211

Behavioural Neurology 16 (2005) 211–216
IOS Press

Auditory hallucinations in acute stroke
Yair Lampla,∗ , Mordechai Lorberboym b , Ronit Gilada , Mona Boazc and Menachem Sadeh a
a

Department of Neurology, Edith Wolfson Medical Center, Holon, Sackler Faculty of Medicine, Tel Aviv University,
Israel
b
Department of Nuclear Medicine, Edith Wolfson Medical Center, Holon, Sackler Faculty of Medicine, Tel Aviv
University, Israel
c
Epidemiology Unit and the Institute for Cardiovascular Research, Edith Wolfson Medical Center, Holon, Sackler
Faculty of Medicine, Tel Aviv University, Israel

Abstract. Auditory hallucinations are uncommon phenomena which can be directly caused by acute stroke, mostly described
after lesions of the brain stem, very rarely reported after cortical strokes. The purpose of this study is to determine the frequency
of this phenomenon. In a cross sectional study, 641 stroke patients were followed in the period between 1996–2000. Each
patient underwent comprehensive investigation and follow-up. Four patients were found to have post cortical stroke auditory
hallucinations. All of them occurred after an ischemic lesion of the right temporal lobe. After no more than four months, all
patients were symptom-free and without therapy. The fact the auditory hallucinations may be of cortical origin must be taken
into consideration in the treatment of stroke patients. The phenomenon may be completely reversible after a couple of months.

1. Introduction
Auditory hallucinations are defined as auditory
experiences without the presence of external stimuli.
Descriptions of hallucinatory displays as being similar
to deficit phenomena after stroke have been documented [1,3,4,17]. Auditory hallucinations are less
commonly seen complications after stroke, mostly
described as happening after ischemic or hemorrhagic
lesions in the brainstem [13,21,25], the thalamus [11,
26] and the left internal capsule [18]. Auditory
hallucinations after cortical strokes are very uncommon, and only few cases were reported describing this
phenomenon. Anegawa et al. [1] reported unilateral
auditory hallucinations after left temporal lobe
ischemia. Augustine et al. [2] reported musical
hallucinations following stroke of the right middle
cerebral artery.
We analyzed in a prospective study all acute stroke
patients who were admitted to our neurology depart∗ Corresponding author: Yair Lampl, MD, Department of Neurology, Edith Wolfson Medical Center, Holon 58100, Israel. Tel.: +972
3 502 8512; Fax: +972 3 502 8681; E-mail: y lampl@hotmail.com.

ment during the last six years and developed post stroke
auditory hallucinations.

2. Patients and methods
Of the 641 patients (401 male and 240 female),
who were admitted to our neurology department under
the diagnosis of stroke during the years of 1996–2001
for primary investigation, 521 fulfilled the inclusion
criteria and were included in the study. The mean
age was 73.2 ± 12.0 years. The inclusion criteria for
auditory hallucination of organic origin were as
follows: the existence of true non-affective hallucination with the inability to maintain any control, distress
or copying mechanism, known neurological origin,
absence of psychiatric disorder and insight into the
unreality of any pathological perspective state.
Auditory hallucinations were defined as post acute
stroke hallucinations if they appeared between the
onset of symptoms and 14 days after the onset of stroke.
Exclusion criteria included those patients with evidence
of an additional disorder of the central nervous system
apart from ischemic stroke, including inflammatory
diseases or infections of the CNS, tumors, and

ISSN 0953-4180/05/$17.00 © 2005 – IOS Press and the authors. All rights reserved

212

Y. Lampl et al. / Auditory hallucinations in acute stroke

neurodegenerative diseases of the brain. Excluded were
also patients taking recreational drugs or alcohol abuse
patients, as well as those taking medications which had
been proven to evoke hallucinations, including beta
blockers or antihypertensive medications. Patients with
past psychiatric history of affective or non-affective
psychoses were excluded as well. Each patient underwent an acute stroke work-up which included repeat
CT scans, carotid duplex examinations, transthorax
and transesophogastric heart echo and comprehensive
blood examinations. Each patient who demonstrated
signs of a hallucinatory disorder underwent a protocol
which included interviews with a neurologist and a
psychiatrist. The questions were mainly directed at
obtaining an exact description of the hallucination,
using the Hamilton Depression Scale [14] and the
Minimental State Examination (MMSE) [12]. The
patients with hallucinations underwent additional
testing with MRI scans and repeat electorencephalography (EEG) during the ictal phase, as well as during
the interictal phase of the hallucinations. Repeat
examinations, including ENT testing, as well as
audiometry and brainstem evaluated potential test
(BEAR) for the auditory hallucinations were carried
out as well. The data from these examinations were
compared with a 40 member aged- and sex-matched
post cortical stroke patient group (mean age 63.2 ±
9.7 years) without hallucinations. The comparison was
performed according to the anatomical characteristics
of each stroke. Each stroke was diagnosed according
to the anatomical location and volume [7].

