García-Pérez et al. BMC Neurology
(2020) 20:232
https://doi.org/10.1186/s12883-020-01819-9

CASE REPORT

Open Access

Delayed extensive brain edema caused by
the growth of a giant basilar apex
aneurysm treated with basilar artery
obliteration: a case report
Daniel García-Pérez*, Irene Panero, Carla Eiriz, Luis Miguel Moreno, Pablo M. Munarriz, Igor Paredes,
Alfonso Lagares and José F. Alén

Abstract
Background: Partially thrombosed giant aneurysms at the basilar apex (BA) artery are challenging lesions with a
poor prognosis if left untreated. Here we describe a rare case of extensive brain edema after growth of a surgically
treated and thrombosed giant basilar apex aneurysm.
Case presentation: We performed a proximal surgical basilar artery occlusion on a 64-year-old female with a partially
thrombosed giant BA aneurysm. MRI showed no ischemic lesions but showed marked edema adjacent to the aneurysm.
She had a good recovery, but 3 months after surgical occlusion, her gait deteriorated together with urinary incontinence
and worsening right hemiparesis. MRI showed that the aneurysm had grown and developed intramural hemorrhage, which
caused extensive brain edema and obstructive hydrocephalus. She was treated by a ventriculoperitoneal shunt placement.
Follow-up MRI showed progressive brain edema resolution, complete thrombosis of the lumen and shrinkage of the
aneurysm. At 5 years follow-up the patient had an excellent functional outcome.
Conclusions: Delayed growth of a surgically treated and thrombosed giant aneurysm from wall dissection demonstrates
that discontinuity with the initial parent artery does not always prevent progressive enlargement. The development of
transmural vascular connections between the intraluminal thrombus and adventitial neovascularization by the vasa vasorum
on the apex of the BA seems to be a key event in delayed aneurysm growth. Extensive brain edema might translate an
inflammatory edematous reaction to an abrupt enlargement of the aneurysm.
Keywords: Basilar apex aneurysm, Hunterian occlusion, Brain edema

Background
Partially thrombosed giant basilar artery (BA) aneurysms
are uncommon vascular lesions with an extremely poor
natural history [1]. Among such lesions, those in the
upper basilar apex are the most challenging to treat, given
that the aneurysm usually incorporates the normal
branches of the upper BA [bilateral posterior cerebral
* Correspondence: dgp.neurosurgery@gmail.com
Department of Neurosurgery, University Hospital 12 de Octubre, Avda de
Córdoba s/n, 28041 Madrid, Spain

arteries (PCAs) and superior cerebellar arteries (SCAs)],
and/or vital perforating arteries [1]. So, these aneurysms
pose high risks for treatment by either microsurgical aneurismal clipping or endovascular coiling [2–5]. Moreover,
bypass is not effective for complex BA aneurysms [6, 7].
BA obliteration proximal to the SCA, which is known
as hunterian occlusion, has been performed for such
unclippable giant BA aneurysms [1, 8, 9]. It has been
proposed that obliterating the direct inflow from the
basilar trunk reduces the hemodynamic stress on the

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García-Pérez et al. BMC Neurology

(2020) 20:232

aneurysm, allowing for complete thrombosis of the
aneurysmal sac and consequent shrinkage of the
aneurysm [1, 10]. However, some cases are refractory to
hunterian occlusion due to the persistence of blood flow
into the aneurysms [10–13]. Perforating artery thrombosis
is another problem that influences outcome [6, 7, 14, 15].
Here, we report the long-term outcome of a complex
BA aneurysm treated by means of surgical occlusion of
the proximal BA. Importantly, several weeks after hunterian occlusion, the patient presented at the emergency
department (ED). Magnetic resonance imaging (MRI)
depicted growth of the partially thrombosed giant basilar
artery aneurysm by intramural hemorrhage, which
caused brain compression and edema, leading to clinical
deterioration.

