Childs Nerv Syst (2003) 19:204–210
DOI 10.1007/s00381-003-0726-0

Luca Massimi
Jacques Moret
Giampiero Tamburrini
Concezio Di Rocco

Received: 23 January 2003
Published online: 25 March 2003
© Springer-Verlag 2003

L. Massimi (✉) · G. Tamburrini
C. Di Rocco
Pediatric Neurosurgery,
Catholic University School of Medicine,
Largo A. Gemelli, 8, 00168 Rome, Italy
e-mail: lucamax30@hotmail.com
Tel.: +39-06-30154587
J. Moret
Service de Neuroradiologie
Interventionnelle,
Fondation Ophtalmologique Rothschild,
Paris, France

C A S E - B A S E D U P D AT E

Dissecting giant vertebro-basilar aneurysms

Abstract Object: Vertebro-basilar
dissecting aneurysms (VDAs) are
very rare in children. Strokes or subarachnoid hemorrhage are characteristic clinical manifestations, but often only non-specific symptoms are
found. Radiological diagnosis may
be difficult to obtain and therapy
hard to perform. We report on a child
who presented with an intracranial
mass effect due to a giant VDA.
Methods: The patient was a 8-yearold girl with right hemiparesis, ataxia, dysphagia and dysphonia and
worsening of her neurological deficits. Neuroimaging discovered a giant dissecting aneurysm arising from
the left vertebral artery and involv-

Background
Introduction
Dissection of intracranial arteries may result in a dissecting aneurysm (aneurysmal dilatation of the artery caused
by the presence of blood within its wall) [49]. The vertebral artery is the most common intracranial site of such a
process, followed by the basilar artery, the internal carotid artery, and the middle cerebral artery [8]. The vertebral arteries also represent the most frequent vessels involved in multiple dissections [30, 51]. Males are more
frequently affected than females [50].
In spite of being increasingly recognized in adults
[25], intracranial vertebro-basilar dissecting aneurysms
(VDAs) are extremely rare in the pediatric population
[19, 35, 37, 41, 43] and their definition is still under discussion. However, they may be associated with severe
morbidity and mortality because of the possibility of

ing the vertebro-basilar junction. Endovascular treatment by coil embolization was performed. The post-operative course initially showed a remarkable improvement in her clinical condition. Afterwards, she developed cerebral hemorrhage and died.
Conclusion: VDAs may have an unusual presentation and their therapy
still remains a challenge. Endovascular embolization is a valid option
but, as it is surgery, it may cause the
death of the patient.
Keywords Dissecting aneurysm ·
Intracranial vertebral artery ·
Therapy · Endovascular
embolization

generating strokes. Strokes are quite frequent in children
with VDAs because of a secondarily reduced distal flow
(narrowing of the arterial lumen as a consequence of the
growth of an intramural hematoma or thrombosis) or embolic phenomena [4, 12, 32]. Subarachnoid hemorrhage
is uncommon in children in comparison with adults [4, 9,
27]. Subarachnoid hemorrhage has not significantly influenced the outcome in some series [49], while in others
it is thought to be responsible for a grim prognosis [33].
Subclinical manifestations may occur [4].
Bilateral dissection and the initial severity of the
stroke are the two deciding factors for poor prognosis in
patients with VDAs [4]. Also, the location may affect the
outcome, since, for instance, basilar artery dissecting aneurysms have a worse prognosis than vertebral ones [8].
According to Yamaura et al. [50], a favorable outcome
can be found in 60% of surgical cases, with moderate to
severe disability in 35%, and a poor outcome in 5%.
Mortality rate has decreased in the last few years [31]

