Photo Essay
Section Editor: Timothy J. McCulley, MD
Horner Syndrome as the Only Focal Neurologic
Manifestation of Hypothalamic Hemorrhage
Cansu B. Sahin, MD, Neeraj Chaudhary, MD, Jonathan D. Trobe, MD
Downloaded from https://journals.lww.com/jneuro-ophthalmology by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3tjcLwhL8g9bZhhig7WeJvju8zbSeqjpGv/JBZKH85NhsMNnPdAwmaw== on 07/23/2019
FIG. 1. Coronal (A) and axial (B) precontrast CT, and axial fluid-attenuated inversion recovery MRI (C) performed on the day of
the fall shows hemorrhage in the right anterior hypothalamus with blood products in the third ventricle.
Abstract: A 70-year-old woman suffered an anterior dorsal
hypothalamic hemorrhage that caused an ipsilateral Horner
syndrome (HS) as the only focal neurologic manifestation. This
is only the second reported case of hypothalamic hemorrhage
producing HS. Because HS was the sole focal neurologic
manifestation, its confirmation with topical apraclonidine drops
was a valuable clue toward prompt localization of the patient’s
confusional state.
Journal of Neuro-Ophthalmology 2018;38:192–194
doi: 10.1097/WNO.0000000000000604
© 2017 by North American Neuro-Ophthalmology Society
A 70-year-old woman seemed confused to her husband
and fell in the bathroom minutes later. Several weeks
earlier, she had been diagnosed with a herpes zoster menin-
goencephalitis and treated with intravenous acyclovir with
nearly complete recovery of mental status.
Departments of Ophthalmology, Neurology, and Radiology
(Neuroradiology), Kellogg Eye Center, University of Michigan, Ann
Arbor, Michigan.
The authors report no conflicts of interest.
Address correspondence to Jonathan D. Trobe, MD, University of
Michigan, Ann Arbor, MI; E-mail: jdtrobe@umich.edu
192
Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.
Brain CT and MRI performed on the day of the fall
revealed an acute intracranial hemorrhage centered in the right
anterior hypothalamus with extension into the third ventricle
(Fig. 1). Head and neck CT angiography was negative. The
hemorrhage was attributed to to an underlying developmental
venous anomaly identified on a brain MRI performed 1
month earlier (Fig. 2).
The patient had been examined by an otolaryngologist
for dizziness 3 days previously without any mention of
ptosis or anisocoria. The patient’s husband had noted right
upper lid ptosis for the first time on the day of
presentation.
Twenty-four hours after the fall, the patient was
confused and slightly somnolent with anisocoria and mild
right upper lid ptosis. In darkness, pupils measured 2.5 mm
in the right eye and 4 mm in the left eye, both constricting
briskly and equally to the direct light of a flashlight held at
about 1 foot from the eyes. All other aspects of the
ophthalmic and neurologic examinations were normal.
Thirty minutes after topical instillation of 2 drops of
apraclonidine 0.5% in each eye, the right pupil measured
5.5 mm and the left pupil still measured 4 mm in
darkness. Apraclonidine also elevated the right upper lid.
It had no effect on the lid position of the left eye.
Sahin et al: J Neuro-Ophthalmol 2018; 38: 192-194

FIG. 2. Axial fluid-attenuated inversion recovery MRI performed 1 month prior to the patient’s presentation with Horner
syndrome caused by thalamic hemorrhage. It shows an anterior thalamic developmental venous anomaly without hem-
orrhage.
This is the second reported case of reversal of
anisocoria after topical instillation of apraclonidine in
a patient with a Horner syndrome (HS) caused by
a hypothalamic hemorrhage. Kauh and Bursztyn (1) re-
ported a patient with HS from a thalamic hemorrhage
that was confirmed by a positive topical apraclonidine
0.5% test performed 96 hours after symptoms developed.
