EFFORTFUL ECHOLALIA
Kazuo Hadano1, Hikaru Nakamura2,3 and Toshihiko Hamanaka2
(1Department of Psychogeriatrics, National Institute of Mental Health (NCNP);
2Department of Neuropsychiatry, Nagoya City University School of Medicine;
3Department of Audiology and Logopedics, Japan College of Rehabilitation
and Welfare Professionals, Nagoya)

ABSTRACT
We report three cases of effortful echolalia in patients with cerebral infarction. The
clinical picture of speech disturbance is associated with Type 1 Transcortical Motor Aphasia
(TCMA, Goldstein, 1915). The patients always spoke nonfluently with loss of speech
initiative, dysarthria, dysprosody, agrammatism, and increased effort and were unable to
repeat sentences longer than those containing four or six words. In conversation, they first
repeated a few words spoken to them, and then produced self initiated speech. The initial
repetition as well as the subsequent self initiated speech, which were realized equally
laboriously, can be regarded as mitigated echolalia (Pick, 1924). They were always aware
of their own echolalia and tried to control it without effect. These cases demonstrate that
neither the ability to repeat nor fluent speech are always necessary for echolalia. The
possibility that a lesion in the left medial frontal lobe, including the supplementary motor
area, plays an important role in effortful echolalia is discussed.
Key words: echolalia, transcortical motor aphasia, compulsive behavior, frontal lobe.

INTRODUCTION
Echolalia (Romberg, 1857), the automatic repetition of speech of the partner in
conversation, occurs in various conditions: (1) in normal children, occurring at a
particular stage of language acquisition; (2) in pathological mental development,
especially in early infantile autism and mental retardation; (3) as a catatonic
symptom in schizophrenic patients; (4) as a partial symptom of dementia in diffuse
brain damage, for example in patients with Alzheimer’s or Pick’s disease; and (5),
in the subject of this paper, echolalia occurring in patients predominantly with
transcortical aphasia caused by a circumscribed lesion of the left hemisphere.
Echolalia as a form of automatic speech (Poeck, 1989) is generally realized
with fluent speech lacking in increased effort, dysarthria (anarthria), decreased
phrase length (agrammatism), and dysprosody (Benson, 1979). The repetition
ability of patients with transcortical aphasia, in which echolalia often occurs, is
by definition well (or normally) preserved (Goldstein, 1915, 1948). However, we
have recently observed nonfluent effortful echolalia combined with slight or
moderate difficulty in repetition in three aphasic patients. Addressed by the
conversation partner, they always repeated very laboriously the few words
spoken to them before answering. Despite full awareness of their echolalia, they
Cortex, (1998) 34, 67-82

68

Kazuo Hadano and Others

were unable to stop it voluntarily, and they felt it forced on them. We present
here a report of three cases with effortful echolalia and consider its implications
in aphasiology.
CASE REPORTS
Case 1
MM, a 68-year-old right-handed housewife educated to the elementary school
level, was hospitalized for rehabilitation therapy. She had been known to be
hypertensive for three years. Three months before admission, she had suddenly
developed a severe speech disturbance and mild right hemiparesis including the
face, and was initially admitted to another hospital and medically treated under
the diagnosis of cerebral infarction.
X-ray Computed Tomography (CT) and Magnetic Resonance Imaging (MRI)
revealed a large circumscribed lesion caused by cerebral infarction involving the
medial frontal lobe including the anterior portion of the cingulate gyrus and the
supplementary motor area (SMA), the superior and middle frontal gyrus, and the
anterior and superior part of the basal ganglia in the left hemisphere. The infarct
was located in the territories of the anterior and middle cerebral artery and the
watershed area between them (Figure 1). The posterior part of the inferior

Fig. 1 – T2-Weighted Magnetic Resonance Imaging (MRI) of Case 1.

