ARTICLE IN PRESS

Case Studies

Anterior Inferior Cerebellar Artery Strokes Based on Variant

Vascular Anatomy of the Posterior Circulation: Clinical Deficits
and Imaging Territories

Melissa M. Chen, MD,* Stephen R. Chen, MD,† Pedro Diaz-Marchan, MD,‡

Donald Schomer, MD,* and Vinodh A. Kumar, MD*

We report imaging findings of 3 patients with anterior inferior cerebellar artery

(AICA) infarcts who presented with atypical clinical findings of cerebellar strokes.
AICA strokes are rare, and diagnosis can be difficult because of the high vari-
ability of the posterior circulation vascular anatomy. We describe the embryology
and variant anatomy of AICA so that clinicians can understand and recognize
the patterns of these infarcts. Key Words: AICA—ischemia—cerebellum—posterior
circulation—variant vascular anatomy.
© 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Introduction clinical case series of AICA strokes have demonstrated

variable clinical presentations.5-7 Lack of a common clin-
The anterior inferior cerebellar artery (AICA) arises from
ical picture unfortunately makes diagnosis difficult in the
the lower half of the basilar artery and is closely asso-
absence of imaging. Previously, a direct correlation had
ciated with the abducens, facial, and vestibulocochlear
been found between variable anatomy of the posterior
nerves. AICA and the cranial nerves together comprise
communicating artery and the prevalence of cerebral
the middle neurovascular complex.1
infarction8 Similarly, the differing AICA stroke presenta-
AICA strokes are the rarest of the posterior circula-
tions can be explained by the variable anatomy of the
tion strokes, representing .1% of all strokes.2-4 The AICA
posterior circulation.
contributes the smallest supply to the cerebellum com-
pared with the other cerebellar arteries. The classically
described symptoms of AICA stroke include presence of
Cases
ipsilateral cerebellar ataxia, Horner syndrome, and in-
volvement of trigeminal, facial, and vestibulocochlear nerves Case 1
with contralateral sensory disturbance. However, A 67-year-old man with diffuse large B-cell lym-
phoma, diabetes, hypertension, and hyperlipidemia who
From the *Diagnostic Radiology, MD Anderson Cancer Center, underwent autologous stem cell transplant 3 months ago
Houston, Texas; †Radiology and Neurosurgery; and ‡Radiology, Baylor
was an inpatient for treatment of pneumonia. During hos-
College of Medicine, Houston, Texas.
Received July 7, 2017; revision received September 30, 2017; accepted
pitalization, the patient developed left facial numbness.
October 11, 2017. Family members also noticed the patient developed a left-
Address correspondence to Melissa Mei Chen, MD, MD Anderson sided facial droop. Magnetic resonance imaging (MRI)
Cancer Center, 1400 Pressler Street, Unit 1482, Houston, TX 77030. revealed an acute infarct in the left middle cerebellar pe-
E-mail: Melissa.mei.chen@gmail.com.
duncle (Fig 1, A) and petrosal surface of the left cerebellum
1052-3057/$ - see front matter
© 2017 National Stroke Association. Published by Elsevier Inc. All
(Fig 1, B). A computed tomography (CT) angiogram of
rights reserved. the head showed a moderate focal stenosis of the lower
https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.10.007 basilar artery (Fig 1, C,D). Occlusion of the left AICA is

Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2017: pp ■■–■■ 1
 ARTICLE IN PRESS
2 M.M. CHEN ET AL.

Figure 1. Case 1 presents a 67-year-old male patient

with acute left facial numbness and facial droop.
Diffusion-weighted magnetic resonance images show in-
creased signal in the left (A) petrosal surface of the
cerebellum and flocullus (B) middle cerebellar pedun-
cle, with low signal on the corresponding Apparent
Diffusion Coefficient (ADC) map (not shown) consis-
tent with an acute infarct. A computed tomography
angiogram showed focal stenosis of the midportion of
the basilar artery (dashed arrow) as seen on the (C)
3-dimensional image and (D) sagittal maximum in-
tensity projections.

