J Neurosurg 70:847-852, 1989

Vascular malformations of the brain stem
DOUGLAS CHYATTE, M.D.

Section of Neurological Surgery, Subsection of Cerebrovascular Diseases, Yale University School of
Medicine, New Haven, Connecticut
v,, Vascular malformations of the brain stem are unusual lesions that may pose a diagnostic and therapeutic
challenge. Seven patients with vascular malformations involving the brain stem were evaluated; six were treated
surgically, with complete obliteration of the lesion in five patients. In five patients symptoms developed only
after a hemorrhage had occurred, and three of these suffered a rebleed before appropriate treatment was given.
Angiography failed to demonstrate lesions in three cases, which did not appear to protect from repeat
hemorrhage since two of the three rebled. There were no operative deaths, and no patients were made
permanently worse after surgery. Useful recovery occurred commonly after appropriate treatment and appeared
to be possible even in patients who had suffered a catastrophic neurological deficit at the time of presentation.
These data indicate that surgical removal of the lesion may be warranted in some patients with symptomatic
brain-stem vascular malformation.
KEY WORDS
arteriovenous malformation
brain stem
9 brain-stem hematoma
9

V

ASCULAR malformations o f the brain stem are
unusual lesions and often present with catastrophic neurological dysfunction. 1,4-7,9-~l, 16,19,23,
24,26,28Because o f their treacherous location, surgical removal of these anomalies has been considered hazardous or impossible.13"16'24'25 Reports of resection of these
lesions are rare and few authors recommend surgical
treatment o f brain-stem malformations, l-3,s,6'8'llA2,14,15,
17,18,21-23,27
Seven patients with vascular malformations involving the brain stem were referred to us for evaluation
and treatment. The angioarchitecture of the lesion and
the clinical presentation led to surgical treatment in six
cases with acceptable management results. Surgical
obliteration appears to be possible for some of these
lesions and can be performed at an acceptable risk.
Summary of Cases

Clinical Presentation and Treatment
A summary o f the clinical aspects of these seven
patients is presented in Table 1. The age at onset ranged
from 16 to 43 years (mean 32 years). Five patients were
male and two were female.
Intracranial hemorrhage was the most c o m m o n
cause of presentation and occurred in five patients.
Three patients, two with malformations limited exclusively to the brain-stem surface and one with a lesion
involving the surface and the intra-axial region, presented abruptly with subarachnoid hemorrhage (SAH).

J. Neurosurg. / Volume 70/June, 1989

9 subarachnoid hemorrhage

9

Two other patients with strictly intra-axial malformations came to medical attention because o f intrinsic
brain-stem hematomas; in both instances, s y m p t o m s
developed insidiously over several weeks. Because o f
the temporal profile of onset in these two patients, one
was thought to have a brain-stem neoplasm and the
other a demyelinating disease before the correct diagnosis was made at surgery. The remaining two patients
presented with progressive brain-stem dysfunction not
related to hemorrhage. This was thought to be due to
"steal" in one case and to venous hypertension or local
mass affect in the other.
All but one patient exhibited a profound neurological
deficit that correctly localized the lesions to the brain
stem. The one exception experienced an SAH not associated with localizing findings. Two patients (Cases 2
and 5) suffered respiratory arrest within 24 hours o f
hospital admission. Both of these patients m a d e useful
recoveries after appropriate therapy.
Angiography failed to demonstrate the malformation
in three patients (in two of these, angiography was
performed more than once). In all three patients the
correct diagnosis was made at the time o f surgery (two
had strictly intra-axial malformations and one had a
malformation limited exclusively to the brain-stem
surface).
Preoperative computerized tomography (CT) and
magnetic resonance (MR) imaging were performed on
all patients and correctly demonstrated the location and
extent of intra-axial involvement in five o f the six
847