Effortful echolalia

69

frontal gyrus containing Broca’s area and the lower part of the pre- and postcentral gyrus in the left hemisphere appeared to be spared. There were some
small lacunar infarctions in the right hemisphere.
She was awake, alert, fully oriented and cooperative during each
examination. She showed only slight emotional lability during the first few
months. Neurological examination demonstrated a mild right hemiparesis
including the face. Orofacial apraxia and severe aphasia were detected as
neuropsychological symptoms. The performance intelligent quotient (IQ) was 66
on the Wechsler Adult Intelligence Scale (WAIS) and 54 with the Kohs Block
Design Test. The Raven’s Progressive Matrices score was 14/36 in the Colored
and 17/60 in the Standard Version.
There was little spontaneous speech, but she responded verbally to questions
from the examiner with a strong tendency to echolalia. She always first repeated
a few words in the question and then produced her response. Accordingly, her
speech consisted of two parts, the echolalic repetition and her self initiated
answer; these corresponded to the “mitigated form of echo’ described by Pick
(1924). Both the echolalic and intentional part were realized nonfluently with
distorted articulation, simplification of grammatical forms (agrammatism),
monotonous intonation (dysprosody), and increased effort (Benson, 1979).
Figure 2 shows the profile of her speech characteristics evaluated with the
Boston Diagnostic Aphasia Examination (BDAE, Goodglass and Kaplan, 1972).
She was always aware of her echolalia, against which she often agonizingly
struggled by closing her eyes tightly and shaking her head violently during her
echolalising. She was nevertheless unable to control it.
Moderate word-finding difficulties and few phonemic paraphasias were
observed on confrontation naming. Auditory comprehension was moderately
disturbed at the semantic level. In the object pointing task, examining auditory
comprehension, she always repeated the stinulus word correctly, but sometimes
pointed to another object. The score on the Token Test (Japanese version) was
36/165. She showed marked difficulties in repeating utterances longer than those
containing four words. She was able to repeat five-digit numbers forward.
Reading aloud and reading comprehension of written words were well preserved,
but those of written sentences were moderately or severely disturbed. She could
write only a few Kana- and Kanji-words. Writing sentences was impossible.
Figure 3 shows the Z-score profile of the Japanese Standard Language Test for
Aphasia (JSLTA, Japanese Society of Aphasiology, 1977).
Her speech performance improved considerably with intensive speech
therapy. Figure 3 shows the JSLTA profile after three months of speech therapy.
The nonfluent speech and effortful echolalia, however, remained unchanged.
The type of aphasia in this patient is not consistent with any typical aphasia
described in classical theory. Loss of speech initiative with echolalia can be
regarded as components of Transcortical Motor Aphasia (TCMA), while
nonfluent agrammatic speech, mildly impaired repetition and moderate
disturbance of auditory comprehension led us to a diagnosis of Broca’s aphasia.
The diagnosis we finally reached was a mixed TCMA and Broca’s aphasia.

70

Kazuo Hadano and Others

Fig. 2 – Speech profile ratings of Case 1 (shown by circles linked with solid lines) and Case 2
(by squares with broken lines). Rating scale profiles of speech characteristics in Boston Diagnostic
Aphasia Examination (BDAE, Goodglass and Kaplan, 1972).

Effortful echolalia

71

Fig. 3 – Z-score profile of Japanese Standard Language Test for Aphasia (JSLTA, Japanese
Society of Aphasiology, 1977) on admission (shown by circles linked with solid lines) and three
months later (by squares with broken lines) of Case 1.

72

Kazuo Hadano and Others

Case 2
MY, an 80-year-old right-handed woman with a high school education, was
hospitalized in order to rehabilitation therapy for aphasia and right sided motor
disturbance. She had a long history of hypertension. A cerebral infarction at the
age of 58 had caused a temporary mild right hemiparesis. At the age of 79,
eleven months before admission, she had been suddenly affected by a second
cerebral infarction, again developing a hemiparesis of the right side and severe
speech disturbance.
X-ray CT and MRI revealed a large lesion in the left hemisphere, including
the inner and anterior portion of the superior frontal gyrus, the subcortical white
matter of the frontal lobe, and the upper part of the insula and the basal ganglia
(Figure 4). The posterior part of the inferior frontal cortex (Broca’s area)
appeared to be largely spared. The left SMA cortex also seemed to be spared,
but the underlying white matter was widely involved. There were no ischemic
lesions in the right hemisphere with the exception of moderate so-called leukoaraiosis.
She was alert, fully oriented and cooperative. Neurological examination
revealed a severe, incomplete, right hemiplegia with forced grasping.
Neuropsychological evaluations detected a severe aphasia, orofacial and
ideomotor apraxias, and constructive disabilities. The Mini-Mental State
Examination (MMSE, Japanese version) score was 16/30 and the Performance

Fig. 4 – T2-Weighted MRI of Case 2.

