Neuroradiology (2002) 44: 133–137
DOI 10.1007/s002340100657

S. Maeshima
H. Toshiro
E. Sekiguchi
R. Okita
H. Yamaga
F. Ozaki
H. Moriwaki
T. Matsumoto
A. Ueyoshi
P. Roger

Received: 6 March 2001
Accepted: 25 April 2001
Published online: 27 October 2001
Ó Springer-Verlag 2001
S. Maeshima (&) Æ T. Matsumoto
A. Ueyoshi
Department of Physical Medicine
& Rehabilitation, Wakayama Medical
University, 811-1 Kimiidera, Wakayama
641-0012, Japan
E-mail: maeshima@waKayama-med.ac.jp
Tel.: +81-73-4472300
Fax: +81-73-4410509
H. Toshiro Æ E. Sekiguchi Æ R. Okita
H. Yamaga Æ F. Ozaki Æ H. Moriwaki
Department of Neurological Surgery,
Hidaka General Hospital,
Wakayama, Japan
P. Roger
School of Communication Sciences
and Disorders, University of Sydney,
Sydney, New South Wales,
Australia

DIAGNOSTIC NEURORADIOLOGY

Transcortical mixed aphasia due to cerebral
infarction in left inferior frontal lobe
and temporo-parietal lobe

Abstract We present a case of
transcortical mixed aphasia caused
by a cerebral embolism. A 77-yearold right-handed man was admitted
to our hospital with speech disturbance and a right hemianopia. His
spontaneous speech was remarkably
reduced, and object naming, word
fluency, comprehension, reading and
writing were all severely disturbed.
However, repetition of phonemes
and sentences and reading aloud
were fully preserved. Although
magnetic resonance imaging (MRI)
showed cerebral infarcts in the left
frontal and parieto-occipital lobe
which included the inferior frontal
gyrus and angular gyrus, single
photon emission CT revealed a
wider area of low perfusion over the
entire left hemisphere except for part

Introduction
Transcortical aphasia is characterized by a relative
preservation of sentence repetition in the context of severe disturbances in the comprehension and/or production of oral language. It is divided into three types:
transcortical motor, sensory and mixed aphasia. Transcortical mixed aphasia (TMA) has only rarely been reported. TMA is characterized by a severely reduced
verbal output and impaired language comprehension in
the presence of echolalic repetition and automatic
completion of open-ended sentences [1, 2]. The localization of lesions producing TMA is variable [3, 4].
Albert et al. [5] reported that the syndrome is seen most
often with diffuse or multifocal pathological changes

of the left perisylvian language
areas. The amytal (Wada) test,
which was performed via the left
internal carotid artery, revealed that
the left hemisphere was dominant
for language. Hence, it appears that
transcortical mixed aphasia may be
caused by the isolation of perisylvian
speech areas, even if there is a lesion
in the inferior frontal gyrus, due to
disconnection from surrounding
areas.
Keywords Aphasia Æ Cerebral
blood flow Æ Repetition Æ Speech
area

that involve both anterior and posterior left hemisphere
cortical association areas but spare the perisylvian
language core. Similarly, Geschwind et al. [1] wrote that
this condition is caused by anterior and posterior lesions
of the left hemisphere when the perisylvian speech area is
intact, and referred to it as ‘the syndrome of isolation of
speech areas’. Therefore, they discussed that repetition is
carried out by the spared left perisylvian area, i.e.,
Heschl’s gyrus–Wernicke’s area, Broca’s area, the inferior left precentral gyrus, and their interconnections [1].
On the other hand, some investigators [6, 7] have suggested that the mechanism which preserves repetition in
transcortical aphasia is linked to an exceptional ability
for repetition of the right hemisphere.
We report a patient with TMA, who underwent an
amytal test to determine hemispheric language domi-

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nance, caused by cerebral infarcts in the left frontal and
parieto-occipital lobe which included Broca’s area
(inferior frontal gyrus).

Case report
The patient was a 77-year-old right-handed farmer with 10 years of
school education. His parents, brothers and sisters were all right
handed. He had a 4-year history of arrhythmia and hypertension, but
no prior history of neurological problems. The patient suddenly
began to exhibit speech disturbance with headache and nausea on 5
March 1997. He was referred for diagnosis to our hospital on 6
March 1997. Initially, he was completely conscious and fully oriented
but manifested a right homonymous hemianopia. Slight paralysis in
the right half of his face was accompanied by minor right hemiparesis, but there was no apparent sensory disturbance.

Neuropsychological findings
The patient spoke little of his own volition, and often demonstrated
echolalia when he was questioned. His phonological structure was
clear. He had severe difficulty with visual recognition of words with
aural compression at the word level, but was able to read aloud
words in both kanji (Chinese-based characters) and kana (syllablebased characters). Agraphia was almost total for both kanji and
kana. Although no paraphasic errors were heard in his spontaneous speech, he made literal paraphasic errors and there was some
Fig. 1. Profile of standard
language test for aphasia

perseveration as he performed picture-description tasks. This was
in contrast to the full preservation of his ability to repeat phonemes
and short sentences.
The standard language test of aphasia [8] was performed
2 weeks after the onset of symptoms, and the results are given in
Fig. 1. In addition, the patient demonstrated buccofacial, ideomotor, ideational and constructional apraxia. On the Wechsler
Adult Intelligence Scale-Revised (WAIS-R), his performance
intelligence quotient (IQ) was 72. Verbal IQ was unmeasurable in
the presence of aphasia.

