J Neurosurg Pediatrics 10:50–55, 2012

A thrombosing, giant, distal posterior cerebral artery
aneurysm in a newborn infant
Case report
Pulat Akin Sabanci, M.D.,1 Yavuz Aras, M.D., 2 Aydin Aydoseli, M.D., 2
Serra Sencer, M.D., 3 Altay Sencer, M.D., 2 Mine Erguven, Ph.D., 4 and Nail Izgi, M.D. 2
Department of Neurosurgery, Karabük State Hospital, Karabük; Departments of 2Neurosurgery and
Radiology, İstanbul Medical Faculty, İstanbul University; and 4Department of Biochemistry, Faculty of
Medicine, Yeni Yüzyıl University, İstanbul, Turkey
1
3

Intracranial aneurysms are extremely rare in infancy. No consensus has yet been developed about the exact
treatment of this rare situation. The authors report the case of a 47-day-old male infant who had multiple seizures on
the same day, leading to the diagnosis of an intracranial aneurysm. The case was managed conservatively with close
imaging follow-up, and the patient had a good recovery. The results of neurological examination were completely
normal at the 5-year follow-up visit.
These rare lesions may be suspected on the basis of clinical findings and correctly diagnosed with current neuroradiological imaging modalities. The authors believe this report contributes valuable imaging data on rare childhood
aneurysms to the literature, as well as emphasizing the importance of clinical and imaging information in therapeutic
decision making in children with intracranial vascular problems.
(http://thejns.org/doi/abs/10.3171/2012.3.PEDS11473)

Key Words
imaging
•

I

•

infancy
treatment

•

•

cerebral aneurysm
vascular disorders

ntracranial aneurysms are thought to occur as a re-

sult of chronic hemodynamic stresses at the branching
points of arteries. This process needs time to produce
aneurysmal changes, and thus intracranial aneurysms are
rare in children and extremely rare in newborns and older
infants.29 Aneurysms in pediatric patients are reported to
represent 0.17%–4.6% of the total number of intracranial
aneurysms in the general population.3,9,12,21,29,30,34 Aneurysms in children younger than 1 year (that is, infants)
have only been described in case reports or in small series.3,19
Abbreviations used in this paper: ACA = anterior cerebral artery;
ACoA = anterior communicating artery; BA = basilar artery; CTA
= CT angiography; DSA = digital subtraction angiography; ICA =
internal carotid artery; ICH = intracerebral hemorrhage; MCA =
middle cerebral artery; MRA = MR angiography; PCA = posterior
cerebral artery; PICA = posterior inferior cerebellar artery; SAH =
subarachnoid hemorrhage; VA = vertebral artery.

50

•

thrombosed aneurysm

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The clinical and radiological presentation, location,
and morphological characteristics of the aneurysms in
infants differ from those found in adults. The differences
include male predominance and a preferential location at
the ICA bifurcation or in the posterior circulation.10,16,22
There are also some cases defined as traumatic or infectious in the literature.3,9 Approximately 73% of the infancy aneurysms appear with initial hemorrhage,3 and these
aneurysms are often smaller than 2.5 cm3. The prognosis of these lesions has improved as a result of improvements in diagnostic techniques such as MRA and CTA,
although there is still a high incidence of bleeding or rebleeding due to a delay in diagnosis.26 Different treatment
modalities can be used for management, such as surgical clipping, resection, cauterization, ligation, or trapping
of the vessel or the parent vessel, endovascular embolization or coiling, and antibiotic therapy (for infectious
aneurysms).17,18,29,32,38 Some cases have been reported in
the literature in which aneurysms in infants have healed
spontaneously by thrombosis.14,15,23,33
J Neurosurg: Pediatrics / Volume 10 / July 2012

