CASE REPORTS

DEVELOPMENT OF A PONTINE CYST AFTER
ENDOVASCULAR COIL OCCLUSION OF A BASILAR ARTERY
TRUNK ANEURYSM: CASE REPORT
Jonathan A. Friedman,
M.D.
Department of Neurologic Surgery,
Mayo Clinic, Rochester, Minnesota

Jon I. McIver, M.D.
Department of Neurologic Surgery,
Mayo Clinic, Rochester, Minnesota

Frederic P. Collignon,
M.D.
Department of Neurologic Surgery,
Mayo Clinic, Rochester, Minnesota

Douglas A. Nichols, M.D.
Department of Radiology, Mayo
Clinic, Rochester, Minnesota

David G. Piepgras, M.D.
Department of Neurologic Surgery,
Mayo Clinic, Rochester, Minnesota
Reprint requests:
Jonathan A. Friedman, M.D.,
Department of Neurologic Surgery,
Saint Mary’s Hospital, 1216
Second Street SW, Joseph 1-229,
Rochester, MN 55905.
Email:
friedman.jonathan@mayo.edu
Received, June 25, 2002.
Accepted, October 30, 2002.

OBJECTIVE AND IMPORTANCE: Cyst formation within the brain parenchyma after
endovascular coil occlusion of an intracranial aneurysm is a previously undescribed
occurrence. We describe a 70-year-old woman who presented with a symptomatic
pontine cyst 1 year after uncomplicated stenting and Guglielmi detachable coil
occlusion of an unruptured basilar artery trunk aneurysm.
CLINICAL PRESENTATION: A 70-year-old woman presented with an episode of transient
dysequilibrium and gait difficulty. Magnetic resonance imaging and cerebral angiography
demonstrated a 15-mm distal basilar artery trunk aneurysm. Endovascular stenting and coil
occlusion of the aneurysm were performed without technical complications. One year
after the initial treatment, the patient developed progressive dysarthria, dysphagia, diplopia, and left hemiparesis. A large pontomesencephalic cyst adjacent to the coiled basilar
aneurysm was identified on magnetic resonance imaging scans.
INTERVENTION: A subtemporal craniotomy and decompression of the pontomesencephalic cyst were performed. The patient’s symptoms of brainstem dysfunction
improved temporarily but recurred within 2 months, necessitating reoperation for cyst
drainage and placement of a cyst-peritoneal shunt.
CONCLUSION: Intra-axial cyst formation after stenting and endovascular occlusion of
an intracranial aneurysm is an unusual occurrence and should be considered in the
differential diagnosis of new neurological deficits after endovascular treatment. The
pathophysiological mechanism of cyst formation in this case is not known.
KEY WORDS: Aneurysm, Basilar artery, Brainstem cyst, Coil occlusion, Endovascular therapy
Neurosurgery 52:694-699, 2003

C

DOI: 10.1227/01.NEU.0000048480.41325.17

omplications of endovascular coil occlusion of cerebral aneurysms include
thromboembolism, aneurysm perforation, catheter-induced arterial vasospasm or
dissection, and coil migration (2, 4, 5, 7, 9, 13,
18, 19, 21, 22, 25–31, 37, 40). Neurological deficits attributable to pressure from the intraaneurysmal coil mass on adjacent neural
structures after endovascular coil occlusion
occur rarely (7, 33, 37). Although supratentorial parenchymal cysts associated with intracranial aneurysms can occur (17, 32, 36), cyst
formation after endovascular aneurysm treatment has not been reported. We describe a
70-year-old woman who developed a symptomatic pontomesencephalic cyst 1 year after
uncomplicated endovascular stenting and coil
occlusion of an unruptured basilar artery
trunk aneurysm.