Effortful echolalia

73

IQ was 62 evaluated with the Wechsler Adult Intelligence Scale-Revised
(WAIS-R) and 49 with the Kohs Block Design Test.
She had virtually no spontaneous speech, but she responded verbally to
questions. Her conversation was limited to simple subjects of daily life, and this
was not easy even with the help of the partner. Her speech was non-fluent with
mild dysarthria, monotonous dysprosody, telegrammic agrammatism, and greatly
increased effort (Benson, 1979). Speech characteristics were assessed by the
rating scale profile of BDAE (Figure 1). She always repeated laboriously a few
words of high informative value contained in the partner’s question, and
subsequently, she made her own answer with a word or two also produced
laboriously (mitigated echolalia, Pick, 1924). She often shook her head with an
agonized look during the echolalic repetition, and appeared to be trying to fight
it. She appeared to feel it forced against her own will. Indeed, she explained
laboriously that she was fully aware of her echolalia but was unsuccessful in
trying to stop it.
The JSLTA profile on admission is shown in Figure 5. Auditory
comprehension was mildly disturbed. The Token Test (Japanese version) score
was 117/165. Repetition was limited to words and to short sentences containing
four words despite echolalia; JSLTA showed moderate disturbance of repetition.
In the confrontation naming test, she demonstrated moderate word-finding
difficulty with some semantic paraphasias. No phonemic paraphasia was
observed either in the test situations or in conversation. Reading aloud and
comprehension of written material, including Kanji- and Kana-words, was
relatively well preserved. Writing both on written confrontation naming and to
dictation was severely impaired. She could write only a few Kanji-words and
several Kana-letters.
Regular speech therapy had little effect, and after two months she
complained of a general malaise with further deterioration of her speech.
Although there were no changes in the MRI-findings, the cause was thought to
be further cerebral ischemia. Loss of speech initiative and nonfluent effortful
echolalia was almost unchanged, but her performance on language tests,
including the JSLTA, showed some deterioration on retesting after six months
(Figure 5).
The clinical picture of aphasia with loss of speech initiative and echolalia is
compatible with Type 1 TCMA (Goldstein, 1915) with the exception of
nonfluent speech and moderate impairment of repetition that may belong to
Broca’s aphasia syndrome.
Case 3
BT, a 63-year-old right-handed man who was a retired official with an
elementary education and a four-year history of diabetes mellitus, developed
acute right-sided motor weakness and aphasia with impairment of consciousness.
Consciousness cleared after a few days, but severe aphasia and mild right
hemiparesis became apparent. He was admitted to our institution two weeks after
the onset and was diagnosed as having a cerebral infarction on the basis of
neurological and neuroradiological findings.

74

Kazuo Hadano and Others

Fig. 5 – Z-score profile (JSLTA) on admission (shown by circles linked with solid lines) and six
months later (by squares with broken lines) of Case 2.

Effortful echolalia

75

Fig. 6 – T2-Weighted MRI of Case 3.

X-ray CT and MRI performed on admission demonstrated a circumscribed
lesion localized to the anterior superior part of the medial frontal lobe, the
anterior part of the basal ganglia, the insula, the posterior part of the inferior
frontal gyrus including Broca’s area, and the lower part of the central gyri in the
left hemisphere (Figure 6). The left SMA was spared.
He was alert, oriented in time and space, and cooperative to examination.
Neuropsychological examination on admission revealed mild orofacial and
ideomotor apraxia, transient constructional disability, and severe aphasia.
Performance IQ (WAIS-R) was 64 and the score on Raven’s Colored
Progressive Matrices was 31/36.
The patient produced hardly any spontaneous utterances. Speech was limited
exclusively to nonfluent repetition of several words contained in the examiner’s
question during the first two weeks after admission (complete echolalia).
Auditory comprehension was severely disturbed on admission, but markedly
recovered four months later. As the speech disturbance gradually improved, his
echolalic repetition came to be nearly always followed by self initiated speech
(mitigated echolalia). His speech, including echolalia, was produced laboriously
with occasional articulatory distortions, short phrase length and monotonous
intonation, and was contaminated with sporadic verbal paraphasias. The rating
profile of his speech characteristics (BDAE) is shown in Figure 7. In spite of the

76

Kazuo Hadano and Others

Fig. 7 – Speech profile ratings (BDAE) on admission (shown by circles linked with solid lines)
and four months later (by squares with broken lines) of Case 3.

