Journal of the Neurological Sciences 313 (2012) 153–159

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Journal of the Neurological Sciences

journal homepage: www.elsevier.com/locate/jns

Audiovestibular loss in anterior inferior cerebellar artery territory infarction: A

window to early detection?
Hyung Lee ⁎
Department of Neurology, Keimyung University School of Medicine, Daegu, Republic of Korea
Brain Research Institute, Keimyung University School of Medicine, Daegu, Republic of Korea

a r t i c l e i n f o a b s t r a c t

Article history: Acute audiovestibular loss is a common neurotological condition that is characterized by sudden onset of severe
Received 29 June 2011 prolonged (lasting days) vertigo and hearing loss and is diagnosed by the presence of canal paresis to caloric
Received in revised form 27 August 2011 stimulation and sensorineural hearing loss on pure tone audiogram. Before 2000, papers on anterior inferior cer-
Accepted 29 August 2011
ebellar artery (AICA) territory infarction focused mostly on associated brainstem and cerebellar findings, without
Available online 13 October 2011
a detailed description of neurotological findings. Since 2000, several reports have demonstrated that acute audio-
Keywords:
vestibular loss is an important sign for the diagnosis of AICA territory infarction. To date, at least eight subgroups
Audiovestibular loss of AICA infarction have been identified according to the pattern of neurotological presentations, among which
AICA territory infarction the most common pattern of audiovestibular dysfunction is the combined loss of auditory and vestibular func-
tions. Because audiovestibular loss may occur in isolation before ponto-cerebellar infarction involving AICA dis-
tribution, audiovestibular loss may serve as a window to prevent the progression of acute audiovestibular loss
into more widespread areas of infarction in posterior circulation (mainly in the AICA territory). Clinician should
keep in mind that acute audiovestibular loss may herald impending AICA territory infarction, especially when pa-
tients had basilar artery occlusive disease presumably close to the origin of the AICA on brain MRA, even if other
central signs are absent and MRI does not demonstrate acute infarction.
© 2011 Elsevier B.V. All rights reserved.

1. Introduction neurotological dysfunction with vertigo and/or hearing loss is an im-

Acute audiovestibular loss is a common neurotological syndrome
characterized by sudden onset of severe prolonged (lasting days) vertigo
and hearing loss. The presence of canal paresis (CP) to caloric stimulation
and sensorineural hearing loss (SNHL) on pure tone audiogram is consid-
ered as a mandatory sign for the diagnosis of acute audiovestiublar loss.
It can occur in isolation (i.e., acute labyrinthitis or labyrinth infarction) or
is associated with other neurological symptoms or signs that in the later
condition are usually accompanied by ischemic stroke in the territory of
the anterior inferior cerebellar artery (AICA) [1,2].
Acute ischemic stroke in the distribution of the AICA is known to
be associated with vertigo, hearing loss, nystagmus, facial weakness,
gait ataxia, and hypalgesia. In 1943, Adams [3] was the first to
completely describe the syndrome associated with the AICA occlu-
sion. Although neurotologic symptoms such as vertigo, tinnitus, and
bilateral hearing loss were early initial symptoms in his patients, neu-
rotological findings have received little attention. Subsequent reports
[4–8] on AICA infarction before 2000 focused mostly on the brainstem
and cerebellar findings or mechanism of stroke without the associat-
ed neurotologic findings. Since 2000, many studies have shown that a
⁎ Department of Neurology, Keimyung University School of Medicine, 194 Dongsan
dong, Daegu 700-712, Republic of Korea. Tel.: + 82 53 250 7835; fax: + 82 53 250 7840.
E-mail address: hlee@dsmc.or.kr.
portant sign for the diagnosis of the AICA [1,9–16]. An extensive neu-
rotological evaluation suggested that CP and SNHL are mainly caused
by ischemia to the inner ear [1,9–16]. This review aims to highlight
recent advances on audiovestibular loss in the AICA territory infarc-
tion and to address their clinical significance. It is especially focused
on isolated audiovestibular loss as a window to early detection of
AICA infarction.
2. Vascular mechanism of AICA territory infarction
The mechanism for AICA occlusion was atherothrombotic in most
cases [5–7]. In a series of nine patients with AICA territory infarction di-
agnosed by brain MRI [7], four diabetic patients had isolated unilateral
AICA infarctions due to basilar artery branch occlusive disease because
these patients had patent basilar artery on angiography. In these pa-
tients, plaque in the basilar artery probably extended into the AICA
or microatheroma blocked the AICA orifice, resulting in isolated
AICA infarction. The other five patients had infarcts extending beyond
AICA territory (i.e., AICA infarct and other infarcts in the posterior circu-
lation). These all had basilar artery occlusion including the AICA level
and reconstitution of the distal basilar artery on angiography. A recent
report also showed similar findings that most patients (82%, 45/55)
with isolated AICA infarction showed normal basilar artery on MRA
and severe basilar artery occlusive disease was more common in

