J Neurol (1998) 245 : 69–76
© Springer-Verlag 1998

Mika Otsuki
Yoshiaki Soma
Akira Koyama
Nahoko Yoshimura
Hiroko Furukawa
Shoji Tsuji

Received: 14 March 1997
Received in revised form:
29 September 1997
Accepted: 15 October 1997

M. Otsuki (Y) · Y. Soma · S. Tsuji
Department of Neurology,
Brain Research Institute,
Niigata University, 1 Bancho,
Asahimachidori, Niigata 951, Japan
Tel.: 81-025-223-6161 (ext. 5183 or 5184),
Fax: 81-025-223-3620
A. Koyama
Department of Neurology,
Kobari Hospital, Japan
N. Yoshimura
Department of Neurology,
Takeda General Hospital, Japan

O R I G I N A L C O M M U N I C AT I O N

Transcortical sensory aphasia
following left frontal infarction

Abstract Two right-handed patients
who exhibited language disability after left frontal infarction are described. The patients spoke fluently
and exhibited excellent repetition
ability from the onset of infarction
without exhibiting any oral apraxia,
but had deficits in auditory comprehension, naming, reading and writing. In both patients, brain magnetic
resonance imaging (MRI) revealed
infarction in the left inferior frontal
gyrus, the middle frontal gyrus and
the anterior part of the lower precentral gyrus. Single photon emission
computed tomography (SPECT) revealed decreased blood flow in the
same regions as those shown to be

infarcted by MRI. The MRI and
SPECT findings and the symptoms
of these patients suggest that left
frontal lesions that encompass Broca’s
area produce fluent aphasia if the
posterior part of the left precentral
gyrus or motor cortex remains intact
and that lesions anterior to Broca’s
area and the middle frontal gyrus
produce a deficit in auditory comprehension of single words as well as
sentences.
Key words Transcortical sensory
aphasia · Fluent aphasia · Frontal
lobe · Auditory comprehension ·
Word comprehension

H. Furukawa
Department of Speech Therapy,
Takeda General Hospital, Japan

Introduction
Concerning language disability following a left frontal
lobe lesion, there is still some debate regarding the relationship between Broca’s area (posterior part of the pars
triangularis and the pars opercularis [9]) and speech nonfluency, and between frontal lesions and comprehension
deficits. The relationship between left frontal lobe lesions
and comprehension deficits in particular is still uncertain.
Regarding the former point, although left frontal lobe lesions are generally known to produce nonfluent aphasia
such as Broca’a aphasia [9], aphemia (or pure anarthria
[18] or apraxia of speech [35]), transcortical motor aphasia and supplementary motor area aphasia [6], the critical
lesion producing speech nonfluency has been much de-

bated [1, 2, 13, 17, 19, 21, 24, 26, 28, 37]. It has become
clear that Broca’s aphasia develops only following lesions
extending beyond Broca’s area; lesions restricted to
Broca’s area alone do not usually cause nonfluency or
persistent speech disorders [2, 13, 24, 25, 32, 36]. Instead,
the left precentral gyrus is now considered a candidate site
for the causative lesion for nonfluent speech. Tonkonogy
and Goodglass [37] suggested that articulatory disorders
are associated with lesions in the left lower motor strip,
including the Rolandic operculum. Knopman et al. [17]
found that persistent nonfluency was associated with lesions in the Rolandic cortical region and the underlying
white matter. These findings, suggesting that the posterior
part of the left precentral gyrus (Brodman area 4) is associated with articulatory disorders, are supported by those
of other investigators [2, 22].

