BRAIN INJURY, 1999, VOL. 13, NO . 11, 927 ±

933

Ca s e rep o rt
Transcortical sensory aphasia due to a left
frontal subcortical haemorrhage
SH IN ICH IR O M A ESH IM A { ,
TOSHIKAZU KUW ATA{ ,
O SA M U M ASU O { , H IR O O YAM A G A{ ,
R Y U JI O K ITA { , F U M IN O R I O Z AK I{ ,
H IR O SH I M O RIW AK I{
and PETER ROGER{
{ Department of Neurological Surgery, Hidaka General Hospital, Wakayama, Japan
{ School of Communication Sciences and Disorders, University of Sydney, NSW,

Australia
(Received 13 May 1999; accepted 8 June 1999 )
A case of transcortical sensory aphasia caused by a cerebral haemorrhage in the left frontal lobe is
presented. A 72-year-old right-handed woman was admitted to the hospital, with a history of acute
onset of speech disturbance and headache. On initial assessment, her spontaneous speech was fluent.
She had no difficulty initiating speech, articulated normally, and did not exhibit logorrhea. Her ability
to repeat phonemes and short sentences (5± 6 words) was fully preserved, however she had severe
difficulty with visual recognition of words, and with aural comprehension at the word level, although
she was able to read words aloud. Computed tomography and magnetic resonance imaging showed
cerebral haemorrhage in the left frontal lobe, involving the superior and middle frontal gyrus. Single
photon emission CT revealed a wider area of low perfusion over the entire left frontal lobe, including
the superior, middle and inferior frontal gyrus. The aphasia symptoms, mainly poor comprehension,
disappeared quickly several weeks after the event. This may have been due to a reduction in the size of
the haematoma and a resolution of the oedema around the haematoma. Clinically, the transcortical
sensory aphasia in this case was indistinguishable from that caused by damage to the posterior language
areas. Further case reports of transcortical sensory aphasia associated with frontal lobe lesions would
help to confirm whether a relatively rapid recovery is characteristic in cases such as this.

Introd uctio n
Transcortical sensory aphasia is characterized by fluent speech, poor comprehension,
and preserved repetition. The lesion responsible for the aphasia is thought to be
located in the posterior language area [1], that is, the left temporo-occipital lobe or
left parieto-occipital lobe, but it has also been found in the basal ganglia [2] and the
thalamus [3]. There have been very few reports of transcortical sensory aphasia
caused by lesions in the frontal lobe [4± 6]. This paper reports on a case of transcorCorrespondence to: Shinichiro Maeshima, M.D., Ph.D., Department of Physical Medicine and
Rehabilitation , Wakayama Medical College, 811-1, Kimiidera, Wakayama 641-0012, Japan.
Brain Injury ISSN 0269± 9052 print/ISSN 1362± 301X online # 1999 Taylor & Francis Ltd
http://www.tandf.co.uk/JNLS/bin.htm
http://www.taylorandfrancis.com /JNLS/bin.htm

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S. Maeshima et al.

tical sensory aphasia caused by subcortical haemorrhage in the left frontal lobe, and
the relationship between the lesion and language deficit is discussed.

Ca s e rep ort
A.N. is a 72 year-old right-handed housewife with 9 years of school education. She
had a history of mild hypertension, but no prior history of neurological problems.
This patient suddenly began to exhibit speech disturbance with headache and
nausea on 5 July 1997. She was referred for diagnosis to the hospital on 9 July
1997. Initially, she was completely conscious with normal orientation. No anomalies were detected in her eyesight or visual fields. Slight paralysis in the right half of
her face was accompanied by minor right hemiparesis, but there was no apparent
sensory disturbance.
Neuropsychological findings
The patient’ s spontaneous speech was fluent. She had no difficulty initiating speech,
articulated normally, and did not have logorrhea. Echolalia was observed, but
phonological structure was clear. Although no paraphasic errors were heard in
her spontaneous speech, she made literal paraphasic errors and there was som e
perseveration as she performed picture-description tasks. This was in contrast to
the full preservation of her ability to repeat phonemes and short sentences (5± 6
words). She had severe difficulty with visual recognition of words and with aural
comprehension at the word level, but she was able to read aloud words in both
Kanji (Chinese-based characters) and Kana (syllable-based characters). Agraphia was
almost total for Kanji but was 60% for Kana. The Western aphasia battery (WAB)
was administered 2 weeks following the onset of symptoms, and the results are
given in table 1. In addition, A.N. demonstrated constructional apraxia but not oral,
ideomotor, or ideational apraxia. On the Weschler Adult Intelligence Scale-Revised
(W AIS-R), her performance intelligence quotient (IQ) was 79. Verbal IQ was
unmeasurable because of the aphasia.
Neuroradiological findings
The computed tomography (CT) scan performed on admission showed a high
density area in the left frontal lobe (figure 1). Magnetic resonance imaging (MRI)
revealed a cerebral haemorrhage in the left frontal lobe, involving the superior and
middle frontal gyrus (figure 2). Cerebral angiography was performed via transTable 1.

I.
II.
III.
IV.
V.
VI.

The scores of the subsets in the Western Aphasia Battery

Spontaneous speech ( /20)
Comprehension ( /10)
Repetition ( /10)
Naming ( /10)
Reading ( /10)
Writing ( /10)

2 weeks post-onset

5 weeks post-onset

16
4.6
10
2.8
3.4
3.8

19
8.75
10
7.8
6.1
8.8

TCS due to left frontal lobe lesion

Figure 1.