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compared with past years [3], but overall mortality still
remains high (26%) [49].
Etiopathogenesis
Although “spontaneous” VDAs have been reported by several authors [12, 23, 37, 45, 50], trivial injuries cannot be
excluded so that the real incidence of “true spontaneous”
dissections remains obscure. Actually, fibromuscular dysplasia [2, 23, 39] and other risk factors, such as inheritance
of intracranial aneurysms [36, 40], connective tissue disorders such as Marfan’s syndrome [35, 36, 38], Moyamoya
disease [48], systemic lupus erythematosus [9], syphilitic
arteritis, poliarteritis nodosa, degeneration of the media [8],
and oral contraceptives [23] are frequently found in cases
of “spontaneous” extra- or intracranial dissections.
Trauma represents the most common predisposing
factor for VDAs during childhood. Posttraumatic dissections can share etiology with one or more of the previously mentioned factors. Posttraumatic VDAs often result from minor cranio-cervical injuries such as blunt
trauma [50], sporting and playing activities or neck manipulation [26, 33]. They may also be secondary to road
accidents or iatrogenic injuries (surgical manipulation or
endovascular procedures).
An initial transintimal bleeding, with secondary hematoma formation into the vessel wall (subintimal, intramedial or subadventitial) is thought to lead to the aneurysmatical dilatation of the artery. Subarachnoid hemorrhage
generally arises from subadventitial dissection (with or
without luminal connection), while arterial lumen occlusion may be the consequence of a subintimal hematoma
[6, 10]. Sometimes, hemorrhage occurs into an atheromatous plaque [6]. Besides atherosclerosis, associated histopathological findings are represented by cystic or mucoid
medial degeneration, adventitial neovascularization, disruption of internal elastic lamina and media [6, 34, 52]. In
particular, disruption of internal elastic lamina seems to
play an important role in the genesis of nonatherosclerotic cerebral dissecting aneurysms [28].
Clinical presentation
The usual clinical manifestations of VDAs in children
are represented by neurological symptoms following
transient ischemic attacks (vertigo, transient loss of consciousness, unilateral facial paresthesia, visual field
defects) or strokes (hemiparesis, cranial nerve palsy,
Wallemberg’s syndrome, ataxia), which result from
brainstem, thalamic, cerebellar or cerebral infarcts [5, 7,
15, 24, 33, 35]. Another possible clinical presentation is
recurrent torticollis [11]. Signs and symptoms of subarachnoid hemorrhage in children are observed less commonly than in the adult population [3, 4, 9, 16].

The main symptoms of VDA in the pediatric age are
severe headaches and neck pain [11, 13, 33, 35]. Headaches are often the first symptom of arterial dissection
and can precede neurological disturbances by days or up
to months [24, 42]. Headaches may be recurrent, steady
or pulsating, and generally ipsilateral to the side of dissection [42, 50]. They may occur acutely and be severe
after a major head injury; in other instances, they may
remain subtle, such as in the case of a minor trauma.
Neck pain is a frequent manifestation of VDAs [33] and
it may also occur as an isolated symptom [21]. This phenomenon is often misinterpreted as being due to musculoskeletal disorders and acquires significance only when
neurological deficits appear [11].
Vertebro-basilar dissecting aneurysms can exert an intracranial mass effect affecting cerebellar, brainstem or
cranial nerve functions [8, 11, 13]: in this instance, a
giant dissecting aneurysm may be found [29].
Evaluation and management
The recognition of VDAs may be delayed because of
nonspecific symptoms and/or difficult differential diagnosis with other cerebral posterior circulation disorders [4,
7]. On these grounds, the proposal of early investigation
for VDA in children with manifestations of a posterior
stroke may be justified [46]. Hemodynamic abnormalities
are frequently found in patients with VDAs [5] and
Doppler ultrasonography represents an effective technique for early evaluation. Computed tomography and
MRI are useful for evaluating associated brain infarcts,
although these investigations may allow, in some cases,
the direct visualization of the lesion and the detection of
some radiological findings of arterial dissection (intimal
flap, intravascular hematoma). Transfemoral angiography
still represents the main diagnostic tool. In fact, there are
several angiographic findings that can suggest VDA: luminal stenosis or occlusion (“string sign”), aneurysmal
dilatation preceding or following a focal narrowing of the
vessel lumen (“pearl and string sign”), true and false
(intramural) lumen producing a double channel (“double
lumen sign”), isolated fusiform dilatation, and intimal
flap [8, 22, 32]. In spite of this, correct angiographic diagnosis may remain difficult to perform because of the
rarity of the specific signs (e.g., double lumen sign, intimal flap) and the misinterpretation of other findings (e.g.,
“string” or “pearl and string” may be considered to be the
consequences of a vasospasm following the rupture of a
saccular aneurysm in patients with associated subarachnoid hemorrhage) [8, 46, 52]. Repeating angiography can
show different images from previous scans [20].
The role of computerized tomographic angiography
and magnetic resonance angiography is still under definition even if some authors propose them as alternative
diagnostic modalities to invasive techniques [17, 22].