70

R

A

L

P
R

Fig. 1 Patient 1: magnetic resonance and single photon emission
computed tomography (SPECT) images. Top (axial view) and bottom left (sagittal view): MRI (1.5 T, T2-weighted images: TR 3500,
TE 90), 6 days post-onset. Bottom right: 99mTc-HMPAO SPECT
axial view, 1 day post-onset (R right, L left, A anterior, P posterior)

Here we describe two patients with fluent aphasia accompanied by difficulty in comprehension, naming, reading and writing but with excellent repetition ability. The
patients had infarction in the left pars opercularis and the
pars triangularis in the inferior frontal gyrus, the middle
frontal gyrus and in the anterior part of the lower precentral gyrus. We discuss their symptoms and the association
with the lesions.

Case reports
Patient 1
A 63-year-old right-handed man was admitted to Takeda General
Hospital on 24 April 1991 because he had noticed difficulty in

L

word finding and in writing. He had been found to have atrial fibrillation several years earlier, but had not been prescribed any drug
therapy. On the evening prior to his admission, the patient’s family had noted that he tried to pour hot water into a covered bowl.
Then he dozed intermittently and went to bed. The next morning
he began to write in his diary as usual, but as he was unable to
write letters or sentences correctly, he consulted the hospital. Physical examination revealed no abnormalities. Neurological examination confirmed him to be alert and his cranial nerves to be intact,
and no paresis, sensory defects or pathological reflexes were detected. He was well oriented and showed no abnormality in praxis.
He was able to imitate both meaningful and meaningless gestures
as presented by examiners, to pantomine, and to use tools correctly. He showed no unilateral spatial neglect, visual agnosia or
constructional disturbance.
Magnetic resonance imaging (MRI) of his brain performed 6
days post-onset (Fig. 1) revealed infarction in the left pars opercularis and in the pars triangularis in the inferior frontal gyrus, the
middle frontal gyrus and the anterior part of the lower precentral
gyrus. The posterior border of the lesion was before the anterior
part of the precentral gyrus, and the lesion extended through deep
white matter to the anterior horn of the left lateral ventricle. 99mTchexamethyl-propyleamine oxime (99mTc-HMPAO) single photon
emission computed tomography (SPECT) performed 1 day postonset (Fig. 1) revealed decreased blood flow in the same regions,
shown to be infarcted by MRI. Re-examination using MRI and

71

Table 1 Results of the
Western Aphasia Battery for
patient 1

Days post-onset

3

32

64

578

793

Spontaneous speech
Information content (10)
Fluency (10)

6
8

6
8

8
8

8
8

8
8

Comprehension
Yes/no questions (60)
Auditory word recognition (60)
Sequential commands (80)
Repetition (100)

45
6
4
80

48
30
8
100

48
32
22
100

57
45
33
97

59
46
46
100

Naming
Object naming (60)
Word fluency (20)
Sentence completion (10)
Responsive speech (10)
Reading (10)
Writing (10)
Praxis (60)
Drawing (30)
Block design (9)
Calculation (24)
Raven’s score (37)

0
1
0
0
2
1
47
17
9
4
11

21
9
4
8
5
5
54
17
8
16
23

36
9
2
10
5
6
57
25
9
16
25

46
9
6
10
7
7
59
22
9
21
19

42
8
8
10
–
–
59
21
9
20
24

Table 2 Results of the token test for patient 1
Days post-onset
Total score (%)

8
3

45
21

80
27

378
32

523
60

793
61

Table 3 Auditory comprehension of single words, naming of the
50 line drawings for patient 1 (ACSW auditory comprehension of
single words)
Days post-onset

3

24

52

92

378

586

ACSW (50)
Naming (50)