694 | VOLUME 52 | NUMBER 3 | MARCH 2003

www.neurosurgery-online.com

CASE REPORT
A 70-year-old woman had been treated at
another hospital for a brainstem stroke 7 years
before the current presentation, with mild stable left hemiparesis and dysarthria. A basilar
artery trunk aneurysm had been identified at
the time of the original ictus and was reidentified on magnetic resonance imaging (MRI)
scans when the patient experienced transient
symptoms of dysequilibrium 2 years before
the current presentation. The patient was referred to our institution after experiencing another, more severe episode of dysequilibrium,
with MRI scans clearly confirming an aneurysmal abnormality in relation to the basilar
artery. There were no current or previous
findings suggesting subarachnoid hemorrhage. The neurological examination demon-

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PONTINE CYST AFTER BASILAR ARTERY TRUNK ANEURYSM COILING

strated mild dysarthria and old left spastic hemiparesis, which
was unchanged in comparison with the patient’s baseline
findings. The most recent head MRI scans revealed an aneurysm arising from the basilar artery and invaginating the
pons, with associated T2-weighted signal changes (Fig. 1); the
aneurysm had increased in size approximately 3 mm, compared with the study performed 2 years previously. Cerebral
angiography confirmed a 13- ⫻ 18-mm aneurysm with a
broad base, arising from the posterior sidewall of the distal
basilar artery trunk (Fig. 2). It was suspected that this aneurysm resulted from a basilar artery dissection, which was the
likely cause of the original brainstem stroke 7 years earlier. No
thrombus within the aneurysm was demonstrated with either
MRI or angiography.
Because of the size and recent enlargement of the aneurysm,
definitive treatment was recommended. Because the aneurysm arose from the posterior wall of the basilar artery trunk
and was embedded in the brainstem, it was considered to be
high risk for surgical clipping; therefore, endovascular coil
occlusion was chosen for therapy. Forty percent focal stenosis
of the basilar artery proximal to the aneurysm neck was noted
at the time of the procedure, as was a wide aneurysm neck.
Because of this stenosis and to facilitate tight coil packing of
the aneurysm, a 3.5- ⫻ 12-mm stent (S670; Medtronic AVE,
Minneapolis, MN) was deployed in the basilar artery, across
the neck of the aneurysm. Twenty-two Guglielmi detachable
coils (Target Therapeutics, Fremont, CA), with a total length of
312 cm, were detached within the aneurysm, resulting in
complete occlusion of the aneurysm fundus and a small neck
remnant (Fig. 2C). Repeat angiography performed 2 months
after the initial coil occlusion demonstrated stable occlusion of
the aneurysm dome, with a persistent neck remnant, and no
further therapy was attempted. Follow-up angiography performed 7 months after the initial treatment revealed enlargement of the neck remnant (Fig. 3A). An additional 13
Guglielmi detachable coils, with a total length of 80 cm, were
detached without difficulty (Fig. 3B). To allow the use of
smaller coils, an angioplasty balloon was inflated within the
stent during coil advancement (balloon-assisted neck
remodeling).

FIGURE 1. T1-weighted sagittal
(A) and T2-weighted axial (B)
MRI scans, demonstrating a 13- ⫻ 18-mm basilar artery trunk aneurysm
projecting posteriorly into the pons and interpeduncular cistern. There is a
minimal amount of T2-weighted signal abnormality in the upper pons,
consistent with edema.

NEUROSURGERY

FIGURE 2. A and B, lateral (A)
and right anterior oblique (B)
views from a right vertebral artery
digital subtraction angiogram,
demonstrating the aneurysm originating from the basilar artery
trunk distal to the origins of the
anteroinferior cerebellar arteries.
The neck of the aneurysm is relatively wide, and there is 40% focal
stenosis of the basilar artery at the
neck of the aneurysm. C, right
vertebral artery digital subtraction
angiogram obtained immediately
after stenting of the basilar artery
and placement of 22 Guglielmi detachable coils, with a total length of 312
cm, through the stent into the aneurysm. There is stagnant contrast material in the interstices of the coil mass inferiorly.