Our case had a positive apraclonidine test within 24 hours
after symptom onset. Until this report, the shortest re-
ported latency between symptom onset in a first-order
(brainstem) HS and a positive apraclonidine test was 3
days. It involved a patient with a dorsolateral pontome-
dullary infarction (2).
We acknowledge that we cannot be certain about the
latency from the onset of the HS to the positive
apraclonidine test. However, we assume that the thalamic
hemorrhage which caused the HS occurred at about the
time of the patient’s fall, which was when her husband
noted right ptosis.
The thalamic hemorrhage in our patient was located
dorsally and anteriorly in the hypothalamus, correspond-
ing to the anatomic location of the paraventricular
nucleus, which controls sympathetic function (3).
Although HS in thalamic hemorrhage has not been fre-
quently described, HS with hypothalamic infarction has
been well documented (4–8). In none of the reported
cases was pharmacologic confirmation of HS provided.
In those reported cases, the infarction also involved the
Sahin et al: J Neuro-Ophthalmol 2018; 38: 192-194
Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.
Photo Essay
overlying thalamus and extended ventrally to damage the
paraventricular nucleus. Infarction was likely caused by
occlusion of a proximal branch of the posterior cerebral
artery.
In previously reported cases of HS in hypothalamic
infarction, the HS has never been the only (or even the
most prominent) neurologic abnormality, usually over-
shadowed by lowered consciousness, ataxia, weakness, or
aphasia. Our case, which was hemorrhagic rather than
infarctive, is distinctive because HS, confirmed with
topical apraclonidine drops, stood out as the only focal
abnormality in a patient with a mild confusional and
somnolent state.
STATEMENT OF AUTHORSHIP
Category 1: a. Conception and design: C. B. Sahin, N. Chaudhary,
and J. D. Trobe; b. Acquisition of data: C. B. Sahin, N. Chaudhary,
and J. D. Trobe; and c. Analysis and interpretation of data: C. B.
Sahin, N. Chaudhary, and J. D. Trobe. Category 2: a. Drafting the
manuscript: C. B. Sahin, N. Chaudhary, and J. D. Trobe and b.
Revising it for intellectual content: J. D. Trobe. Category 3: a. Final
approval of the completed manuscript: C. B. Sahin, N. Chaudhary,
and J. D. Trobe.
REFERENCES
1. Kauh CY, Bursztyn L. Positive apraclonidine test in Horner
syndrome caused by thalamic hemorrhage. J Neuroophthalmol.
2015;35:287–288.
193
 Photo Essay
2. Lebas M, Seror J, Debrouker T. Positive apraclonidine test
36 hours after acute onset of Horner syndrome in
dorsolateral pontomedullary stroke. J Neuroophthalmol.
2010;30:12–17.
3. Martin JH. The Hypothalamus and Regulation of Bodily
Functions. Neuroanatomy Text Book and Atlas. 4th edition. New
York, NY: McGraw-Hill, 2012:365.
4. Rossetti AO, Reichhart MD, Bogousslavsky J. Central
Horner’s syndrome with contralateral ataxic hemiparesis:
a diencephalic alternate syndrome. Neurology.
2003;61:334–338.
194
Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.
5. Stone WM, de Toledo J, Romanul FC. Horner’s syndrome due to
hypothalamic infarction. Arch Neurol. 1986;43:199–200.
6. Gieraerts K, Casselman L, Casselman J, Vanhooren G.
Tuberothalamic infarction causing a central Horner syndrome
with contralateral ataxia and paraphasia. Acta Neurol Belg.
2015;115:727–729.
7. Austin CP, Lessell S. Horner’s syndrome from hypothalamic
infarction. Arch Neurol. 1991;48:332–334.
8. Faust-Socher A, Greenberg G, Inzelberg R. Thalamic-
hypothalamic infarction presenting as first-order Horner
syndrome. J Neurol. 2013;260:1673–1674.
Sahin et al: J Neuro-Ophthalmol 2018; 38: 192-194