13
0

14
3

19
8

26
22

42
25

43
33

The maximum score is 50. The ACSW and naming ability were assessed using 50 words/line drawings selected at random from
among common Japanese words from training cards for aphasics
[29] (cf. Appendix)

was strikingly poor. His naming ability was also severely impaired. Sometimes he seemed unable to recognize that he had already recalled the target word. When he tried to recall the word
“bow” upon viewing the line drawing representing a bow, he said
“Well, what is this? It’s something… draws a bow… drawing a
bow… Ah… I’m sorry I cannot recall the name of it, although I
have certainly seen one before”. He was able to read aloud both
kana (Japanese phonograms) and kanji (Japanese morphograms),
although without comprehension, rendering him unable to point
out objects represented by written words or follow written directions. In addition, he was unable to write either kana or kanji correctly owing to difficulty in generation of the characters in both
dictation and spontaneous writing.
His speech remained fluent from the onset and remained unchanged throughout of the course of his disorder, that is for a period of several years. Although he showed gradual improvement in
all aspects of language ability, his deficits have still persisted several years after onset.
Patient 2

99mTc-HMPAO SPECT performed 1.5 years post-onset revealed
the same findings.
His speech was fluent, well articulated and grammatically correct, he spoke with normal volume and speed, and he had neither
oral apraxia nor any facial weakness. However, he sometimes gave
irrelevant answers to the examiners’ questions. Otherwise, his
speech was circumlocutory, he was unsuccessful in generating target words and he sometimes exhibited verbal paraphasias. He also
exhibited echolalia. In order to assess his language ability formally, we applied the Western Aphasia Battery (WAB) [14]
(Table 1), Japanese version [34], and the token test [12, 33] (Table
2). In addition to these formal examinations, in order to assess his
auditory comprehension and naming abilities, in particular for single words, we used 50 line drawings representing single nouns that
were selected from among common Japanese words for the language training of aphasics (Sasanuma’s cards) [29] (Table 3, cf.
appendix). According to the results of these examinations, his ability to select the appropriate line drawing, when asked to point to it,

A 63-year-old right-handed bishop had difficulty in word finding
after awakening on the morning of 11 May 1993. He had been
working as a bishop and was in good health, except that he suffered
from hypertension and diabetes mellitus, both of which were well
controlled. He was admitted to Tsubame Rousai Hospital on the
afternoon of the day of onset. Physical examination revealed no
abnormal findings. Neurological examination revealed that he was
alert and that all cranial nerves were intact. He showed no paresis
in his extremities, pathological reflexes or sensory defects. He was
lively and cooperative. He had no problems in everyday life except
for the language impairments. He showed no abnormality in
praxis. He was able to imitate both meaningful and meaningless
gestures presented by the examiners, pantomime and use tools correctly. Unilateral spatial neglect, visual agnosia and constructional
disturbance were not detected.
Brain MRI performed 10 days post-onset (Fig. 2) revealed infarction in the left pars opercularis and pars triangularis in the inferior frontal gyrus, the middle frontal gyrus and the anterior part

72

R

L

L

R
A

P

Fig. 2 Patient 2: magnetic resonance and SPECT images. Top (axial view) and bottom (left) (sagittal view): MRI (1.5 T, T2-weighted
images: TR 3400, TE 102), 10 days post-onset. Bottom (right):
123I-IMP SPECT axial view, 13 days post-onset. Small hyperintense areas scattered in the right putamen could be interpreted as
dilated Virchow-Robin spaces
of the lower precentral gyrus. The posterior border of the lesion
was a part of the anterior aspect of the precentral gyrus, and the lesion extended to the anterior horn of the left lateral ventricle. Assessment of the regional cerebral blood flow by N-isopropyl-p-[123I]
iodoamphetamine (123I-IMP) SPECT performed 13 days post-onset revealed a decrease in blood flow in the same regions as those
shown to be infarcted by MRI (Fig. 2). Re-examination by MRI
performed 2 years post-onset and 123I-IMP SPECT performed 10
months post-onset revealed the same findings.
His spontaneous speech was fluent, well articulated, prosodic
and grammatical; no phonemic errors were found, and he exhibited
no oral apraxia or facial weakness. However, his narrative was irrelevant and exhibited numerous verbal paraphasias. He showed
frequent perseveration as well as verbal paraphasia. When he was
asked “What‘s troubling you?” although he had never been a merchant, he answered, “Well, I have felt sick since yesterday so I
have not managed my shop well because I could not manage the
merchandise well, so I could not do it well…”. His fluent but irrelevant speech persisted from the onset for several months. In order
to assess his language ability formally, we applied the WAB [14],
Japanese version [34] (Table 4), and the token test [12, 33] (Table