Case presentation
A 64-year-old female presented with cephalea, left ptosis
and diplopia. Neurological examination detected left
oculomotor nerve palsy. Computed tomography (CT) revealed a partially thrombosed giant aneurysm at the tip
of the BA (Fig. 1). The aneurysm projected posteriorly,
significantly distorting the midbrain. An angiogram was
performed, revealing a giant aneurysm at the basilar
apex. Importantly, angiogram showed good collateral
flow to the posterior circulation through at least one robust posterior communicating artery (PCoA).
The patient underwent BA surgical occlusion. The BA
was accessed using a pterional craniotomy and a transsylvian approach. The clip placement was selected on
visual inspection after identifying a perforator-free zone
of the BA between the origins of the anterior inferior
cerebellar arteries (AICAs) and SCAs. Electrophysiological monitoring of evoked potentials (EPs) showed no
decrease of motor evoked potentials (MEPs) or somatosensory evoked potentials (SSEPs). Post-surgery angiography demonstrated stagnant flow in the dome of the
aneurysm, now filling from the PCoAs (Fig. 1). Antiplatelet treatment with aspirin was initiated. Postoperatively, the patient developed a decreased level of
consciousness and right hemiparesis. MRI demonstrated
a marked reduction in the size of the giant aneurysm
(Fig. 2). In addition, MRI showed no ischemic lesion
next to the aneurysm given that no infarct was observed
on diffusion-weighted MR imaging. High signal on T2weighted images of the brain stem adjacent to the
aneurysm was interpreted as edema. Over the following
weeks she showed progressively increased strength and
improved mentation, and was transferred to an acute rehabilitation facility. Prior to discharge, she was ambulating independently.
Three months after BA occlusion, she was referred to
our institution because of progressive gait instability,
urinary incontinence, worsening right hemiparesis, binge

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eating behaviour and memory difficulties. Plain CT scan
demonstrated ventricular dilatation (Fig. 3). MRI showed
high signal at the periphery of the aneurysm on T1weighted imaging, which was interpreted as a fresh
intramural clot (Fig. 4). Aneurysm dissection caused severe brain-stem compression and obstructive hydrocephalus. Increased brain edema was also evident on
MR images. Obstructive hydrocephalus was treated by a
ventriculoperitoneal shunt placement.
Long-term follow-up has extended for 5 years. The patient has made an excellent recovery and the hemiparesis
has almost resolved. Left oculomotor palsy was completely recovered. Follow-up MR imaging demonstrated
a marked reduction in the size of the giant aneurysm
with no filling of the aneurysm sac, and filling of the
upper BA via the PCoAs (Fig. 5). Intramural hematoma
resolved and brain edema markedly diminished.

Discussion
Surgical alternatives for thrombosed giant upper BA
aneurysm

In the present report, we assessed the radiological and
neurological results of a partially thrombosed giant
upper BA aneurysm treated with BA proximal occlusion.
Microsurgical aneurysmal clipping or endovascular
coiling of partially thrombosed giant BA aneurysms result in high complication rates [16]. Proximal BA occlusion is safer and more effective than other therapies [9].
The aim of the surgery is the occlusion of the BA without impairment of brainstem perforators, while maintaining collateral blood flow to the posterior circulation
by PCoAs. We performed a right pterional transsylvian
approach. Advantages of the transsylvian approach are
its widespread familiarity among neurosurgeons, less
temporal lobe retraction, potential for visualization of
the opposite P1, and larger surgical field compared with
the subtemporal approach [17]. When a choice is possible, the senior author usually prefers the right side approach. It reduces the risk of injury of the dominant
lobe and facilitates clipping for right handed surgeons,
which is the case. Although the patient presented a left
oculomotor palsy, the objective of the surgery was not to
decompress the third cranial nerve, but only find a safe
region to place a clip in the basilar trunk.
Early complication following hunterian occlusion

Flow redirection to the BA apex from the anterior circulation is supposed to reduce the hemodynamic burden
and to promote intra-aneurysmal thrombosis, thus reducing the size of the aneurysm [1, 8, 9]. In agreement, a
few days after surgery, digital subtraction angiography
(DSA) and MR angiography showed a markedly reduced
intra-aneurysmal flow. However, our patient developed a
decreased level of consciousness and right hemiparesis

