J Neurosurg 89:667–670, 1998

Cavernous sinus syndrome during balloon test occlusion of
the cervical internal carotid artery
Report of two cases
DEMETRIUS K. LOPES, M.D., ROBERT A. MERICLE, M.D., AJAY K. WAKHLOO, M.D., PH.D.,
LEE R. GUTERMAN, PH.D., M.D., AND L. NELSON HOPKINS, M.D.
Department of Neurosurgery and Toshiba Stroke Research Center, School of Medicine and Biomedical
Sciences, State University of New York at Buffalo, Buffalo, New York
U The authors report the occurrence of ipsilateral transient cavernous sinus syndrome during balloon test occlusion (BTO)
of the cervical internal carotid artery (ICA) and discuss the involved pathomechanisms.
The authors reviewed their series of 129 BTOs of the ICA performed between 1989 and 1996. Two patients developed
facial paresthesias and transient palsies of the third through sixth cranial nerves during test occlusion of the cervical ICA.
The tests were performed prior to planned permanent carotid artery occlusion for the treatment of a neck sarcoma in one
patient and a giant cavernous carotid artery aneurysm in the other. The patients’ symptoms resolved with deflation of the
balloon. When the balloon was subsequently inflated above the inferior cavernous sinus artery (ICSA), one of the patients
complained of mild facial discomfort. There was no contralateral weakness or mental status change during test occlusion
in either patient. Angiography demonstrated good filling of the ipsilateral intracranial circulation via collateral vessels of
the circle of Willis.
In these two cases, the cranial nerves in the cavernous sinus were likely supplied by the ICA via the meningohypophyseal trunk and the ICSA. In each case, there was excellent blood supply to the ipsilateral cerebral hemisphere; however,
there was probably inadequate retrograde filling of the cranial nerve collateral vessels located where the meningohypophyseal trunk and ICSA originated. These cases emphasize the importance of a patent external carotid artery–ICA connection for successful cervical carotid artery occlusion. Neurological examination during BTO was critical to interpret the
clinical manifestations caused by the hemodynamic changes.

KEY WORDS • balloon test occlusion • carotid artery • cavernous sinus syndrome •
endovascular therapy • neurological deficit

B

ALLOON test occlusion (BTO) was introduced by

Serbinenko7 in 1974. This endovascular technique
is commonly performed to evaluate the tolerance
of the central nervous system to carotid artery occlusion.
We reviewed our series of 129 BTOs of the internal carotid artery (ICA) that were performed from 1989 to 1996.
Two patients developed ipsilateral transient palsies of the
third through sixth cranial nerves during test occlusions.
The tests were performed before planned permanent carotid artery occlusion for the treatment of a neck sarcoma
in one patient and a giant cavernous carotid artery aneurysm in the other. The interpretation of this finding and its
implications are discussed.
Case Reports
Case 1
History. This 20-year-old man with rhabdomyosarcoma
of the right parapharyngeal space and infratemporal fossa
(Fig. 1) was admitted for BTO of the right ICA prior to
J. Neurosurg. / Volume 89 / October, 1998

surgical resection. The patient complained of decreased
hearing on the right side and occasional episodes of dizziness that were most often postural in nature.
Examination. On examination, the patient had a lobulated retromandibular mass extending to the mastoid process
and a right-sided facial nerve paralysis, but no other neurological deficits. Right ICA angiography demonstrated
filling of the anterior and posterior communicating arteries. Angiograms of the left vertebral artery and the left
ICA did not show any abnormalities. There was no appreciable compression of the ICA.
Balloon Test Occlusion. In preparation for the test occlusion, intravenous heparin (5000 U) was administered and
topical nitropaste was applied to the chest wall. A pediatric Swan–Ganz catheter (Edwards Laboratories Inc.,
Anasco, Peurto Rico) was placed and inflated in the right
cervical ICA at the C1–2 vertebral level (Fig. 2, position
1). Heparinized saline was slowly infused through the distal lumen of the balloon catheter. After 10 minutes of ICA
occlusion, the patient began to complain of pain in the
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D. K. Lopes, et al.