Table 4 Results of the Western Aphasia Battery for patient 2
Days post-onset
Spontaneous speech
Information content (10)
Fluency (10)
Comprehension
Yes/no questions (60)
Auditory word recognition (60)
Sequential commands (80)
Repetition (100)
Naming
Object naming (60)
Word fluency (20)
Sentence completion (10)
Responsive speech (10)
Reading (10)
Writing (10)
Praxis (60)
Drawing (30)
Block design (9)
Calculation (24)
Raven’s score (37)

1

41

8
7

–
–

45
22
10
82

54
55
80
99

8
0
0
5
5.5
2.5
42
30
9
12
31

45
8
10
10
–
6.9
–
–
–
–
–

73

Table 5 Results of the token test for patient 2
Days post-onset

2

75

135

225

1 019

Total score (%)

29

76

81

78

82

Table 6 Auditory comprehension of single words, naming of the
50 line drawings for patient 2
Days post-onset

2

6

75

225

ACSW (50)
Naming (50)

17
0

41
9

48
47

50
50

5), which revealed significant impairment of auditory comprehension and naming and writing abilities, but intact repetition. We
also used pointing and naming tasks using the 50 line drawings
(Sasanuma’s cards) [29] (cf. appendix) in order to assess his auditory comprehension and naming ability, particularly of single
words (Table 6). His ability to select and point to the appropriate
line drawing when he was asked to do so was severely impaired,
and he sometimes insisted that he had never heard words such as
book or fish presented by the examiners. His ability to name objects was also strikingly poor, and he sometimes gave a strange response during the task of naming objects; although he had already
correctly recalled a target word, he was not able to recognize it and
wondered aloud about the recalled word, for example, when he
tried to recall the word “desk”, he said “Well,… what is this? Let’s
see… desk… ah? what? desk? what is a desk? It’s nonsense! Ah,
I’m sorry… I cannot recall the name of this though I know what it
is”. He was able to read aloud both kana and kanji correctly; however, he had difficulty in comprehending their meaning. His writing contained numerous phonemic errors in kana, and he showed
difficulty in generating kana and kanji characters both in dictation
and spontaneous writing.
Follow-up assessments revealed rapid improvement in his performance in the task of pointing to single words (Table 6), followed by improvement in naming ability; however, his auditory
comprehension remained deficient as revealed by the token test
and has never improved to higher than 82% correct answers even
1019 days post-onset (Table 5).

Discussion
We have described two patients with language disability
after left frontal lesions. The patients’ spontaneous speech
was well articulated with normal volume and speed,
prosodic and grammatically correct from the onset, and
remained unchanged for several months to years. Regarding verbal output, two contrasting forms of “fluent” and
“nonfluent” have been defined [3, 4, 15]. We have adopted the term “fluent” only when a patient’s speech fulfilled
the following criteria: normal volume, normal speed, good
articulation, correct prosody, grammatical accuracy and
sufficient phrase length without any phonemic errors or
any hesitation or elaboration in searching for phonemes.
On the basis of these criteria, the speech of each patient
described here was fluent.
However, the patients gave inappropriate responses to
the examiner’s commands, and they sometimes repeated
the examiner’s utterances with excellent mimicry but

