J Neurosurg 107:161–164, 2007

Reversible cortical auditory dysfunction caused by
cerebral vasospasm after ruptured aneurysmal
subarachnoid hemorrhage and evaluated by
perfusion magnetic resonance imaging
Case report
SADAHARU TABUCHI, M.D., PH.D., MITSUTOSHI KADOWAKI, M.D.,
AND TAKASHI WATANABE, M.D., PH.D.
Department of Neurosurgery, Institute of Neurological Sciences, Tottori University School of
Medicine, Yonago, Japan

PA 52-year-old woman developed subarachnoid hemorrhage (SAH) caused by a ruptured right internal carotid artery
(ICA) aneurysm. Because of the aneurysm configuration, the authors decided to delay surgery and instead undertook
serial imaging studies of the aneurysm. The patient remained alert but developed acute bilateral deafness on Day 7. Audiological examination and auditory brainstem responses suggested that the hearing disturbance was cortical in origin.
Three-dimensional computed tomography (CT) angiography showed severe vasospasm in the right middle cerebral artery (MCA) and moderate vasospasm in the left ICA and MCA. Three-tesla magnetic resonance (MR) imaging was
performed 2 days after the onset of symptoms. Diffusion-weighted and T2-weighted MR images showed an acute infarction in the right insular cortex caused by vasospasm. Perfusion-weighted MR imaging, particularly mean transit
time mapping, revealed hypoperfusion in both temporal lobes including the auditory cortex and right auditory radiation.
The vasospasm was treated with induction of mild hypertension and hypervolemia. Follow-up MR images, 3D CT angiograms, and audiometry performed 2 weeks after the first examination showed recovery of vasospasm and resolution
of perfusion abnormality and hearing disturbance. On Day 26, the aneurysm was successfully occluded with clips and
the patient was discharged with no deficits. To the authors’ knowledge, this is the first reported case of reversible cortical auditory dysfunction purely due to bilateral cerebral vasospasm detected using perfusion MR imaging after SAH.
(DOI: 10.3171/JNS-07/07/0161)
KEY WORDS • auditory agnosia • cortical auditory dysfunction • cortical deafness •
perfusion-weighted magnetic resonance imaging • subarachnoid hemorrhage • vasospasm

C

ORTICAL deafness is a rare symptom that is most of-

ten associated with cerebral infarction and is caused
by bilateral lesions of the auditory cortex or its radiations.6,11 We encountered a case of acute deafness of cortical origin secondary to vasospasm after SAH. We identified the ischemic lesions in both temporal lobes with the
aid of PW MR imaging. The patient’s symptoms and perfusion abnormality resolved after cessation of vasospasm.
To our knowledge this is the first report of reversible cortical auditory dysfunction caused purely by cerebral vasospasm after SAH.
Case Report
Presentation and Examination. This 52-year-old rightAbbreviations used in this paper: CT = computed tomography;
DW = diffusion-weighted; ICA = internal carotid artery; MCA =
middle cerebral artery; MR = magnetic resonance; MTT = mean
transit time; PW = perfusion-weighted; rCBV = regional cerebral
blood volume; SAH = subarachnoid hemorrhage.

J. Neurosurg. / Volume 107 / July, 2007

handed woman was admitted to our institution with SAH
caused by a ruptured right ICA aneurysm. Computed tomography scans showed diffuse thick SAH with no other
lesions such as an old infarction or hemorrhage. Clinically,
the SAH was evaluated as Grade I according to the World
Federation of Neurological Societies system. Cerebral angiography demonstrated a blisterlike aneurysm located at
the distal ICA. It was unrelated to arterial branching, and
could therefore be classified as an anterior wall aneurysm.
Imaging Studies and Treatment. Because of the risk of premature rupture during early surgery, delayed surgery was
scheduled and the patient underwent serial imaging of the
aneurysm. During follow-up, she was alert; however, she
developed acute bilateral deafness on Day 7 even though
she had no history of hearing impairment. Because of the
deafness, verbal communication was difficult. Although
spontaneous speech and some recognition of verbal and
nonverbal sounds existed, moderate bilateral hearing loss
and an auditory agnostic component were present and communication was confined to writing. The patient’s ability to
read and write and execute written tasks was preserved. The
161