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Fig. 1 Preoperative computed tomography (CT) and digital subtraction angiography (DSA) demonstrated a basilar apex giant aneurysm
occupying the interpeduncular fossa. a-d: Plain and contrast enhanced CT showed a giant calcified basilar artery aneurysm causing brain-stem
compression. e-k: Diagnostic DSA with a right vertebral artery (VA) injection showing a basilar artery (BA) tip aneurysm. The diameters of the
blood lumen measured 2.5 × 1.5 cm. The aneurism projected posteriorly into the interpeduncular cistern. A left robust PCoA was observed (red
arrow in f). Based on the angiographic anatomy, trial balloon test occlusion was not required. Anteroposterior (g) and lateral (h) DSA with right
VA injection showed partial filling of the aneurysm sac due to thrombosis. The aneurysm was wide-necked, with incorporation of both posterior
cerebral arteries (PCAs) and superior cerebellar arteries (SCAs) into the neck (3D reconstructions, I-K). l-q: Postoperative DSA confirmed occlusion
of the BA and filling of the top of the BA via the posterior communicating arteries (PCoAs) bilaterally (red arrows in L-O). DSA also revealed
continued filling of the PCAs and SCAs through the PCoAs. Stagnant flow was also visible in the aneurysm, indicating a high likelihood of
aneurysm thrombosis. In fact, there was a marked decrease in the diameter of the contrast filling in aneurysm blood lumen

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Fig. 2 Postoperative magnetic resonance imaging (MRI) did not
detect ischemic complications. a-c: Sagittal nonenhanced T1weighted images (T1WI) exhibited a newer clot, expressed as a
sickle-shaped high signal intensity area (red arrows), on the outer
surface of the intraluminal old thrombus. d-i: Fluid-attenuated
inversion recovery (FLAIR) MRI depicted a thrombosed giant
aneurysm severely compressing the brainstem in the backward
direction. In addition, we observed marked edema surrounding the
basilar apex (BA) aneurysm and involving the midbrain, thalamus
and left internal capsule. The sickle-shaped high signal intensity
structure was also observed on FLAIR images (red arrow in F). j-o:
Diffusion weighted imaging (DWI) showed no high-intensity lesions,
thus excluding ischemic complications. p-r: Sagittal (sag), coronal
(cor) and axial (ax) maximum intensity projection (MIP)
reconstructions of magnetic resonance angiography (MRA) showed
a > 50% decrease of the aneurysm blood lumen

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Fig. 3 Follow up computed tomography (CT) detected a marked
increase in the size of the supratentorial ventricular system together
with clinical symptoms suggestive of hydrocephalus. a-b: Postsurgical changes secondary to a pterional craniotomy and a
transsylvian approach, with pneumocephalus and blood remnants in
the surgical site. c-d: Plain CT performed at the emergency
department 3 months after surgical basilar artery occlusion. The
supratentorial ventricular system was markedly increased in size
compared to the previous study. We also noticed low attenuation
periventricular changes around the lateral ventricles (LVs), thus
suggesting transependymal edema. e-f: A right parieto-occipital
ventriculoperitoneal shunt was placed, with the proximal catheter
arising from the occipital horn of the right LV. Notice the decrease
in the size of the supratentorial ventricular system in comparison
with the previous study

following hunterian occlusion. By far, the most common
cause of surgical morbidity of the aneurysms treated
with BA occlusion is infarction of the perforating arteries territory, which supplies the mesencephalon as well
as the hypothalamus and thalamus [6, 7, 14, 15]. Surgical
occlusion of thalamoperforators could even impair the
so-called rostroreticular activation system and lead to