Effortful echolalia

77

Fig. 8 – Z-score profile (JSLTA) on admission (shown by circles linked with solid lines) and four
months later (by squares with broken lines) of Case 3.

78

Kazuo Hadano and Others

echolalia, his repetition was not complete and was limited to sentences
containing six words. He was fully aware of his own echolalic behaviour and
tried to check it, accompanied by expressions of frustration, to little effect.
Figure 8 shows his JSLTA Z-score profile.
The aphasia improved with intensive speech therapy. Figures 7 and 8 show
his speech performance after four months. While auditory and reading
comprehension, confrontation naming and reading aloud improved considerably,
the dominant characteristiss of his speech disturbance, i.e. nonfluency and
mitigated echolalia, did not substantially recover.
The clinical picture of the language disturbance is almost consistent with a
mixed transcortical aphasia in the acute stage and Type 1 TCMA subsequently.
DISCUSSION
The speech disturbance demonstrated in the three patients reported here can
be summarized as mitigated echolalia (Pick, 1924) realized with nonfluent
speech (Benson, 1979). In echolalia, as well as in self initiated speech, they
spoke only a few words of high informative value which were produced
laboriously with distorted articulation (dysarthria, anarthria), short phrase length,
simplification of grammatical forms (agrammatism), and monotonous intonation
(dysprosody). Except for the echolalia, pathological automatic expressions
including so-called completion phenomena (Stengel, 1947) were not observed in
the patients. They were also completely aware of their own echolalic repetition,
against which they openly struggled without being unable to control it.
Echolalia is a form of automatic speech (Poeck, 1989), and is therefore
manifested as non-effortful fluent speech in general. We propose here the term
“effortful echolalia” for the echolalic behaviour observed in our patients.
Although the combination of the terms “effortful” and “echolalia” may appear
contradictory, it nevertheless fits the phenomenon observed clinically.
If this terminology sounds strange to some aphasiologists, it may be as a
result of excessive acceptance of the theoretical concept of disconnection, for
example, the Wernicke-Lichtheim schema in aphasiology. Disconnectionists
have asserted that echolalia corresponds to selectively preserved repetition, and
consequently, they have identified mixed transcortical aphasia with predominant
echolalia as a syndrome of “isolation of the speech area” (Goldstein, 1915;
Geschwind, Quadfasel and Segarra, 1968). Goldstein (1915, p. 456) described
two necessary conditions for the occurrence of echolalia: first, the presence of an
intact, prompt functioning speech apparatus, and second, an isolation of this
from the remaining areas of the brain, i.e., from the so-called concept field
(Begriffsfeld). He asserted consequently that true echolalia is never caused by a
lesion in the speech area itself. Geschwind et al. (1968) modified Goldstein’s
“isolation” hypothesis concerning the connecting pathway (the arcuate
fasciculus) between the anterior and posterior speech area, and applied this
explanation to their case of CO-intoxication with mixed transcortical aphasia
exhibiting marked echolalia. Although this hypothesis has been widely accepted
in modern aphasiology (Whitaker, 1976; Assal, Regli, Thuillard et al., 1983;