S. Tabuchi, M. Kadowaki, and T. Watanabe

FIG. 1. A: Audiogram obtained at the onset of deafness, showing moderate hearing loss bilaterally. Solid line denotes
the left ear; dashed line, the right ear. B: Tracings of auditory brainstem responses demonstrating a normal pattern of all
components from wave I through V in both ears. HL = hearing level; Li = left side; ms = msec; nHL = normal hearing
level; Ri = right side.

external auditory meatus, tympanic membrane, and vestibular function were normal. Conservative air conduction
audiometry demonstrated moderate hearing loss bilaterally
(Fig. 1A). Auditory brainstem responses showed normal
waveforms and latencies from wave I to V, indicating intact
auditory pathways (Fig. 1B). Therefore, we obtained 3D
CT angiograms, 3-tesla PW MR images, and DW images.
The 3D CT angiograms demonstrated severe vasospasm in
the right MCA and moderate vasospasm in the left MCA,
ICA, and basilar artery (Fig. 2A). The DW and T2-weighted images obtained 2 days after the onset of symptoms
revealed high signal intensity at the right insular cortex, indicating acute infarction due to vasospasm (Fig. 2B). Measurement of MTT and rCBV showed mild hypoperfusion in
both temporal lobes including the auditory cortex (Brodmann areas 22, 41, and 42), the right auditory radiation, and
both occipital lobes (Fig. 2C). The right side was more
extensively involved than the left. Left-sided areas included part of the Heschl gyrus and the parietal lobe, suggesting
that the hearing difficulty originated in the cortex. Vasospasm was treated with induction of mild hypertension and
hypervolemia. Follow-up MR images, 3D CT angiograms,
and audiometry performed 2 weeks after the first examination showed recovery of vasospasm and resolution of perfusion abnormality and hearing disturbance (Fig. 3). The
patient’s hearing loss improved gradually and comprehension and identification of verbal sounds as well as environmental sounds and music normalized within 1 month.
During 3 weeks of follow-up, the shape and size of the aneurysm changed from blisterlike to enlarged and saccular.
On Day 26, the aneurysm was successfully occluded with
clips.
162

Posttreatment Course. The patient’s postoperative course
was satisfactory and the patient was discharged with no
neurological deficits. When the patient was discharged
from the hospital, her Wechsler Adult Intelligence ScaleRevised and standard language test of aphasia scores were
within the normal ranges.

Discussion
The clinical syndrome of cortical deafness in a woman
with bitemporal infarction was described by Wernicke and
Friedlander11 in 1883. Cortical deafness and auditory agnosia are usually related to each other and are frequently associated with aphasia.2,3 Severe auditory deficit due to bilateral cerebral lesions is relatively rare. This condition is
generally known as “cortical deafness” because in most
cases damage to both temporal or temporoparietal lobes is
observed, including the primary auditory cortex (Broadmann areas 41 and 42) on both transverse gyri (Heschl).
The literature contains reports of a number of cases of cortical deafness in children and adults, some congenital and
others occurring as a result of cerebral infarction or cerebral
hemorrhage.1–3,5,6,9–11 In cortical deafness, auditory signals
cannot be perceived in the cortex and audiometry reveals
severe bilateral hearing loss. Because our case was atypical
and demonstrated moderate bilateral hearing loss as well as
an auditory agnostic component, we have used the term
“cortical auditory dysfunction” instead of cortical deafness.
Among the several causes of cortical deafness, there has
been only one previously reported case in which SAH precipitated deafness.7 In that case, an old infarction was diagnosed in the left temporal lobe before the occurrence of
J. Neurosurg. / Volume 107 / July, 2007

Cortical auditory dysfunction due to cerebral vasospasm

FIG. 2. Neuroimages. A: Three-dimensional CT angiogram
obtained at the onset of deafness showing severe vasospasm in the
right MCA and moderate vasospasm in the left MCA, ICA, and
basilar artery. B: Three-tesla MR imaging performed 2 days after
onset of deafness. The DW (DWI) and T2-weighted (T2WI) imaging sequences show high signal intensity at the right insular cortex, indicating acute infarction due to vasospasm. C: Perfusionweighted MR images showing the MTT delay in both temporal
lobes including the auditory cortex, the right auditory radiation, and
both occipital lobes. Left-sided areas included part of the Heschl gyrus and the parietal lobe.