0022-510X/$ – see front matter © 2011 Elsevier B.V. All rights reserved.
doi:10.1016/j.jns.2011.08.039
154 H. Lee / Journal of the Neurological Sciences 313 (2012) 153–159

patients with posterior circulation infarcts in addition to AICA infarct
[16]. Rarely emboli originating from cardiac or atheromatous plaque
in the proximal artery lodge in the AICA orifice result in AICA infarction
[5,17] (Fig. 1). Overall, isolated AICA infarcts are usually caused by
basilar branch occlusive disease, whereas infarcts extending beyond
AICA territory are mostly due to basilar artery occlusive disease [5–7,16].
3. Audiovestibular loss as an important sign for the diagnosis of
AICA territory infarction
The internal auditory artery (IAA) irrigates the cochlea and vestibular
labyrinth, and occlusion of the IAA causes a loss of auditory and vestibu-
lar function (i.e., audiovestibular loss), resulting in hearing loss and ver-
tigo, so-called labyrinthine (inner ear) infarction. IAA infarction mostly
occurs due to thrombotic narrowing of the AICA itself, or in the basilar ar-
tery at the orifice of the AICA [5–7]. Because the inner ear is not well vi-
sualized on routine MRI, a definite diagnosis of labyrinthine infarction
with audiovestibular loss is not possible unless a pathological study is
done. Hearing loss has been traditionally considered as a less common
sign of AICA territory infarction. There are at least two possible explana-
tions. First, patients may not be aware of their hearing loss during an at-
tack of vertigo and vomiting when the unilateral hearing loss is mild or
the severity of associated vertigo is severe. Second, neurologists have
not included the audiogram as a routine diagnostic tool for the evalua-
tion of AICA infarction. However, more than 90% (11/12) of patients
with AICA infarction diagnosed by brain MRI had acute SNHL, which is
accompanied by acute vertigo and CP (i.e., audiovestibular loss) [1]. Sev-
eral recent papers [1,9–16] emphasized that AICA infarction commonly
accompanied inner ear involvement and labyrinthine infarction with
audiovestibular loss is an important sign for the diagnosis of AICA infarc-
tion. When audiovestibular loss occurs, infarction of the brainstem and/
or cerebellum in the territory of the AICA is usually associated. However,
AICA infarction rarely causes isolated audiovestibular loss without brain-
stem or cerebellar signs (i.e., isolated labyrinthine infarction), in which
case an acute infarct may still be seen on brain MRI [12]. Thus, clinicians
should be aware of the possibility of AICA infarction, particularly in older
patients with acute audiovestibular loss and vascular risk factors, even
when other brainstem or cerebellar signs are absent.
4. Isolated audiovestibular loss before AICA territory infarction:
frequency and clinical implication
When vertigo or hearing loss is associated with other brainstem or
cerebellar signs, the diagnosis of AICA infarction is easily made.

Fig. 1. Three common vascular mechanisms in AICA territory infarction. A. Infarcts on brain MRI are localized to the middle cerebellar peduncle and anterior cerebellum, which is
typically known to be supplied by the AICA (A-1), and brain MRA shows no vascular compromise in the basilar artery (A-2). B. Brain MRI shows multiple infarcts in the posterior
circulation (B-1), in addition to AICA territory infarction (B-2), and brain MRI shows poorly visualized basilar and distal vertebral arteries (B-3). C. The infarcted area on brain MRI is
consistent with AICA territory (C-1). Initial MRA shows moderate stenosis of the lower basilar artery, presumably close to the origin of the AICA (C-2), but follow-up MRA 10 days
after the onset of symptoms shows no stenosis of the basilar artery (C-3), suggesting complete recanalization. This patient had paroxysmal atrial fibrillation and emboli originating
from the cardiac probably lodge in the AICA orifice, resulting in AICA infarction. AICA: anterior inferior cerebellar artery.
 H. Lee / Journal of the Neurological Sciences 313 (2012) 153–159 155

