ORIGINAL CONTRIBUTION

Fourth Nerve Palsy, Homonymous Hemianopia, and
Hemisensory Deficit Caused by a Proximal Posterior
Cerebral Artery Aneurysm
Jennifer K. Hall, MD, Dina A. Jacobs, MD, Tammy Movsas, MD, and Steven L. Galetta, MD

A 21-year-old man developed an ipsilateral fourth nerve
palsy, contralateral hemianopia, and contralateral hemisensory deficit as manifestations of a proximal right posterior
cerebral artery aneurysm. This unusual constellation of
signs reflects the involvement of the structures that run in
the ambient cistern. The fourth nerve palsy and homonymous hemianopia are attributed to compression by the aneurysm. The hemisensory loss is ascribed to compromise of
thalamoperforate arteries emanating from a thrombosed
portion of the aneurysm.
(J Neuro-Ophthalmol 2002;22: 95–98)

C

isterns are CSF-filled spaces with membranous borders that surround the brainstem. The ambient cistern
lies dorsolateral to the midbrain. Structures contained
within this cistern include the posterior cerebral artery
(PCA), the anterior choroidal artery, the optic tract, and the
trochlear nerve (1,2). The PCA runs through the ambient
cistern, giving off thalamic perforating arteries and anterior
and posterior temporal branches. The trochlear nerve
emerges dorsally from the midbrain medial to the superior
cerebellar peduncle and courses anteriorly through the ambient cistern. The optic tract courses posteriorly around the
cerebral peduncles, through the ambient cistern, to the lateral geniculate nucleus of the thalamus, with some fibers
passing to the pretectal nucleus. We report a patient who
presented with a fourth nerve palsy, contralateral hemianopia, and contralateral hemisensory deficit owing to a proximal PCA aneurysm.

CASE REPORT
In May 2000, a 21-year-old previously healthy man
presented with the acute onset of left-sided numbness and a
decrease in vision. During the preceding year, the patient
Department of Neurology, University of Pennsylvania School of
Medicine, Philadelphia, Pennsylvania, USA.
Address correspondence to Steven L. Galetta, MD, Department of
Neurology, 3 East Gates, 3400 Spruce Street, Philadelphia, PA 19104,
USA

J Neuro-Ophthalmol, Vol. 22, No. 2, 2002

had had constant bifrontal throbbing headaches associated
with nausea. On the day prior to admission, he developed
numbness of the left arm lasting for 1 hour. As the day progressed, he experienced a severe headache associated with
nausea and vomiting. One hour later, he noted the onset of
visual blurriness in his left visual field, left arm numbness,
and intermittent vertical diplopia worse in left gaze.
The patient had no known past medical problems and
was on no medications. His family history was significant
for fatal cerebral aneurysms in an 18-month-old cousin and
his maternal grandfather. His neurologic examination on
presentation to the neurosurgery service was significant for
a left homonymous hemianopsia. There was intermittent
rhythmic jerking of his left arm. He had decreased sensation
to light touch in his left face, arm, and leg. Brain magnetic
resonance imaging revealed a partially thrombosed aneurysm originating from the proximal right PCA (Fig. 1A and
B) and an acute infarct involving the right thalamus (Fig.
1C). No subarachnoid hemorrhage was present. A lumbar
puncture was normal.
A cerebral angiogram (Fig. 2A) confirmed the presence of a 2-cm partially thrombosed aneurysm at the right
P2/P3 segment. The aneurysm lay just distal to the takeoff
of the posterior temporal artery. The right P1 segment was
hypoplastic. There was a fetal origin of the right PCA,
which derived from the right internal carotid artery. There
was collateral filling of the right PCA from the left PCA.
The patient underwent intracranial coil embolization of the
PCA aneurysm with sacrifice of the parent vessel. A
postembolization angiogram (Fig. 2B) demonstrated good
closure of the aneurysm with preservation of the right posterior temporal artery located proximal to the aneurysm.
Neuro-ophthalmic examination performed immediately after embolization revealed 20/20 visual acuity in OU.
The patient could identify only 3/10 Ishihara color plates
OD and 2/10 OS but had a history of congenital color blindness. Confrontation fields revealed a mildly incongruous
left homonymous hemianopia, which was later confirmed
by Goldmann perimetry (Fig. 3). Also present was a mild
right hypertropia that increased in left gaze and on right
DOI: 10.1097/01.WNO.0000018242.84472.33

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FOURTH NERVE PALSY, HOMONYMOUS HEMIANOPIA, AND HEMISENSORY DEFICIT

FIG. 1. A: Axial T2 magnetic resonance imaging (MRI)
demonstrates a right posterior cerebral artery aneurysm (arrow) compressing the posterolateral aspect of
the right midbrain. B: Axial gradient echo MRI reveals
signal of old clotted blood in a partially thrombosed
aneurysm. C: Axial FLAIR MRI demonstrates a right thalamic infarct (arrow).

head tilt. Pupils reacted briskly to light bilaterally, and there
was no afferent pupillary defect. Ophthalmoscopy was normal. The left homonymous hemianopia resolved within
several months, as did the right hypertropia and left hemisensory deficit. The patient had a normal follow-up computerized perimetry in October 2000.