FIG. 1. Case 1. Contrast-enhanced computerized tomography
scans demonstrating a large mass in the right parapharyngeal space
and infratemporal fossa.

right orbit and face. Approximately 10 minutes later, after
a total of 20 minutes of temporary occlusion, he developed a complete right-sided ophthalmoplegia. The balloon was deflated and the patient’s symptoms resolved
completely within 3 minutes.
To determine whether these transient deficits had developed as a result of diminished perfusion of the cavernous
arterial branches from the ICA to the third through sixth
cranial nerves, the test was repeated using a nondetachable silicone balloon (Interventional Therapeutics Corp.,
Fremont, CA) placed just above the origin of the inferior
cavernous sinus artery (ICSA) (Fig. 2, position 2). After
10 minutes, the patient experienced mild facial numbness
but less severe symptoms of paresthesia and no ophthalmoplegia. Once again, his symptoms resolved after balloon deflation. No evidence of right hemispheric signs or
symptoms occurred during any portion of the BTO.
Case 2

This 28-year-old man presented with a severe headache
and diplopia.
Examination. The patient’s physical examination was
remarkable for a left sixth cranial nerve paresis. Cerebral
angiography performed immediately before BTO demonstrated a giant aneurysm arising from the cavernous portion of the left ICA (Fig. 3).
Balloon Test Occlusion. Before BTO, intravenous heparin was administered and nitropaste was applied. A pediatric Swan–Ganz catheter was placed and inflated in the
left cervical ICA at the C1–2 vertebral level. Heparinized
saline was slowly infused through the distal lumen of the
balloon catheter. After 2 or 3 minutes of carotid occlusion,
the patient complained of pain and pressure involving his
left eye and, subsequently, of left facial numbness.
Worsening of the left sixth cranial nerve paresis was evident after 10 minutes of occlusion, and complete ophthalmoplegia occurred after 20 minutes. The balloon was
deflated and the patient returned to baseline within 2 minutes. The BTO was repeated in the same region of the ICA
and the same symptoms started after 10 minutes of occlusion. There was no left hemispheric dysfunction throughout the procedure. We did not attempt test occlusion of the
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FIG. 2. Case 1. Schematic illustration of the two positions in
which the balloon was placed for test occlusion. Position 1:
Cervical ICA at the C1–2 vertebral level. Position 2: Above the
origin of the cavernous ICA branches. Abbreviations: CS = carotid
siphon; MHT = meningohypophyseal trunk; OA = ophthalmic
artery.

supraclinoid portion of the ICA. To demonstrate collateral circulation, a right carotid angiogram was obtained
while the left cervical ICA was still occluded by the balloon. There was patency of the anterior communicating
artery with filling of the left cerebral hemisphere. A left
vertebral artery angiogram demonstrated filling of the
middle cerebral artery bilaterally via the posterior communicating arteries. The giant left carotid cavernous
aneurysm was not visualized during either injection, indicating that the reversed flow in the ICA did not reach the
cavernous segment where the meningohypophyseal trunk
and ICSA are located. The BTO re-sults suggested poor
perfusion of the meningohypophyseal trunk and ICSA
with balloon occlusion below these vessels.
We elected to perform a left extracranial–intracranial
arterial bypass prior to ipsilateral ICA balloon occlusion.
Angiography performed through the bypass graft during
simultaneous high-cervical BTO revealed some retrograde flow to the cavernous segment, but no filling of the
aneurysm. No symptoms developed after permanent balloon occlusion. On postoperative evaluation, the patient’s
left sixth cranial nerve paresis was improving. His neurological status remained otherwise unchanged. Magnetic
resonance imaging of the head demonstrated a thrombosed left cavernous ICA aneurysm.
J. Neurosurg. / Volume 89 / October, 1998

Cavernous sinus syndrome during balloon test occlusion

FIG. 3. Case 2. Left ICA angiogram, lateral view, showing a
giant aneurysm at the cavernous portion of the left ICA.

Discussion
To our knowledge, cavernous sinus syndrome has never
been reported during BTO of the cervical ICA. Debrun, et
al.,1 reported a case of third nerve paresis after multiple
balloons were placed in the cavernous sinus to occlude
carotid–cavernous fistulas, which may have been related
to local mass effect and balloon compression of the cranial
nerve. We suggest that the cavernous sinus syndrome in
our patients resulted from poor retrograde filling of the
ICA cavernous segment. The same mechanism has been
reported to cause transient monocular blindness in a
patient with an ophthalmic artery originating from the
cavernous sinus segment.3 The monocular ischemic syndrome has been also reported as a result of rapid heparinized saline infusion, which causes a total or partial
replacement of blood above the occlusion, not allowing
adequate retrograde flow.6 In each case, we specifically
kept the infusion rate very slow and even discontinued the
infusion without improvement in the neurological deficit.
The deficit occurred only after the cervical (C1–2 vertebral level) ICA balloon was inflated and completely resolved immediately after balloon deflation. This was tested by several inflations with the same outcome. If the
symptoms had been related to an embolic event, they
would likely not have disappeared spontaneously after
balloon deflation.

