J Neurosurg 108:1245–1248, 2008

Cerebellar hemorrhage and subsequent venous infarction
followed by incomplete transvenous embolization of dural
carotid cavernous fistulas: a rare complication
Case report
RENG-JYE LEE, M.D., CHIH-FENG CHEN, M.D., SHIH-WEI HSU, M.D.,
CHUN-CHUNG LUI, M.D., AND YEH-LIN KUO, M.D.
Department of Diagnostic Radiology, Chang Gung Memorial Hospital–Kaohsiung Medical Center,
Chang Gung University College of Medicine, Taiwan

PEndovascular therapy for dural carotid cavernous fistulas (CCFs) is generally accepted to be safe and effective. The
authors report a rare complication of hemorrhage and subsequent venous infarcts of the pons and cerebellum after transvenous embolization.
This 41-year-old man presented with a severe left frontal headache, congestion of the left conjunctiva, blurred vision,
and photophobia. Cerebral angiography demonstrated a right dural CCF. The patient underwent transvenous embolization of the cavernous sinus but had the initial complication of cerebellar hemorrhage. One month later, he developed
progressive dizziness, ataxia, and right-sided weakness. Magnetic resonance imaging revealed severe cerebellar and
pontine edema. The cause was a residual fistula combined with delayed occlusion of the inferior petrosal sinus. The fistula was obliterated after repeated embolizations. The patient’s symptoms gradually resolved, and there was no evidence of recurrence during the 4-year follow-up period.
Incomplete transvenous embolization of a dural CCF can result in life-threatening vascular complications due to redistribution of shunt flow. Early recognition of redistributed drainage and preventive placement of coils at the origin of
draining veins during the procedure could avert this rare complication. (DOI: 10.3171/JNS/2008/108/6/1245)
KEY WORDS • brainstem ischemia • dural arteriovenous fistula •
postoperative complications • therapeutic embolization • venous infarction
URAL arteriovenous malformations account for 10–
15% of all intracranial arteriovenous malformations12 and most commonly involve the cavernous,
transverse, and sigmoid sinuses.9 A dural CCF consists of
arteriovenous shunting between the carotid artery and the
cavernous sinus. In recent years, transvenous embolization
of dural CCFs has become widely accepted as a safe and
effective therapeutic method. We report the case of a patient with a dural CCF who received transvenous embolization and who experienced the rare complications of intraprocedural cerebellar hemorrhage and late-onset venous
infarcts.

D

Case Report
History and Examination. This 41-year-old man presented with left-sided visual disturbances and diplopia accompanied by a 3-month history of nausea and vomiting. He
Abbreviations used in this paper: CCF = carotid cavernous fistula; ICA = internal carotid artery; IPS = inferior petrosal sinus; MR =
magnetic resonance; NBCA = N-butyl-2-cyanoacrylate; SPS = superior petrosal sinus.

J. Neurosurg. / Volume 108 / June 2008

also had a severe left frontal headache, photophobia, and a
sensation of bruit behind the eyeball, which developed over
1 month. On examination, a neurologist observed conjunctival chemosis, ptosis, anisocoria, and abducent nerve palsy. Magnetic resonance angiography was performed, and
the findings suggested a CCF. Digital subtraction cerebral
angiography then showed a dural CCF. The dural branches
of the left ICA (Fig. 1 left) and the external carotid artery
were connected to the cavernous sinus. Also visualized
were a retrograde shunt with an engorged left inferior ophthalmic vein, the left sphenoparietal sinus, and the SPS.
First Embolization. Transvenous embolization of the cavernous sinus was performed through the left internal jugular
vein and the IPS with the patient in a state of general anesthesia. Embolization was achieved using a microcatheter
(FasTracker 18, Target Therapeutics/Boston Scientific) and
16 fibered microcoils (Vortex, Target Therapeutics/Boston
Scientific). Follow-up angiography showed substantially reduced shunt flow, but residual flow was present.
To completely occlude the shunts, NBCA was added
through the microcatheter. Immediately after NBCA injection, the patient’s heart rate and blood pressure transiently
rose from 70 to 90 bpm and from 100/50 to 140/70 mm Hg,
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R. J. Lee et al.