Effortful echolalia

79

Bogousslavsky, Regli, and Assal, 1988; Grossi, Trojano, Chiacchio et al., 1991),
some have raised objections to it (Brown, 1975; Liebaldt, Scheller und Schleip,
1975; Rapcsak, Krupp, Rubens et al., 1990).
Our three cases with effortful echolalia provide evidence against the
“isolation” hypothesis. Disability of repetition and nonfluency indicate that their
“speech apparatus” was far from a state of “intact, prompt functioning”.
Accordingly, we conclude that the ability to repeat and to produce fluent speech
are not always necessary conditions for echolalia. Effortful echolalia undermines
a basic premise of the “isolation” hypothesis.
Effortful echolalia may be analogous to a forced grasping reaction induced in
an incompletely paretic hand, which is an automatic and compulsive movement
evoked against the limitation of the motor disturbance. Although forced grasping
occurred only in Case 2, this analogy leads us to believe that this type of
echolalia is not only a form of automatic speech, but is also a compulsive
speech phenomenon (Scheller, 1969; Kornyey, 1975). Indeed, all our patients
expressed facial and gestural resistance to their echolalic repetition, and two
commented that it occurred against their will.
Some recent neuropsychological studies of compulsive behaviour have
emphasized its relationship with frontal lobe damage, for example, “compulsive
manipulation of tools” (Mori and Yamadori, 1982), and “utilization” and
“imitation behaviour” (Lhermitte, 1983, Lhermitte, Pillon and Serdaru, 1986).
Scheller (1969) developed an understanding of echolalia as forced behaviour in
speech and named this situation “loss of freedom” (Freiheitsverlust). Based on
Kleist’s (1934) investigations, he asserted that the syndrome of “loss of
freedom,” including forced grasping, sucking (oraler Einstellreflex), gaze
(Zwangsblicken), reading (Zwangslesen) as well as repeating (echolalia), is
caused by a pathological process in the frontal lobe. Lhermitte et al. (1986)
proposed the term “environmental dependency syndrome” as a special
manifestation of the loss of personal autonony caused by frontal lobe damage:
this may correspond to Scheller’s concept of “loss of freedom” (1969). The
imitation behaviour (Lhermitte et al., 1986) seems to us to be a modified form
of echopraxia that is a forced imitation of gesture or behaviour in classical
symptomatology. Echolalia as a special form of “loss of freedom” is generally of
a compulsive nature. We consider that this attribute may be essential for the
occurrence of echolalia and that the effortful echolalia in our patients
demonstrated this situation most clearly.
It is not easy to diagnose the type of aphasia in our patients. Loss of speech
initiative is a definitive characteristic of TCMA, while nonfluency and impaired
repetition are generally considered as indispensable symptoms constituting
Broca’s aphasia syndrome. Goldstein (1915) described two types of TCMA in
his voluminous monograph on transcortical aphasias: Type 1 TCMA can be
regarded as an insufficient form of Broca’s aphasia with relatively preserved
repetition, better than spontaneous speech, caused by partial dysfunction of the
“motor field”; and Type 2 is characterized by severely impaired speech initiation
and intact repetition without dysfunction of the “motor field,” probably
corresponding to Luria’s “dynamic aphasia.” Accordingly, Type 1 TCMA in
itself may be interpreted as intermediate between Type 2 TCMA and Broca’s

80

Kazuo Hadano and Others

aphasia with respect to the symptom of aphasia as well as to the site of lesion.
Furthermore, no clear boundary can be fixed between Type 1 TCMA and
Broca’s aphasia, and a continuum is more likely (Rubens, 1976). Rubens (1975)
stated, on the basis of his own observations and descriptions in the literature,
that repetition improves disproportionately to spontaneous speech, despite initial
total speechlessness, if the lesion is limited mainly to the mesial frontal area, but
that, when there is a combination of superficial mesial and deep capsular lesions,
repetition falls to the level of spontaneous speech and the disturbance is not
distinguishable from severe Broca’s aphasia.
Our patients with effortful echolalia may also indicate the presence of this
continuum. The Z-score JSLTA profile confirmed that auditory comprehension
and repetition were disturbed to a mild or moderate degree in each of our
patients. Case 3, with mild impairment of repetition in the chronic stage, falls
within Type 1 TCMA, because the severely disturbed comprehension in the
acute stage improved remarkably. We are unable to reach a diagnosis of Type 1
TCMA in Cases 1 and 2, because comprehension in Case 1 and repetition in
Case 2 were moderately impaired. We conclude that Cases 1 and 2 lie between
Type 1 TCMA and Broca’s aphasia on the above-mentioned continuum.
The cerebral lesion common to our patients was in the inner side and
subcortical white matter of the frontal lobe and the anterior portion of the basal
ganglia in the left hemisphere. Traditional localization theory in
neuropsychology, in which aphasic nonfluency is attributed to Broca’s area in
the posterior part of the left inferior frontal gyrus (Dejerine, 1914), can explain
the nonfluent speech in case 3 only. Another hypothesis, which locates the
nonfluency in the lower part of the left pre- and post-central gyri (Knopman,
Selnes, Niccum et al., 1983), could not account for the findings in Cases 1 and
2. Naeser, Palumbo, Helm-Estabrooks et al. (1989) hypothesized that persistent
nonfluency is caused by combined lesions of two subcortical white matter areas
in the left hemisphere: the most rostral portion of the medial subcallosal
fasciculus, located in the lateral angle of the frontal horn (extremely deep to
Broca’s area), and the periventricular white matter near the body of the lateral
ventricle, deep to the lower motor/sensory cortex area for the mouth. This
subcortical hypothesis may explain the nonfluent speech in our patients.
A lesion of the medial portion of the left frontal lobe seems to be of
importance in the occurrence of effortful echolalia. Some authors have claimed
that damage to the supplementary motor area (SMA) in the left medial frontal
lobe is associated with echolalia (Kornyey, 1975; Rubens, 1975), but others have
not observed echolalia in cases with lesions including the SMA (Racy, Jannotta
and Lehner, 1979; Masdeu, Schoene and Funkenstein, 1978). Ross (1980)
reported two cases (his Cases 2 and 3) with TCMA due to damage to the left
SMA, but he observed echolalia only in Case 3. There are also some reports of
patients with the left medial frontal lesion including the SMA who exhibited
TCMA, forced grasping or grasp reflex, and the “alien hand” sign, i.e.
apparently purposeful movements dissociated from conscious volition (Goldberg,
Mayer and Toglia, 1981; McNabb, Carrol and Mastaglia, 1988). These authors
suggested an association between these compulsive movements or behaviours
independent of conscious volition and damage to the SMA and related areas in