The patient was in unchanged clinical condition until 13
months after the initial endovascular treatment, when she
presented to the hospital complaining of gradual but progressive gait ataxia, diplopia, dysarthria, and worsening left hemiparesis. Cerebral angiograms demonstrated no change in the
appearance of the coiled aneurysm or the small neck remnant,
compared with the immediate posttreatment angiograms obtained after the second coiling procedure (Fig. 3C). Head MRI
scans demonstrated a large cyst involving the majority of the
pons and lower midbrain immediately posterior to the coiled
aneurysm, with associated increased T2-weighted signal
within the brainstem (Fig. 4). The aqueduct of Sylvius seemed
to be compressed by the cystic mass, with resultant
hydrocephalus.
A right ventriculoperitoneal shunt was placed, with resolution of the hydrocephalus on MRI scans but without radiological changes in the size of the pontine cyst or the abnormal
signal in the brainstem. The patient’s dysarthria and dysphagia continued to progress. Two weeks after the ventricular
shunting procedure, a right subtemporal craniotomy and fenestration of the pontomesencephalic cyst were performed,
with frameless stereotactic guidance. The coiled aneurysm

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FRIEDMAN ET AL.

FIGURE 3. A, right vertebral artery
digital subtraction angiogram obtained 7 months after the initial endovascular procedure, demonstrating
compaction of the coils in the base of
the aneurysm and the development of
a 4- ⫻ 8-mm broad-based neck remnant. Thirteen additional Guglielmi
detachable coils were advanced
through the stent into the neck remnant. B, immediate posttreatment
right vertebral artery digital subtraction angiogram, demonstrating a
small residual neck remnant. C, right
vertebral artery digital subtraction
angiogram obtained 5 months after
the second coiling procedure, demonstrating a stable appearance of the small
remaining neck remnant, compared with B (allowing for slight differences in
obliquity).

was observed to be projecting into the anterior aspect of the
pons, but no direct communication with the cyst was identified. After incision in the lateral aspect of the pons, there was
egress of an oily-appearing, yellow fluid under modest pressure. The walls of the cyst cavity were amber-colored, and a
biopsy of the cyst wall demonstrated gliotic changes without
inflammation. A drain was not placed because the cyst was
widely opened.
Postoperatively, the patient experienced substantial early
neurological improvement. Her dysarthria, dysphagia, and
walking improved substantially, and MRI scans obtained 1
week postoperatively demonstrated good decompression of
the brainstem cyst. The improvement was only temporary,
however, and within 2 months the patient was readmitted
with recurrent and progressive symptoms of disturbed gait,
speech, swallowing, and vision. The examination revealed
spastic quadriparesis, spastic dysarthria, dysphagia, and severely affected eye movements, with bilateral intranuclear
ophthalmoparesis. Repeat MRI scans demonstrated recurrence of the pontomesencephalic cyst to its previous size and
extensive surrounding T2-weighted signal abnormalities in
the pons, mesencephalon, and medulla. The hydrocephalus
remained decompressed, and the mass of the coiled basilar
artery aneurysm remained unchanged in appearance.

696 | VOLUME 52 | NUMBER 3 | MARCH 2003

FIGURE 4. A to C, T1-weighted
sagittal (A), spin density-weighted
axial (B), and T2-weighted axial (C) MRI scans from an examination performed 6 months after the second coiling procedure, demonstrating a
cystic-appearing mass occupying the majority of the pons and expanding
the pons posterior to the coil mass. The mass is slightly hyperintense to
cerebrospinal fluid in A, hyperintense to cerebrospinal fluid in B, and
isointense to cerebrospinal fluid in C. The findings were thought to be
most consistent with a cerebrospinal fluid-filled cystic space with a high
protein content. The mass of the coiled aneurysm was not significantly
larger than the mass of the aneurysm before treatment (allowing for artifacts secondary to the metallic stent). D, fluid-attenuated inversion recovery axial MRI scan obtained inferior to the cystic pontine mass, demonstrating an extensive T2-weighted signal abnormality involving the
inferior pons, extending into the middle cerebellar peduncles bilaterally,
and the midbrain, which was thought to be consistent with edema and/or
ischemic changes.