D. Chyatte
p a t i e n t s who u n d e r w e n t surgical exploration. I n one
p a t i e n t (Case 1) the C T a n d M R studies were both
i n t e r p r e t e d as s h o w i n g a n i n t r a - a x i a l lesion o f the tect u m ; however, surgical e x p l o r a t i o n revealed that the
m a l f o r m a t i o n was l i m i t e d to the b r a i n - s t e m surface.
O f the five p a t i e n t s w h o p r e s e n t e d with hemorrhage,
three experienced a repeat h e m o r r h a g e before appropriate t r e a t m e n t was given. T w o o f the three patients
w h o suffered r e c u r r e n t h e m o r r h a g e s had n o r m a l angiograms.
Results of Treatment
Six o f the seven p a t i e n t s u n d e r w e n t surgery. I n five
p a t i e n t s c o m p l e t e o b l i t e r a t i o n o f the lesion was
achieved. This was c o n f i r m e d b y postoperative angiogr a p h y i n patients i n w h o m the m a l f o r m a t i o n was visible
o n the preoperative a n g i o g r a m . O n e p a t i e n t (Case 6),
with a n intra-axial p o n t i n e m a l f o r m a t i o n , required reo p e r a t i o n because the m a l f o r m a t i o n was n o t identified
or obliterated at the t i m e o f the first surgery. A n o t h e r
p a t i e n t (Case 7) h a d a residual s y m p t o m a t i c malform a t i o n after e n d o v a s c u l a r e m b o l i z a t i o n a n d was
treated with surgical excision. All six p a t i e n t s who
u n d e r w e n t surgery recovered; however, two had in-

creased neurological deficits i m m e d i a t e l y following surgery. At their postoperative follow-up e x a m i n a t i o n , five
patients showed i m p r o v e m e n t over their preoperative
status. T h e surgical p a t i e n t who was worse (Case 3)
deteriorated after g a m m a - b e a m irradiation, a n d her
poor neurological f u n c t i o n appears to be related to
radiation rather t h a n to her initial surgery. Three of the
six patients w h o were treated surgically have r e t u r n e d
to their p r e m o r b i d o c c u p a t i o n s . T w o of the three patients who were u n e m p l o y e d after surgery were n o t
e m p l o y e d before their illness. All b u t o n e o f these patients (Case 3) are sufficiently i n t a c t to be employable.
O n e p a t i e n t (Case 4) with a m i x e d surface a n d intraaxial m a l f o r m a t i o n was referred for stereotaxic Bragg
peak p r o t o n b e a m irradiation. However, he was n o t
treated because this did n o t a p p e a r to be financially
feasible. H e r e m a i n s e m p l o y e d b u t c o n t i n u e s to experience progressive neurological deterioration.

Representative Cases
Case 2
This 56-year-old r i g h t - h a n d e d m a n was well until 1
m o n t h before a d m i s s i o n w h e n he n o t e d the onset of

TABLE 1
Clinical summary of seven patients with vascular malformations of the brain stem *
Case Age,~- Lesion
Type of
Presentation
No. Sex Location.t Hemorrhage
1 36, F quadrigem- SAH • 2 abrupt headache,
Parinaud's syndrome
inal plate
2
3

4
5

6

7

Angiographic
Findings
normal • 2

Treatment

supracerebellar,
subtentorial
resection
small malformation retromastoid resection
SAH • 1 abrupt headache,
56, M lateral
fed by PICA
respiratory arrest
medulla
malformation fed
suboccipitaltransvermian
21, F 4th ventricle SAH x 2 abrupt headache,
by penetrating
surgical exploration
rt VI, VII spastic
& brachium
arteries
without resection,
ataxic quadriparesis
pontis
gamma-beam radiation
large AVM fed
none
progressive tremor,
35, M midbrain
none
by basilar
diplopia, quadripaperforators
resis, ataxia
normal
suboccipital evacuation of
22, M medulla
medullary subacute, ascending
hematoma & resection of
quadriparesis, ataxia,
hemamalformation
toma x 1 bilat V, VII, IX, X, XII;
respiratory arrest
normal • 2
1: subtemporal, transsubacute, progressive
42, M pons
pontine
tentorial evacuation
quadriparesis &
hemaof hematoma
toma x 2 dysarthria
2: repeat evacuation of hematoma & resection of
malformation
1:
embolization
subacute
headache,
dural
fistulae
43, M medulla
none
w/PVA
nausea, vomiting,
w/venous varix
2: suboccipital excision
hemiparesis, ataxia
at craniocervical
of recurrent
junction
malformation

Follow-Up
Results
improved Parinaud's
syndrome; employed
(field biologist)
neurologically
normal;
working (farmer)
progressivebrain-stem
dysfunction beginning
6 mos after irradiation;
not employed
progressive deficit;
employed (mechanic)
improved;mildly spastic
ataxicgait &
dysarthria; not employed
improved; mild dysarthria & rt hemiparesis;
employed (executive)

improved; mild rt
hemiparesis; not
employed

* SAH = subarachnoid hemorrhage; PICA = posterior inferior cerebellarartery; AVM = arteriovenous malformation; PVA = polyvinylalcohol.
Roman numerals indicate cranial nerves affected.
t Age (years) at treatment.
:~In Cases 1 and 2 the lesion was limited exclusivelyto the surface of the brain stem; in Cases 3 and 4 the lesion was intra-axial with involvement
of the brain-stem surface; in Cases 5 and 6 the lesion was exclusivelyintra-axial; in Case 7 the lesion was predominantly a dural fistula.
848