Effortful echolalia

81

the left medial frontal lobe. In our patients the MRI-findings showed that the left
SMA was damaged cortically in Case 1 and subcortically in Case 2, but was
spared in Case 3, so that the lesion responsible for effortful echolalia does not
appear to lie solely in the left SMA. Our experience and the literature indicate
that the medial frontal lobe, including the SMA, may play an important role in
the occurrence of the echolalia of a compulsive nature that we have described
here as an effortful type, but we are still unable to limit the responsible lesion
solely to the left SMA.
REFERENCES
ASSAL, G., REGLI, F., THUILLARD, F., STECK, A., DERUAZ, J.-P., et PERENTES, E. Syndrome d’isolement
de la zone du langage. Etude neuropsychologique et pathologique. Revue Neurologique, 139: 417424, 1983.
BENSON, D.F. Aphasia, Alexia, and Agraphia. New York: Churchill Livingstone, 1979.
BOGOUSSLAVSKY, J., REGLI, F., and ASSAL, G. Acute transcortical mixed aphasia. A carotid occlusion
syndrome with pial and watershed infarcts. Brain, 111: 631-641, 1988.
BROWN, J.W. The problem of repetition: A study of “conduction” aphasia and the “isolation” syndrome.
Cortex, 11: 37-52, 1975.
DEJERINE, J. Sémiologie des Affections du Système Nerveux. Paris: Masson et Cie, 1914.
GESCHWIND, N., QUADFASEL, F.A., and SEGARRA, J.M. Isolation of the speech area. Neuropsychologia, 6:
327-340, 1968.
GOLDBERG, G., MAYER, N.H., and TOGLIA, J.U. Medial frontal cortex infarction and the alien hand sign.
Archives of Neurology, 38: 683-686, 1981.
GOLDSTEIN, K. Language and Language Disturbances. New York: Grune and Stratton, 1948.
GOLDSTEIN, K. Die transkorticalen Aphasien. Ergebnisse der Neurologie und Psychiatrie, 2: 349-629,
1915.
GOODGLASS, H., and KAPLAN, E. The Assessment of Aphasia and Related Disorders. Philadelphia: Lea
and Febiger, 1972.
JAPANESE SOCIETY OF APHASIOLOGY (Ed.) Standard Language Test for Aphasia. Tokyo: Hohmeido,
1977.
GROSSI, D., TROJANO, L. CHIACCHIO, K., SORICELLI, A., MANCI, L., POSTIGLIONE, A., and SALVATORE, M.
Mixed transcortical aphasia: Clinical features and neuroanatomical correlates. A possible role of the
right hemisphere. European Neurology, 31: 204-211, 1991.
KNOPMAN, D., SELNES, O.A., NICCUM, N., RUBENS, A.B., YORK, D., and LARSON, D. A longitudinal study
of speech fluency in aphasia: CT-correlates of recovery and persistent nonfluency. Neurology, 33:
1170-1178, 1983.
KORNYEY, E. Aphasie transcorticale et écholalie: Le problème de l’initiative de la parole. Revue
Neurologique, 131: 347-363, 1975.
LHERMITTE, F. “Utilization behaviour” and its relation to lesions of the frontal lobe. Brain, 106: 237-255,
1983.
LHERMITTE, F., PILLON, B., and SERDARU, M. Human autonomy and the frontal lobe. Part 1: Imitation
and utilization behaviour: A neuropsychological study of 75 patients. Annals of Neurology, 19: 326334, 1986.
LHERMITTE, F. Human autonomy and the frontal lobe. Part 2: Patient behaviour in complex and social
situations: The “environmental dependency syndrome”. Annals of Neurology, 19: 335-343, 1986.
LIEBALDT, G.T., SCHELLER, H., und SCHLEIP, I. Zur Frage der anatomischen Lokalization echolalischer
Phaenomene in ZNS. Ein Beitrage zur Pathologie der Spontaneitaet der menschlichen Sprache.
Nervenarzt, 46: 422-433, 1975.
MASDEU, J.C., SCHOENE, M.D., and FUNKENSTEIN, H. Aphasia following infarction of the left
supplementary motor area. Neurology, 28: 1220-1223, 1978.
MCNABB, A.W., CARROL, W.M., and MASTAGLIA, F.L. “Alien hand” and loss of bimanual coordination
after dominant anterior cerebral artery territory infarction. Journal of Neurology, Neurosurgery and
Psychiatry, 51: 218-222, 1988.
MORI, E., and YAMADORI, A. Compulsive manipulation of tools and pathological grasp phenomenon.
Clinical Neurology, 22: 329-335, 1982.
NAESSER, M.A., PALUMBO, C.L., HELM-ESTABROOKS, N., STIASSNY-EDER, D., and ALBERT, M. Severe
nonfluency in aphasia. Role of the medial subcortical fasciculus and other white matter pathways in
recovery of spontaneous speech. Brain, 112: 1-38, 1989.
PICK, A. On pathology of echographia. Brain, 47: 417-429, 1924.