without comprehension; this is typical of echolalia consistent with a deficit in auditory comprehension. Patient 1
consistently showed a deficit in comprehension both of
single words and sentences for several years. He was unable to achieve a score of more than 60% on the token test
even 793 days post-onset, and he still showed a score of
less than 43/50 in the auditory comprehension of single
words pointing task 586 days post-onset. Regarding the
pointing task used for the assessment of auditory comprehension of single words, as presented in the appendix, all
of the words were selected from among common Japanese
words used at high frequency, and control subjects are
easily able to point to all of the correct drawings corresponding to the single words presented. Thus, the score of
43/50 clearly demonstrates an apparent deficit in the auditory comprehension of single words. Patient 2 also showed a deficit in auditory comprehension, and he was not
able to achieve more than 82% in the token test even 1019
days post-onset, which indicated that his deficit in auditory comprehension of sentences was persistent. Regarding the comprehension of single words of patient 2, although he showed a milder disability and more rapid improvement compared with patient 1, his deficits remained
at least until the examinations performed 75 days post-onset, and they cannot be interpreted as transient or negligible. The results of the formal examinations using the WAB
and the token test also indicated that these two patients
had comprehension disabilities persisting for months to
years. The clinical symptoms of the two patients were identical in that they exhibited fluent speech unaccompanied
by oral apraxia and exhibited intact repetition, but with
deficits in comprehension, naming, reading and writing
from the onset, and all of these symptoms were persistent.
Among the established terminology of aphasia, transcortical sensory aphasia (TCSA) identified by Lichtheim
[20] in his schema of speech disorders is characterized by
fluent speech with poor comprehension but intact repetition, and naming, reading, and writing are usually found
to be seriously impaired [4, 16]. Thus, the symptoms of
our patients clearly met the established and well-accepted
diagnostic criteria for TCSA from onset to several months
post-onset. The mechanisms producing the symptoms in
our patients remain unclear, nor do we know whether the
TCSA in these patients following left frontal infarction is
exactly the same as the well-known and established TCSA
following a left posterior lesion. Therefore, at present it
seems prudent to discriminate the TCSA of our patients
following a left frontal lesion from classic TCSA following a left posterior lesion. The most important point we
want to emphasize here is not one of terminology but the
fact that there are patients with frontal lobe lesions exhibiting fluent aphasia, whose symptoms are seemingly
typical of TCSA.
In most cases, TCSA is known to arise following left
posterior lesions, specifically at the temporo-parieto-occip-

74

Fig. 3 Schemas of the lesions of the patients. Axial views and reconstructions of the lateral views of the brain made according to
Damasio’s templates [11]

ital junction [16], posterior to Wernicke’s area and sometimes with extension inferiorly and/or posteriorly [5].
However, there are quite a few reports regarding patients
with TCSA occurring following other lesions, including a
left thalamic lesion [10, 23], a left anterior basal ganglionic lesion [40], and a left frontal lesion [7, 30]. Figure
3 shows the extent of the lesions in our two patients, in the
left inferior frontal gyrus, the middle frontal gyrus, and
the anterior part of the lower precentral gyrus. The lesions
in our patients did not extend to the posterior part of the
precentral gyrus. Therefore, we agree with the hypothesis
[2, 17, 22, 32, 37] that fluent aphasia occurs following
left frontal lesions, even those which encompass Broca’s
area, only when the posterior part of the precentral gyrus
(motor cortex area 4, as defined by Brodmann) remains
intact.

