FIGURE 1. Case 1. Hess charts 1 month after cardiac catheterization show vertical deviation, a left hypertropia.

phy and MRI. Diplopia continued for 10 months, and the
patient was referred to our clinic. Examination showed
skew deviation with a 12-prism diopter left hypertropia.
Diplopia disappeared within another 6 months.
● CASE 3: In June 1996, a 72-year-old woman had cardiac
catheterization to check for aortic dissection. She experienced diplopia right after the procedure and came to our
clinic 3 days later. A neuro-ophthalmologic examination
disclosed internal ophthalmoplegia on the right side with
accompanying skew deviation; a 6-prism diopter right hypertropia. No lesion was seen in the brain stem on the neuroimages. Her ocular disorders were resolved in 1.5 months.
The major complications of cardiac catheterization are
death, myocardial infarction, and cerebral stroke, which
occur in only 0.1% to 0.3% of patients.4 Ocular complications after cardiac catheterization are rare, with patients
having been reported with retinal artery occlusion,1 glaucoma,2 and cortical blindness3 associated with cardiac
catheterization.
Skew deviation comprises a group of ocular movement
disorders caused by the disturbance of prenuclear inputs,5
which caused vertical misalignment. Skew deviation has
been reported in association with a variety of lesions in the
vestibular organ or its nerve, brain stem, or cerebellum.
Ischemia of the medial longitudinal fasciculus at the brain
stem may result in unilateral internuclear ophthalmoplegia
with skew deviation, usually ipsilateral hypertropia. Transient skew deviation may occur in patients with basilar
artery insufficiency. Patients with skew deviation usually
recover well, except when the disorder is caused by head
injury.

VOL. 132, NO. 2

All three patients reported here complained of diplopia
immediately after cardiac catheterization. Ocular movement disorders had characteristics of skew deviation and
recovered spontaneously. The patients had high-risk backgrounds for vascular damage, and microvascular ischemia
might have occurred in the brain stem. Neuroimaging,
however, detected no lesions.
REFERENCES

1. Loewenstein A, Goldstein M, Roth A, Lazar M. Cilioretinal
artery occlusion during coronary catheterization. Acta Ophthalmol Scand 1999;77:717–718.
2. Mandak JS, Minerva P, Wilson TW, Smith EK. Angle closure
glaucoma complicating systemic atropine use in the cardiac
catheterization laboratory: a rare but reversible complication.
Cathet Cardiovasc Diagn 1996;39:262–264.
3. Kinn RM, Breisblatt WM. Cortical blindness after coronary
angiography. Cathet Cardiovasc Diagn 1991;22:177–179.
4. Baim DS, Grossman, W. Complications of cardiac catheterization. In: Bain DS, Grossman W, editors. Cardiac catheterization, angiography, and intervention, 5th ed. Baltimore:
Williams and Wilkins, 1996:17–38.
5. Leigh RJ, Zee DS. Skew deviation and the ocular tilt reaction
(OTR). The neurology of eye movements, 3th ed. New York:
Oxford University Press, 1999:463– 465.

Optic Tract Compression from
Dolichoectatic Basilar Artery
Medhat F. Guirgis, MD, Byron L. Lam, MD, and
Steven F. Falcone, MD

BRIEF REPORTS

283

PURPOSE: To report a case of optic tract compression

caused by a dolichoectatic basilar artery
DESIGN: Observational case report.
METHODS: A 74-year-old man with progressive loss of
vision over 13 years and no other neurologic signs or
symptoms was found to have bilateral optic nerve head
pallor and a left homonymous hemianopia.
RESULTS: Magnetic resonance imaging and angiography
revealed a severe dolichoectatic basilar artery compressing the right optic tract.
CONCLUSION: Basilar artery dolichoectasia may rarely
cause compression of the optic tract and progressive
visual loss. (Am J Ophthalmol 2001;132:283–286.
© 2001 by Elsevier Science Inc. All rights reserved.)

F

USIFORM BASILAR ARTERY ANEURYSMS OR DOLICHOEC-

tatic basilar arteries most often cause compression of
the facial and trigeminal nerves, resulting in hemifacial
spasm and trigeminal neuralgia, respectively.1 Ocular motility disorders are also not uncommon when compression
of the oculomotor nerve or abducens nerve occurs.1,2
However, visual pathway compression from basilar artery
aneurysm is extremely rare, with few reported cases of
chiasmal compression producing a bitemporal hemianopia.3 We report a patient with a homonymous hemianopia caused by dolichoectatic basilar artery compression
of the optic tract.
A healthy 74-year-old man was evaluated in May 2000
for gradual, painless progressive loss of vision over the past
Accepted for publication Jan 5, 2001.
From the Bascom Palmer Eye Institute, Miami, Florida (M.F.G.,
B.L.L.), and the Department of Radiology, University of Miami, Miami,
Florida (S.F.F.).
Inquiries to Byron L. Lam, MD, Bascom Palmer Eye Institute, 900 NW
17th St, Miami, FL 33136; fax: (305) 326-6474.