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Management of VDAs may be challenging.
Most of authors recommend heparin immediately after ischemic damage and, subsequently, anticoagulant
oral therapy; however, this type of treatment is not universally accepted, in particular in cases of subarachnoid
hemorrhage or large cerebral infarcts [3, 17, 18, 47, 52].
In cases of subarachnoid hemorrhage, surgical or endovascular treatment should be performed, if possible (e.g.,
vasospasm), acutely or subacutely to reduce the risk of
rebleeding even if a second rupture occurs as late as
more than 1 month after the first [12, 27].
The goal of an urgent or elective invasive treatment
for VDAs is to prevent bleeding or rebleeding, to avoid
or reduce ischemic irreversible damages and, if necessary
(giant aneurysm), to achieve neural decompression. The
surgical techniques include clipping, trapping, and wrapping [8, 27, 50]. Clipping or ligature aim at obtaining an
arterial occlusion as proximal as possible to the dissection
site. Trapping is useful if, after proximal occlusion, further aneurysmal growth is observed due to blood flow
from the contralateral circulation. It is important to carry
out a test occlusion (the balloon must be placed proximal
to the aneurysm) before clipping or trapping to evaluate if
the dissected artery is the dominant vessel, and if its occlusion is not tolerated by the patient [44, 50]. When anatomical or functional conditions do not allow clipping or
trapping of the VDA, wrapping can be performed, but the
effectiveness of this maneuver is still unknown [12].
Thanks to the special clips available nowadays, it is possible to make an external clipping in some cases [27].
Additional surgical procedures include opening the
aneurysm and thrombectomy (neural decompression in
case of giant aneurysms), performing in situ or extra-/intracranial bypass (if collateral circulation is not able to
supply parent vessel occlusion), and resecting the dissected arterial segment with end-to-end anastomosis or
an autologous vein graft.
Surgery of VDAs may be very difficult to perform,
especially when dissecting aneurysms arise above the origin of the PICA [50] because of the risk of incidental
damage to the vertebral perforating arteries [12].
In cases of unclippable aneurysms, endovascular techniques represent an effective option [14, 43]. In recent
years, thanks to technological advances and increased
experience in the field, endovascular treatment has indeed become an efficient and safe alternative to surgical
treatment [4, 11, 12]. Avoiding the heavy approach of
craniotomy and direct manipulation of aneurysm are the
principal advantages of this type of procedure [11]. Nevertheless, endovascular treatment may fail (e.g., in cases
of aneurysm with a wide neck) [35], and transient or permanent complications have also been described [12].
The most frequent endovascular technique modality
for treating VDAs is balloon occlusion [11, 12, 14, 47].
Via a transfemoral approach, a detachable balloon is positioned at the dissection site to prevent luminal recanaliza-

tion from collateral arteries, and to reduce the risk of the
occlusion of the perforating vessels. There are several
variants of simple balloon occlusion: one or two detachable silicone balloons may be used as the sole embolic
agent or in combination with fibered platinum coils; if a
single balloon is used, it may be inflated with hydroxyethyl methacrylate to achieve good solidification before
its detachment [12]. The absence of a secondary embolism is one of main advantages of balloon occlusion.
Detachable coil embolization is an interesting alternative to balloon occlusion [1, 4, 25]. Several kinds of coil
are available and they are used more and more in adults
thanks to their greater ductility in comparison with balloons [4, 12, 25]. According to some authors [11], the
risk of embolism due to the slow flow of the vessel occluded by detachable coils may be reduced by treating
the aneurysm with histoacryl resin. Both balloon occlusion and coil embolization require a test occlusion before
they are performed.