FIG. 1. Left: Lateral left ICA angiogram demonstrating an early opacifying left cavernous sinus (arrow), bilateral IPSs,
the left inferior ophthalmic vein (arrowhead), and the left sphenoparietal sinus (double arrows). Right: Left ICA angiogram, obtained after the fibered microcoils and NBCA deployment, showing a substantial reduction in shunt flow. The residual shunt flow was drained by the IPS (arrowhead), SPS (arrow), and deep cerebellar veins (double arrows).

respectively. Postembolization angiography demonstrated
residual shunt flow draining to the left IPS, the SPS, and the
deep cerebellar veins (veins of the lateral recess) (Fig. 1
right). The procedure was then halted.
The patient’s headache and eye pain resolved after embolization, but dilation of the left pupil and the abducent
nerve palsy persisted. On the 2nd day, MR imaging revealed an acute hemorrhagic lesion of the left cerebellum with
peripheral edema (Fig. 2).
Second Embolization. One month after embolization, the
patient suffered progressive dizziness, ataxia, and right-sided weakness. An MR imaging study revealed severe edema
in the left pons and cerebellum (Fig. 3 left). Subsequent angiography showed occlusion of the left IPS with progressive engorgement of the SPS and deep cerebellar veins,
which were mainly supplied by the left ICA through residual shunts (Fig. 3 right).
Because of the occlusion of the left IPS, repeated attempts at transvenous embolization failed. Transarterial
embolization through the left ICA obliterated only part of
the fistulous flow. For complete occlusion of the fistula,
trapping of the left ICA was planned after a balloon occlusion test. The patient well tolerated the test occlusion for 30
minutes. Four detachable balloons were then used to occlude the left ICA and the fistula (Fig. 4).
Postembolization Course. After embolization, the patient’s symptoms gradually resolved, and he was discharged home after rehabilitation. At 2-year follow-up,
MR imaging showed regression of the edema and cerebellar atrophy (Fig. 5). During the 4-year clinical follow-up
period, the patient exhibited mild weakness of the right
limb. Ataxia and dysmetria remained and were stable.
Discussion
For patients with dural CCF and mild symptoms, observation alone or carotid jugular compression4 provides an
opportunity for the fistula to close. For patients with severe
symptoms, various treatment options are available. Sur1246

gical obliteration of the involved dural sinus is not favored
because severe complications have been observed.14 Transarterial particle-based embolization of the feeding arteries
may be associated with a high recurrence rate. Transarterial application of NBCA10 and transvenous embolization6,11
have been good alternatives for the treatment of dural fistulas. Direct transvenous NBCA injection combined with
coil deployment, as in our case, can achieve complete oc-

FIG. 2. Axial T2-weighted MR image, obtained 1 day after embolization, demonstrating acute hemorrhage in the left cerebellum
with peripheral edema.

J. Neurosurg. / Volume 108 / June 2008

Cerebellar venous infarcts following dural fistula embolization

FIG. 3. Left: Axial T2-weighted MR image, acquired 1
month after the first embolization, revealing the edematous
change over the left pons and the deep cerebellum. Right:
Lateral ICA angiogram showing progressive engorgement
of the left SPS (arrow) and deep cerebellar veins (arrowhead). Late occlusion of the left IPS is also noted.

clusion of complex dural fistulas.15 Radiosurgery offers another choice for patients who are hesitant to receive endovascular therapy.2
Reported complications after transvenous embolization
of a dural CCF include deterioration of ocular motor dysfunction,1,13 transient visual loss,3 embolic stroke,3 and metachronous dural arteriovenous fistula.7 We report the rare
postembolization complication of a posterior fossa hemorrhage and delayed venous infarcts.

In our case, venous infarcts and hemorrhage of the left
cerebellum and pons were closely related to the venous
drainage pathways. Huang5 and Lasjaunias and Berenstein8
have illustrated anatomical variations of venous drainage in
the posterior cranial fossa. They described 2 main channels
that drain the deep cerebellar hemispheres. The first group
of channels drains to the hemispheric or vermian veins and

FIG. 4. Right common carotid artery angiogram, obtained after
the left ICA was trapped, showing good collateral flow into the left
cerebral hemisphere and the absence of fistulas.

FIG. 5. Two-year follow-up axial T2-weighted MR image revealing reduced volume of the left pons and the cerebellum due to
the regression of edema.