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DISCUSSION
We report a patient with a right fourth nerve palsy,
left homonymous hemianopia, and left hemisensory deficit
as manifestations of a proximal right PCA aneurysm. Figure 4 demonstrates the relationship of the aneurysm to the
© 2002 Lippincott Williams & Wilkins

HALL ET AL.

J Neuro-Ophthalmol, Vol. 22, No. 2, 2002

FIG. 3. Goldmann visual fields reveal an incongruous left
homonymous hemianopia.

The right fourth nerve palsy and left incongruous
homonymous hemianopia were probably caused by aneurysmal compression of adjacent pathways (Fig. 4).
Visual field loss due to optic tract lesions is unusual.
In a series of 100 patients with homonymous hemianopsias,
Smith (3) reported that only 3% were due to optic tract lesions. He noted that tract hemianopsias were very difficult
to diagnose by perimetry. The author’s clues to picking up a

FIG. 2. A: Cerebral angiogram reveals a 2-cm partially
thrombosed aneurysm at the P2/P3 segment (arrow).
B: Postembolization angiogram demonstrates nonfilling of
the coiled aneurysm (arrow).

adjacent structures in the ambient cistern. The patient’s left
hemisensory deficit was due to a right thalamic infarction.
Although the thalamic perforators usually branch off from
the parent PCA proximal to the location of this patient’s
aneurysm, it is likely that the perforators were located distal
to the aneurysm because of the hypoplastic P1 segment.
These perforators were either compressed by the aneurysm
or, more likely, occluded by partial thrombosis within the
aneurysm. The intermittent rhythmic tremor of his left arm
was probably caused by ischemia to the ventrolateral
nucleus of the thalamus.

FIG. 4. Drawing of the lateral brainstem demonstrates
compression of the optic tract medially and the fourth cranial (trochlear) nerve laterally by a proximal posterior cerebral artery (PCA) aneurysm.

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FOURTH NERVE PALSY, HOMONYMOUS HEMIANOPIA, AND HEMISENSORY DEFICIT

tract lesion were “extreme incongruity, a negative optokinetic response, and evidence of neurologic disease in neighboring structures” (3).
Two other series have reviewed the optic tract syndrome (4,5). Savino et al. (4) documented 21 patients with
lesions of the optic tract. They reiterated the importance of
associated neurologic findings in identifying the optic tract
as the site of the lesion (4). Without other associated neurologic findings, it would be easy to attribute a homonymous hemianopia to another location in the retrochiasmal
visual pathway. Savino et al. (4) also noted that the classic
tract field defect was extremely incongruous (4). The associated neurologic findings in their series included headache,
change in cognition, sixth nerve palsy, hemiparesis, and
paresthesias (4). None of the patients in their series had the
same constellation of symptoms as our patient. Newman
and Miller (5) described a series of 10 patients with optic
tract lesions. They noted that an afferent pupillary defect
(APD) would not be observed unless there was significant
asymmetry in the degree of visual field loss between the
two eyes (5). Therefore, the absence of an APD in our patient does not preclude an optic tract lesion. Their series did
report one patient with an arteriovenous malformation
(AVM) in the right ambient cistern who presented with a
left homonymous hemianopia, left hemiparesis, and left hemisensory loss, but no fourth nerve involvement was noted.
Another patient in that series with an AVM in the ambient
cistern presented with a mild fourth nerve palsy. However,
a hemianopia did not develop until after surgical resection
of the AVM (5). Ohtsuka et al. (6) described another case of
bilateral fourth nerve palsies secondary to an arachnoid cyst
of the quadrigeminal cistern with extensive compression of
both ambient cisterns.
The young age of our patient and the location of his
aneurysm are two other noteworthy features. The incidence

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of intracranial aneurysms has been reported as approximately 3% in people age 20 years and younger (7). PCA
aneurysms are generally uncommon (7–9), accounting for
only 0.26% to 1.0% of intracranial aneurysms (9). Of these,
only 13% are PCA aneurysms occurring distal to the posterior temporal branch (9). However, in the pediatric population, higher frequencies of aneurysms located in the posterior circulation have been noted (10). Meyer et al. (10)
found a rate of 46% in their study of 24 aneurysms in patients aged 18 years or younger. However, large series have
not substantiated this observation (10). Meyer et al. (10)
also observed a male predominance among pediatric intracranial aneurysm patients.
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© 2002 Lippincott Williams & Wilkins