SAH; hence, cortical deafness was caused by vasospasm
contralateral to this old temporal lobe infarction. Evaluation of cerebral blood flow was not performed in that case.
In the present case, it is noteworthy that cortical auditory
dysfunction was caused purely by bilateral cerebral vasospasm after SAH; no existing lesions were present.
J. Neurosurg. / Volume 107 / July, 2007

FIG. 3. A: Three-dimensional CT angiogram obtained 2 weeks
after the first examination showing recovery of vasospasm. B and
D: Resolution of the hearing disturbance is seen on the audiogram
(B) and that of the perfusion abnormality is seen on the PW MR images (D). C: Magnetic resonance images showing only a small
area of infarction in the right insular cortex.

163

S. Tabuchi, M. Kadowaki, and T. Watanabe
Magnetic resonance imaging including DW and PW imaging sequences is a very promising technique to assess
ischemia and brain damage in SAH. Perfusion-weighted
imaging is a useful new tool in the treatment of patients
with SAH, particularly those with cerebral vasospasm, and
the temporary neurological deficits correlate well with the
location of perfusion changes.4 In this study, hypoperfused
regions corresponding to the responsible foci were demonstrated on PW images. Rordorf et al.8 reported that small
ischemic lesions on DW images were seen to be encircled
by a large area of increased MTT in all patients with symptomatic vasospasm. Our data were consistent with this finding.
To the best of our knowledge, this is the first case in
which transient cortical auditory dysfunction caused by
vasospasm after SAH has been detected in both temporal
lobes on PW MR images. This case suggests that transient
ischemia involving the bilateral auditory cortices and auditory radiations can cause reversible cortical auditory dysfunction.
Acknowledgment
We thank Mr. Eijiro Yamashita (Department of Radiology, Tottori University Hospital) for processing and analyzing the data from
the PW images.
References
1. Arimura Y, Ohi T, Shimizu K, Shiomi K, Sugimoto S, Matsukura
S, et al: [A case of cortical deafness following bilateral putaminal
hemorrhage.] No To Shinkei 54:521–525, 2002 (Jpn)
2. Godefroy O, Leys D, Furby A, De Reuck J, Daems C, Rondepierre P, et al: Psychoacoustical deficits related to bilateral sub-

164

cortical hemorrhages. A case with apperceptive auditory agnosia.
Cortex 31:149–159, 1995
3. Graham J, Greenwood R, Lecky B: Cortical deafness—a case report and review of the literature. J Neurol Sci 48:35–49, 1980
4. Hertel F, Walter C, Bettag M, Morsdorf M: Perfusion-weighted
magnetic resonance imaging in patients with vasospasm: a useful
new tool in the management of patients with subarachnoid hemorrhage. Neurosurgery 56 (1 Suppl):28–35, 2005
5. Hood LJ, Berlin CI, Allen P: Cortical deafness: a longitudinal
study. J Am Acad Audiol 5:330–342, 1994
6. Mendez MF, Geehan GR Jr: Cortical auditory disorders: clinical
and psychoacoustic features. J Neurol Neurosurg Psychiatry
51:1–9, 1988
7. Ogane K, Fujii Y, Hatanaka M: [A case of subarachnoid hemorrhage complaining of deafness.] No To Shinkei 50:443–446,
1998 (Jpn)
8. Rordorf G, Koroshetz WJ, Copen WA, Gonzalez G, Yamada K,
Schaefer PW, et al: Diffusion- and perfusion-weighted imaging in
vasospasm after subarachnoid hemorrhage. Stroke 30:599–605,
1999
9. Szirmai I, Farsang M, Csuri M: Cortical auditory disorder caused
by bilateral strategic cerebral bleedings. Analysis of two cases.
Brain Lang 85:159–165, 2003
10. Tanaka Y, Kamo T, Yoshida M, Yamadori A: ‘So-called’ cortical
deafness. Clinical, neurophysiological and radiological observations. Brain 114:2385–2401, 1991
11. Wernicke C, Friedlander C: Ein Fall von Taubheit in Folge von
doppelseitiger Laesionen des Schlafenlappens. Fortschr Med 1:
177–185, 1883
Manuscript submitted June 23, 2006.
Accepted November 7, 2006.
Address reprint requests to: Sadaharu Tabuchi, M.D., Ph.D., Department of Neurosurgery, Institute of Neurological Sciences, Tottori University School of Medicine, 36-1 Nishi-cho, Yonago 6838504, Japan. email: stabuchi@grape.med.tottori-u.ac.jp.

J. Neurosurg. / Volume 107 / July, 2007