Journal of

J Neurol (1987) 234 : 421-423

Neurology
© Springer-Verlag 1987

Short communications

Cerebral blood flow in thalamic aphasia
A. M. Fasanaro 1, D. L. A. Spitaleri 1, R. Valiani 1, A. Postiglione 2, A. Soricelli 3, L. Mansi 3, and D. Grossi 4
1Divisione di Neurologia, Ospedale A. Cardarelli, Via A. Cardarelli, 1-80131 Napoli, Italy
2Istituto di Medicina Interna e Malattie dismetaboliche, II. Facolt/~ di Medicina e Chirurgia, Napoli, Italy
3Cattedra di Medicina Nucleare, Istituto di Scienz Radiologiche, II. Facolt~t di Medicina e Chirurgia - Servizio di Medicina Nucleare,
Istituto Nazionale dei Tumori, Fondazione Pascale, Napoli, Italy
4Clinica Neurologica, II. Facolth di Medicina e Chirurgia, Napoli, Italy

Summary. A 59-year-old man is reported, who became aphasic

We report the results obtained in a patient with thalamic

after left thalamic infarction, shown by CT. His speech was
fluent, with reduced voice volume, impaired auditory and
reading comprehension, verbal paraphasias but intact repetition skills. A single photon emission computed tomography
(SPECT) scan to measure regional cerebral flow (rCBF)
showed a reduction of flow in the parietotemporal areas of the
left hemisphere. It is suggested that thalamic aphasia could
result from structural subcortical damage with a homolateral
functional cortical deficit leading to the specific aphasic disturbance.

aphasia due to an ischaemic stroke, where the regional blood

Key words: Thalamus - Aphasia - rCBF - SPECT

flow was investigated by single photon emission computed
tomography (SPECT) using xenon 133 (133Xe) [8].

Case report
The patient under study was a 59-year-old, right-handed, male
farm worker, who had received primary education. No relevant previous disease was reported. The patient was admitted
after sudden onset of right-sided weakness and difficulty in
speaking. The initial examination showed a mild right-sided
hemiparesis with homolateral hypoaesthesia and no visual
field defects; the patient was alert and cooperative. There was

Introduction
Language disturbance following thalamic lesions, first described by D6jerine and Roussy [4] and Hillemand [7], has
been confirmed by anatomoclinical studies, as well as by
neuropsychological evaluation in thalamotomy patients [3].
The disorders can be grouped into extrapyramidal deficits,
deficits in word access, and comprehension defects. Thalamic
stimulation performed during stereotaxic surgery has indicated that the posterior part of the left thalamus (the pulvinar
and the ventrolateral nucleus) plays a definite role in language
[9, 14], so that an aphasic disorder occurs if this region is
damaged.
More recent observations have been reported by Cappa
and Vignolo [1], Mazaux and Orgogozo [11] and Puel et al.
[15] in subjects with spontaneous pathology (haemorrhagic or
ischaemic strokes). The clinical features of thalamic aphasia,
as appears from these reports, resemble in some aspects the
semantic aphasia described by Luria [10] for damage of the associative parietal cortex, and the dynamic aphasia described
as arising from lesions of the premotor frontal cortex, and
the transcortical aphasias [1]. From a pathophysiological viewpoint it has been hypothesized that the thalamic lesion implies
a disturbance of the focusing and alerting of neuronal complexes in the posterior temporal and parietal lobes, as the
pulvinar projects extensively to these regions [5, 16]. It is,
therefore, of interest to investigate such patients by dynamic
and structural methods, in order to see whether or not
dynamic changes could be related to language impairment.
Offprint requests to: A. M. Fasanaro

Table 1. Results of the aphasia examination test (Battery of Neuropsychological Centre of the University of Milan)
A. Oral expression

Picture naming
Automatic series

Fluent, dysprosodic speech with
verbal paraphasias, stereotypy,
of limited communicative
efficacy
60% Correct
100% Correct

B. Comprehension
Words
40% Correct
Words of the same semantic group 20% Correct
Sentences
70% Correct
C. Repetition
Letters
Words
Neologisms
Sentences

