripheral vascular
disease, hyperhydrosis are other more benign causes such as cluster headache, Raeder
syndrome should alert the clinician toward requiring further
Surgery for thyroid and parathyroid disease
investigations.11 Enquiries should be made about any recent neck
Carotid and aortic/subclavian aneurysm manipulation or activity resulting in prolonged neck extension
and dissection
and rotation. Clinical cases have been noted following chiro-
Cervical rib practic treatment, prolonged insertion of ceiling tiles, a novice
Osteophytes windsurng, and so on.
Postganglionic Postsurgical/iatrogenic
Trauma
Cluster/migraine headaches INVESTIGATIONS
Internal carotid artery dissection/aneurysm Traditionally, conrmation of Horner syndrome was per-
Jugular venous ectasia formed using topical cocaine 4% or 10% and hydroxyampheta-
Fibromuscular dysplasia mine 1% localization. Recently, the use of apraclonidine 1% has
Skull base lesions
been advocated as a viable alternative to cocaine largely because
of the difculty in accessing cocaine legally. Hydroxyamphetamine
Nasopharyngeal tumor
has also become unavailable commercially. Neuroimaging has
Otitis media largely overtaken pharmacological testing for investigating the site
Cavernous sinus mass/inflammation/infection of lesion causing Horner syndrome.14
Internal carotid arteritis
Those in bold type are the more common causes. Pharmacological
AVM indicates arteriovenous malformation; PICA, posterior inferior In an eye unaffected by Horner syndrome, noradrenaline
cerebellar artery. is normally released and reuptaken at postganglionic sympa-
thetic nerve endings. This is blocked by cocaine. Therefore, in a
normal eye, noradrenaline accumulates and results in prolonged
dilatation. In a Horner syndrome pupil, there is no noradrenaline
other, thought to be due to pressure of the cerebrospinal uid in
the syrinx on the sympathetic bers running down the midbrain.
Although the above signs describe Horner syndrome, in
clinical practice, it is other features on history and examination
that will guide further investigation and management. This is
highlighted below with photographs of some clinical cases the
author (J.L.C.) has been involved with. A central Horner syn-
drome is unlikely to be in isolation because of the close prox-
imity of other structures within the hypothalamus, brainstem,
and spinal cord10 (Supplementary Digital Content 3; http://
links.lww.com/APJO/A15). Patients may present with vertigo, FIGURE 2. Alternating Horner syndrome in a quadriplegicVlying
ataxia, contralateral loss of pain and temperature sensation, on left side, lying on right side.

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Asia-Pacific Journal of Ophthalmology & Volume 1, Number 3, May/June 2012
released, and therefore, the cocaine has no effect15 (Fig. 3).
Evaluation of cocaine has shown that 0.8 mm of anisocoria after
instillation of cocaine 10% makes Horner syndrome highly
likely with a mean odds ratio of 1050:1.16
Hydroxyamphetamine potentiates the release of noradren-
aline from postganglionic nerve endings resulting in pupil di-
latation. In a postganglionic lesion, the neuron is destroyed, and
there is no noradrenaline to be released, and hence, the Horner
pupil will not dilate. In a preganglionic lesion, both pupils
will dilate as noradrenaline is still present in the unaffected
postganglionic neuron.17 Hydroxyamphetamine must be in-
stilled 72 hours after the cocaine test because cocaine blocks
the effectiveness of hydroxyamphetamine.7 It takes 1 week for
the noradrenaline stores to be depleted, and so instilling hydro-
xyamphetamine within 1 week of the onset of Horner syndrome
may result in spurious results.18 These potential limitations mean
that, in an acute setting, the use of pharmacological testing to
localize a Horner lesion may not be practical, and hence, neu-
roimaging may be more appropriate.