3. Results
521 patients (340 male and 181 female) were
primary included in the study. All were interviewed for
having hallucinations. 16 (3%) patients had at least
one kind of hallucinations (visual, auditory or tactile).
Of these, 4 (2 male and 2 female) had auditory hallucinations. All cases of hallucinations occurred after
cortical stroke. No patient demonstrated post stroke
hallucinations after an infarction of the brain stem or
subcortical structures.
In all four patients with auditory hallucinations,
the hallucinations had the same characteristics which
consisted of two main features: (1) hearing familiar
persons, mostly family members speaking to the patients or between themselves or (2) hearing themselves
in their own voice speaking. The data of patients is
shown in Table 1.

4. Case descriptions
4.1. Patient No. 1
A 67-year-old right handed woman was admitted
to the hospital due to sudden onset of headache,
dizziness and auditory hallucinations which appeared
two days prior to hospitalization. She kept complaining
of hearing her sister and neighbor continuously speaking between them and was convinced that she, herself,
was saying things, events that other members of the
family denied the presence of any speech by the patient.
She had long-standing history of good health and no
previous psychiatric event.
On admission, the patient was alert, well orientated
as to time and place and had no speech or language
difficulties. On the left side, mild hemiparesis and
hemihypoesthesia was found. The deep tendon reflexes
were brisker on the same side and accompanied by
pyramidal signs.
In the next three weeks, the patient demonstrated
continued vivid and clear auditory hallucinations. The
hallucinations were complex, consisting of three types:
(1) family members and neighbors speaking to her – the
content of the speech was about sharing information
regarding family members, including past information
about a pet dog, having no threatening or frightening
components and was not emanating from an external
source; (2) the family members speaking with other
persons, not about her, but projecting her ideas; and (3)
hearing herself speaking in her own voice. She defined
the last two incidents as unpleasant and threatening.
The patient always declared that the spoken information
came only from the right side.
Mental status tests were normal, including Waschler
Adult test (WAT) (91 percentile) (27), Mini Mental
State Examination (MMSE) (29/30) [12], digit span
test, drawing a clock [24] and Trail Making Test [23].
Audiometric and repeat psychiatric examinations were
normal. Electroencephalo-graphical examination revealed normal background with persistent appearance
of waves in the right mid-temporal region without
epileptic discharge. On the BEAR test, symmetrical
BTT values <0.2 mg were found. On repeat CT scan
and MRI, an acute lesion of the right temporal area
was demonstrated. The infarction involved the right
temporal auditory region (Broadman area 41, 42)
(Fig. 1) and the post auditory area (interictal)
(Broadman 22). SPECT HMPAO imaging demonstrated a hypoperfusion located in the middle and the
posterior temporal lobe of the right side. The patient

Y. Lampl et al. / Auditory hallucinations in acute stroke

213

Table 1
No.

Age

Sex

Handedness

1

67

F

Right

2

56

F

Right

3

72

F

Left

4

32

M

Right

Neurological symptoms
and/or complaints
Hemiparesis, dizziness,
headache
Headache
−

Left hemiparesis,
left hemihypoesthesia

was treated with haloperidol with good effects. Four
months later, the medication could be discontinued
successfully.
4.2. Patient No. 2
A 56-year-old right handed woman with wellcontrolled hypertension and diabetes mellitus, was
reported as having an episode of syncope, sudden
headache and auditory hallucination following the
syncope. A family member noted the abnormal event,
but the patient refused to leave the house for medical
attention. The family members were confused by
her complaints of “telling them all what she thought”
without actually hearing any of her words. She told
them also that she heard both her sisters speaking the
whole time between them, leaving her out, without their
being physically present in the room. On neurological
examination, no deficit was found. After admission,
she continued to describe two types of hallucinations:
(1) hearing herself in her own voice speaking in a well
constructed manner; and (2) hearing her near relations
discussing things above her head. The hallucinations
consisted of very frightening characters. She did not
define her condition as anxious, but as bizarre and unpleasant. The hallucinations occurred when she was
not awake, and the voice was not of an external source.
On repeat psychiatric examination, no abnormality was found. Neurocognitive tests, including WAT
(93 percentile), MMSE test (30/30), drawing a clock
and trail making test, were all normal. Audiometric
and evoked potential tests were within normal limits.
During an episode of hallucination and interactive
period, EEG examination showed no epileptic discharges with intermittent spikes in the mid and posterior right temporal region on a normal background. The
BEAR examination showed a difference in the BTT of
0.3 msec between the right and left ear.
CT scan demonstrated two hypodense areas – an
acute lesion of the right temporal post auditory region