90% Correct
100% Correct
90% Correct
100% Correct

D. Reading aloud
Letters
Words
Neologisms
Sentences
Reading comprehension

60% Correct
50% Correct
0% Correct
0% Correct
10% Correct

E. Writing
Spontaneous
Dictation
Copying

0% Correct
0% Correct
0% Correct

422
a paucity of spontaneous speech; when prodded, however, the
patient produced almost fluent speech with stereotypy, neologisms, verbal and phonemic paraphasias. Voice volume was
reduced and dysprosody was evident. He was able to understand very simple commands such as "close your eyes", but
failed in more complicated commands. Repetition was normal; naming of objects was impaired; he could no longer read
or write. Attempts at figure drawing and copying produced
illegible marks that did not resemble the model; he was, however, able to group similar figures.
About 20 days after the onset he was subjected to a complete aphasia examination test (aphasia test of the University
of Milan), which demonstrated a profile consistent with transcortical sensory aphasia (Table 1). Furthermore, the general
neuropsychological examination showed the presence of constructional apraxia and of long-term memory impairment.
E E G showed slow rhythms in the parietotemporal areas.
CT scan of the brain showed an ischaemic area confined to
the left thalamus (Fig. 1). A SPECT scan to measure regional
cerebral flow (rCBF) was carried out using a brain dedicated

Fig. 1. CT scan showing an area of decreased density in the capsularthalamic region of the left hemisphere

32 phototubes SPECT scanner (Tomomatic 32, Medimatic,
Copenhagen) and m X e gas (20mCi/1). Measurements of
rCBF (ml/min per 100 g) were performed in one axial slice
(+ 5 cm from the orbitomeatal line). After the inhalation for
i rain of 133Xe and a 3-min period of exhalation, the rCBF was
calculated according to specially designed algorithms [2]. The
SPECT scan revealed a reduction of rCBF in the parietotemporal areas of the left hemisphere (Figs. 2, 3).
The patient was discharged on the 30th hospital day without any improvement in his language abilities. Three months
after discharge a second aphasia test was performed, which
showed an improvement of naming and comprehension as
well of reading tasks. Writing and drawing abilities were still
severely impaired.

Discussion
The present case and others from the literature indicate that a
left thalamic lesion is followed by an aphasic picture characterized by dysarthric, dysprosodic non-fluent speech with diminished volume of voice, absence of phonemic paraphasias,
presence of verbal paraphasias, preserved verbal repetition
with impairment of aural and reading comprehension. We
conclude that the profile of the aphasia suggests a sensory
transcortical aphasia, in agreement with previously reported
cases [1, 6].
The evaluation of cerebral blood flow by SPECT in our patient showed a significantly low perfusion in the parietotemporal region of the left hemisphere; this area is the one expected for transcortical sensory aphasia, and it is congruent
with the E E G findings. These data are in agreement with the
hypothesis that structural thalamic damage is associated with
a functional deficit in the homolateral cortical regions.
Furthermore, the data are in agreement with the findings obtained in patients with subcortical lesions where the metabolic
activities have been investigated employing positron emission
tomography using the fluoro-deoxyglucose-F18 method [12,
13]. Indeed these patients showed diminished metabolic activ-

Figs.2, 3. Cerebral blood flow (CBF) in a patient with thalamic aphasia following an ischaemic stroke. Reduction of CBF (> 15%) is observed in
the left temporal region as compared with the right temporal lobe

423
ity in cortical regions, while the CT scan demonstrated only a
subcortical homolateral lesion. Hence thalamic aphasia can
result from subcortical damage leading to the extrapyramidal
signs, and from a functional cortical deficit leading to a specific aphasic disturbance.
It seems possible that following structural thalamic damage
a disturbance of thalamocortical connections would occur,
producing an intrahemispheric vertical disconnection, from
which an aphasic syndrome could follow. The analogy between transcortical aphasia and thalamic aphasia suggests that
in both cases the connections between areas involved in languages, not the areas themselves, are damaged.

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Received October 6, 1986 / Accepted November 3, 1986