Neuroradiological findings
Computed tomography (CT) and magnetic resonance imaging
(MRI) of the brain revealed left frontal and parieto-occipital
infarcts (Fig. 2). The right carotid angiogram revealed a persistent
primitive hypoglossal artery (PPHA) originating from the cervical
portion of the internal carotid artery (ICA) at C2 level [9]. The right
vertebral angiogram revealed a hypoplastic vertebral artery; the
basilar artery and posterior inferior cerebral artery were not seen.
The posterior communicating artery and the left vertebral artery
were not visualized. The left carotid angiogram did not show any
abnormal findings. Single photon emission CT 2 weeks after onset
revealed a wider area of low perfusion over the entire left hemisphere except for part of the left perisylvian language areas (Fig. 3).
On March 31, the amytal test (Wada test) was performed via
transfemoral catheterization of the left ICA to determine hemispheric language dominance. The patient was instructed to raise
both arms, and a dose of 100 mg sodium amobarbital in a 10%
saline solution was hand-injected. The drug effect was confirmed by

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Fig. 2. MRI of the brain revealed the left frontal and parietooccipital infarcts
the presence of hemiplegia. Before the injection, the patient was
able to repeat a short sentence of four to five words and read a few
words aloud. For 5 min following the injection, he could not repeat
or read any words. After a certain interval his repetition ability
recovered. These results suggested that the left hemisphere was
dominant for language functions, including repetition.
Clinical course
Spontaneous speech was still limited 3 months later. However,
there was some improvement in the patient’s ability to name and to
Fig. 3. SPECT 2 weeks from
the onset revealed a wider area
of low perfusion over the entire
left hemisphere except for part
of the left perisylvian language
area

describe scenes. Paraphasia had also disappeared. Auditory verbal
comprehension had improved remarkably, but was still poor at the
sentence level. Agraphia did not improve.

Discussion
Spontaneous speech was markedly reduced in this
patient, and he often demonstrated echolalia. His object
naming, comprehension, reading, and writing were also
severely disturbed. However, as discussed above his
ability to repeat and read phonemes and short sentences

136

aloud was fully preserved. His language disorder was
thus classified as TMA. As mentioned previously, TMA
has rarely been reported. Although Bougouslavsky et al.
[10] reported four cases of TMA among 1,200 patients
with acute cerebrovascular disorders, the symptoms
disappeared over a period of several weeks in all cases.
It has classically been considered that in transcortical
aphasia, repetition is carried out by the spared left
perisylvian area, i.e., Heschl’s gyrus–Wernicke’s area,
Broca’s area, the inferior left precentral gyrus, and their
interconnections [1]. In support of this, several neuropathological and radiological studies have shown that
transcortical aphasia can result from acute brain lesions
surrounding the speech area, thus potentially disconnecting the intact perisylvian language zone from the
peripheral brain areas that may be essential for meaning
and intention [11]. TMA is associated with diffuse or
multifocal brain pathology; two simultaneous but independent vascular lesions (one anterior, in the precentral–
central cortex, and the other, in the temporo-occipital
cortex); or single vascular lesions in the left frontoparietal region [7]. We have previously reported a case
with TMA due to subcortical hemorrhage in the left
parietal lobe [12] and a case following a left fronto-parietal infarct caused by vasospasm after subarachnoid
hemorrhage [13], and have also speculated that TMA
was caused by functional isolation of the perisylvian
speech area due to disconnection from surrounding areas. We have, therefore, stressed the importance of
SPECT in the detection of lesions responsible for
aphasia [14]. In 1999, we reported a case of TMA in
which the lesion was situated in the left frontal lobe
including the inferior frontal lobe [15]. We could not
explain the preservation of repetition in this case, as this
patient had not only isolation of perisylvian speech areas
but also a lesion in the left inferior frontal gyrus.
Recently, the role of the left inferior frontal lobe has
been discussed. Anarthria, the core symptom of nonfluent aphasia, does not occur in response to exclusive

damage in the inferior frontal lobe, but it does occur as a
result of lesions in the lower part of the precentral gyrus
[16, 17]. There have been some reports of fluent aphasia
caused by lesions in the frontal lobe including the inferior frontal lobe, as in this case [18, 19]. A relationship
between frontal lobe lesions and difficulty in comprehension has been reported [20, 21]. A PET study by
Peterson et al. [22] showed that an increase in the blood
flow in the frontal lobe is necessary for word understanding. Schaffler et al. [23] reported a case in which
electrical stimulation to Broca’s area caused poor comprehension. Some authors [24] have suggested that repetition in transcortical aphasia is carried out by either
the non-dominant (usually the right) hemisphere, or by
joint activity of non-involved left hemisphere structures
and the intact right hemisphere [25]. Kezuka et al. [26]
pointed out that the literature contains case reports [25,
27, 28] which provide indirect support for the importance of the contralateral (spared) hemisphere in language repetition, and that despite significant damage to
the central language zone, the patients described in these
papers exhibited a relative preservation of repetition. In
fact, some cases of transcortical mixed aphasia were
noted to be associated with extensive reductions in blood
flow and metabolism in the cerebral hemisphere including the perisylvian speech area. Bando et al. [6]
performed the Wada test in a patient with transcortical
sensory aphasia and suggested a fundamental role of the
non-dominant (right) hemisphere in language repetition
using this data. Berthier et al. [7] suggested that the
spared contralateral hemisphere may subserve residual
repetition in some transcortical aphasia patients with a
lesion within or outside the speech-dominant perisylvian
area.
The results of the Wada test indicated that the function of repetition lateralized in the left hemisphere in the
case. Thus, we suspected that the repetition might be
carried out by the perisylvian speech area except for the
inferior frontal lobe, rather than the right hemisphere.

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