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Spontaneous Thrombosis of an Unruptured
Saccular Aneurysm Causing MCA Infarction
Anton Fomenko, Anthony M. Kaufmann

ABSTRACT: Spontaneous complete thrombosis of an unruptured intracranial aneurysm leading to ischemic stroke is rare. We present a
case of a 56-year-old man who suffered an acute left middle cerebral artery (MCA) infarction, attributable to complete thrombosis of an
unruptured saccular MCA bifurcation aneurysm with occlusion of the parent artery. The presenting hemiparesis and aphasia partially
improved over a long hospital rehabilitation stay. Follow-up imaging demonstrated no recanalization of the aneurysm or parent vessels.
To the best of our knowledge this is the first documented case of isolated MCA territory infarction due to complete spontaneous thrombosis
of a saccular aneurysm.

RÉSUMÉ: Thrombose spontanée d’un anévrisme sacculaire non-rupturé ayant causé un infarcissement de l’artère cérébrale moyenne. Les cas
spontanés de thrombose totale d’un anévrisme sacculaire non-rupturé menant à un accident vasculaire cérébral (AVC) ischémique sont rares. Nous voulons ici
présenter le cas d’un homme de 56 ans victime d’un infarcissement aigu de l’artère cérébrale moyenne (ACM) gauche ayant été causé par la thrombose totale
d’un anévrisme sacculaire non-rupturé. À noter que des manifestations d’hémiparésie et d’aphasie ont en partie diminué à la suite d’un long séjour de réadaptation
à l’hôpital. Un examen de suivi par imagerie n’a pas révélé de recanalisation de l’anévrisme ou des vaisseaux sanguins principaux. À notre connaissance,
il s’agit là du premier cas documenté d’infarcissement d’une ACM isolée provoqué par une thrombose spontanée et totale d’un anévrisme sacculaire.

Keywords: Stroke, neuroimaging, aneurysms
doi:10.1017/cjn.2016.282

INTRODUCTION
The prevalence of unruptured intracranial aneurysms (UIA) as
an incidental finding has been cited from less than 1% to as high as
9% depending on study methodology and patient demographics.1
Studies have found some degree of intra-aneurysmal thrombosis
in up to 9% of patients with ruptured and unruptured aneurysms.1
Only a few cases document spontaneous thrombosis of an UIA
resulting in ischemic stroke.2-4 To the best of our knowledge our
case is unique in describing complete thrombosis of an MCA
bifurcation unruptured aneurysm with occlusion of the parent
artery and resulting ischemic stroke of its entire vascular territory.
CASE REPORT
A 56-year-old right-handed man was admitted to hospital for
acute-onset global aphasia and dense right hemiparesis. His past
medical history was notable only for smoking and acid reflux. He
had awoken in the morning feeling well and was witnessed by his
wife leaving for work without incident. The patient’s coworkers
called the ambulance in the afternoon after noticing sudden confusion, unintelligible speech and unsteadiness. On admission to
the emergency department vital signs were within normal limits.
On initial neurological examination the patient was alert and
had flaccid hemiplegia of his right face, arm and leg. He had
neglect of his right visual field and severe receptive and expressive aphasia. Relevant bloodwork such as partial thromboplastin
time, international normalized ratio, and liver function tests were
all normal.
Initial computed tomography (CT) scans demonstrated a
thrombosed MCA aneurysm (1.8 × 1.3 × 1.0 cm) with associated

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Can J Neurol Sci. 2016; 43: 856-858

occlusion of the left MCA at its bifurcation (Figure 1). There was no
evidence of subarachnoid hemorrhage or intracerebral blood. There
was loss of grey-white differentiation in the left insular, frontal and
parietal lobes. The initial Alberta Stroke Program Early CT score
was 2, indicating an established stroke with diffuse MCA involvement. As such, stroke mitigation by endovascular or surgical
revascularization was not pursued. The next day magnetic resonance
imaging (MRI) and MR angiography (MRA) confirmed a large area
of ischemic acute infarction in the left MCA territory and extremely
poor opacification of distal left MCA branches (Figure 2).
The patient had an uncomplicated hospital stay in the neurosurgical ward, was started on acetylsalicylic acid and clopidogrel,
and was eventually transferred to the stroke rehabilitation unit.
Prolonged Holter monitor demonstrated no evidence of arrhythmia, an Echocardiogram showed no intracardiac abnormality, and
carotid CT Angiogram (CTA) showed no significant stenosis.
Follow-up CTA performed 2 and 9 months post-stroke showed no
intra-aneurysmal flow and no change in the morphology of the
aneurysm dome, wall or thrombus. Partial recanalization of the
M1 segment was seen at the MCA bifurcation, though with persistent attenuation of distal MCA branches (Figure 3). Therefore
continued surveillance with serial neuroimaging and clinical
follow-up is planned.

From the University of Manitoba, Section of Neurosurgery, Winnipeg, Manitoba, Canada
(AF, AMK).
RECEIVED OCTOBER 13, 2015. FINAL REVISIONS SUBMITTED MARCH 16, 2016. DATE
OF ACCEPTANCE MAY 6, 2016.
Correspondence to: Anton Fomenko, Section of Neurosurgery, University of Manitoba,
Winnipeg, Manitoba, Canada. Email: fomenkoa@myumanitoba.ca

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Figure 1: Initial uninfused (A) and infused (B) CT demonstrating
hyperdensity at the left MCA bifurcation representing an acutely
thrombosed aneurysm with occlusion of the parent vessel and early
MCA territory infarction.

