(2021) 15:111
Kinouchi et al. J Med Case Reports
https://doi.org/10.1186/s13256-020-02574-8

Open Access

CASE REPORT

Basilar artery occlusion presenting
as sudden bilateral deafness: a case report
Tomoya Kinouchi1* , Keisuke Ishitani2, Shinichi Uyama1, Tadashi Miyamoto1, Naomi Fujimoto3
and Hiromi Ueta1

Abstract
Background: Most sudden-onset hearing loss is due to otolaryngologic- and very rarely to cerebrovascular disease.
We report a woman with sudden bilateral sensorineural hearing loss. This case suggests that even in the absence of
brainstem or cerebellar signs, magnetic resonance imaging (MRI) and MR angiography (MRA) should be performed
since such studies may reveal signs of life-threatening vertebrobasilar artery occlusion.
Case presentation: A 73-year-old Japanese woman with a history of hypertension, hyperlipidemia, and atrial fibrillation who suffered bilateral deafness with vertigo and vomiting was transferred from a local hospital to our department. On admission her consciousness was clear and vertigo was absent. Neurological examination revealed only
bilateral sensorineural hearing loss. Head computed tomography (CT) returned no significant findings. The next
morning she gradually developed severe drowsiness. Diffusion-weighted MRI demonstrated acute cerebral infarction
in the brainstem and bilateral cerebellum; MRA showed basilar artery occlusion due to a cardioembolic thrombus.
Revascularization was obtained by endovascular treatment. However, her condition worsened progressively during
the following hours. CT revealed new brainstem lesions, massive cerebellar swelling, and obstructive hydrocephalus.
She died on the second day after her admission.
Conclusions: When hearing loss is due to vertebrobasilar occlusive disease, the prognosis is very poor. We suggest
that vertebrobasilar stroke be suspected in patients with bilateral sensorineural hearing loss who present with risk factors for stroke such as atrial fibrillation and other neurologic signs.
Keywords: Sudden bilateral deafness, Bilateral sensorineural hearing loss, Vertebrobasilar artery occlusion,
Endovascular treatment
Introduction
The prognosis of patients with sudden-onset sensorineural hearing loss, an inner ear disorder, is relatively good. It
tends to be due to idiopathic sudden deafness, Meniere’s
disease, or a perilymphatic fistula. More rarely it is attributable to vertebrobasilar ischemia. The incidence of
vertebrobasilar ischemia in sudden sensorineural hearing loss is approximately 1.2% [1]. The anterior-inferior
*Correspondence: k‑tomoya@xg8.so‑net.ne.jp
1
Department of Neurosurgery, Tokushima Municipal Hospital, 2‑34,
Kitajyosanjima‑cho, Tokushima 770‑0812, Japan
Full list of author information is available at the end of the article

cerebellar artery (AICA) which originates from the
basilar artery (BA) is implicated in acute audiovestibular dysfunction. Sudden bilateral deafness due to AICA
ischemia is associated with multiple brainstem signs or
symptoms and rarely with a single factor.
When hearing loss is due to vertebrobasilar occlusion,
the prognosis is very poor. We report a woman who presented with only bilateral hearing loss without vertigo
and vomiting. Consequently, initially we did not suspect
specific anomalies including vertebrobasilar impairment. However, angiography revealed occlusion of lower
third of the BA. Based on the experience reported here,
we suggest that patients with sudden bilateral hearing

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loss be subjected to MRI and MRA studies because they
may reveal signs of life-threatening vertebrobasilar artery
occlusive disease.

Case presentation
A 73-year-old Japanese woman with a history of hypertension, hyperlipidemia, and atrial fibrillation (AF) with
a CHA2DS2-VASC score of 3 developed bilateral hearing
loss with vertigo and vomiting and was brought to a local
hospital. Her home medications included 5 mg daily of
atorvastatin. The diagnosis was sudden deafness and she
was transferred to our emergency department. At that
time her consciousness was clear. She had no significant
family, social, environmental, or employment history.
She did not smoke or take alcohol. Her blood pressure
was 147/72 mmHg, her pulse rate was 78 beats/minute
with AF, and her temperature 36.8 °C. One year earlier
she interrupted anticoagulant therapy because she experienced recurrent epistaxis.
She reported only bilateral hearing loss without vertigo and vomiting. Dysarthria, weakness, ataxia, diplopia,
dysphagia, and Horner syndrome were absent. As computed tomography (CT) returned no specific findings
(Fig. 1) she returned home and was scheduled for audiometry on the next day.
The next morning her consciousness decreased progressively and she returned to our hospital. At the
time of admission she was severely drowsy. Her Glasgow Coma Scale (GCS) score was 7 (E2V1M4) and
the National Institute of Health Stroke Scale (NIHSS)
score was 33. We found the normal pupil reflexes,
symmetrical facial responses and withdrawal of both
arms and legs to painful stimuli. Her general physical examination was unremarkable. Her blood pressure was 170/90 mmHg, her pulse rate was 80/minute
with AF, and her temperature 36.4 °C. Her laboratory test results showed a white blood cell count of