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Fig. 4 Magnetic resonance imaging (MRI) obtained on readmission to the hospital after temporary symptom relief. MRI demonstrated a large
thrombosed aneurysm compressing the brainstem, with a hyperintense area indicating the presence of an acute clot within the aneurysm,
besides markedly increased brain edema surrounding the enlarged aneurysm. a-b, e-f, i: Sagittal and axial nonenhanced T1-weighted images
(T1WI) exhibited a high signal in the posterior portion of the aneurysm, suggestive of a fresh intraluminal thrombus (red arrows) as well as new
intramural hematoma (green arrows; a-b), which caused a significant mass effect on the brainstem and third ventricle. The hyperintense areas on
the images were located mainly on the contralateral side to the patent lumen. High signal on T1WI progressively decreased during follow up
period (e-f, i), thus suggesting that no new hemorrhages happened. An intimal flap (yellow arrows in a-b, e-f) separated the true lumen and the
false lumen. c, g, j: Axial fluid-attenuated inversion recovery (FLAIR) images showed a marked increase in brain edema in comparison with the
previous MRI study. Intraluminal and intramural hematomas evolution were also detected on FLAIR images. d, h, k: Sagittal (sag), coronal (cor)
and axial (ax) maximum intensity projection (MIP) reconstructions of magnetic resonance angiography (MRA) confirmed progressive thrombosis
and reduced contrast filling in the residual blood lumen of the giant basilar apex aneurysm

coma or somnolence. So, all of the thalamoperforators
should be preserved during neurosurgical procedures regardless of their caliber [18]. Accordingly, our clip placement was selected on visual inspection of a perforatorfree zone to ensure safe clip application [9]. However,
perforator territory infarction (PTI) can occur even without direct injury of the parent artery or occlusion of perforators [14]. PTI is usually diagnosed on diffusionweighted imaging (DWI). Larger aneurysm size, basilar
artery aneurysms and localization in the interpeduncular
cistern (IPC) are significantly related to PTI, which has a
negative impact on outcome [6, 7, 14, 15]. Postoperative
DWI revealed neither ischemic nor hemorrhagic complications. So, no ischemic complication associated with insufficient perfusion caused by BA obliteration seemed to
be related with the clinical worsening in our patient.
Consequently, the patient’s motor deficit was attributed

to aneurysm thrombosis, increased brain edema and
mass effect. Therefore, the patient gradually improved as
brain edema progressively resolved and the aneurysm reduced in size.
Delayed complication following hunterian occlusion

Several weeks after hunterian occlusion, our patient presented with clinical deterioration and radiological obstructive hydrocephalus. The occurrence of obstructive
hydrocephalus due to an intracranial aneurysm is rare,
whereas the basilar bifurcation is their most common location [19–22]. Neuroimaging findings demonstrated a
stable reduced aneurysm lumen but a new intramural
hemorrhage (IMH) which caused aneurysmal growth and
severe midbrain compression. Coexistence of luminal narrowing and aneurysmal external contour dilatation have
been considered helpful in detecting aneurysm dissection

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Fig. 5 Follow-up magnetic resonance imaging (MRI) showed almost complete thrombosis of the lumen of the aneurysm and progressive
reduction of the aneurysmal external contour. a, e, i, m: Sagittal T1-weighted images (T1WI) showed resolution of the intramural hematoma, no
new intraluminal fresh thrombus and progressive decrease in the maximum external diameter of the aneurysm, thus alleviating brainstem
compression. b, f, j, n: Axial fluid-attenuated inversion recovery (FLAIR) and/or T2-weighted images (T2WI) showed progressive resolution of brain
edema. c, g, k, o: Sagittal, coronal and axial maximum intensity projection (MIP) reconstructions of magnetic resonance angiography (MRA)
showed no filling of the aneurysm sac, and filling of the upper basilar apex via both posterior communicating arteries (PCoAs). d, h, l, p: Sagittal,
coronal and axial MIP reconstructions of contrast enhanced 3-dimensional time of flight (3D-TOF). Although no filling of the aneurysm was found,
a marked gadolinium enhancement is noted around the top of the basilar artery, representing the old intraluminal thrombus. The maximum
external diameter of gadolinium enhancement decreased over the follow-up period (red arrows)