Thrombosing aneurysm in a newborn
Case Report

This 47-day-old male infant was admitted because
of repeated bouts of generalized seizures. His prenatal
history and delivery were normal, and the family history
was also unremarkable. He was first brought to a private
local clinic, where transcranial ultrasonography and cranial CT were performed. He was then sent to our institution with the diagnosis of intracerebral hematoma. On
physical examination, the sole pathological finding was a
bulging anterior fontanelle. There was no history or evidence of head injury. He had no external skin lesion. The
results of routine serum tests were within normal limits,
and blood cultures were negative for microbial growth.
The child’s body temperature remained within normal
levels throughout his hospitalization. On cranial CT, a
round lesion with a 2.5-cm diameter and sharp calcific
borders was observed in the left perimesencephalic cistern. There was evidence of a hyperdense clot in the left
sylvian cistern and the left leaflet of the tentorium, with
edema and sulcal/local ventricular effacement in the left
occipital lobe (Fig. 1). A tentative diagnosis was made of
a ruptured intracranial aneurysm and infarction in the
PCA territory due to compression.
Given that the patient was neurologically stable, a
conservative approach was chosen and further neuroradiological imaging was planned. Cranial MRI (Fig. 2)
and MRA (not shown) were carried out. The MRI study
showed the vascular lesion to have a complex internal
signal and intraaneurysmal enhancement possibly compatible with partial or ongoing thrombosis. On the other
hand, occipital edema and leptomeningeal enhancement
due to ishemic edema were also detected. Because complex flow hindered the exact diagnosis on MRI and MRA,
an intracranial CTA study was planned after family consent was obtained.
The CTA study, which was performed on the second
day of admission, showed total filling of the aneurysm
and provided valuable information by showing that the
lesion was located in the distal PCA zone and the parietooccipital artery was not visible; this was thought to
account for the infarction (Fig. 3).
The patient was treated conservatively with antiepi-

Fig. 1. Noncontrast CT images obtained at admission showing a
round lesion in the left perimesencephalic cistern measuring 2.5 cm
(left) and local subarachnoid clot and hypodense edema in the left occipital lobe (right).

J Neurosurg: Pediatrics / Volume 10 / July 2012

Fig. 2. Axial T2-weighted (left) and contrast-enhanced T1-weighted
(right) MR images showing the aneurysm to have a complex flow pattern (loss of signal void) and intraaneurysmal enhancement suggesting
low flow and ongoing thrombosis. There is also edema and ischemic
infarction in the left occipital lobe.

leptic drugs and supportive therapy and was seizure free
with no new neurological signs. On the 5th day of admission, cerebral DSA was performed for definitive diagnosis of the aneurysm and to assess the current status of the
thrombotic process. On DSA, the carotid artery circulation was found to be normal. Left vertebral artery injection showed slow flow in the left PCA and lack of opacity in the aneurysm, suggesting total thrombosis (Fig. 4).
The patient was hospitalized for another 10 days and was

Fig. 3. Axial maximum intensity CTA image revealing enhancement
in the aneurysm located in the distal PCA and loss of the parieoto­
occipital artery.

51

P. A. Sabancı et al.

Fig. 4. Anteroposterior view digital subtraction angiogram obtained
after left VA injection showing slow flow in the left PCA and lack of opacity in the aneurysm, suggesting total thrombosis.

then discharged because there were no new seizures. The
fontanel was soft and he was functioning within expected
normal developmental limits for his age.
Brain MRI performed shortly before discharge demonstrated total thrombosis of the aneurysm and early
signs of atrophy in the affected regions of the left cerebral
hemisphere. At the 1-, 3-, and 6-month follow-up visits,
the child was found to be neurologically normal, demonstrated age-appropriate development, and had had no
new seizures on a regimen of antiepileptic drug therapy.
Follow-up brain MRI performed at the 1-year follow-up
visit showed no sign of the aneurysm, suggesting total
thrombosis followed by obliteration and atrophy in the
parietooccipital region (Fig. 5).
As of this writing, the patient is 5 years old and attending nursery school. His neurological examination findings
are completely normal. The 5-year control cranial MR images were similar to the those obtained at 1-year follow-up,
with left parietooccipital atrophy.