Location
of stroke
Right temporal
lobe
Right temporal
Lobe,
right occipital
lobe (old lesion)
Right temporal
lobe
Right insula, right
temporal lobe

Treatment
symptoms
Haloperidol

Period of
risk factors
4 months

Vascular

Haloperidol and
Carbamazepine

1 months

Hypertension,
diabetes mellitus

Haloperidol and
Carbamazepine
Resperidone
Carbamazepine

2 months

Hypertension,
hyperlipidemia
Smoking

3 months

−

and a fixed lesion of the lateral periventricular region
of the occipital lobe (Fig. 2). The patient was successfully treated with haloperidol combined with
carbamazepine. The medications were discontinued
one month after the onset of treatment.
4.3. Patient No. 3
A 72-year-old left handed woman, suffering from
hypertension, and hyperlipidemia, was examined by a
psychiatrist after sudden onset of auditory hallucinations. According to her husband, she was in good health
when she went to sleep, and during the night awoke,
complaining of headache and saying that she heard her
mother speaking in the other room. She was aware
of the fact that her mother had died several years ago
and that this phenomenon was illogical; and therefore,
became very frightened and confused. One day later,
the patient complained of hearing herself telling what
she has to do and discussing problems about which she
had no insight. She has a suspicion that the voice did
not come from an external source, but was not sure.
The commands consisted of short phrases of 2–3 words
and were constructed well grammatically.
In the emergency room, no abnormalities were
found on the neurological examination. The psychiatric
examination revealed no pathology, apart form the
auditory hallucination and severe anxiety state.
Audiometric and evoked potential tests were normal.
On EEG examination, slowing of the background in
the tetra wave rate (more on the right side), but without
epileptic discharge, was found during and after the
hallucination period. BEAR examination was symmetrical with BTT less than 0.2 msec. On repeat brain CT
scan, acute ischemic infarct of the middle upper region
of the right temporal lobe was found.
She started a combined haloperidol and carbamazepine therapy which had very good efficacy. After
one week, the auditory hallucinations disappeared, and

214

Y. Lampl et al. / Auditory hallucinations in acute stroke

the anti-psychotic treatment was discontinued. A trial
of discontinuing the anti-convulsive medication two
months later was successful.
4.4. Patient No. 4
A healthy 32-year-old right-handed man, who was
a smoker and had no vascular risk factors, was admitted to the hospital after the appearance of weakness
of the left side combined with auditory hallucinations.
He awoke one morning hearing himself speak that he
feels bad. He called to his wife who immediately called
an emergency care ambulance. During the transport to
the hospital, he was very anxious, irritated and told the
attendants for the entire transport time that he heard his
wife and his children speaking to him about his condition. The neurological examination revealed moderate
left hemiparesis with hemihypoesthesia.
On the following days, the auditory hallucinations
became more intense and were concentrated in two
main topics: (1) hearing himself speak about his
condition without any real verbal speech and (2) hearing his wife and older daughter discuss with him about
non-medical issues. The messages were very specific
and very well constructed. He was only partially aware
of the unreality of the hallucinations, plus very irritated,
nervous and apprehensive. He has the feeling that the
information came from an internal source,but also from
an external one. CT scan showed involvement of the
right insula and right superior temporal gyrus and part
of the surrounding area 22.
Psychiatric examination did not reveal any
abnormality, apart from the hallucinations. Neurocognitive tests (WAT – 94 percentile, MMSE – 30/30) were
normal. Audiometric and evoked potentials, as well
as repeat EEG examinations which showed a normal
background with intermittent slowing on the right
anterio-temporal area, were all normal. BEAR BTT
was symmetrical at 0.25 msec. On brain CT scan,
infarction of the right insula and right superior
temporal gyrus and the surrounding Broadman area 22
was found (Fig. 3).
Two weeks after admission, the hallucination
symptoms disappeared. The patient was transferred to
a rehabilitation center where he stayed for the next
five weeks. A combination therapy of resperidonecarbamazepine was continued for the next three
months. The patient continued to act normally, having
only moderate motor impairment. Unfortunately, one
year later he was admitted again to the hospital with
a recurrent stroke of the contralateral temporal lobe
expressed as a central bilateral deafness.