However, partial ischemia of the AICA may give rise to isolated verti-
go or hearing loss because the IAA is an end artery with minimal col-
laterals from other major arterial branches, and the cochlea and
vestibular apparatus are supplied by different branches of the IAA
[18,19]. There have been several case reports [9,13,14] indicating
that acute audiovestibular loss may be an impending sign of AICA ter-
ritory infarction. In one study [15], 8% (4/43) of patients with docu-
mented AICA territory infarction on brain MRI initially experienced
an isolated audiovestibular loss with a normal brain MRI. Another
similar study showed that in 30% (9/29) of patients with acute
SNHL (mainly combined with vertigo) due to posterior circulation is-
chemic stroke, an isolated audiovestibular loss had been the initial
presenting symptom, up to 10 days before other delayed neurological
deficits [20]. In a more recent study [16], in approximately 16%
(13/82) of patients with AICA territory infarction on brain MRI,
acute vertigo/auditory disturbance (mostly hearing loss) in isolation
had been the initial symptoms within 1 month before the infarction.
Although the above three studies were somewhat different in meth-
odology, all of these data suggested that 8–30% of patients with posteri-
or circulation stroke (mainly AICA territory) had acute audiovestibular
loss before more widespread infarction and this symptom may come
to be viewed as an opportunity to prevent an impending posterior cir-
culation stroke. Because most patients with prodromal audiovestibular
disturbances had an evidence of focal or diffuse segment of reduced
blood flow in the basilar artery presumably close to the origin of the
AICA [1,11,16], prodromal vertigo and/or hearing loss before AICA in-
farction may be explained by the assumption that an atheromatous pla-
que within the basilar artery may have extended into the AICA ostia. By
this mechanism, decreased blood flow in the affected AICA might cause
transient episode of selective ischemia to the inner ear, resulting in iso-
lated prodromal audiovestibular disturbance, because the inner ear re-
quires high-energy metabolism and has little collateral circulation
[18,19]. Although there are as yet no systematic data on what a high-
risk factor suggesting impending stroke is or what interventions
might be beneficial at the stage of isolated audiovestibular loss, patients
with prodromal audiovestibular disturbance were more likely to have
focal or diffuse stenosis of the basilar artery presumably close to the or-
igin of the AICA than patients without audiovestibular disturbance
[1,11,16]. This finding emphasized that AICA infarction should be con-
sidered, particularly in elderly patients with vascular risk factors and
acute audiovestibular loss, even when MRI does not demonstrate
acute infarction in the brain. At this stage, clinicians should consider a
further investigation and proper managements to prevent progression
of acute audiovestibular loss into a more widespread posterior circula-
tion stroke, mainly in the territory of the AICA. Because current diagnos-
tic methods (including MRI) cannot confirm labyrinthine infarction
among the acute audiovestibular loss syndrome, clinicians should con-
sider all the clinical evidences when attempting to determine the etiol-
ogy of acute audiovestibular loss rather than emphasizing that MRI is
the best way to distinguish viral from vascular etiology [21]. Fig. 2 illus-
trates the MRI findings in a patient with acute audiovestibular loss as a
prodromal sign of AICA territory infarction. The diffusion-weighted MRI
was normal at the time of acute isolated audiovestibular loss. The site of
injury responsible for isolated audiovestibular loss was probably local-
ized to the inner ear or vestibular nerve.
5. Which of the anatomical structures supplied by the AICA is
more sensitive to ischemia?
AICA territory infarction is diagnosed on brain MRI or CT by in-
volvement of at least one of the following anatomical structures
such as middle cerebellar peduncle, lateral inferior pontine area, or
anterior cerebellar hemisphere [5]. Amarenco et al. showed that ap-
proximately 80% of patients with AICA infarction showed symptoms
or signs indicative of lateral pontine dysfunction including facial
weakness or crossed sensory loss [7]. High incidence of pontine dys-
function in AICA territory infarction may be explained by the fact
that the pontine area supplied by the AICA has little collateral circula-
tion, but the cerebellar hemisphere has a rich anastomotic network
originating from other cerebellar arteries including the posterior infe-
rior or superior cerebellar arteries [5,7,22]. Thus, involvement of the
lateral inferior pons and middle cerebellar peduncle is considered as
a radiological hallmark for the diagnosis of the AICA infarction. How-
ever, recent papers after 2000 have contradictive findings [1,16]. All
but one (11/12, 92%) patients with AICA territory infarction had a
audiovestibular loss with CP and SNHL on presentation, which is
mostly resulted from injury to the inner ear, but symptoms and
signs suggestive of pontine dysfunction were found in only 50% of pa-
tients [1]. In the largest series to date on the audiovestibular symp-
toms of AICA infarcts (82 patients), 60% had audiovestublar loss