Figure 2: MR sequences demonstrating (A) acute left MCA territory
infarction on diffusion weighted imaging (B) and complete occlusion of
distal MCA vessels at its bifurcation on MRI time of flight 3-D
reconstruction.

Figure 3: Follow-up CT Angiogram 11 weeks post-stroke
demonstrating unchanged aneurysmal geometry and intensity, with
partial recanalization of a distal M2 segment.

DISCUSSION
The natural history of thrombosed aneurysms is not well
known. The presence of partial thrombosis has not generally been
shown as protective against aneurysm rupture, although it has
been associated with distal embolization leading to transient
ischemic attacks and infarction. Exceptional case reports have
demonstrated spontaneous complete thrombosis of cerebral

Volume 43, No. 6 – November 2016
https://doi.org/10.1017/cjn.2016.282 Published online by Cambridge University Press

aneurysms which, despite being angiographically silent, may not
necessarily protect against future rupture.5 There are only a few
cases in the literature documenting spontaneous complete
thrombosis of an UIA with occlusion of the parent artery and
resulting ischemic stroke. Brownlee2 described thrombosis of an
anterior communicating artery aneurysm in a 66-year old woman,
resulting in fatal ischemic infarctions. Whittle3 described
successful aneurysmectomy and thrombectomy of a giant intracavernous carotid aneurysm that had thrombosed and occluded the
carotid artery. Cohen4 described a series of three patients where
completely thrombosed aneurysms caused distal infarcts in the
anterior communicating, PICA and PCA territories, respectively.
Several theories of the pathophysiology of aneurysm thrombosis have been proposed based on animal and computational
models. German and Black5 used an in vivo canine model to
demonstrate that higher rates of spontaneous aneurysm thrombosis were associated with a narrower aneurysm orifice and more
voluminous dome. Kikut6 studied patterns of intra-aneurysmal
blood flow with diaphanoscopy in explanted human specimens
and found three distinct zones within the aneurysm: one with
turbulence, one with nearly normal flow and one region near the
apex of the dome where flow was nearly stagnant. Preliminary
simulations of intra-aneurysmal hemodynamics have also been
conducted with the aid of increasingly sophisticated threedimensional computer algorithms. Mathematical models of
MCA aneurysms from images acquired by three-dimensional
CTA have shown an inverse relationship between the dome-toneck ratio of the aneurysm and the average intraluminal flow
velocity.7 This may help explain the higher rates of thrombosis in
large and giant aneurysms. In addition, areas of stasis and
recirculation were consistently found at the tip of the dome, a
common area of observed thrombosis. Intra-aneurysmal platelet
aggregation in portions of the aneurysm with relatively stagnant
intraluminal flow may thereby foster an environment for
thrombosis.
Recurrent intramural hemorrhages are another potential
mechanism underlying aneurysmal thrombosis. Neuroimaging
studies have found acute clots at the periphery of thrombosed
giant aneurysms, and surgical series of large or giant aneurysms
commonly cite intramural or intraluminal thrombosis as a pathological finding in up to 60% of treated lesions. The fragile vasa
vasorum that encapsulates large aneurysms may bleed into the
subadventitial aneurysmal wall, contributing to intramural
thrombosis. This mechanism is analogous to the neovascularized
membrane of a chronic subdural hematoma bleeding and contributing to the enlargement of the collection. In a series of ten
patients with giant aneurysms imaged with MRI, nine (90%)
showed areas of T1 hyperintensity, suggestive of fresh clot distal
to the parent vessel and within the thrombus. Three of five patients
administered gadolinium showed partial or complete rim
enhancement at the margin of thrombus, suggestive of extravasation consistent with the aforementioned theory.8,9 Pathological studies have also revealed intrathrombotic capillary channels
with endothelial lining surrounded by staged clots, suggesting that
intra-aneurysmal thrombus may neovascularize, bleed and
thereby enlarge from within. In our case, the aneurysm was
homogeneously hyperdense on uninfused CT, indicating an acute
event, while the MRI demonstrated a recent blood product age.
There was no evidence of longstanding or organized thrombosis,
making this etiology unlikely.

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Complete occlusion of the aneurysm with thrombus is associated with a very low risk of future rupture.9,10 However, delayed
recanalization of the dome has been described in a case report of
completely thrombosed PCA aneurysm, which was subsequently
treated with trapping and aneurysmectomy.9,10 Similarly, studies
have reported aneurysm rupture following thrombosis induced by
flow diversion (FD) treatment.9,10 Follow-up imaging is therefore
important to identify any aneurysm recanalization that may
warrant treatment.
In summary, we present a unique case of an unruptured MCA
bifurcation aneurysm presenting with an acute stroke due to
complete thrombosis of the aneurysm and parent vessel. Factors
contributing to thrombosis in this case are unknown but may
include flow stasis within the dome of a large unruptured
aneurysm. Thromboembolic workup was negative. Late 9-month
follow-up imaging revealed no intra-aneurysmal flow, but did
demonstrate partial recanalization of the parent vessel. Continued
clinicoradiological surveillance is planned.

DISCLOSURES
Anton Fomenko and Anthony Kaufmann do not have anything
to disclose.

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https://doi.org/10.1017/cjn.2016.282 Published online by Cambridge University Press

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