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Computed tomography scan performed on admission showed a high density area in the left frontal lobe.

femoral catheterization of the internal carotid artery 5 days after admission, and did
not reveal any lesions. Single photon emission CT (SPE CT), 6 days after admission,
revealed a wider area of low perfusion over the entire left frontal lobe including the
left superior, middle, and inferior frontal gyrus (figure 3a) with sparing of the
precentral gyrus.
Clinical course
Spontaneous speech was still limited 3 weeks later. However, there was some
improvement in the patient’ s ability to nam e and to describe scenes. Paraphasia
had also disappeared. Auditory verbal comprehension had improved remarkably,
but was still poor at the sentence level. Agraphia had also improved significantly.
The scores of the WAB 5 weeks after the onset are shown in table 1. SPECT
revealed an improvement in the diminished cerebral blood flow in the frontal lobe
(figure 3b). All signs of aphasia had completely resolved 8 weeks after the onset of
symptoms.

D is c us s io n
The language symptoms in this patient can be sum marized as follows. Spontaneous
speech was fluent, although literal paraphasic errors were observed. Disturbance of
auditory comprehension was evident, and echolalia was sometimes observed.
Repetition was excellent. The patient’ s ability to read aloud was good, but she
was not able to understand what she was reading. The separation between reading
aloud and comprehension was, thus, obvious. Moderate to severe disturbances in

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Figure 2.

S. Maeshima et al.

Magnetic resonance imaging revealed cerebral haemorrhage in the left frontal lobe, involving the superior
and middle frontal gyrus.

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(a)

(b)
Figure 3. Single photon emission CT (a) 6 days after admission, revealing a wider area of low perfusion over the
entire left frontal lobe including the left superior, middle, and inferior frontal gyrus, and (b) 5 weeks after the
onset, revealing an improvement in the diminished cerebral blood flow in the frontal lobe.

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S. Maeshima et al.

object naming and writing were also observed. These characteristics were considered to represent transcortical sensory aphasia in the classical classification.
Patients with transcortical sensory aphasia usually retain not only repetition but
also the ability to read aloud. Repetition and reading aloud are activities that can
be carried out without any appreciation of the meaning of the corresponding
phonemes as they are input auditorily or visually [5]. It seems that this case also
fits this description. In contrast, nam ing and reading comprehension are activities
which require interconversion processing of phonemes and meaning. In this case,
the difficulties in the auditory comprehension of words and sentences indicate that
there was a disorder involving interconversion processing in both the phoneme
processing system and the semantic processing system.
The lesion responsible for transcortical sensory aphasia is generally considered to
be in the posterior language area surrounding Wernicke’s area. Kertesz et al. [1],
reporting the results of a neuroradiological study using CT scan, placed responsible
lesions in the left temporo-occiptal lobe or left parieto-occipital lobe. Others have
located the responsible lesion in the left basal ganglia or the internal capsule [2].
Yamadori et al. [6] have reported three cases of transcortical sensory aphasia caused
by lesions in the frontal portion of the left basal ganglia. They have also reported
lesions in the deep white matter of the anterior horn of the left lateral ventricle. In
cases of transcortical sensory aphasia caused by thalamic lesions, damage to thalamocortical projection fibres has been determined to be more responsible for symptoms
of the aphasia than damage to the thalamus itself [5]. In this case, the lesion was
located in the white matter in the anterior horn of the left lateral ventricle and the
middle frontal gyrus. Furthermore, in the cerebral blood flow (CBF) study using
SPECT, no abnormalities in the left temporo-occipital lobe or parieto-occipital
lobe were observed, but extensive reduction of the CBF in the cortex and subcortex
of the middle frontal gyrus to the inferior frontal gyrus, including a part of Broca’ s
area, was observed.
It is known that anarthria, the core symptom of non-fluent aphasia, does not
occur in Japanese in response to exclusive damage in Broca’ s area, but it does occur
as a result of lesions in the lower part of the precentral gyrus [7, 8]. There have been
some reports of fluent aphasia caused by lesions in the frontal lobe including Broca’ s
area, as in this case [4, 9, 10], but the CBF was not examined in these cases. It is
presumed that the individual described in this case did not exhibit any non-fluent
aphasia sym ptoms, because the CBF to the precentral gyrus was maintained.
In recent years, a relationship between frontal lobe lesions and difficulty in
comprehension has been reported. Yoshimura and Soma [11], who have exam ined
comprehension difficulties in Broca’ s aphasia, have reported that if lesions spread
ahead of Broca’ s area, poor comprehension in spoken and written language occurs.
Otsuki et al. [10] have reported that, in aphasia caused by lesions located in the
frontal lobe, the lower and further outward the lesion spreads from the superior
frontal gyrus, the more ability to understand deteriorates. This gives considerable
weight to the connection between lesions in the middle frontal gyrus cortex/
subcortex and semantic understanding disturbance (semantic aphasia). A PET
study by Peterson et al. [12] demonstrated that an increase in the blood flow in
the frontal lobe occurred during the performance of word comprehension tasks.
Schaffler et al. [13] have reported a case in which electrical stimulation to Broca’ s
area caused poor comprehension. The aphasia sym ptoms in this case, notably the
poor comprehension, disappeared quickly several weeks after the pathopoiesis. This

TCS due to left frontal lobe lesion

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may have been caused by a reduction in the size of the haematoma and a resolution
of the oedema around the haematoma. An improvement was observed in the
diminished cerebral blood flow in the frontal lobe, by SPECT. From the current
case, one could not identify distinct differences between the transcortical sensory
aphasia som etimes caused by damage to the posterior language area and that caused
by damage to other sites. The patient is this case showed a relatively rapid recovery
of language function. As the literature contains few case reports of transcortical
sensory aphasia associated with frontal lobe lesions, additional cases would be of
value in determining whether rapid recovery was, in fact, a more general characteristic of this particular condition.
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