Fig. 2. MRI findings in a patient with acute audiovestibular loss as a prodromal sign of AICA territory infarction. (A and B) Axial diffusion-weighted brain MRI 1 day after the onset of
sudden right-sided hearing loss and vertigo was normal, but MRA (C) shows severe stenosis of the proximal portion of the basilar artery presumably close to the origin of the AICA
and the distal right vertebral artery. One day later, the patient complained of exacerbation of vertigo and hearing loss on the right ear. On examination, there were bidirectional
gaze-evoked nystagmus and dysmetria on the right limb. (D and E) Follow-up axial diffusion-weighted MRI demonstrated hyperintense foci involving the right middle cerebellar
peduncle and the right anterior cerebellum. AICA: anterior inferior cerebellar artery.
156 H. Lee / Journal of the Neurological Sciences 313 (2012) 153–159
with CP and SNHL, whereas facial weakness or crossed sensory loss
suggesting pontine dysfunction was found in only 28% (23/82) of pa-
tients [16]. Complete AICA infarction involving the middle cerebellar
peduncle, lateral pons, and anterior inferior cerebellum was found
in only 16% (13/82) of patients [16]. Thus, although pontine signs
are key features differentiating AICA infarction from more common
benign disorders involving the inner ear, they are less common than
previously thought. As noted above, the labyrinth requires high-
energy metabolism and the IAA is an end artery with minimal collat-
erals from the otic capsule so the labyrinth is especially vulnerable to
ischemia [18,19,22]. By contrast, the retrocochlear acoustic nerve has
an abundant collateral blood supply arising from the lateral medul-
lary artery, arteries supplying adjacent dura matter and petrous
bone, and the inferior lateral pontine artery [18,23,24]. Overall, recent
prospectively gathered evidence suggests that the inner ear is a com-
monly affected site during AICA territory ischemia, as well as, the
brainstem although current imaging techniques including MRI did
not permit the visualization of the inner ear.
6. Vestibular dysfunction in AICA territory infarction
With AICA territory infarction, the most common pattern of vestibu-
lar dysfunction is a combination of peripheral (i.e., unilateral CP),
and central signs (e.g., asymmetrically impaired smooth pursuit, bidirec-
tional gaze-evoked nystagmus, or impaired modulation of the vestibular
responses using visual input) that was observed in approximately 65%
(53/82) of a large series of consecutive cases [16]. These findings occur
because the AICA supplies peripheral vestibular structures such as the
inner ear and vestibulocochlear nerve, in addition to central vestibular
structures [5,7]. Because AICA supplies both peripheral and central ves-
tibular structures, the site(s) responsible for producing vertigo with
AICA infarction is difficult to determine in an individual patient. Howev-
er, most patients with AICA infarction have a unilateral decrease to CP,
suggesting dysfunction of the peripheral vestibular structures at least
in part. Occasionally, patients with vertigo have normal caloric re-
sponses, in which case the vertigo likely originates from ischemia to cen-
tral vestibular structures.
7. Spectrum of audiovestibular loss in AICA territory infarction
(Table 1)
Nearly all patients (80/82, 98%) with AICA infarction have acute pro-
longed (more than 24 h) vertigo and vestibular dysfunction of peripheral,
central, or combined origin [16]. So far, there are eight subgroups of
AICA territory infarction according to the pattern of neuro-otological pre-
sentations [16,25]. First (group 1), acute prolonged vertigo with audio-
vestibular loss is the most common subgroup of audiovestibular
dysfunction in AICA territory infarction. Second (group 2), acute pro-
longed vertigo but without documented audiovestibular loss is also a
common presentation in AICA territory infarction. In this condition, verti-
go originates from dysfunction of the central vestibular structure. Third
Table 1
Spectrums of audiovestibular loss in AICA territory infarction.