J. Neurosurg. / Volume 70~June, 1989

Vascular malformations of the brain stem
intermittent double vision. On the day of admission he
experienced the abrupt onset of headache.
On examination, he preferred to sleep but was easily
aroused. His neurological examination was otherwise
normal. A C T scan showed blood in the fourth ventricle
and in the subarachnoid space around the brain stem.
Shortly after admission, he became obtunded and suffered a respiratory arrest. H e was intubated and a
ventriculostomy was placed for cerebrospinal fluid
drainage resulting in rapid improvement. Eventually,
the ventriculostomy was converted to a ventriculoperitoneal shunt. Angiography showed a small vascular
lesion filling f r o m the left posterior inferior cerebellar
artery (PICA).
At surgery, the left lateral medulla was approached
through a left retromastoid craniectomy. The lesion
itself was a "transistor"-shaped vascular malformation
on the surface o f the medulla. It was fed from pial
branches rather t h a n from the subarachnoid portion of
the PICA that coursed past the lesion. The malformation was cauterized and removed. The patient tolerated
surgery without neurological incident and m a d e an
uneventful recovery. At follow-up examination, he was
neurologically n o r m a l and had returned to his previous
occupation as a farmer.

Case 4
This 35-year-old left-handed mechanic presented
with a 5-year history of progressive intention tremor
involving the right a r m and leg, diplopia, unsteady gait,
right arm and leg weakness, and intermittent headache.
He had no k n o w n episodes of intracranial hemorrhage.
On examination, he had a left medial longitudinal
fasciculus deficit, m a r k e d intention tremor in both the
fight arm and fight leg, and a mild right hemiparesis.
He was able to walk with assistance but, in addition to
his tremor, he had a spastic ataxic gait. Both plantar
responses were extensor and he had generalized hyperreflexia. A C T scan (Fig. 1) and angiograms (Fig. 2)

FIG. 1. Case 4. Contrast-enhanced computerized tomography scan showing an arteriovenous malformation involving
the midbrain.

showed a large mixed surface and intra-axial malformation involving the midbrain. His progressive symptoms were believed to be due to arterial "steal." He was
not judged to be a suitable candidate for surgery or
endovascular embolization and was referred for Bragg
peak proton b e a m irradiation; however, this treatment
was not possible because o f financial considerations.
He continued to show progressive deterioration.

FIG. 2. Case 4. Left vertebral anteroposterior (left) and lateral (center) subtraction angiograms and left carotid
subtraction angiogram (right) showing an arteriovenous malformation involving the upper brain stem.

J. Neurosurg. / Volume 70~June, 1989

849

D. Chyatte

FIG. 3. Case 6. Magnetic resonance image showing a fluidfilled cystic lesion of the pons.

Case 6

This 42-year-old fight-handed man had previously
been healthy until he insidiously developed a progressive gait disturbance, tingling in the hands and feet,
tremulousness, slurred speech, and right-arm weakness
6 weeks before admission. On examination he had mild
dysaxthria and fight-sided hemiparesis involving the
face, arm, and leg. Deep-tendon reflexes were hyperactive throughout and the right plantar response was
extensor. His gait was ataxic. A C T scan showed a nonenhancing hypodense lesion in the pons, and M R imaging revealed a cystic lesion in the pons with a "fluid
level" (Fig. 3). Angiography was normal.
A left subtemporal transtentorial approach was used
to expose the pons, which appeared to be enlarged.
The pons was opened revealing a cystic cavity filled
with hemorrhagic fluid which was drained. No other abnormalities were found and several biopsy samples of
the cyst wall were taken. Histological examination of
these samples showed no evidence of abnormality. Immediately following surgery the patient's right-sided
weakness was somewhat worse, but this gradually improved. Progressive gait difficulties, dysarthria, tremulousness, tingling in the hands and feet, and right-sided
weakness recurred several weeks after surgery. On neurological examination 8 weeks after surgery, his condition was somewhat worse than at his preoperative
examination. Repeat CT and M R studies showed a recurrent h e m a t o m a in the pons. Angiography was again
normal.
Reexploration o f the pons was performed through
the same exposure. The previous incision in the pons
was enlarged and the h e m a t o m a evacuated. A cluster
o f tangled blood vessels was found in the wall of the
hematoma cavity which was coagulated and removed.
The patient's condition was no worse following the
second operation and thereafter it gradually improved.
At his last follow-up examination, his only residual
deficit was a mild right-sided hemiparesis and dysar850