Adrenaline 1:1000 or phenylephrine 1% has also been
used to localize a Horner pupil. One percent phenylephrine
has been found to be comparable to hydroxyamphetamine in terms
of sensitivity and specicity and is readily available in most
ophthalmic practices.19 The dilator pupillae muscle develops
denervation hypersensitivity when it is deprived of its motor
supply. Therefore, it will display heightened sensitivity to any
adrenergic neurotransmitter. In a preganglionic lesion, this does
not occur because the postganglionic neuron is intact, and
so neither pupil will dilate (Supplementary Digital Content 4;
http://links.lww.com/APJO/A16). The adrenaline is rapidly de-
stroyed by monoamine oxidase produced by the postganglionic
neuron. In a postganglionic lesion, however, the Horner pupil will
dilate because of the absence of monoamine oxidase. The ptosis
may also improve. This explains why Horner syndrome can im-
prove with stress and the release of endogenous catecholamines.19
Apraclonidine 1% has recently been described as an alter-
native to cocaine for the diagnosis of Horner syndrome. It was
rst described by Morales et al20 in 2000. Apraclonidine is
primarily an >2 agonist acting on the ciliary body to decrease
aqueous production. However, it also exhibits weak >1 activity
causing pupil dilation. It is proposed to work because of de-
nervation hypersensitivity and upregulation in the number of
>1 receptors in a Horner pupil, which results in dilation with
instillation compared with no change or even constriction in
the unaffected eye.20 However, it is not clear at what point after
the onset of the Horner syndrome that this hypersensitivity
FIGURE 3. Right traumatic Horner syndrome from brachial plexus
injury after a motorbike accident. Note that only the normal left
pupil dilated on instillation of cocaine 10% drops.
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Horner Syndrome
FIGURE 4. Bilateral iatrogenic Horner syndrome after bilateral
surgical sympathectomies for peripheral vascular disease.
occurs. The majority of case series that have shown success with
apraclonidine have tested patients at least 1 month after the
onset of symptoms, and although they have shown favorable
results, the series of patients were small.21Y24 Other case reports
have shown mixed results, with 1 patient having a positive apra-
clonidine test only 36 hours after a dorsolateral pontomedullary
stroke25 and yet another with a negative apraclonidine test
16 days after an internal carotid artery dissection.26 There has
also been concern due to recent reports of serious idiosyncratic
adverse effects of apraclonidine, especially in children younger
than 6 months. Adverse effects include excessive drowsiness,
bradycardia, hypertension, and decreased oxygen saturations.27
Its use in children is therefore contraindicated. These prelimi-
nary results suggest that cocaine 10% for conrmation of Horner
syndrome is still the criterion standard. However, given the
difculty in its access, it would be reasonable to use apracloni-
dine as an alternative in adults, keeping in mind that, early in
the disease process, denervation hypersensitivity may not have
occurred, leading to false negatives.
Neuroimaging
Although neuroimaging can be extremely useful in helping
to determine the etiology of Horner syndrome, it is very im-
portant that the imaging is targeted. It would be expensive and
time consuming to try and image the entire oculosympathetic
pathway. This again highlights the need and importance of
taking an adequate history and examination to help determine
the site of the suspected lesion along the pathway.
If suspecting a central lesion, magnetic resonance imaging
(MRI) T magnetic resonance angiography (MRA) is the imaging
of choice that avoids the beam hardening artifact of computed
tomography (CT) and allows clear resolution of the hypothala-
mus and midbrain structures. Diffusion-weighted imaging can
also be useful in diagnosing stroke.11 In a preganglionic Horner
syndrome, if a lung, anterior neck, or mediastinal mass is sus-
pected on history, a contrast-enhanced CT is the imaging of
choice. If there are brachial plexus or cervical/upper thoracic
neurological symptoms or signs, an MRI should be consid-
ered.11 Magnetic resonance angiography or CT angiography
(CTA) has largely superseded traditional angiography and is
appropriate if suspecting a carotid artery dissection.10,11 Given
the urgency of this diagnosis, it is often practically easier to
obtain a CTA. In infants, where there is no reasonable expla-
nation for Horner syndrome on history such as birth trauma,
the current recommendation for investigation is urine catechol-
amine testing and MRI of the brain, neck, and chest looking
for neuroblastoma.28
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Gao and Crompton Asia-Pacific Journal of Ophthalmology & Volume 1, Number 3, May/June 2012

TABLE 2. Breakdown of Site of Lesion in Horner Syndrome TABLE 4. Neuroimaging Approach

Case Series
Central MRI T MRA
n Stroke Diffusion-weighted imaging
Site of lesionVpharmacologically tested Preganglionic
Central 2 Neck/mediastinal/lung pathology Contrast-enhanced CT
Preganglionic 3 Brachial plexus/spinal cord MRI
Postganglionic 11 Postganglionic
Site of lesionVpresumed based on history/examination Carotid dissection MRA or CTA
Central 20 Infants MRI + urine catecholamines
Preganglionic 17
Postganglionic 12 drome, which differs from other case series, which have shown
Unknown 12 a much lower prevalence of central Horner syndrome.12,13 Per-
Total 77 haps this reects the tertiary nature of the referral pattern in our
series from a major neurosciences and trauma hospital.