82

Kazuo Hadano and Others

POECK, K. Klinische Neuropsychologie (2. Auflage). Stuttgart: Georg Thieme Verlag, 1989.
RACY, A., JANNOTTA, F.S., and LEHNER, L.H. Aphasia resulting from occlusion of the left anterior
cerebral artery. Report of a case with an old infarct in the left rolandic region. Archives of
Neurology, 36: 221-224, 1979.
RAPCZAK, S.Z., KRUPP, L.B., RUBENS, A.B., and REIM, J. Mixed transcortical aphasia without anatomic
isolation of the speech area. Stroke, 21: 953-956, 1990.
ROMBERG, M.H. Lehrbuch der Nervenkrankheiten der Menschen (Dritte Auflage), Berlin: Verlag von
August Hirschwald, 1857.
ROSS, E.D. Left medial parietal lobe and receptive language functions: Mixed transcortical aphasia left
anterior cerebral artery infarction. Neurology, 30: 144-151, 1980.
RUBENS, A.B. Aphasia with infarction in the territory of the anterior cerebral artery. Cortex, 11: 239-250,
1975.
RUBENS, A.B. Transcortical motor aphasia. In H. and H.A. Whitaker (Eds.), Studies in Neurolinguistics,
Vol. 1. New York: Academic Press, 1976, pp. 293-303.
SCHELLER, H. Zur Anthropologie der Verhaltensstoerungen bei Stirnhirnprozessen (Aspontaneitaet,
Greifen, Sperren, Echosymptome als Freiheitsverlust). Nervenarzt, 40: 557-560, 1969.
STENGEL, E. A clinical and psychological study of echo-reactions. Journal of Mental Science, 93: 598612, 1947.
TONKONOGY, J., and GOODGLASS, H. Language function, foot of the third frontal gyrus, and Rolandic
operculum. Archives of Neurology, 38: 486-490, 1981.
WHITAKER, H. A case of the isolation of the language function. In H. and H.A. Whitaker (Eds.), Studies
in Neurolinguistics, Vol. 2 New York: Academic Press, 1976, pp. 1-58.
Kazuo Hadano, M.D., Department of Psychogeriatrics, National Institute of Mental Health (NCNP), 1-7-3 Kohnodai, Ichikawa, Chiba,
272, Japan. E-mail: hadano@ncnp-k.go.jp

(Received 15 February 1997; accepted 15 July 1997)