presumably related to atherosclerotic plaque embolizing
from the basilar artery.
Case 2
A 65-year-old female patient presented with acute onset
of right facial numbness, vertigo, and medical history of
diabetes, hypertension, and hyperlipidemia. The emer-
gency room (ER) staff diagnosed the patient with Bell palsy
and did not obtain imaging on her initial visit. The diag-
nosis of acute infarct was specifically dismissed in the initial
visit, given the lack of cerebellar dysfunction. A week later,
the patient presented to the ER with persistent vertigo and
right facial numbness. On examination, she had sus-
tained nystagmus on leftward and upward gaze and a few
beats of nystagmus on rightward gaze. Romberg was un-
steady while standing with eyes open and she demonstrated
mild dysmetria and very unsteady gait. Hearing was grossly
intact with finger rub. A non–contrast-enhanced CT re-
vealed a round hypodensity in the right middle cerebellar
peduncle (Fig 2, A), with evidence of prior lacunar in-
farcts in the left putamen and bilateral frontal centrum
semiovale. MRI showed diffusion-weighted signal abnor-
mality (Fig 2, B) and Fluid-Attenuated Inversion Recovery
(FLAIR) hyperintense signal (Fig 2, C) in the right middle
cerebellar peduncle, consistent with an acute infarct.

Figure 2. Case 2 presents a 65-year-old female patient with right facial numbness and vertigo. (A) Unenhanced computed tomography of the brain shows
hypodensity in the right middle cerebellar peduncle. (B) MRI FLAIR axial image of the brain demonstrates an expansile FLAIR hyperintensity in the right
middle cerebral peduncle with (C) mildly increased diffusion-weighted signal with low ADC (not shown), compatible with an acute infarct.
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AICA STROKES BASED ON VARIANT VASCULAR ANATOMY
Figure 3. Case 3 presents a 62-year-old male patient
with worsening mental status changes, psychosis, and
confusion. (A) Unenhanced computed tomography of
the brain ordered from the emergency room showed a
round hypodensity in the left middle cerebellar pedun-
cle. (B) High diffusion-weighted signal with low ADC
(not shown) confirmed the presence of an acute infarct.
Case 3
A 62-year-old male patient presented with worsening
mental status changes, psychosis, and confusion with
medical history of hypertension. He had walked into his
family’s home and started shooting his gun. The pa-
tient’s family brought him into the ER for evaluation and
potential transfer to senior care living. Given his altered
mental status, hearing could not be tested. A noncontrast
CT of head was performed, and a round hypodensity in
the left middle cerebellar peduncle was found (Fig 3, A).
The patient had evidence of extensive small vessel isch-
emic changes and prior lacunar infarcts. An MRI confirmed
the presence of acute infarction in the left middle cer-
ebellar peduncle (Fig 3, B).
Discussion
In our study, the patients presented with 2 patterns of
infarcts. Two of our patients presented with focal infarct
in the middle cerebellar peduncle. The second pattern was
a diffuse pattern including the middle cerebellar pedun-
cle and petrosal surface of the cerebellum. The initial
presenting symptoms were either related to cranial nerve
deficits or nonspecific symptoms. Cerebellar stroke was
not clinically suspected and was discovered incidental-
ly on imaging. All of the patients had risk factors for
atherosclerosis that included hypertension, diabetes, and
hyperlipidemia.
AICA Embryology and Variant Anatomy
Embryologically, the AICA develops as a branch of the
longitudinal neural system, a plexus of discontinuous
vessels. In week 5, neural channels coalesce to form the
basilar artery at the embryonic stage.9 Initially, the an-
terior circulation predominantly supplies the posterior fossa
through the vertebrobasilar anastomoses.10 As the neural
structures in the posterior fossa develop, the transverse
arteries from the longitudinal channel enlarge to meet
the demands of the cerebellum and brain stem. Superiorly,
3
the dominant transverse arteries become the superior cer-
ebellar arteries (SCAs). In the mid to lower basilar segment,
the dominant transverse arteries develop into AICA. De-
pending on the recruitment of the transverse arteries, SCA,
AICA, and Posterior Inferior Cerebellar Artery (PICA) vari-
ants can develop. Duplicated SCA and AICA result from
co-dominant recruitment of multiple transverse arteries.
The variable takeoffs of AICA from the basilar artery are
related to the recruitment of higher or lower transverse
arteries during the embryologic stage.11
The embryologic development helps to explain the vari-
able anatomy of the posterior circulation. A normal
vertebrobasilar system is often the exception, with a recent
study finding that only 35% of patients had normal
vertebrobasilar system. The most common posterior cir-
culation variant is an absent PICA with blood supply
coming from a well-developed ipsilateral AICA, also known
as the AICA–PICA complex, or from the contralateral PICA.
Approximately 29% of the variant anatomy in the pos-
terior circulation is related to AICA agenesis.12 Previously,
Martin et al found that AICA arose as a single trunk in
72%, as duplicate arteries in 26%, and as triplicate ar-
teries in 2% of cerebellopontine angles.1,13
The AICA runs along the ventral surface of the pons
near the abducens, facial, and vestibulocochlear nerves,
and courses near the lateral recess, foramen of Luschka,
cerebellopontine fissure, middle cerebellar peduncle, and
petrosal cerebellar surface. The AICA is divided into 4
segments: the anterior pontine, lateral pontine,
flocculopeduncular, and cortical segments.1
Branches from the lateral pontine segment of the AICA
give rise to nerve-related arterial branches, including the
labyrinthine (internal auditory) artery, the recurrent per-
forating arteries, and the subarcuate artery. In the most
recent anatomic studies, AICA consistently gives off the
internal auditory artery in 98% of patients. Only in rare
cases does the internal auditory artery arise directly from
the basilar artery. As a result, some have suggested naming
it the cerebellolabyrinthine artery.11 The cerebellolabyrinthine
trunk gives off the subarcuate artery that can anastomose
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4 M.M. CHEN ET AL.