The patient was returned to the operating room for reexploration and shunting of the cyst, with frameless stereotactic
guidance. The cyst was easily entered through its mid-right
lateral wall, at the level of the tentorial notch. Aspiration
yielded return of a very thick yellow fluid with a measured
protein level of 4300 mg/dl; residual fluid coagulated in the
syringe (Froin’s syndrome). Exploration within the cyst failed
to demonstrate exposure of the coiled aneurysm or inflammatory changes. A valveless cyst-peritoneal shunt was then constructed. Surgery was again followed by significant improvement of the patient’s neurological deficits. At the 3-month
follow-up examination, the patient’s symptoms remained stable, but repeat MRI scans revealed cyst enlargement. Because
of the satisfactory clinical condition of the patient, no further
treatment was performed.

DISCUSSION
Indications for surgical versus endovascular repair of intracranial aneurysms continue to evolve. Endovascular techniques are particularly valuable for aneurysms that are diffi-

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PONTINE CYST AFTER BASILAR ARTERY TRUNK ANEURYSM COILING

cult to approach directly, including aneurysms of the midbasilar artery trunk. Although a craniotomy is avoided,
endovascular coil occlusion of an intracranial aneurysm is an
invasive procedure associated with morbidity and uncertainties regarding permanent aneurysm obliteration. The most
common causes of procedural morbidity and death related to
endovascular therapy are thromboembolism, intraprocedural
aneurysmal rupture, catheter-related arterial vasospasm or
dissection, and coil migration (2, 4, 5, 7, 9, 13, 18, 19, 21, 22,
25–31, 37, 40). To our knowledge, intra-axial cyst formation
after endovascular coil occlusion of an intracranial aneurysm
has not been previously described.
Endovascular coil occlusion has been moderately successful
in relieving pretreatment neurological symptoms attributable
to aneurysmal mass effect (12, 15, 18, 22, 23, 38, 39). However,
in rare cases the coil mass itself can exert pressure on adjacent
brain parenchyma or cranial nerves, causing new neurological
deficits or worsening of preexisting symptoms of aneurysmal
mass effect (12, 14, 18, 20, 22, 23, 37). Aneurysms of the
posterior fossa may cause brainstem compression (1, 3, 6, 8, 10,
11, 24). Tateshima et al. (37) described one case of worsening
symptoms of brainstem compression after endovascular coil
occlusion of a basilar tip aneurysm. In contrast, although the
presenting neurological symptoms of the pretreated aneurysm
for our patient might have been related to brainstem compression or focal ischemia caused by aneurysm enlargement before
endovascular treatment, the dramatic development of progressive brainstem dysfunction and its recurrence after the
first operation seemed clearly attributable to the enlarging cyst
within the brainstem.
The cause of formation of this intra-axial cyst deep to the
coiled aneurysmal mass remains uncertain. It is possible that
the mass effect from the aneurysm itself was the basis for
development of the cyst and that the coiling procedure was
incidental to cyst formation. This is unlikely, because of the
long history of the aneurysm’s existence and the absence of the
cyst in two MRI studies performed in the 2 years before
endovascular treatment. Also, the cyst progressed clinically
and radiologically despite nearly complete coil occlusion of
the aneurysm. The development of the cyst after aneurysm
treatment and the infratentorial location differentiate this case
from a few previous reports of parenchymal supratentorial
cysts associated with untreated aneurysms (17, 32, 36). However, the operative and pathological findings of nonspecific
gliosis are consistent with the biopsy findings for a perianeurysmal cyst reported by Sato et al. (32).
Although endovascular therapy seems likely to be the underlying cause of cyst formation in this case, the pathophysiological
mechanism is unclear. A series of small chronic ischemic events
could have resulted in cyst formation; however, the patient’s
symptoms seemed consistent with gradual cyst enlargement,
rather than discrete events typical of ischemic phenomena. If a
small area of parenchyma adjacent to the aneurysm was infarcted, it might have served as a focus of least resistance for
accumulation of exudate from the aneurysm, which occurred
during thrombus formation and maturation.