[23]. In the present report, we had switched the parent
artery from the basilar artery to the PCoAs. Thus, it could
be argued that the changes in the direction and the
diameter of the parent arteries might have resulted in a
focal elevation of wall shear stress on the posterior
aneurysm wall, and that these hemodynamic changes
might have been associated with the subsequent wall dissection [24]. Nevertheless, BA ligation has been described
to reduce and change the flow of an aneurysm, allowing
complete organization of the thrombus and avoiding
hemodynamic injury to the aneurysm wall [10]. So, it
seems that surgical intervention can stabilize several aneurysms, but can cause rupture in others. In this sense, preoperative computational flow dynamics simulation might
help to predict postoperative intraluminal flow and so,
help to establish the best strategy [24]. However, we consider that increased wall shear stress due to hemodynamic
changes was unlikely to be the mechanism that enabled
IMH because the hemorrhage occurred at the periphery

of the aneurysm wall within the clot, but far from the patent lumen, as previously documented [25].
Pathophysiological mechanisms underlying thrombosed
aneurysm enlargement

Literature supports persistent growth of completely
thrombosed giant aneurysms [26–29]. Different pathomechanisms have been reported. On the one hand,
intrathrombotic vascular channels development and
consequent intrathrombotic hemorrhages have been
proposed [30]. On the other hand, growth of these giant
aneurysms might be attributable to neovascularization
and recurrent intramural hemorrhages [25, 26, 28, 31].
As shown in Fig. 4, we observed that the thrombosed
portion grew due to both, hemorrhage into the
thrombus and in the aneurismal wall. IMH is considered
to be caused by the rupture of the vasa vasorum or
newly formed wall vessels [29, 32]. The strong peripheral
contrast enhancement that we observed (Fig. 5) could be

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(2020) 20:232

attributed to the highly vascularized arterial wall [26].
Numerous factors are thought to trigger neovascularization, such as an intra-aneurysmal thrombus [33]. In fact,
most growing intracranial giant aneurysms contain a
thrombus within the aneurysm sac [34]. Our case supports this concept, and suggests that the rapid formation
of an intra-aneurysmal thrombus following BA occlusion
may have promoted mural damage, helping to trigger
neovascularization and the growth of capillaries. Our report suggests that the thrombotic process started right
after the surgical proximal occlusion and not at distance.
This would also explain the significant edema and worsening of clinical condition that developed following BA
occlusion. Delayed worsening of the thrombosis and
new IMH would have led to hydrocephalus and a new
neurological worsening (supplementary Figure 1). We
conclude that neovascularization processes and repeated
minor hemorrhages into the aneurysm thrombus and
wall led to the delayed increased mass effect, increased
edema and consequently, deterioration in our patient’s
neurological condition.
Very few reports describe giant aneurysms presenting
with massive cerebral edema and clinical deterioration
[35, 36]. The authors proposed that an abruptly enlarged
aneurysm compromised blood supply to the adjacent
brain tissue and caused ischemia and subsequent edema
due to a loss of vasoresponsivity and breakdown of the
blood-brain barrier [35, 36]. The present case presented
with extensive edema following aneurysm growth, but
no ischemic lesions next to the aneurysm were observed
on DWI. Nakayama and colleagues reported a case of
spontaneous rapid growth of a partially thrombosed
giant basilar artery aneurysm caused by intramural
hemorrhage. With conservative treatment, her ataxia
and urinary incontinence resolved [36]. In contrast,
Heros and Kolluri reported two cases of giant left middle
cerebral artery aneurysm presenting with rapidly progressing hemiparesis and aphasia. CT showed recent
intraaneurysmal thrombosis and massive edema and
swelling of the cerebral hemisphere. In both patients,
surgical resection of the aneurysm was accomplished,
but the outcome was disastrous [35]. Alternatively, the
enhancing wall and the edematous reaction of the adjacent brain parenchyma might be a sign for an inflammatory pathomechanism [25, 37, 38], although the role of
vasa vasorum concerning the rim enhancement might
also account for these findings. Medical, i.e. antiinflammatory treatment (such as steroids), could have
been proposed given the likelihood of an inflammatory
pathomechanism (either causative or reactional).
IMHs have the same signal evolution on MRI, and signals are likely to appear isointense or unrecognizable
within 2 months [39, 40]. The resolution of intramural
hemorrhagic signals in our case indicate cessation of

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intramural hemorrhage. During the long-term follow-up,
we have also observed progressive brain edema resolution, decrease in the residual blood lumen and marked
shrinkage of the aneurysm, together with improvement
of the neurological condition, highlighting that thrombosis and shrinkage might be dynamic processes. We
propose that, once hemodynamic factors following hunterian ligation had been stabilized, block of the blood
flow to intrathrombotic vascular channels promoted absorption of the organized thrombus and shrinkage of the
aneurysm.