The relationship between the frontal lobe lesions and
comprehension disability is not well established. Posterior
lesions, i.e. temporo-parieto-occipital lesions rather than
frontal lesions, are widely accepted as causing deficits in
comprehension and syndromes such as Wernicke’s aphasia and classic TCSA [16]. However, it is also known that
comprehension deficits are inevitable in patients with
Broca’s aphasia following left frontal lesions. Some investigators have suggested that grammatical deficits result
from frontal lesions [38, 39], and this would explain why
our patients showed deficits in understanding sentences.
However, this is not sufficient to explain why they also
showed deficits in single word comprehension. The patients described by Soma et al. [32], who had lesions exclusively restricted to Broca’s area, showed a deficit in the
auditory comprehension of sentences but not of single
words. Our patients exhibited deficits in the comprehension of both, which suggests that lesions extending anterior to Broca’s area and to the middle frontal gyrus, as in
our patients, cause a deficit in the comprehension of both
single words and sentences. This speculation is consistent
with the impairment of auditory comprehension of single
words observed in patients with typical Broca’s aphasia
when the lesions extend anterior to Broca’s area [41]. A
similar case of TCSA following left frontal lesions reported by Sato et al. [30] also involved extensive lesions
of the middle frontal gyrus. In a report on comprehension
ability in patients with left medial frontal lesions [27], it
was concluded that a deficit in the auditory comprehension of single words occurred when the lesions extended
laterally to the middle frontal gyrus from the left medial
frontal lesions. Thus, it is possible that the lesions in the
anterior part of the left inferior frontal gyrus and in the left
middle frontal gyrus play an important role in the comprehension of single words.
However, this conclusion should not be accepted without further consideration of the other possible interpretations of our patients’ symptoms. First, when considering
the candidate site for the causative lesion of the deficits,
we must consider whether the deficits depend only on lesion size or on the specific lesion site. Regarding the former, Selnes et al. [31] found a negative correlation between lesion volume and word comprehension at both 1
month and 6 months post-onset. However, this was not
found in the cases presented here, since patient 1 showed
more severe and more persistent disability than patient 2,
even though his lesion was smaller. Thus, we can presume
that the deficits in our patients were affected by the lesion
site or other individual factors. Second, we must investigate the possibility that the deficits can be ascribed either
only to the visible lesions revealed by MRI or to remote
effects via the connection with the posterior part of the
cortex. Neither possibility can be ruled out, as white matter involvement was evident on MRI images for both patients, and there might have been some remote effects, at
the early stage after onset, on the posterior cortex whose

75

function is associated with the process of word comprehension. However, our patients showed persistent deficits
in comprehension for several months, and there is no general consensus that invisible remote effects would persist
for so long. Thus, we speculate that the lesions in the left
frontal lobe themselves caused the comprehension deficits
of sentences and single words.
Regarding the role of the left frontal lobe, Binder et al.
[8] found, using functional MRI in conjunction with a
pure-tone processing task as a control condition, that use
of a semantic-processing task revealed activation in this
region as well as in the left posterior region. They deduced that the left frontal component may incorporate
mechanisms facilitating access to the posterior information store. Our observation that the deficits in comprehension occurred following left frontal lesion is consistent
with their hypothesis that, in addition to the posterior regions, the left frontal lobe plays an important role in comprehension or semantic processing.
One symptom observed in our patients was that they
tended to exhibit better comprehension ability in conver-

sation and yes/no questions than in the pointing task. We
cannot quantitatively clarify this tendency or interpret this
observation with confidence because little information is
available regarding the differences in the comprehension
abilities that arise depending on the modalities for the assessment of comprehension. Most standard and formal
aphasia batteries adopt the pointing task as a measure of
the comprehension of single words. However, the results
of the pointing task can easily be affected by impairments
of other functions, one of which seems to be the mode of
response. The lower degree of comprehension ability in
the pointing task than in conversation or in yes/no questions indicates that our patients’ deficits in the pointing
task reflect not only pure comprehension deficits but also
disabilities dependent on the mode of response. One factor that affects responses is apraxia; however, our patients
did not exhibit apraxia, and therefore it is not a factor in
their comprehension deficits. Thus, this issue requires further investigation.