NEUROSURGERY

Exacerbation of direct mechanical compression from the aneurysm by the coiled mass would have been expected to cause
earlier sustained symptoms of brainstem dysfunction, before
substantial parenchymal loss and secondary cyst formation. Additionally, the progressive symptomatic enlargement of the cyst
argues for an ongoing pathophysiological process, rather than
encephalomalacia attributable to a prior insult. However, we
cannot exclude the possibility of a water hammer-type effect of
the aneurysm on the adjacent tissue, perhaps attributable to
conversion of the pulsatile sac to a semirigid mass after coiling,
which transmitted a pulsatile wave throughout the brainstem,
causing cystic encephalomalacia. Studies by Sorteberg et al. (34,
35) have demonstrated alterations of intra-aneurysmal pressures,
pressure amplitudes, and flow after coiling, although it is unclear
how these changes might affect extra-aneurysmal structures.
Normal pulsations from the basilar artery could have been transmitted to the brainstem via the coil mass. Before endovascular
treatment, the same pulsations might have exerted less pressure
on the brainstem, because of the more compliant nature of the
aneurysm sac.
On the basis of extensive investigations of the pathophysiological features of syringomyelia in Chiari I malformations, Heiss et
al. (16) postulated a piston-like effect of the cerebellar tonsils at
the foramen magnum, increasing cerebrospinal fluid pressure in
the spinal subarachnoid space and causing cerebrospinal fluid to
enter the cord parenchyma across the cord surface. A similar
mechanism of cyst formation might be postulated in the present
case, with the pulsatile coiled aneurysm acting as the piston,
partially occluding the subarachnoid space at the pontine level
and increasing cerebrospinal fluid pressure caudally. However,
the cyst fluid in our case was highly proteinaceous, as opposed to
that of the hydromyelic spinal cord.
An alternative hypothesis of inflammation around the aneurysm wall after endovascular stenting and coil occlusion,
with secondary involvement of the adjacent pontine parenchyma, seems unlikely, on the basis of the MRI appearance
and the gliotic histological features of the cyst wall. Similarly,
subclinical hemorrhage seems highly unlikely, on the basis of
the clinical profile, the postcoiling angiographic appearance,
and the absence of direct communication between the aneurysm and the cyst, as observed during surgery.
Although this complication is likely to be a rare occurrence,
cumulative experience with endovascular coil occlusion of
large or giant posterior fossa aneurysms is also relatively
limited. As more experience with endovascular treatment of
such lesions is accumulated, it should become clear whether
intraparenchymal cyst formation is a recurring complication,
and perhaps its underlying pathophysiological mechanisms
can be elucidated. Cyst formation should be considered in
cases with delayed brainstem findings after endovascular coil
occlusion of an aneurysm in the posterior fossa.

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Acknowledgments
We are deeply indebted to Charles M. Strother, M.D., for thoughtful review of
the manuscript and to Mary Soper for assistance with manuscript preparation
and figure reproduction.

COMMENTS

F

riedman et al. describe a unique case of symptomatic cyst
formation within the parenchyma of the brainstem after stentassisted coil embolization of a basilar artery aneurysm. Although
there have been reports of supratentorial parenchymal cysts de-