Group 1 Group 2
Presented with vertigo + +
Combined audiovestibular loss + −
Normal audiovestibular function − +
Prodromal audiovestibular disturbance − −
Isolated SNHL (normal caloric and VEMPs responses) − −
Isolated CP (normal hearing and VEMPs responses) − −
Isolated VEMPs abnormality (normal caloric and VEMPs responses) − −
Associated with other neurological symptoms or signs + +
AICA: anterior inferior cerebellar artery; SNHL: sensorineural hearing loss; CP: canal paresis; VEMPs: vestibular evoked myogenic potentials.
(group 3), acute prolonged vertigo with audiovestibular loss is some-
times preceded by an episode(s) of transient vertigo/auditory distur-
bance, which is considered as a prodromal sign of impending AICA
territory infarction. Fourth (group 4), AICA infarction rarely presented
with acute prolonged vertigo and isolated auditory loss without vestibu-
lar loss (i.e., SNHL without CP). Fifth (group 5), AICA infarction rarely pre-
sented with acute prolonged vertigo and isolated superior vestibular loss
without auditory loss (i.e., CP without SNHL). Sixth (group 6), AICA in-
farction rarely presented with acute prolonged vertigo and isolated infe-
rior vestibular loss without auditory or superior vestibular loss (i.e.,
abnormal vestibular evoked myogenic potential without CP or SNHL).
Seventh (group 7), AICA infarction rarely presented with acute prolonged
vertigo and isolated audiovestibular loss without any other neurological
symptoms/signs. Eighth (group 8), AICA infarction rarely presented
with nonvestibular symptoms including tingling sensation on the face
and/or extremities, gait ataxia, or cerebellar dysmetria and normal audio-
vestibular function. Overall, AICA territory infarction can produce a broad
spectrum of neuro-otological presentations, in which the most common
pattern of audiovestibular dysfunctions is the combined loss of auditory
and vestibular function. Selective loss of vestibular or cochlear func-
tion is infrequently observed. The pattern of inner ear involvement in
AICA territory infarction is shown in Fig. 3.
8. Clinical implication of a broad spectrum of audiovestibular loss
in AICA territory infarction
When patients with risk factors for stroke developed acute onset
of isolated prolonged vertigo without accompanying hearing loss or
other neurological symptoms, ischemic damage to the superior ves-
tibular labyrinth due to anterior vestibular artery (AVA) infarction is
reasonably suspected because the lumen of the AVA is small and
has little collateral circulation [18,19,22]. A previous report [18] also
supported this assumption because approximately 50% of patients
with isolated episodic vertigo of a vascular cause (i.e., vertebrobasilar
insufficiency) had unilateral CP, which is commonly localized to the
inner ear (i.e., superior vestibular labyrinth). However, recent finding
did not support this assumption because only four (5%) patients
showed isolated vestibular labyrinthine involvement at the time of
AICA infarction [16]. Thus, although isolated AVA infarction may
serve as a mechanism of isolated vascular vertigo, the incidence
would be low. Isolated involvement of the cochlea was also an un-
common manifestation of AICA infarction, which was observed in
only 3% of patients [16]. Unlike inner ear dysfunction of a viral
cause, which can commonly present as an isolated vestibular (i.e.,
vestibular neuritis) or cochlear loss (i.e., sudden deafness), labyrin-
thine dysfunction of a vascular cause rarely results in isolated loss of
vestibular or auditory function. Thus, when sudden onset of isolated
prolonged vertigo or hearing loss occurred in patients with vascular risk
factors, vascular compromise to the inner ear was less likely considered.
However, when the combined audiovestibular loss occurred in patients
with prolonged vertigo, the vascular cause was highly suspected.
Group 3 Group 4 Group 5 Group 6 Group 7 Group 8
+ + + + + −
+ − − − + −
− − − − − +
+ − − − − −
− + − − − −
− − + − − −
− − − + − −
+ + + + − +
 H. Lee / Journal of the Neurological Sciences 313 (2012) 153–159 157