References
1. Alexander MP, Benson DF, Stuss DT
(1989) Frontal lobes and language.
Brain Lang 37 : 656–691
2. Alexander MP, Naeser MA, Palumbo
C (1990) Broca’s area aphasia: aphasia
after lesions including the frontal operculum. Neurology 40 : 353–362
3. Benson DF (1967) Fluency in aphasia:
correlation with radioactive scan localization. Cortex 3 : 73–394
4. Benson DF (1979) Aphasia, alexia and
agraphia. Churchill Livingstone, New
York
5. Benson DF (1988) Classical syndromes
of aphasia. In: Boller F, Grafman J
(eds) Handbook of neuropsychology.
Elsevier, Amsterdam New York Oxford, pp 267–280
6. Benson DF (1993) Aphasia. In: Heilman KM, Valenstein E (eds) Clinical
Neuropsychology, 3rd edn. Oxford
University Press, New York, pp 29
7. Berthier ML, Starkstein SE, Leiguarda
R, Ruiz A, Mayberg HS, Wagner H,
Price TR, Robinson RG (1991) Transcortical aphasia. Brain 114 : 1409–1427
8. Binder JR, Rao SM, Hammeke TA,
Frost JA, Bandettini PA, Jesmanowicz
A, Hyde JS (1995) Lateralized human
brain language systems demonstrated
by task subtraction functional magnetic
resonance imaging. Arch Neurol 52 :
593–601
9. Broca P (1863) Discussion. Bull Soc
Anat Paris Ser 2 : 379–385

10. Cappa SF, Vignolo LA (1979)
“Transcortical” features of aphasia following left thalamic hemorrhage. Cortex 15 : 121–130
11. Damasio H, Damasio A (1989) Lesion
analysis in neuropsychology. Oxford
University Press, New York, pp 185–
218
12. De Renzi E, Vignolo LA (1962) The
token test: a sensitive test to detect receptive disturbanc in aphasics. Brain
85 : 665–678
13. Henderson VH (1985) Lesion localization in Broca’s aphasia. Implications
from Broca’s aphasia without hemiparesis. Arch Neurol 42 : 1210–1212
14. Kertesz A (1982) The Western Aphasia
Battery. Grune & Stratton, New York
15. Kertesz A, Harlock W, Coates R
(1979) Computer tomographic localization, lesion size and prognosis in
aphasia and nonverbal impairment.
Brain Lang 8 : 34–50
16. Kertesz A, Sheppard A, MacKenie R
(1982) Localization in transcortical
sensory aphasia. Arch Neurol 39 :
475–478
17. Knopman DS, Selnes OA, Niccum N,
Rubens AB, Yock D, Larson D (1983)
A longitudinal study of speech fluency
in aphasia: CT correlates of recovery
and persistent nonfluency. Neurology
33 : 1171–1178
18. Lecours AR, Lhermitte F (1976) The
“pure form” of the phonetic disintegration syndrome (pure anarthria):
anatomo-clinical report of a historical
case. Brain Lang 3 : 88–113

19. Levine DN, Mohr JP (1979) Language
after bilateral cerebral infarctions: role
of the minor hemisphere in speech.
Neurology 29 : 927–938
20. Lichtheim L (1885) On aphasia. Brain
7 : 433-484
21. Masdeu JC, O’Hara RJ (1983) Motor
aphasia unaccompanied by faciobrachial weakness. Neurology 33 : 519–
521
22. Mazzocchi F, Vignolo LA (1979) Localization of lesions in aphasia: clinical
CT correlations in stroke patients. Cortex 15 : 627–654
23. Minematsu K, Sugimoto K, Sone K,
Miyashita M, Yamaguchi T (1983)
Transcortical sensory aphasia following left thalamic hemorrhage-report of
two cases (in Japanese, with an English
summary). Jpn J Stroke 5 : 364–370
24. Mohr JP, Pessin MS, Finkelstein S,
Finkelstein HH, Duncan GW, Davis
KR (1978) Broca aphasia: pathologic
and clinical. Neurology 28 : 311–324
25. Mori E, Yamadori A, Furumoto M
(1989) Left precentral gyrus and
Broca’s aphasia: a clinicopathologic
study. Neurology 39 : 51–54
26. Ojemann GA, Whitaker HA (1978)
Language localization and variability.
Brain Lang 6 : 239–260
27. Otsuki M, Soma Y, Onodera O, Tsuji
S (1995) Auditory comprehension in
transcortical motor aphasia due to medial lesions of the left frontal lobe (in
Japanese, with an English summary).
Brain Nerve 47 : 1081–1085