Discussion

In large aneurysm series, aneurysms in pediatric
patients account for only 0.17%–4.6% of the total case
series.3,9,12,21,29,30,34 Male predominance as well as more
frequent involvement of the posterior circulation and distal branches are reported (in comparison with adult case
series).9,12,29
Aneurysms also tend to be larger in children.8 The reported sizes of aneurysms in infants vary between 1 mm
and 9 cm.35 The largest infantile aneurysm was measured
52

Fig. 5. Axial T2-weighted MR image obtained at 1-year follow-up
examination showing no sign of the aneurysm and revealing atrophy in
the occipital cortex.

as 8 × 9 cm. This huge aneurysm of the PCA was reported
by Ventureyra et al.36 The case involved a 6-month-old
boy with progressive macrocephaly and anemia. A giant
PCA aneurysm was diagnosed. The lesion was clipped
and excised in 2-stage surgery, and the infant was reported to have an uneventful recovery.36 Reviewing pooled
data in their 1997 publication, Tekkök and Ventureyra35
note that the majority (60.9%) of 41 infantile aneurysms
were large (1–2.5 cm) and 19.5% were giant (larger than
2.5 cm). In our case, the infantile aneurysm was located
in the distal PCA territory and was giant, in accordance
with the features described in the literature for similar
lesions.
Different studies report different aneurysm localizations in children. Sencer et al.30 reported on a series of 14
patients—including 2 with double aneurysms—in 2008.
There were 15 anterior circulation aneurysms (6 ICA, 5
MCA, 2 ACoA, 2 ACA) but only 1 posterior circulation
(basilar tip) lesion. In Lv and colleagues’ 2009 article18
describing 25 cases of endovascularly treated aneurysms,
10 patients (40%) had anterior circulation aneurysms (5
MCA, 2 ACA, 2 ACoA, 1 ICA) and 15 had posterior circulation lesions (9 VA, 1 basilar tip, 1 BA, 4 PCA). In
2009 Liang et al.17 reported on a series of 24 patients with
25 aneurysms; 9 patients (36%) had posterior circulation
aneurysms (3 BA, 2 VA, 4 PCA); 16 patients had anterior
circulation lesions (7 ICA, 5 MCA, 2 ACoA, 2 ACA). In a
recent (2010) study by Sanai and colleagues,29 there were
31 anterior circulation aneurysms (14 ICA, 11 MCA, 3
ACoA, 3 ACA) and 12 posterior circulation aneurysms
J Neurosurg: Pediatrics / Volume 10 / July 2012