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PONTINE CYST AFTER BASILAR ARTERY TRUNK ANEURYSM COILING

veloping after coil embolization, this report is the first to describe
such a lesion in the brainstem. The contents of the cyst were
extremely proteinaceous, and the biopsy of the cyst wall demonstrated gliotic change without inflammation. The cyst was
adequately treated with drainage followed by shunting.
The authors postulate several theories regarding the pathophysiology of the cyst, and we agree that none of these theories adequately explain the cyst’s development. We have had
extensive experience with intracranial stents in animal models, and histological studies have shown that those perforating
vessels “jailed” by the struts of the stent remain patent. The
interval between stent implantation and sacrifice with removal of the stent in these studies has been relatively shortterm (1 mo), so the long-term results in humans can only be
inferred. Although the vessel may remain patent, its autoregulatory capacity may be lost. Over time, chronic hypoperfusion could lead to changes resulting in encephalomalacia and
a breakdown of the blood-brain barrier. This in turn could set
up a transudative process that gradually forms a Froin’s-type
collection. We freely admit that this explanation comes no
closer to adequately defining the cyst’s development than the
theories described by the authors, but we anticipate a growing
understanding of intracranial stenting with future studies.
Jay U. Howington
L. Nelson Hopkins
Buffalo, New York

T

he authors present a case of pontine, intraparenchymal
cyst formation after combined stenting and embolization
of an upper basilar trunk aneurysm. The figures clearly demonstrate the time course of clinical and neuroradiological
events. The etiology underlying the cyst formation is unclear,
although the authors do provide an excellent discussion of the
possible pathophysiological mechanisms. It is interesting to
note that all previous case reports of aneurysms with associated parenchymal cysts involved large or giant lesions, generally with thrombosis or calcification. These findings may
well underscore the authors’ supposition that coiling changed
the aneurysmal “pulsatile sac” to a “semirigid mass” and that
this might have influenced subsequent cyst formation. The
therapeutic strategies, i.e., stenting and coiling of the large
aneurysm embedded in the upper brainstem, as well as the
drainage of the pontine cyst, were well chosen.
Bernd Richling
G. Michael Lemole, Jr.
Salzburg, Austria
Andreas Gruber
Vienna, Austria

T

his very interesting case report describes a 70-year-old
woman who developed a very large, symptomatic pontine
cyst 1 year after stenting and endovascular coil occlusion of a
large mid-basilar artery aneurysm. The authors do not know
the etiology of this cyst formation but present some interesting
hypotheses. These include subclinical ischemic events related
to the aneurysm coiling, exacerbation from direct mechanical
compression of the coiled aneurysm causing parenchymal loss
and cyst formation, pulsatile force from arterial pressure on a
semirigid coil mass affecting the adjacent brain tissue causing
cystic encephalomalacia, and peri-inflammatory changes
around the aneurysm secondary to endovascular therapy. All
of these are speculative, however, and the formation of this
pointine cyst may be coincidental and not related at all to the
therapy.
Nonetheless, this is a very interesting, well-documented
case report with a good description of the surgical pathology.
To my knowledge, there have been no prior reports describing
this type of association. It will be interesting to see whether
other reports describing a similar association of developmental pontine cysts after endovascular coiling of aneurysms arise
in the future.
Randall T. Higashida
Interventional Neuroradiologist
San Francisco, California

T

he authors report a very unusual outcome after stenting
and coiling of a basilar aneurysm in a 70-year-old woman.
The development of a symptomatic pontine cyst 1 year after
treatment is unusual. It is unlikely that the mass of coils is
related to a mechanical cause. The Discussion reviews most of
the possible etiologies, including ischemic events produced by
various mechanisms. The only aspect that has not been taken
into consideration is the electrical nature of the detachment of
the Guglielmi detachable coils; Martin et al. (1) considered this
mechanism likely to be responsible for injury to adjacent neural tissue without cystic development in one of their patients.
This incident is exceptional enough not to be regarded as a
predictable complication but rather as an additional reason to
carefully follow patients by means of magnetic resonance
imaging and magnetic resonance angiography after complete
exclusion of an aneurysm mass.
Pierre Lasjaunias
Paris, France

1. Martin D, Rodesch G, Alvarez H, Lasjaunias P: Preliminary results of
embolisation of nonsurgical intracranial aneurysms with GD coils: The 1st
year of their use. Neuroradiology 38[Suppl 1]:S142–S150, 1996.

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