FIG. 4. Case 7. Contrast-enhanced computerized tomography scan showing a vascular lesion at the craniocervical
junction.
thria. He has returned to his previous occupation as a
business executive.
Case 7

This 43-year-old right-handed man had suffered transient episodes of severe right-sided headaches, nausea
and vomiting, blurred vision, and transient right-arm
weakness for several years before admission. Five days
before admission he again developed severe right-sided
headache, nausea and vomiting, and later the gradual
onset of fight-sided arm and leg weakness. Over the
next several days his condition progressively worsened
instead of improving as previously. He was noted to be
lethargic at times. There was no history of trauma and
he was otherwise well.
On examination, the patient was lethargic, but could
easily be aroused. He had a moderate amount of weakness in the right arm and leg, worse distally than proximally, and the arm was weaker than the leg. He had
generalized hyperreflexia, and both plantar responses
were extensor. Sensation to pinprick and touch and
proprioception were severely affected on the right side
of the body. Testing of the cranial nerves and visual
fields was normal. A C T scan with and without contrast
enhancement did not show any evidence of hemorrhage, but revealed a large enhancing lesion at the
craniocervical junction (Fig. 4). There was no hydrocephalus. A lumbar puncture was traumatic but not
xanthochromic. Angiography revealed dural fistulae filling exclusively from the left external carotid artery with
large venous varices surrounding the medulla (Fig. 5).
Endovascular embolic obliteration of the dural fistulae using polyvinyl alcohol was performed shortly
after admission. Although he initially improved, hiccups and worsening right-sided weakness appeared 3 or
4 weeks after embolization. Repeat angiography showed
that the dural fistulae were still patent, now filling not
from the left external carotid circulation but via extradural branches of the left vertebral artery. Direct intraJ. Neurosurg. / Volume 70 / June, 1989

Vascular malformations

of the brain stem

FIG. 5. Case 7. Subtracted external carotid angiogram,
anteroposterior view, showing a dura-based arteriovenous
shunt with intradural venous varices.
dural arterial shunting into the venous varices was now
apparent from the left anterior inferior cerebellar artery.
Surgical exposure o f the lesion was achieved through a
midline suboccipital approach. The dural fistulae were
identified and cauterized. Numerous small arterial
channels from arterial pial vessels and larger vessels
traveling in the subarachnoid space and fourth ventricle
supplied arterial blood to the venous varices. These
were cauterized and sectioned and the venous varices
were removed. On the right side of the medulla, a varix
was deeply embedded into the substance of the brain.
Efforts to dissect this out o f the brain stem were judged
to be injudicious, and this varix was thrombosed with
the neodymium:yttrium-aluminum-garnet (Nd:YAG)
laser and an aneurysm clip was applied across its venous
outflow.
Postoperatively, the patient developed transient bilateral vocal cord paralysis which required tracheostomy for a short period of time. His hemiparesis has
gradually improved and at last follow-up examination
was substantially better than at the time of admission.
He is fully ambulatory and has no cranial nerve deficits
at this time. Postoperative angiography showed no residual arteriovenous malformation.
Discussion

Vascular malformations of the brain stem are unusual lesions. The Cooperative Study 19found that 2% of
all intracranial vascular malformations involve the
brain stem. This series confirms the observation of
others that brain-stem malformations most commonly come to medical attention only after intracranial
hemorrhage has occurred. LS,l3-15,19,23,24,29Young adults
appear to be affected most often. Subarachnoid hemorrhage occurs more frequently than intra-axial hematoma; however, both are commonly accompanied by
severe neurological dysfunction which usually localizes
the lesion to the brain stem. Less frequently, brain-stem
malformations produce progressive neurological dysfunction not related to identifiable intracranial hemorrhage. Although the risk of hemorrhage from asymptomatic lesions is unknown, these findings and those
J. Neuroxurg. / Volume 70/June, 1989