Table 3 shows the breakdown of etiologies in our case
A recent review of 52 patients referred for neuro- series. Vascular causes accounted for 18 cases with an equal
ophthalmology evaluation of Horner syndrome by Almog et al29 number of stroke and carotid dissections. There were 13 cases
found that, in two thirds of patients, the cause of Horner syn- of trauma in adults and 2 in childrenVboth birth trauma. There
drome will already be known at the time of the rst consulta- were 6 cases of surgical/iatrogenic Horner syndromeVthese
tion. These etiologies consisted of surgery or trauma to the neck, cases being as a result of intervention in the anterior neck. There
head, or chest; dorsolateral medullary stroke; or carotid dissec- were 7 tumors, 6 cases of migraine/cluster headache, and the
tion. Of the remaining third of patients, one half of these will miscellaneous cases of syringobulbia and multiple sclerosis.
have clinical clues that will allow localization of the lesion, Twenty-two patients had an unknown etiology for Horner syn-
and in these patients, targeted imaging will usually nd the le- drome after investigation, which is a similar percentage to other
sion. In the rest of the patients, nontargeted imaging will rarely studies.12,13,29
nd a responsible lesion. However, it is still necessary because The majority of the patients did not require any further
life-threatening lesions such as malignancy can be detected. intervention or follow-up once diagnosis was established. There
This highlights that although all of the above investigations were a few patients who underwent ptosis surgery, but the ma-
are at a clinicians disposal, not all are necessary or appropriate jority of patients were not troubled by the anisocoria.
for each patient. With a thorough history and examination, it
may be possible to avoid any investigations in up to two thirds CONCLUSIONS
of patients and only targeted investigations for one sixth. Our approach to a patient presenting with suspected Horner
syndrome would be to rst take a thorough history and exami-
nation looking for associated symptoms or signs that will help
CASE SERIES localize the site of a lesion. The presence of Horner syndrome
From 1979 to 2010, one of the authors (J.L.C.) has seen should be conrmed through the clinical features described but
more than 70 patients with Horner syndrome. A retrospective also with topical cocaine 10% if possible, as this still remains the
review of the case notes of these patients was performed. A total criterion standard. Given the concerns with safety, apraclonidine
of 77 patients were identied with Horner syndrome. Fifty-three is not recommended in young children and/or infants. If cocaine
of these patients had cocaine testing, which conrmed the di- is not available, apraclonidine is a reasonable alternative in
agnosis. The remainder were diagnosed based on clinical history adults. However, one should be aware that there may be false
and examination. Sixteen of the patients underwent pharmaco- negatives early in the disease process.
logical testing with either hydroxyamphetamine or phenyleph- If there is enough information on history and examination
rine to localize the lesion. Table 2 shows the breakdown of this to explain the diagnosis, no further investigations are required.
testing. In the majority of patients, history and examination alone However, if a diagnosis cannot be made although there are lo-
were enough to localize the lesion. There was an even distribution calizing signs, targeted imaging as outlined in Table 4 should
between central, preganglionic, and postganglionic Horner syn- be performed. The timing of imaging will depend on the sus-
pected diagnosis. For example, carotid artery dissection is an
urgent diagnosis to be excluded, and a suspected Pancoast tumor
TABLE 3. Breakdown of Etiology in Horner Syndrome Case is also relatively urgent.
Series Finally, if there are no clues as to making a diagnosis,
topical phenylephrine may be useful in differentiating postgan-
Cause N glionic lesions, although patients often end up requiring non-
Trauma 15 selective imaging from the upper chest to the brain. Although
Surgery/iatrogenic 6 this has a low yield, it can rarely detect life-threatening lesions
Vascular 18 and so is still worthwhile. Given the limited availability of
Tumor 7 hydroxyamphetamine, phenylephrine is preferred.
Migraine/cluster headache 6
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