Figure 4. Anterior inferior cerebellar artery (AICA) variant anatomy. (A) Normal AICA variant. (b) AICA variant: complete distal agenesis with com-
pensatory hypertrophy of the superior cerebellar and posterior cerebellar arteries. (C) AICA variant: regression of the caudal portion with the compensatory
hypertrophy of the distal branches of the superior cerebellar and posterior cerebellar arteries. (D) AICA variant: duplicated AICA.

with the middle meningeal artery. This results in a dis-
tinct collateral pathway for the AICA different from the
PICA and SCA. In contrast to the SCA and PICA, which
typically are reconstituted by leptomeningeal collaterals,
meningeal dural-based collaterals can be seen to recon-
stitute AICA.14
Higher variability exists in the more distal AICA. The
AICA typically bifurcates near the facial vestibulocochlear
complex into a rostral and caudal branch. The rostral trunk
courses laterally above the flocculus to reach the surface
of the middle cerebellar peduncle and the cerebellar pontine
fissure. The rostral AICA can form anastomosis with the
marginal branch of the SCA, particularly if the margin-
al artery is large.
The caudal AICA terminates at the flocculus in 40%
of cases. In the other 60% of cases, the caudal trunks course
caudal to the flocculus and are frequently associated with
the lateral portion of the fourth ventricle, supplying the
associated choroid plexus. The distal branches can anas-
tomose with PICA and feeds the flocculus and inferior
petrosal surface of the cerebellum. In 18% of cases, the
AICA supply to the cerebellum can be significant, even
replacing the PICA in 13% of cases.1,15
AICA typically supplies the inferolateral pons, middle
cerebellar peduncle, petrosal surface of the cerebellum in-
cluding the flocculus, inner ear, and rarely the lateral
medulla. The core territory is the middle cerebellar
peduncle.16 The perforating branches of the marginal branch
of the SCA can also supply the middle cerebellar peduncle.1
Heterogeneous clinical presentations for AICA strokes
can be explained by this variation in anatomy and col-
lateral circulation. Proximal AICA occlusion with a “normal
anatomy” including a dominant and full caudal and rostral
branch pattern (Fig 4, A) will result in a diffuse pattern
of infarct that involves the middle cerebellar peduncle, floc-
culus, and petrosal surface of the cerebellum (Case 1).
Proximal AICA strokes with complete distal agenesis
of the affected AICA (Fig 4, B) can result in cranial nerve
deficits of the abducens, facial, and vestibulocochlear nerves,
and infarcts in the territory of the labyrinthine or audi-
tory artery can present with hearing loss. An isolated infarct
in this territory could be undetectable on imaging due
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AICA STROKES BASED ON VARIANT VASCULAR ANATOMY
to the small nature of the affected structures. The more
distal territory of the middle cerebellar peduncle, the floc-
culus and petrosal surface of the cerebellum would not
be affected because branches of the SCA and PICA would
supply these regions.
The AICA infarct isolated to the middle cerebellar pe-
duncle (Cases 2 and 3) can be attributed to the commonly
found atretic pattern of the caudal AICA (Fig 4, C). In
this variation, the marginal branch of the SCA likely sup-
plies the flocculus and petrosal surface of the cerebellum,
and PICA feeds the caudal territory.
Isolated middle cerebellar peduncle stroke (Cases 2 and
3) could also be seen with a duplicated AICA (Fig 4, D)
in the setting where occluded rostral AICA supplies the
cerebellar peduncle and the nonoccluded duplicated caudal
AICA supplies the petrosal cerebellum and flocculus.