Conclusions
Growth of a surgically treated and thrombosed giant
aneurysm demonstrates that discontinuity with the initial parent artery does not always prevent progressive
enlargement. The development of transmural vascular
connections between the intraluminal thrombus and
neovascularized adventitial wall appears to be a key
event in delayed aneurysm growth. Extensive brain
edema might translate an inflammatory edematous reaction to abrupt enlargement of the aneurysm. Conservative management is recommended.
Supplementary information
Supplementary information accompanies this paper at https://doi.org/10.
1186/s12883-020-01819-9.
Additional file 1 Figure S1. Comparison between postoperative
magnetic resonance imaging (MRI) and a new MRI obtained on
readmission to the hospital after temporary symptom relief. A-C: Sagittal
nonenhanced T1-weighted images (T1WI) exhibited a newer clot,
expressed as a sickle-shaped high signal intensity area, on the outer surface of the intraluminal old thrombus. D-I: Fluid-attenuated inversion recovery (FLAIR) MRI depicted a thrombosed giant aneurysm severely
compressing the brainstem in the backward direction. In addition, we observed marked edema surrounding the basilar apex (BA) aneurysm and
involving the midbrain, thalamus and left internal capsule. The sickleshaped high signal intensity structure was also observed on FLAIR images. J: Axial maximum intensity projection (MIP) reconstructions of magnetic resonance angiography (MRA) showed a decrease of the aneurysm
blood lumen. K: Axial MIP reconstructions of contrast enhanced 3dimensional time of flight (3D-TOF). A marked gadolinium enhancement
is noted around the aneurysm, representing the new intraluminal
thrombus. L-N: Sagittal nonenhanced T1WI exhibited a high signal in the
posterior portion of the aneurysm, suggestive of a fresh intraluminal
thrombus as well as new intramural hematoma, which caused a significant mass effect on the brainstem and third ventricle. O-T: Axial FLAIR
images showed a marked increase in brain edema in comparison with
the previous MRI study. Intraluminal and intramural hematomas evolution
were also detected on FLAIR images. U: Axial MIP reconstructions of MRA
confirmed reduced contrast filling of the blood lumen of the giant basilar
apex aneurysm. V: Axial MIP reconstructions of 3D-TOF showed gadolinium enhancement around the aneurysm, representing the intraluminal
and intamural thrombus.
Abbreviations
AICA: Anterior inferior cerebellar artery; BA: Basilar artery; CT: Computed
tomography; DWI: Diffusion-weighted imaging; DSA: Digital subtraction
angiography; ED: Emergency department; EPs: Evoked potentials;
IPC: Interpeduncular cistern; IMH: Intramural hemorrhage; MRI: Magnetic
resonance imaging; MEPs: Motor evoked potentials; PTI: Perforator territory

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infarction; PCA: Posterior cerebral artery; PCoA: Posterior communicating
artery; SSEPs : Somatosensory evoked potentials; SCA: Superior cerebellar
artery

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12.

Acknowledgements
Not applicable.
13.
Authors’ contributions
DGP drafted the manuscript. DGP, IPan, CE and LMM collected and analyzed
the data. PMM, IPar, AL and JAA revised the case report critically for
important intellectual content. All authors read and approved the final
manuscript.
Funding
None.

14.

15.

Availability of data and materials
Additional data and material would be made available upon request.
Ethics approval and consent to participate
Not applicable.

16.

Consent for publication
Written informed consent was obtained from the patient for publication of
this case report and any accompanying images. A copy of the written
consent is available for review by the Editor of this journal.

17.

18.

Competing interests
The authors declare that they have no competing interests.

19.

Received: 1 April 2020 Accepted: 3 June 2020

20.

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