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8.8 × 109/l, hemoglobin of 14.7 g/dl, platelet count of
268 × 109/l, blood urea nitrogen 11.3 mg/dl, and creatinine of 0.58 mg/dl, as well as a normal liver function
test result. Diffusion-weighted imaging (DWI) revealed
acute multifocal lesions involving the bilateral cerebellar hemispheres and pons and the posterior circulation.
The DWI posterior circulation Acute Stroke Prognosis Early CT Score (DWI-pc-ASPECTS) was 7 (Fig. 2a,
b). The susceptibility vessel sign was noted in the BA
on T2*-weighted images (Fig. 2c). Magnetic resonance
angiography (MRA) and 3D CT angiography (CTA)
showed occlusion of the V3–4 segments of the bilateral vertebral arteries (VA) and the BA (Fig .2d, e). As
conservative treatment was thought to be ineffective we
started edaravone infusion (30 mg intravenously, twice
a day) and performed endovascular treatment.
Transfemoral cerebral angiography showed occlusion of the V4 segment of the left VA just proximal
to its union with the BA (Fig. 3a, b). Left common
carotid angiography demonstrated retrograde blood
flow into the BA and the bilateral superior cerebellar artery (SCA) via the left posterior communicating
artery (PcomA); the proximal side was obstructed to
the union area. Two-pass 5MAX ACE (Penumbra Inc.,
Alameda, USA) using a direct aspiration first-pass technique was successful. While the BA trunk was completely reperfused, the right AICA and SCA remained
occluded (Fig. 3c).
Her past history of untreated AF and current angiographic findings strongly suggested a cardioembolic
thrombus-induced basilar artery occlusion; we did not
perform echocardiography. Postoperatively she was
comatose; brain CT showed a large brainstem infarct
and upward herniation (Fig. 4) and she died on the second day after admission. Whole body and brain autopsy
was not performed.

Fig. 1. Brain computed tomography showed no new lesions in the area of the cerebellar hemispheres and brainstem

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Fig. 2. Diffusion-weighted brain MRI showing acute multifocal lesions involving the bilateral cerebellar hemispheres (a, b). The susceptibility vessel
sign was noted in the middle portion of the basilar artery on the T2*-weighted image (c). The V3 segment of the right VA, the V4 segment of the left
VA, and the lower third of the BA were occluded on MRA and 3D-CTA images (d, e)

Fig. 3. Anteroposterior left vertebral angiography revealed BA trunk occlusion (a). Anteroposterior left common carotid angiograms showed
reverse flow into the BA and SCA through the PcomA (b). Post-thrombectomy, the last anteroposterior left vertebral angiogram demonstrated total
recanalization of the BA trunk and residual occlusion of the right AICA and SCA (c)

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Fig. 4. Postoperative brain CT demonstrated progressive infarction and transtentorial upward herniation

Discussion
We showed a woman who presented with only bilateral
hearing loss without vertigo and vomiting caused by
embolic occlusion of lower third of the BA. When hearing loss is due to vertebrobasilar occlusion, the prognosis
is very poor. We suggest that patients with sudden bilateral hearing loss be subjected to MRI and MRA studies
because they may reveal signs of life-threatening vertebrobasilar artery occlusive disease.
Sudden-onset sensorineural hearing loss usually suggests
an inner ear disorder, e.g. Meniere disease, acute labyrinthitis, autoimmune inner ear disease, or a perilymphatic fistula.
Most sudden-onset sensorineural hearing loss is unilateral. The reported incidence of vertebrobasilar ischemia in
patients with sudden sensorineural hearing loss is approximately 1.2–8.0% [1, 2]. Vertebrobasilar artery occlusion was
implicated in 6% of patients with acute sensorineural hearing loss [3]; 1.4% of patients with vertebrobasilar impairment presented with bilateral hearing loss [4]. Strokes
associated with BA occlusion elicit numerous neurological
symptoms or signs. Huang et al. [4] reported 7 patients with
bilateral sudden deafness due to vertebrobasilar occlusive
disease, 4 of them suffered vertigo only at onset. We suspect
that vertebrobasilar ischemia is often overlooked.
Our patient had no symptoms of brainstem and cerebellar involvement. Among vascular causes, ischemic stroke
in the territory of the AICA, a branch of the BA, is the
leading cause of sensorineural hearing loss [5, 6]. Usually the internal auditory artery (IAA) originates from the
AICA and the inner ear receives its sole supply from the
IAA. Strokes in the AICA territory have been shown to
be associated with occlusion of a BA branch [7–9]. At the
time of admission to our hospital, our patient presented
with only bilateral hearing loss without vertigo and vomiting, consequently, initially we did not suspect specific
anomalies including vertebrobasilar impairment. However,
angiography revealed occlusion of lower third of the BA.