5. Discussion
Auditory hallucinations have been rarely described
after stroke, mostly after brain stem infarction [13,25].
Hallucinations of the non-peduncular type after cortical
lesions are also supposed to be very uncommon. Most
of the studies stress an association between the location of the cortical stroke in the dominant hemisphere
and the appearance of auditory hallucination [15]. In
the presented cases, all infarctions were localized on
the right side of the brain. In three of the patients, the
right side location was the non-dominant hemisphere.
Whereas, the fourth patient was a 72-year-old female
with characteristics of left-handedness on examination,
but suspicion of a history of attempts to change hand
dominance during early childhood. This raises the
possibility that auditory hallucinations are associated
with cortex lesions of the non-dominant hemisphere in
contrast to the common assumption otherwise.
The explanation for post stroke auditory hallucination can be based on the development models of this
phenomenon. Two main theories of the etiology of
hallucinations are presently under discussion: the
‘stimulation theory’ and the ‘inhibition theory’. The
stimulation theory explains the origin of auditory
hallucination as being caused by seizures or electrical
and neurochemical stimulators. The inhibition theory
is based on destruction of normally inhibitory
function, resulting in a disinhibition phenomenon [5]
that involves a reduced corticocortical connectivity
neural network. Brasic [5] provided a model of
auditory hallucinations by showing that excessively
pruned attractor networks become functionally
fragmented, and thatpruning back-propagation stimulation of speech perception leads to spontaneous output.
Using neuroimaging methods, Levitan et al. [19]
showed that the severity of auditory hallucinations
was significantly associated with smaller left anterior
superior gyrus volume, thereby demonstrating a deficit
of corticocortical connection tissue. Rajarethinam et
al. [22] discovered similar findings in schizophrenic
patients having auditory hallucinations and proposed
that these anatomical abnormalities and dysfunction of
primary auditory cortex may play a role in production
of this perceptual disorder.
Since all presented patients resemble those having
pathological inner speech, an explanation based on the
mechanism of pathological thinking in words can also
be discussed. One theory of of auditory hallucination is based on the model of pathological endogenous
language production process of perception leading to

Y. Lampl et al. / Auditory hallucinations in acute stroke

creation of inner speech [8]. It is postulated that the
unusual phenomenon of thinking in words is a result of
the brain tissue destructive process of the inner speech
monitory center associated with the frontal generating
area [20].
The infarcted areas in all of our patients involve
overlapping brain locations, which were found to
be involved in patients with auditory hallucinations
in several neuroimaging studies [6,9,27,29]. Most
functional imaging studies have concentrated on
psychotic schizophrenic patients. Using fMRI, Dierks
et al. [19] found an increase of blood oxygen
level dependent signal in the Heschel’s gyrus during
patients’ auditory hallucinations. Change in the
cerebral blood flow and metabolism was also shown in
the superior temporal gyrus and in the cingulate gyrus,
using PET and SPECT techniques [27]. However, in
rare cases of patients suffering from auditory hallucinations caused by stroke, hypoperfusion was found in
the temporal lobe, indicating a decrease of blood flow
in those areas [9,29].
The data from this studyreveal that auditory hallucinations can be isolated sequelae of strokes located in
the dominant temporal lobe. This phenomenon seems
to be more frequent than suspected and must be taken
into consideration when handling patients with acute
onset of auditory hallucinations.

[2]

[3]
[4]

[5]
[6]
[7]
[8]

[9]

[10]

[11]

[12]

[13]

[14]

6. Conclusion
[15]

This prospective study demonstrated an uncommon
post stroke manifestation of auditory hallucinations
(>1%). This form of perceptual disturbance cannot be
explained by psychiatric or epileptogenic means, but
is a consequence of vascular tissue damage or tissue
dysfunction and should be taken into consideration in
the clinical evaluation of brain infarction involving the
temporal lobe.

[16]

[17]
[18]

[19]

Acknowledgment
We wish to extend our appreciation to Ms. Judy
Brandt for her skillful English editing and word
processing expertise and contributions.

[20]

[21]

[22]

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