Case report
A 8-year-old girl, with a 4-month history of ingravescent dysphagia
and anorexia, was admitted to our Pediatric Neurosurgery Department on February 2001 because of an obvious deterioration in her
neurological condition, characterized by dysphonia, right facial
nerve palsy, right brachio-crural hemiparesis, gait disturbance, and
remarkable weight loss. There were no congenital or acquired risk
factors for VDA. No history of minor or major cranio-cervical injuries, headache or neck pain was reported. Physical examination revealed right facial nerve palsy, end-position nystagmus, left soft
palate palsy, dysphonia, right spastic hemiparesis with overexcitable deep tendinous reflexes. Neuroimaging (CT scan, MRI, angioCT scan with 3D reconstructions) indicated an extra-axial, oval,
sharp-edged, expansive process of nearly 4 cm in diameter, with
contrast enhancement. The mass lesion was compressing the brain
stem and the fourth ventricle, and induced an obvious displacement
of the basilar artery. It protruded through the occipital foramen caudally, and caused an angulation of the bulbopontine junction within
the prebulbar cistern rostrally. Flow void was valuable within the
lesion; there was hypertensive triventricular hydrocephalus
(Fig. 1). Cerebral angiography showed a giant dissecting aneurysm
of the left vertebral artery extending to the vertebro-basilar junction
(Fig. 2). The contralateral vertebral artery was hypoplasic.
Clinical signs and symptoms improved following antiedemic
therapy. An endovascular treatment was suggested because of the
complexity of the lesion, which appeared to prevent effective surgical therapy. The young patient underwent a partial embolization
of the aneurysm with mechanically detachable coils. The choice of
a partial embolization was based on the necessity of avoiding the
risk that the complete thrombosis of the aneurysm and the possible
consequent rapid increase in volume might induce the blocking of
the posterior circulation and/or the rupture of the aneurysm wall.
Forty-eight hours after the intervention, the girl showed further
improvement in her neurological deficits. However, 3 days after
the endovascular treatment, she experimented a sudden worsening
of her neurological condition with the abrupt loss of consciousness
and onset of coma. An urgent CT scan showed tetrahemoventriculus, acute hypertensive hydrocephalus, and subarachnoid hemorrhage. The girl underwent an urgent right frontal external ventriculostomy and a cerebral angiography, which showed the embolization of the aneurysm; neither of the vertebral arteries could be visualized (Fig. 3A). A few hours later, after a further worsening of

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Fig. 1 T1-weighted A axial
and B sagittal MRI, C T1weighted coronal MRI after gadolinium, and D T2-weighted
sagittal MRI demonstrating a
posterior cranial fossa round
mass lesion, dislocating and severely compressing the brain
stem

Fig. 2A, B Digital cerebral
angiography. A Lateral and
B oblique views show a voluminous aneurysm of the terminal segment of the left vertebral
artery, extending to the vertebro-basilar junction

the clinical condition with bradycardia, a new CT demonstrated
signs of rebleeding with an increase in the amount of blood within
the ventricular system and the subarachnoid spaces (Fig. 3B). A
new cerebral angiography suggested the fissuration of the posterior wall of the aneurysm (Fig. 4A) and its caudal dislocation
through the occipital foramen due to endocranial hypertension
(Fig. 4B). Unfortunately, death occurred a few hours later.

Conclusion
Giant VDAs are very rare in childhood and hard to recognize; these lesions may insidiously progress making
their management a real challenge. Endovascular tech-

niques are an effective therapeutic option when the aneurysms are unclippable, although they carry significant
risk, as demonstrated by the immediate good outcome of
our young patient followed by her death later. Like surgical treatment, lethal complications may occur after endovascular treatment, due to the possibility of hemorrhage,
the possible progression of the artificially induced
thrombosis, and the occlusion of the perforating branches supplying the brainstem.

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Fig. 3 ACerebral angiography
(left ICA, lateral view) after
endovascular treatment demonstrates the aneurysm excluded
by coils and the basilar artery
anteriorly dislocated; vertebral
arteries are not visible. B CT
scan after rebleeding showing
tetrahemoventriculus, subarachnoid hemorrhage and hypertensive hydrocephalus (axial
view)

Fig. 4A, B Cerebral angiography after rebleeding. A The
lateral view (right ICA) shows
contrast medium passing into
the ventricular system from the
posterior wall of the aneurysm.
B Imaging without bone subtraction: the aneurysm protrudes through the occipital
foramen

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