reported by others suggest that the risk o f recurrent
hemorrhage from symptomatic lesions in the absence
of definitive therapy is substantial. 1,27
The presentation and treatment o f patients in this
series were related to the lesion angioarchitecture. T w o
patients (Cases 1 and 2) had malformations limited
exclusively to the brain-stem surface. Both lesions received arterial blood from branches of the vertebrobasilar system at the pial surface or in the subarachnoid
space and, as a consequence, the bulk of these lesions
was limited to the pial surface o f the brain stem or the
subarachnoid space. Both manifested abruptly with
SAH. Surgical excision was technically feasible and well
tolerated. In two other patients (Cases 3 and 4), the
malformations received arterial supply both from intraaxial penetration arteries and from surface arteries.
Abrupt presentation with SAH occurred in one (Case
3). In two patients (Cases 5 and 6), the malformations
were entirely intra-axial and were fed exclusively by
penetrating branches of the vertebrobasilar system.
Both of these lesions caused intra-axial hematoma leading to insidious, progressive brain-stem dysfunction.
This temporal profile is not c o m m o n l y associated with
intracranial hemorrhage and may lead even the most
astute clinicians away from the correct diagnosis. 24'27
Finally, in one patient (Case 7), arteriovenous shunting
from the external carotid and extracranial vertebral
arteries occurred in the dura and was associated with
large intradural venous varices. Sources o f arterial
shunting from the intradural vertebrobasilar system
became apparent after partial treatment. The angioarchitecture and presentation o f this lesion were similar
to those of spinal dural arteriovenous malformations. 2~
Although angiography remains the cornerstone o f
diagnosis in patients with suspected intracranial vascular malformations, this series is unique in the high
incidence of negative angiography. Failure to demonstrate the vascular malformation on preoperative angiography may occur because of small lesion size or
because the lesions are not filling at the time of angiography. Regardless of the cause, in this series rebleeding occurred at the same high incidence both in patients
whose vascular malformations could not be demonstrated on angiography and in those with angiographically demonstrable malformations. Decisions regarding
therapeutic intervention, therefore, cannot be based
exclusively on whether a vascular malformation is seen
on angiography. Both CT and M R studies complement
angiography and better define the anatomy o f these
lesions. In particular, the extent of intra-axial malformations can often be predicted based on the M R or CT
images. Despite these high-resolution studies, the operative findings m a y differ from those predicted.
The results o f this series show that, despite a catastrophic neurological presentation, useful recovery is
c o m m o n after appropriate treatment. In this series,
even patients who presented with respiratory paralysis
eventually recovered. Overall, six o f the seven patients
were treated surgically and complete obliteration o f the
vascular malformation was achieved in five patients.
851

D. C h y a t t e
There were no deaths, and no significant morbidity was
related to surgical intervention. Patients with small
intra-axial malformations tolerated surgical resection
without additional permanent neurological deficits.
These results, which are somewhat better than those
reported by others, most likely reflect patient differences
rather than fundamental variations in surgical technique. 1'5'6'23 S u r g e r y a p p e a r s to be w a r r a n t e d in s o m e
p a t i e n t s with b r a i n - s t e m v a s c u l a r m a l f o r m a t i o n s . Alt h o u g h s o m e m a l f o r m a t i o n s m a y l e n d t h e m s e l v e s to
surgical resection, i n j u d i c i o u s efforts to resect lesions
with extensive i n t r a - a x i a l c o m p o n e n t s m a y result in
disaster. 6 F o r these m a l f o r m a t i o n s , s o m e success has
b e e n r e p o r t e d w i t h h i g h - e n e r g y i r r a d i a t i o n ; however, as
o u r Case 3 illustrates, this m o d e o f t r e a t m e n t is not
w i t h o u t risk. 25 R a d i a t i o n t h e r a p y does a p p e a r to lower
t h e l o n g - t e r m d a n g e r o f r e p e a t h e m o r r h a g e , b u t this
effect is n o t i m m e d i a t e a n d m a y leave the p a t i e n t
u n p r o t e c t e d for several years. Little is k n o w n a b o u t the
l o n g - t e r m c o n s e q u e n c e s o f this t y p e o f t r e a t m e n t . End o v a s c u l a r e m b o l i z a t i o n is u s u a l l y n o t possible because
o f t h e a n a t o m i c a l a n d flow characteristics o f these
lesions. Surgical r e s e c t i o n s h o u l d be c o n s i d e r e d for
symptomatic brain-stem malformations before other
m o d e s o f t r e a t m e n t are e x p l o r e d .
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Manuscript received May 17, 1988.
Accepted in final form October 24, 1988.
Address reprint requests to: Douglas Chyatte, M.D., Section of Neurological Surgery, 333 Cedar Street, New Haven,
Connecticut 06510.
J. Neurosurg. / Volume 70~June, 1989