Clinical Presentations of AICA Infarcts
Commonly reported clinical presentations include hearing
loss, vertigo, nystagmus, vertigo, diplopia or gaze palsy,
nausea, vomiting, crossed sensory loss, and Horner
syndrome.1,7,17,18 With AICA stroke, the reported inci-
dence of hearing loss is highly variable, with reports ranging
from 30% to 100% of patients. Although there is consis-
tent contribution of AICA to the internal auditory artery,
collateral supply to the labyrinthine artery from the middle
meningeal and occipital artery via the subarcuate artery
might be protective for some patients. In addition, pa-
tients who experience other symptoms such as vertigo and
vomiting may be distracted and unaware of more subtle
hearing loss from cochlear injury.5 Horizontal diplopia is
related to abducens nucleus involvement.7 Dysphagia can
be seen when the infarct involves the lateral medulla.19
The middle cerebellar peduncles are composed of white
matter tracts from the contralateral pontine nuclei as part
of the corticopontocerebellar pathway. As a result, lesions
confined to the middle cerebellar peduncle can result in
limb ataxia, difficulty with speech, and difficulty walking.
The cerebellar pathways decussate twice, and therefore
the symptoms will be ipsilateral to the lesion.
Etiology of AICA Infarcts
AICA strokes are most likely secondary to atheroscle-
rosis from basilar branch occlusive disease due to risk
factors such as hypertension, diabetes, and hyperlipid-
emia. Isolated bilateral AICA strokes can occur in the setting
of basilar occlusive disease, which has been described in
the literature.20 Anastomoses from PICA or superiorly from
the posterior communicating artery can provide collat-
eral flow to the cerebellum. Other causes include cardiac
embolism and more rarely, there has been a single case
report of giant cell arteritis.7 Although AICA is not typically
visualized on MRA or CTA, vascular imaging can char-
acterize the nature of basilar artery disease.19
5
CT and MRI Patterns of AICA Infarcts Territories
Three main MRI imaging patterns can be seen in AICA
strokes. A normal MRI can occur if only the labyrin-
thine segment of the AICA is affected. The true territory
of the AICA is the middle cerebellar peduncle, and so
an isolated to the middle cerebellar peduncle is the second
pattern of acute infarct. The diffuse pattern of infarct in-
volving the petrosal surface of the cerebellum, flocculus,
lateral medulla, and middle cerebellar peduncle is likely
less common than the former patterns because the normal
variant of AICA is rare.
Imaging Differential Diagnosis of AICA Infarcts
The more diffuse pattern of AICA stroke is easily rec-
ognized as a vascular distribution. However, AICA strokes
isolated to the middle cerebellar peduncle can be a di-
agnostic challenge for radiologists. Other differential
considerations for T2/Fluid-Attenuated Inversion Recov-
ery hyperintense lesions in the middle cerebellar peduncle
lesion include inflammatory, infectious, metabolic,
neurodegenerative, and neoplastic etiologies.
Conclusion
AICA strokes are the rarest of the posterior circula-
tion strokes and are clinically underdetected given the
lack of typical cerebellar signs and variable presenta-
tion. The embryology of the posterior circulation contributes
to the high anatomic variability in the vasculature. As a
result, the patterns of AICA infarct include a radiographi-
cally normal study, focal infarct of the middle cerebellar
peduncle, or a diffuse pattern that can include the pe-
trosal surface of the cerebellum, flocculus, lateral medulla,
and middle cerebellar peduncle.
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