76

28. Racy A, Jannotta FS, Leslie H, Lehner
MS (1979) Aphasia resulting from occlusion of the left anterior cerebral
artery. Arch Neurol 36 : 221–224
29. Sasanuma S, Ito M, Watamori T,
Fukusako Y, Monoi S (1978) Speech
therapy for aphasics (in Japanese).
Igakushoin, Tokyo
30. Sato M, Goto T, Watanabe K (1991)
Transcortical sensory aphasia and
palilalia following left frontal lesion: a
case report (in Japanese, with an English summary). Jpn J Neuropsychol 7 :
202–208
31. Selnes OA, Niccum N, Knopman DS,
Rubens AB (1984) Recovery of single
word comprehension: CT-scan correlates. Brain Lang 21 : 72–84

32. Soma Y, Otuski M, Yoshimura N,
Maruyama K, Tsuji S (1994) Fluent
aphasia associated with lesions in
Broca’s area (in Japanese, with an
English summary). Neurol Med
(Tokyo) 41 : 385–391
33. Spellacy FJ, Spreen O (1969) A short
form of the token test. Cortex 5 : 390–
397
34. Sugishita M, Tagawa K, Nagata K,
Kaga K, Makishita H, Motomura M
(1986) The Western Aphasia Battery
(Japanese edn). Igakushoin, Tokyo
35. Sugishita M, Konno K, Kabe S,
Yunoki K, Togashi O, Kawamura M
(1987) Electropalatographic analysis of
apraxia of speech in a left hander and
in a right hander. Brain 110 : 1393–
1417
36. Tanabe H, Ohigashi Y (1982) Broca’s
area and Broca’s aphasia (in Japanese,
with an English summary). Brain
Nerve 34 : 797–804
37. Tonkonogy J, Goodglass H (1981)
Language function, foot of the third
frontal gyrus, and Rolandic operculum.
Arch Neurol 38 : 486–490

Appendix
List of words and samples of line drawings [29] used for the pointing and naming task of single nouns:
Card 1: (1) lion, (2) ladder, (3) pine tree, (4) kettle, (5) pan, (6) iron,
(7) chest, (8) umbrella, (9) shirt (10) fish
Card 2: (1) mirror, (2) aeroplane, (3) bow, (4) squirrel, (5) butterfly, (6) deer, (7) chair, (8) hammer, (9) giraffe, (10) chicken
Card 3: (1) eggplant, (2) brush, (3) shoes, (4) pumpkin, (5) desk,
(6) radish, (7) swallow, (8) cow, (9) bucket, (10) slippers
Card 4: (1) comb, (2) melon, (3) lunch box, (4) bullet train, (5) bag,
(6) cat, (7) TV, (8) lotus rhizome, (9) chimney, (10) electric fan
Card 5: (1) peach, (2) toilet, (3) rocket, (4) saw, (5) bottle, (6) Japanese wooden doll, (7) fan, (8) ogre, (9) yacht, (10) crab

38. Von Stockert T (1972) Recognition of
syntactic structure in aphasic patients.
Cortex 8 : 323–334
39. Von Stockert T, Bader L (1976) Some
relations of grammar and lexicon in
aphasia. Cortex 12 : 49–60
40. Yamadori A, Ohira T, Seriu M, Ogura
J (1984) Transcortical sensory aphasia
produced by lesions of the anterior
basal ganglia area (in Japanese, with an
English summary). Brain Nerve 3 : 261–
266
41. Yoshimura N, Soma Y (1993) The correlation between the auditory comprehension capability and brain lesion site
in patients with Broca’s aphasia: a CT
study (in Japanese, with an English
summary). Higher Brain Function Res
13 : 224–229