Thrombosing aneurysm in a newborn
(3 basilar tip, 3 BA, 3 PCA, 2 VA, 1 PICA). According to
these 4 relatively recent studies, despite some controversies, one can say that most common site for intracranial
childhood aneurysms is the ICA, and a greater proportion of cerebral aneurysms are found in the posterior circulation in children than in adults. Huang et al.9 found
similar results in his 2005 literature review, and they also
stressed the importance of 4-vessel angiography during
the diagnostic evaluation of young patients presenting
with SAH. Our patient’s aneurysm was also located in
the posterior circulation.
The diagnosis of an aneurysm and its sequelae, such
as ICH, may be quite difficult on clinical grounds when
dealing with a child who is unable to communicate. Neonatal patients with aneurysms usually present with signs
such as irritability, vomiting, lethargy, apnea, cyanosis,
seizures, and loss of consciousness. The most specific
sign that points to the CNS is seizure.35 In the present
case, the admitting sign was seizure.
The most important first step in diagnosing an infantile ICH is transcranial ultrasonography. With accuracy, sensitivity, and specificity all exceeding 88%, ultrasonography is an invaluable diagnostic tool. It not only
demonstrates the location and size of the hemorrhage but
also delineates the sizes and possible secondary distortion of the ventricular system. It is noninvasive and can
be repeated serially without the need for sedation.35 The
patient in the present case was referred to our clinic after
diagnosis of ICH by means of ultrasonography. Computed tomography and MRI are also useful in the diagnosis
of intracranial aneurysms in infants and yielded valuable
information in our case. Although CT is very sensitive
for acute hemorrhage, it is not specific enough to identify
the cause of the hemorrhage. It may show a focal hyperdense mass with or without enhancement in addition to
the hemorrhage. In our case, CT showed the aneurysm
and border calcifications, which may be attributed to
ongoing thrombosis and capsule organization. Magnetic
resonance imaging successfully revealed internal flow
dynamics of the aneurysm; however, MRA was nondiagnostic due to complex internal flow. Computed tomography angiography, a relatively new noninvasive vascular
imaging tool that is particularly helpful in young children,
also yielded important data in our case. Although the use
of noninvasive vascular imaging did not replace the use of
DSA in our case, it provided valuable baseline data about
the aneurysm and the final diagnosis of total thrombosis could be made by angiography. DSA remains the gold
standard for aneurysms, but only experienced centers can
perform this procedure safely in very young children. Although noninvasive imaging is important in the diagnosis
of childhood aneurysms, DSA remains the gold standard
for decision making with respect to treatment.19
There are also pioneering articles representing infants
with intracerebral aneurysms in the past when modern
radiological techniques were unavailable. Jane11 reported
the case of a 1-year-old boy with a large PICA aneurysm
in 1961. The radiological tests performed for this case
were roentgenogram and pneumoencephalogram. These
tests revealed that the boy had moderate hydrocephalus,
and this was interpreted as a large extracerebellar tumor.
J Neurosurg: Pediatrics / Volume 10 / July 2012

A twist-drill biopsy was performed, and a few cubic centimeters of reddish-brown material was aspirated. During
the following 4 days the boy continued to be irritable and
vomited frequently, and he died despite lateral ventricle
tapping. At autopsy it was discovered that the pathology
provoking the hydrocephalus was not a cerebellar tumor
but rather a left PICA aneurysm. When compared with
today’s modern era, the radiological techniques of those
days were so limited that the pathological condition could
not be accurately diagnosed preoperatively. With the help
of modern technological developments, we are now able
to diagnose an intracranial aneurysm preoperatively. In
light of the developments over the past 50 years, thinking
about what will happen in next 50 years is a bit frightening.
Despite the high perioperative mortality as mentioned by Huang et al.9 and Sencer et al.,30 better results
have been achieved in children with aneurysmal SAH
than in adults. This can be attributed to the increased
plasticity of the childhood cerebrum and the repair capabilities of the maturing brain. Also, the lack of mostly
age-related vascular pathological changes may play a role
in the favorable results.30
Our patient had an uneventful course with conservative management and made a very good clinical recovery under close clinical and radiological follow-up. The
relatively high reported perioperative mortality and the
difficulty related to surgical treatment of young children
also point to the importance of correct therapeutic decision making.
In routine clinical practice for the management of aneurysmal SAH, we believe early surgery or endovascular
treatment (generally but not precisely defined as less than
48–96 hours after SAH) is the gold standard. Aneurysm
treatments, including surgical clipping or endovascular
coiling, are typically advocated when the risk of rupture
is considered to exceed the therapeutic risks.20 Intracranial
aneurysms are challenging to manage clinically. Watchful waiting exposes the patient to continued risk of aneurysm rupture, progressive mass effect on critical neural
structures, local thrombosis causing small perforating
artery infarcts, or distal embolization of thrombus causing large-vessel infarction.8,20 The key point supporting
the conservative management in the present case was the
evidence of partial or ongoing intraaneurysmal thrombosis on the 1st-day MRI and MRA studies. This finding led
us not to behave in an aggressive manner. Factors thought
to affect aneurysm progression and risk of rupture include
aneurysm size, location, and morphological characteristics. Increasingly, factors such as hemodynamics and the
perianeurysmal environment are also being recognized as
possible contributors to aneurysm growth and evolution.20
Partial thrombosis is common (50%–60% of cases)
in giant aneurysms.24,28 However, complete thrombosis of
an intracranial aneurysm is extremely rare.5–7,25,31 It was
reported to occur in 1%–2% of ruptured intracranial aneurysms especially the ones with larger than 2.5 cm in
diameter.4,8 The exact mechanism of spontaneous thrombosis is still unknown, but there are theories concerning
local arterial wall damage, vasospasm, systemic hypotension, and relatively narrow neck.2,4
53