The most consistent branches of the cavernous portion
of the ICA are the meningohypophyseal trunk, ICSA, and
the capsular arteries of McConnell (Table 1).2,4,5,8,9 The
lack of perfusion of the meningohypophyseal trunk and
ICSA presumably accounted for the transient dysfunction
of the third through sixth cranial nerves. When ICA occlusion was performed above the origin of the ICSA, the
symptoms diminished significantly. In both cases, the
external carotid artery (ECA) circulation appeared normal
on angiography. There are multiple and highly variable
connective channels between both ICAs and between the
ICA and ECA that usually protect cranial nerve function
during BTO. The rich basilar plexus, which is composed
of cavernous ICA branches, connects to its contralateral
counterpart and meningeal branches of the ECA and to the
ophthalmic and vertebral arteries; it has been termed the
“rete mirable.”9 Collateral flow through a patent circle of
Willis was sufficient to provide perfusion of the hemisphere during the occlusion test; however, there was probably inadequate retrograde filling of cranial nerve collateral vessels at the level of the meningohypophyseal trunk
and the ICSA. Whether the patients’ neurological symptoms would have persisted with permanent occlusion of
the carotid artery is unknown. The potential for ICA collateralization with branches of the ECA and contralateral
ICA exists and permanent occlusion could possibly result
in enlargement of preexisting connective channels prior to
irreversible neurological injury. In Case 2, the patient’s
tolerance to permanent occlusion after extracranial–intracranial arterial bypass had been performed may have
resulted from an increase in ICA retrograde flow, increased perfusion through preexisting connective channels, or both.
Conclusions
Neurological examination with detailed evaluation of
cranial nerve function during BTO is critical for the interpretation of clinical manifestations due to hemodynamic changes. Thorough knowledge of neuroanatomy and
blood flow dynamics is essential for accurate interpretation of BTO findings. The current technology for assessment of cerebral blood flow during BTO is inadequate to
evaluate blood supply to cranial nerves. We should be
aware of the possibility of insufficient connections between the ECA and ICA and between both ICAs prior to
high-cervical ICA occlusion.

TABLE 1
Anatomy of cavernous ICA branches*
Cavernous ICA Branches

Secondary Branches

Vascular Territory

meningohypophyseal trunk

inferior hypophyseal artery

posterior lobe of pituitary gland;
floor of sella turcica
third & fourth cranial nerves; roof of
cavernous sinus; tentorium; falx
sixth cranial nerve
gasserian ganglion; floor of cavernous
sinus
floor of sella turcica

tentorial artery
ICSA

dorsal meningeal artery
NA

capsular arteries of McConnell

NA

Connections

contralat inferior hypophyseal artery
contralat tentorial artery
contralat dorsal meningeal artery
middle meningeal artery
contralat capsular & inferior hypophyseal arteries

* Data provided in this table obtained from References 2, 4, 5, 8, and 9. Abbreviation: NA = not applicable.

J. Neurosurg. / Volume 89 / October, 1998

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D. K. Lopes, et al.
Acknowledgment
We thank Paul H. Dressel for preparation of the figures and illustration.
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3. Hurst RW, Goldberg HI: Transient monocular blindness in
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5. Krisht A, Barnett DW, Barrow DL, et al: The blood supply of

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the intracavernous cranial nerves: an anatomic study. Neurosurgery 34:275–279, 1994
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258–262, 1994
7. Serbinenko FA: Balloon catheterization and occlusion of major
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Manuscript received February 2, 1998.
Accepted in final form May 29, 1998.
Address reprint requests to: Demetrius Klee Lopes, M.D.,
Department of Neurosurgery, 3 Gates Circle, Buffalo, New York
14209–1194.

J. Neurosurg. / Volume 89 / October, 1998