13 years. The patient had no systemic disease and had
uneventful bilateral cataract extraction with intraocular
lens implantation in 1996. He had no history of malnutrition, smoking, excessive alcohol intake, or toxic exposure.
Best-corrected visual acuity was RE: 20/70 and LE: 20/40,
with no relative afferent pupillary defect. On Ishihara
color plate testing, the patient identified RE: 9 out of 15
plates and LE: 8 out of 15 plates, and on Hardy–Rand–
Rittler pseudoisochromatic color plate testing, he identified only the control plate for each eye. Goldmann
perimetry revealed a dense, left homonymous hemianopia
with constriction of the remaining right hemifields (Figure 1). Extraocular movements, ocular alignment, and
the rest of the cranial nerve examination were all
normal. Both optic nerve heads had marked diffuse
pallor. Magnetic resonance imaging and angiography
showed a dolichoectatic basilar artery compressing and
displacing the right optic tract and adjacent brain tissue
(Figure 2).
Homonymous hemianopia is rarely caused by aneurysmal compression of the optic tract. Savino and associates
reviewed 21 patients with optic tract syndrome and found
aneurysm as the origin in only 14% of the cases, with
suprasellar neoplasms as the predominant cause (71%).4 Of
the rare reports in which direct aneurysmal impingement
of the optic tract was evident, an artery of the circle of
Willis has nearly always been implicated.5 However, our
patient demonstrates that severe basilar artery dolichoectasia may rarely cause compression of the optic tract,
resulting in homonymous hemianopia and optic atrophy.
The dramatic superior displacement of the right optic tract
was easily identifiable by magnetic resonance imaging and
angiography. This optic tract displacement also produced

FIGURE 1. Goldmann visual fields of (right) right eye and (left) left eye show a left homonymous hemianopia. The remaining right
hemifields are constricted and depressed.

284

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AUGUST 2001

FIGURE 2. Magnetic resonance imaging and arteriogram. (Top left) Maximum intensity projection coronal angiogram from axial
acquired three-dimensional time-of-flight angiogram shows the basilar artery in an “S” configuration ascending from left to right.
Note the superiorly displaced ectatic basilar artery tip and the right posterior cerebral artery (white arrow). (Top right) Source image
from three-dimensional time-of-flight angiogram (TR ⴝ 28, TE ⴝ 6.7, NEX ⴝ 1, slice thickness ⴝ 1 mm) shows the basilar tip
(asterisk) well to the right of midline and posterior to the optic tract. A portion of the right optic tract (hollow white arrow) is
thinned and displaced anteriorly. (Bottom left) T1-weighted fat saturation axial image at the level of the optic tracts (TR ⴝ 665,
TE ⴝ 16, NEX ⴝ 2, slice thickness ⴝ 3 mm) reveals a normal appearing left optic tract (white arrow). The right optic tract is not
visualized because it is thinned and displaced superiorly. (Bottom right) T1-weighted coronal image at the level of the mid-optic
tracts (TR ⴝ 634, TE ⴝ 16, NEX ⴝ 2, slice thickness ⴝ 3 mm) shows normal left optic tract (white curved arrow) and the ectatic
basilar artery (white arrowhead) that causes cephalad displacement of the adjacent brain and the right optic tract.

secondary distortion of the optic chiasm, which contributed to the optic atrophy and the decrease in visual acuity.
Of interest, our patient had no other neurologic signs or
VOL. 132, NO. 2

symptoms despite a basilar fusiform aneurysm of such
magnitude. Unfortunately, the condition of the patient is
not treatable, and the prognosis is uncertain.

BRIEF REPORTS

285

REFERENCES

1. Smoker WRK, Corbett JJ, Gentry LR, et al. High-resolution
computed tomography of the basilar artery: 2. Vertebrobasilar
dolichoectasia: clinical-pathologic correlation and review.
AJNR 1986;7:61–72.
2. Kasner SE, Liu GT, Galetta SL. Neuro-ophthalmologic aspects of aneurysms. Neuroimag Clin N Am 1997;7:679 – 692.
3. Rush JA, Balis GA, Drake CG. Bitemporal hemianopia in
basilar artery aneurysm. J Clin Neuro-ophthalmol 1981;1:
129 –133.
4. Savino PJ, Paris M, Schatz NJ, Orr LS, Corbett JJ. Optic tract
syndrome: a review of 21 patients. Arch Ophthalmol 1978;
96:656 – 663.
5. Versavel M, Witmer JP, Matricali B. Giant aneurysm
arising from the anterior cerebral artery and causing an
isolated homonymous hemianopia. Neurosurgery 1988;22:
560 –563.