Misery perfusion in the bilateral AICA territories was
due to insufficient supply from the PcomA-mediated
retrograde collateral pathway. Because the inner ear
requires a high-energy metabolism and the IAA is an end
artery with little collateral circulation from the otic capsule, the inner ear is particularly vulnerable to ischemia
[10–14]. The vestibular structure is relatively well supplied by a rich network of anastomosing vessels from the
posterior inferior cerebellar artery (PICA), the SCA, and
the VA [15–17]. AICA hypoperfusion associated with
BA occlusion can result in selective damage and elicit
cochlear dysfunction, leading to bilateral sensorineural
hearing loss. Our patient suffered acute progression of
ischemia to the bilateral cerebellum and the pons of the
posterior circulation and she manifested severe symptoms of brainstem involvement.
Many patients with vertebrobasilar occlusive disease
have a poor outcome and experience truncal ataxia,
quadriplegia, locked-in syndrome, coma, and death [4,
18, 19]. Before the onset of transient vertigo, nausea and/
or tinnitus, 8–16% of patients with AICA territory infarction manifest acute audiovestibular disturbance [4, 11,
20]. Therefore, especially older patients with suddenonset sensorineural hearing loss and episodic central
nervous system symptoms or signs and a history of atherosclerosis or embolism must be carefully evaluated.
Our patient had a history of untreated AF. The delivery
of recombinant tissue plasminogen activator (rtPA) has
been the standard of care in patients with acute ischemic
stroke. However, rtPA must be administered within
4.5 h of stroke onset. To address acute ischemic stroke
due to intracranial large-vessel occlusion, endovascular
treatment by mechanical thrombectomy has been recommended [21, 22]. A meta-analysis [23] found that endovascular thrombectomy was effective when performed
within 6–24 h after the onset of ischemic stroke as long
as the region was still ischemic and not yet infarcted.

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There is no sufficient evidence for the effectiveness of
this treatment in patients with BA occlusion. We found
no recommendations for using both rtPA and endovascular thrombectomy at the posterior circulation in our
patient. Yoon et al. [24] and Kim et al. [25] reported that
they obtained a good clinical outcome when they treated
patients with a DWI-pc-ASPECTS of 6 or less by endovascular reperfusion therapy. Although endovascular
treatment revascularized the vertebrobasilar artery in
our patient, it was too late to prevent the expansion of
irreversible ischemic damage. We suggest that the early
diagnosis and proper management of audiovestibular
events may provide a window to prevent the progression
of infarction to larger areas of the posterior circulation.

Conclusion
Ours is a rare case of sudden bilateral sensorineural hearing
loss due to embolic occlusion of the vertebrobasilar artery,
the AICA, and the PICA. The delayed diagnosis of ischemic
stroke in the posterior circulation can be life-threatening.
Therefore, an early diagnosis and the proper management
of hearing impairment may provide a window to prevent
the progression of infarction to larger areas of the brainstem
and cerebellum. Clinicians must consider the possibility of
vertebrobasilar occlusive disorder especially in patients with
sudden bilateral hearing impairment, with risk factors for
stroke and the manifestation of other neurologic signs.
Acknowledgements
Not applicable.
Authors’ contributions
KI, SU, TM, NF, and HU participated in the patient management. All authors
read and approved the final manuscript.
Funding
None.
Availability of data and materials
Not applicable.
Ethics approval and consent to participate
Not applicable.
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-in-Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of Neurosurgery, Tokushima Municipal Hospital, 2‑34, Kitajyosanjima‑cho, Tokushima 770‑0812, Japan. 2 Department of Otolaryngology,
Takamatsu Red Cross Hospital, Kagawa, Japan. 3 Department of Neurosurgery,
Tokushima Kensei Hospital, Tokushima, Japan.
Received: 4 May 2020 Accepted: 3 November 2020

Page 5 of 5

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