P. A. Sabancı et al.
Black and German1 suggested that a ratio of aneurysm volume (in mm3) to neck surface (in mm2) greater
than 28:1 is associated with spontaneous thrombosis.
Roach27 suggested that aneurysms with a dome-to-neck
ratio greater than 4 were prone to thrombosis, while those
with a dome-to-neck ratio lower than 2.5 tended to rupture. “The bigger the aneurysm, the greater the thrombosis possibility” is a widely accepted theory, but there are
also reports contradicting these ratios.8
Another factor that may play a role in spontaneous
thrombosis of aneurysms is the contrast media used in
angiography. Although the underlying mechanism is not
well understood, some consider that nonionic contrast
media may interfere with clotting (endothelium, platelets,
and red blood cells) and in this way activate coagulation
and thrombosis.7 Some other authors explain the mechanism by intermittent vasospasm caused by the contrast
agent.4,14 Supporting these theories are some reported
cases in which intracranial aneurysms completely disappeared after diagnostic angiography.4,14,37
Kasliwal et al.13 reported a case of 3-week-old neonate with a right-side giant cavernous ICA aneurysm. The
aneurysm was found to be totally thrombosed on DSA
before planning definitive treatment. Follow-up showed
that the patient was doing well 2 years after the diagnosis.
The authors speculated that spontaneous thrombosis can
occur in a neonatal intracranial aneurysm possibly due to
changing hemodynamics at this young age. Because of
this unstable condition, they stressed the importance of
repeated DSA or MRA before embarking on any form of
treatment.13
The question remains as to why almost all cerebral
aneurysm patients have similar factors, as described
above, but only a small portion of them have spontaneous thrombosis. The rarity of the condition hampers discovery of the exact pathophysiology. It must be kept in
mind that the small number of patients in these series
limits the identification of factors affecting these favorable outcomes. Every kind of data concerning childhood
intracranial aneurysm is valuable and more information
is needed.

Conclusions

Although endovascular or microsurgical treatments
options are being debated nowadays, we preferred the
conservative method for the patient described in this case
report. We believe close clinical observation as well as
current radiological imaging facilitated our treatment
strategy in this infant with a spontaneously thrombosing
intracranial aneurysm. Instead of using formulaic treatment algorithms, we must not forget that every patient is
unique and every patient needs personalized treatment.
Disclosure
The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this
paper.
Author contributions to the study and manuscript preparation
include the following. Conception and design: Sabanci, S Sencer,
A Sencer. Acquisition of data: Sabanci. Analysis and interpretation
of data: Sabanci, S Sencer, A Sencer. Drafting the article: Sabanci,

54

S Sencer, A Sencer. Critically revising the article: all authors.
Reviewed submitted version of manuscript: all authors. Approved
the final version of the manuscript on behalf of all authors: Sabanci.
Study supervision: Sabanci, S Sencer, A Sencer, Erguven, Izgi.
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Manuscript submitted November 1, 2011.
Accepted March 13, 2012.
Please include this information when citing this paper: published online June 8, 2012; DOI: 10.3171/2012.3.PEDS11473.
Address correspondence to: Pulat Akın Sabancı, M.D., Karabük
Devlet Hastanesı, Beyin ve Sinir Cerrahisi Kliniği, Karabük, Turkey. email: sabanci.akin@gmail.com.

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