Loss of motivation for speaking with bilateral lacunes in
the anterior limb of the internal capsule
B. Croisile*,

E. Henry*,

M. Trillet*,

G. Aimard*

Introduction
Summary

Language disorders, differing from classical cortical aphasia, are frequent after subcortical lesions’. Bilateral lesions in the basal ganglia are
sometimes responsible for behavioral alterations without dementia. The most dramatic is
the loss of self psychic activation’-6, when patients show inertia for all behavioral activities,
but it is easily reversible after external stimulation. We report a patient who only lost the
motivation for speaking. CT scan showed bilateral lacunes, mainly in the anterior limb of the
internal capsule. This case emphasizes the role
of activating cortico-subcortical loops.

A 76-year-old man suddenly presented with
loss of motivation for speaking. He had no
aphasia, depression
or dementia,
but he did
not want to speak with other people. CT scan
showed hypodensities,
presumably
lacunes,
mainly in the anterior limb of the two internal
capsules. Global behavioral changes with loss
of self psychic activation have been reported,
but in our patient the disturbance
was restricted to oral language. The role of activating cortico-subcortical
loops is discussed.
Key words: psychic akinesia,
motivation,
speaking.

internal

capsule,

Case report

Our patient, a 76-year-old man, right-handed,
retired master-builder, with systemic hypertension, had no familial or personal history of psychiatric disorders. In December 1987 he suddenly presented with a mild right hemiparesis
and his wife noticed that he spoke less than
usually. There was no headache, no dysarthria,
no word-finding difficulty, no paraphasia and no
oral comprehension deficit.
His first medical consultation was in March
1988. Since 4 months he had lost desire for
speaking with other people but he was not so
reluctant once conversation was engaged. When
he took previously one hour for his shopping he
* Department

of Neurology (Pr Trillet and Pr Aimard),

now spent only ten minutes because he avoided
his friends with whom he did not want to speak.
He told no more jokes. The loss was limited to
speaking as he had usual motivation for previous activities which were fully preserved: dining, dressing, washing, reading, writing, gardening, watching television. He demonstrated
no anxiety or special feeling about his loss of
motivation for speaking. He had no compulsive
behavior, no personality change and his affect
was normal. Using DSM III and MADRS criteria there was no depression. Attention and orientation were normal. Apart from mild dysprosody his language examination was normal: fluoral
articulation,
word-naming,
ency ,

H6pital Neurologique.

Lyon, France

Address for correspondence and reprint requests: Dr. Croisile. Department of Neurology (Pr Trillet and Pr Aimard),
Neurologique, 59 boulevard Pinel, 69394 Lyon cedex 3, France
Accepted 10.4.89
C/in Neurol Neurosurg

Hepital

1989. Vol91-4

325

Fig. I. Contrast-enhanced CT. Lacunes of the left and right
anterior Jimbs of the internal capsule and near the two
frontal horns (the left side of the patient is on the right of the
photograph).

expression
and comprehension , repetition,
writing, reading aloud, oral spelling, calculation. There was no frontal semiology and all
Luria’s series were normal, He could learn and
recall digits, words and pictures; he could summarize the story of the various books he was
reading (five/week). There was no constructional or limb apraxia.
CT scan showed bilateral hypodensities in the
anterior limb of the internal capsule with perhaps ~~vo~v~rnent of the putamen but limited to
its anterior aspect (Fig. 1). There were hypodensities near the two frontal horns, at the entrance of the anterior limb of the internal capsule, and the left sylvian fissure was enlarged.
CT scan was performed four months after the
onset but these h~ode~sities were presumably
lacunes or infarctions more than sequels from
hematoma,
R5seussioo

Our patient presented with an unusual symptom
which cannot be related to dementia, depres324

sion or aphasia. He had no deficit in intellectual
or cognitive functioning. His specific loss of interest toward speaking was easily reversible by
external stimulations, and conversation was
therefore normal. This is not consistent with
aphemia, mu&m, transcortical motor aphasia
or frontal syndrome7. Left-sided lesions. involving the anterior limb of the internal capsule. the
head of the caudate nucleus and the putamen
have been related with dysarthria, right hemiparesis, dysprosody and atypical aphasia”. Patients
with right-sided lesions in the same sites had
often dysarthria or dysprosody’. Our patient
had only a mild dysprosody; the disturbance of
the oral speech was not aphasic and did not
resemble the clinical pictures of subcortical
aphasia’. In fact he demonstrated a behavioral
syndrome limited to speech rather than a true
aphasia,
Pure psychic akinesia (or athymhormia syndrome) corresponds with the loss of drive and
i~itiative~.~. Patients show dramatic reduction of
their usual activities with a flattened affect.
They stay for hours doing nothing and they do
not take part in sport or in social activities. Mild
extrapyramidal symptoms are sometimes present, but there is no reduction of motor abilities.
Physical and intellectual capacities are always
normal, as are neuropsychological tests. Some
patients have compulsive activities: mental
counting, verbal and motor stereotypes or obsessive cotlecting2~“~‘. fn only one patient this
was similar to an obsessive neurosis with intense
anxiety and a magic-like clue5. In all cases the
lack of initiative is also present in language. As
in our case, patients talk only if asked and they
do not try to engage conversation whereas neuropsycholog~~al evaluation failed to demonstrate aphasia, except dysprosody or defect in
speech fluency. For Laplane ef al. 2v5this capacity
to maintain normal activities after stimulation
shows that psychic akinesia is different from
frontal lobe syndrome or subcortical dementia,
and corresponds to the loss of self psychic activation.
Pure psychic akinesia is the consequence of
lesions in the basal ganglia after carbon monoxide poisoning, wasp sting or vascuiar disease,
Lesions are bilaterally located: in the gbbus
pailidus2,3.5,in the head of the caudate nuclei4 or
in the striatum6. These structures are also in-

volved in subcortical diseases with motor or cognitive disturbances (Parkinson’s disease, Huntington chorea, progressive supranuclear palsy).
In our patient, as far as we can rely upon the
resolution of the CT scan, the anterior limbs of
the internal capsule seemed to be mostly damaged with little extension into the gray-matter
nuclei. There was a hypodensity near the left
frontal horn. The interpretation can be related
to (1) disconnection of fibre pathways in the
white matter anterior limb and to (2) some damage to the adjacent caudate nuclei and putamens. The globus pallidus was not involved. In
the anterior limb of the internal capsule the
major pathways are: prefrontal corticopontine
tract, projections from the head of the caudate
nucleus to the putamen, anterior thalamic radiation connecting the frontal premotor and motor cortex and the prefrontal cortex with respectively ventral anterior, ventral lateral and dorsomedian thalamic nuclei’.
Five circuits linking cortex and basal ganglia
have been described”.“. Three are of interest in
our case. The lateral orbitofrontal and dorsolatera1 prefrontal cortex have projections on the
caudate nucleus, followed by connection with
the rostra1 part of globus pallidus which in turn
projects to the dorsomedian and ventral anterior thalamic nuclei. These nuclei send efferents
toward prefrontal cortex. Ventral limbic striaturn receives efferents from the limbic cortex,
mainly the anterior cingulate cortex. Then,
through globus pallidus, ventral striatum is the
origin of input to the dorsomedian thalamic nucleus which in turn projects largely to the anterior cingulate cortex.
Bilateral lesions in any part of these three

cortico-subcortical loops may result in loss of
drive2-6. In our patient there is mainly interruption of white matter pathways linking nuclei in
these cognitive and limbic loops. The occurrence of a specific defect with the activation of
speech suggests that the lesions do not involve
equally the fibres but only those specifically concerned with motivation for speech.
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