Fig. 3. Schematic diagram of the patterns of inner ear involvement in AICA territory infarction according to type of involved artery. A. The arterial supply to the inner ear. B. Internal
auditory artery occlusion results in combined loss of cochlear and vestibular functions (i.e., SNHL, CP, and abnormal VEMP). C. Main cochlear artery occlusion causes selective loss of
cochlear function (isolated SNHL). D. Anterior vestibular artery occlusion causes selective loss of superior vestibular function (isolated CP only). E. Posterior vestibular artery occlu-
sion causes selective loss of inferior vestibular function (abnormal VEMP only). F. No involvement of the internal auditory artery results in normal cochlear and vestibular functions.
Hatched region indicates area of lesion. SNHL: sensorineural hearing loss, CP: canal paresis, VEMP: vestibular evoked myogenic potentials.

9. Long-term outcome of audiovestibular loss with CP and SNHL imbalance gradually improve with central compensation. However,
a recent report [20] showed that most patients (17/21, 81%) with lab-
In audiovestibular loss of a vascular cause, it was previously yrinthine infarction after at least 1 year follow-up showed improved
thought that hearing loss is usually permanent, but dizziness and hearing loss partially or completely. A recovery rate of 81% is above

Fig. 4. MRI and progress of audiovestibular dysfunction in a patient with AICA territory infarction who had severe hearing loss initially, but showed normal hearing level on the last
follow-up. A. Axial diffusion-weighted MRI demonstrates acute infarcts involving the right middle cerebellar peduncle. B. Initial pure tone audiogram reveals severe hearing loss
(80 dB) with 40% speech discrimination in the right ear. Hearing levels in decibels (dB) (American National Standards Institute, 1989) are plotted against stimulus frequency on
a logarithmic scale. C. Initial video-oculographic recordings of bithermal caloric tests disclose the left CP (84%). D. Follow-up testing performed 4 years after the onset of symptoms
shows a complete recovery of hearing loss in the right ear. E. Follow-up caloric test performed 4 years after the onset of symptoms also shows normal caloric response on the left
side. AICA, anterior inferior cerebellar artery; CP, canal paresis; Vmax, maximal velocity of slow phase of nystagmus.
158 H. Lee / Journal of the Neurological Sciences 313 (2012) 153–159

Fig. 5. MRI and progress of audiovestibular dysfunction in a patient with AICA territory infarction who had profound hearing loss at initial and last follow-up. A. Axial diffusion-
weighted MRI demonstrates acute infarcts involving the right middle cerebellar peduncle and right anterior cerebellar hemisphere. B. Initial pure tone audiogram reveals profound
hearing loss on the right side. Hearing levels in decibels (dB) (American National Standards Institute, 1989) are plotted against stimulus frequency on a logarithmic scale. C. Initial
video-oculographic recordings of bithermal caloric tests show a right CP (64%). D. Follow-up testing performed 6 years after the onset of symptoms shows persistent hearing loss
with no interval change. E. Follow-up caloric test performed 6 years after the onset of symptoms shows normal caloric responses on the right side. AICA, anterior inferior cerebellar
artery; CP, canal paresis; Vmax, maximal velocity of slow phase of nystagmus.

the spontaneous recovery rate (40%–69%) reported for idiopathic
SNHL [26,27], but is similar to the recovery rate (61%–89%) of idio-
pathic SNHL after steroid treatment [28–30]. Although there are no
systematic studies on factors predicting poor outcome in patients
with SNHL of a vascular cause, the improvement rate of hearing loss
in patients with profound hearing loss was significantly lower than
that in patients with less than profound hearing loss (40% vs 94%)
[20]. This is consistent with previous studies focusing on idiopathic
sudden SNHL [31–33]. Similar to hearing loss of a vascular cause, CP
of a vascular cause may also be normalized. A recent paper [34]
showed that 67% of patients with CP associated with posterior circula-
tion ischemic stroke after at least 1 year follow-up showed normalized
caloric response. Furthermore, all patients after more than 5 years
follow-up after the onset of vertigo showed normalized caloric response
[34]. Overall, recent data suggests that audiovestibular loss associated
with posterior circulation ischemic stroke often has a good long-term
outcome. Illustrative cases of good outcome with complete recovery
of audiovestibular loss and poor outcome with no recovery of SNHL of
a vascular cause are shown in Figs. 4 and 5, respectively.
Conflict of interest
I have no conflict of interest.
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