Acute Asymmetric Upper Nasal
Quandrantanopsia Caused by a
Chiasmal Colloid Cyst in a Patient
with Multiple Sclerosis and Bilateral
Retrobulbar Neuritis
Hanspeter E. Killer, MD, Josef Flammer, MD,
Barbara Wicki, MD, and Rudolf H. Laeng, MD
PURPOSE: To report a patient with multiple sclerosis and

a history of sequential bilateral retrobulbar neuritis, who
developed new onset of highly asymmetric upper quadrantanopsia.
DESIGN: Interventional case report.
METHOD: A 36-year-old woman with multiple sclerosis
and bilateral retrobulbar neuritis developed an acute
asymmetric upper nasal quadrantanopsia.
RESULTS: Magnetic resonance imaging of the brain revealed a cyst that caused chiasmal compression and
bilateral visual field defects.
CONCLUSION: New onset of bilateral visual field defects
in a patient with diagnosed multiple sclerosis is likely to
be caused by a new attack of the demyelinating disease.
In this case, a newly diagnosed chiasmal colloid cyst was
the cause of visual field defects. (Am J Ophthalmol
2001;132:286 –288. © 2001 by Elsevier Science Inc.
All rights reserved.)

Accepted for publication Feb 13, 2001.
From the Department of Ophthalmology (H.E.K., B.W) and the
Department of Pathology (R.H.L.), Kantonsspital Aarau, Aarau, Switzerland, and the Department of Ophthalmology, School of Medicine,
University of Basel, Basel, Switzerland (J.F).
Presented at the North American Neuro-Ophthalmology Society
Meeing March 26 –30, 2000, Mont Tremblant, Quebec, Canada.
Inquiries to Hanspeter E. Killer, Augenklinik, Kantonsspital Aarau,
5000 Aarau, Switzerland; fax: 062-838-44-26; e-mail: killer@ksa.ch

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ETROBULBAR NEURITIS IS OFTEN THE FIRST CLINICAL

manifestation of multiple sclerosis. Loss of vision in
bilateral retrobulbar neuritis may be of acute onset, but it
can progress over several days. Pain on eye movements is a
frequent complaint in this condition. Different patterns of
visual field defects in patients with bilateral retrobulbar
neuritis have been reported. They include central, paracentral, and coecocentral scotomas, nerve fiber bundle
defects, and hemianopic and quadrant defects.1
● CASE: A

36-year old woman was found to have a
sensorimotor hemisyndrome in 1991. Magnetic resonance
imaging (MRI) of the brain revealed multiple small- and
medium-sized white matter lesions predominantly in the
periventricular region. Cerebrospinal fluid examination
was positive for oligoclonal bands. Based on the clinical
findings, the result of the MRI, and the oligoclonal bands
in the cerebrospinal fluid, the diagnosis of multiple sclerosis was made. In 1994, the patient suffered from acute loss
of vision in the left eye (LE) that was accompanied with
pain on eye movements. Ophthalmologic examination
revealed best-corrected visual acuity of RE: 20/20 and LE:
counting fingers at 20 cm. Kinetic visual field testing with
the Goldmann perimeter was normal RE, but it showed a
central scotoma in the left visual field. The optic disk in
the left eye was slightly swollen. Fundus examination of
the right eye was normal. The visual acuity of the left eye
improved to 20/400 after 4 months.
Two years later, the patient suffered sudden loss of
vision in the right eye that again was accompanied by pain
on eye movements. Visual acuity measured RE: 20/40 and
LE: 20/400. Examination of the right fundus was unremarkable, and the left optic disk appeared pale. Despite
high-dose intravenous methylprednisolone therapy, SoluMedrol (Pharmacia & Upjohn AG, Dübendorf, Switzerland) 250 mg every 6 hours for 3 days, visual acuity in the
right eye deteriorated progressively to counting fingers at
4 m. Three months later, the patient was again admitted to
the hospital because of new onset “darkening” in the left
eye. Kinetic perimetry with the Goldmann perimeter
revealed a nasal quandrantanopsia LE and a discrete
superonasal field defect RE. Both optic disks were atrophic.
A relapse of multiple sclerosis causing bilateral simultaneous visual field loss was suspected, and a repeat MRI was
performed to identify active plaques. Instead of new white
matter lesions, a mass compressing the chiasm with left
mediolateral localization was noted (Figure 1). A transphenoidal excision was performed, and the histologic
diagnosis of a colloid cyst was made (Figure 2). In both
eyes, rapid and substantial improvement in the upper nasal
visual field occurred.
Retrobulbar neuritis manifests with sudden and sometimes progressive monocular loss of vision and is often
accompanied with pain on eye movements. In many cases
of demyelinating disease, bilateral retrobulbar neuritis is
the first clinical manifestation. When retrobulbar neuritis

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