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R. J. Lee et al.
later to the torcula herophili or tentorial sinus. The second
group drains to the veins of the lateral recess, the petrosal
vein, and later to the SPS. The present case fits the second
drainage pathway.
The cerebellar hemorrhage that occurred immediately
after NBCA-assisted embolization could have been due
to high pressure in the cavernous sinus. Aihara et al.1 have
described high intracavernous sinus pressure during embolization, which resulted in cranial nerve palsy. In our
first embolization procedure, occlusion of the main venous
drainage outlets, such as the inferior ophthalmic vein, the
sphenoparietal sinus, and the contralateral cavernous sinus, was achieved. At the same time, the microcatheter partially occluded the left IPS. Residual shunt flow might then
have been redirected to the SPS and the deep cerebellar
veins, causing cerebellar hemorrhage.
High intrasinus pressure after partial obliteration of the
drainage pathways can be dangerous and can lead to subsequent complications.7 In our patient, the same mechanism may also account for the delayed onset of the cerebellar and pontine venous infarcts. Nonobliterated shunt
flow combined with late occlusion of the draining IPS
resulted in focal cerebellar congestion and edema 1 month
later.
To prevent such complications, it might be helpful to recognize redistributed venous channels on serial angiograms
during the procedure. In our case, selective placement of
coils at the SPS origin could avoid this rare complication.
Detachable coils such as Guglielmi detachable coils are
preferable because they are retrievable and easy to advance
to the desired position.
Conclusions
We report the rare complication of transvenous embolization in association with a dural CCF. Redistributed
residual blood flow through the fistula can result in cerebellar hemorrhage and venous infarcts. To avoid this complication, early recognition of redistributed shunt flow and
selective placement of coils at the origin of draining veins
during the procedure could be helpful.
References
1. Aihara N, Mase M, Yamada K, Banno T, Watanabe K, Kamiya K,
et al: Deterioration of ocular motor dysfunction after transvenous
embolization of dural arteriovenous fistula involving the cavernous sinus. Acta Neurochir (Wien) 141:707–710, 1999
2. Guo WY, Pan DH, Wu HM, Chung WY, Shiau CY, Wang LW,
et al: Radiosurgery as a treatment alternative for dural arteriove-

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nous fistulas of the cavernous sinus. AJNR Am J Neuroradiol
19:1081–1087, 1998
3. Halbach VV, Higashida RT, Hieshima GB, Hardin CW, Pribram
H: Transvenous embolization of dural fistulas involving the cavernous sinus. AJNR Am J Neuroradiol 10:377–383, 1989
4. Halbach VV, Higashida RT, Larsen DW, Dowd CF, McDougall
CG, Hieshima GB, et al: Treatment of dural arteriovenous fistulas, in Maciunas RJ (ed): Endovascular Neurological Intervention. Park Ridge, IL: American Association of Neurological Surgeons, 1995, pp 217–246
5. Huang YP: Veins of the posterior fossa, in Salamon G (ed): Radiologic Anatomy of the Brain. Berlin: Springer-Verlag, 1976,
pp 332–390
6. Kiyosue H, Hori Y, Okahara M: Treatment of intracranial dural arteriovenous fistulas: current strategies based on location and hemodynamics, and alternative techniques of transcatheter embolization. Radiographics 24:1637–1653, 2004
7. Kubota Y, Ueda T, Kaku Y, Sakai N: Development of a dural arteriovenous fistula around the jugular valve after transvenous embolization of cavernous dural arteriovenous fistula. Surg Neurol
51:174–176, 1999
8. Lasjaunias P, Berenstein A: Surgical Neuroangiography. Vol 3.
Berlin: Springer-Verlag, 1990, pp 268–278
9. Lasjaunias P, Chiu M, ter Brugge K, Tolia A, Hurth M, Bernstein
M: Neurological manifestations of intracranial dural arteriovenous malformations. J Neurosurg 64:724–730, 1986
10. Liu HM, Huang YC, Wang YH, Tu YK: Transarterial embolization of complete cavernous sinus dural arteriovenous fistulae with
low-concentration cyanoacrylate. Neuroradiology 42:766–770,
2000
11. Mullan S: Treatment of carotid-cavernous fistulas by cavernous sinus occlusion. J Neurosurg 50:131–144, 1979
12. Newton TH, Cronqvist S: Involvement of dural arteries in intracranial arteriovenous malformations. Radiology 93:1071–1078,
1969
13. Roy D, Raymond J: The role of transvenous embolization in the
treatment of intracranial dural arteriovenous fistulas. Neurosurgery 40:1133–1144, 1997
14. Tu YK, Liu HM, Hu SC: Direct surgery of carotid cavernous fistulae and dural arteriovenous malformations of the cavernous sinus. Neurosurgery 41:798–805, 1997
15. Wakhloo AK, Perlow A, Linfante I, Sandhu JS, Cameron J, Troffkin N, et al: Transvenous n-butyl-cyanoacrylate infusion for complex dural carotid cavernous fistulas: technical considerations
and clinical outcome. AJNR Am J Neuroradiol 26:1888–1897,
2005
Manuscript submitted June 6, 2007.
Accepted August 16, 2007.
Address correspondence to: Yeh-Lin Kuo, M.D., Department of
Diagnostic Radiology, Chang Gung Memorial Hospital–Kaohsiung
Medical Center, Chang Gung University College of Medicine, 123
Ta-Pei Road, Niaosung Hisan, Kaohsiung Hsien, 833, Taiwan.
email: silingcgmh@adm.cgmh.org.tw.

J. Neurosurg. / Volume 108 / June 2008