456 Warren et al.

Expressive language
disorder after infarction of
left lentiform nucleus
JD Warren1 BMedSc MBBS (Hons), HB Smith2 BApplSc (Speech
Path)1, LA Denson3 BA (Hons) DipAppPsych MPsych, HM
Waddy1 MB FRACP
1

Department of Neurology, Royal Adelaide Hospital, Adelaide, Australia
Department of Speech Pathology, Royal Adelaide Hospital, Adelaide,
Australia
3
Department of Clinical Neuropsychology, Royal Adelaide Hospital, Adelaide,
South Australia
2

Summary A 53 year old bilingual woman presented with apraxia of
speech and writing in English and German after ischaemic infarction
of the left posterior lentiform nucleus. Detailed language
assessment revealed impairments of articulation, verbal fluency,
auditory repetition, interpretation of complex semantic relationships,
formulation of definitions and verbal short-term memory. The case
illustrates the role of the basal ganglia in speech planning, word
retrieval and verbal short-term memory. © 2000 Harcourt Publishers
Ltd
Journal of Clinical Neuroscience (2000) 7 (5), 456–458 © 2000 Harcourt Publishers Ltd
DOI: 10.1054/ jocn.1999.0238, available online at http://www.idealibrary.com on

Keywords: speech apraxia, verbal memory, basal ganglia

Received: 7 May 1999
Accepted: 18 June 1999
Correspondence to: Dr JD Warren, Department of Neurology, Royal Adelaide
Hospital, Adelaide, South Australia, 5000. Tel.: +61 8 8222 5500; Fax: +61 8
8223 3870.

INTRODUCTION
The diversity of brain regions implicated in expressive language
disorders, ranging from Broca’s aphasia through speech apraxia to
anarthria, was emphasised recently by Donnan et al.1 A putative
centre for the articulation of human speech has been identified in
the anterior insula of the dominant hemisphere.2,3 A number of
reports have described dysphasia, apraxia of speech or dysarthria
after lesions involving the basal ganglia.4–9 However, in most cases
other deficits (facial palsy, hemiparesis, neglect, Gerstmann’s
syndrome, frontal signs) have accompanied the language disorder,
and the role played by the basal ganglia in speech articulation and
expressive language in general remains to be clarified.9 We report
a bilingual patient in whom ischaemic infarction of the left posterior lentiform nucleus presented as an apparently isolated apraxia
of speech and writing affecting both languages.

towards the end of longer words. She used the right hand
normally when manipulating tools and utensils, and had no weakness of hand-grip or sensory symptoms. There was a past history
of hypertension and diabetes mellitus. Medications were perindopril, metformin and gliclazide.
On examination, she was alert and fully orientated. Her estimated premorbid IQ (Wechsler Adult Intelligence Scale III) was
103.10 Speech and language functions were assessed using the
Robertson Dysarthria Profile, Mount Wilga High Level Language
Test, Boston Diagnostic Aphasia Examination and Western
Aphasia Battery. She was able to initiate and sustain phonation
normally; however, she had difficulty coordinating pitch and
volume changes. Her speech had inappropriate intonations and
rhythms in both English and German, which were slow and staccato in quality, and words were not clearly articulated. She had
particular difficulty with complex sounds such as approximates,
glides and liquids (‘j’, ‘ch’, ‘r’ and ‘l’), English and German sound
combinations (such as ‘str’ and ‘spl’) and multisyllabic words (for
example, ‘calendar’ and ‘caterpillar’). She made occasional sound
omissions (for example, ‘Moday’ for ‘Monday’). Repetition and
reading aloud were hesitant and marred by errors similar to those
in spontaneous speech. Formation of letters when writing was
often awkward, inaccurate or duplicated (Fig. 1, top), punctuation
marks were sometimes omitted and three attempts were required
to sign her name correctly.
She was able to name and categorise common objects normally.
Vocabulary, syntax and grammar were preserved when speaking
and writing. However, she could generate only 7 spontaneous
English words beginning with the letter ‘S’ in a 3-min period
(predicted 30–54 words), and tended to reiterate these when asked
to perform the same task in German. She had difficulty producing
concise definitions for words such as ‘handle’ or ‘lottery’,
constructing a sentence using specific content words (for example,
‘crop’, ‘although’, ‘drought’), and listing the components of a
complex sequential task (such as making a cup of coffee). She
performed one to five stage spoken commands promptly, making a
single error on the last item of the five-stage task in the Western
Aphasia Battery subtest. On the Similarities subtest of the Wechsler
Adult Intelligence Scale, in which she was required to describe the
common property of a series of paired items (for example, ‘tablechair’; ‘eye-ear’), her performance was moderately impaired (age
score 4; predicted 11). She also had difficulty interpreting complex
semantic and grammatical relationships (for example, ‘Is your
sister your father’s daughter or your daughter’s father?’; ‘Car is to
wheels as hand is to …?’), whether spoken or written.
On testing immediate recall of verbal stimuli, digit span was
mildly impaired (maximum 4 forwards, 2 backwards; age score 5,

CASE STUDY
A 53 year old right-handed woman of German ancestry presented
to hospital because she had been unable to express herself clearly
since waking that morning. Although she was able to formulate
her thoughts, her speech was halting and effortful, with occasional inappropriate or nonsense words. She experienced similar
difficulties in her first language, German, as well as English,
which she had spoken fluently since childhood. She also noted
difficulty forming letters when writing, tended to add letters inappropriately to the ends of words and legibility deteriorated
Journal of Clinical Neuroscience (2000) 7(5), 452–464

Fig. 1 Examples of the patient’s hand-writing 24 h (top) 2 months (bottom)
after onset of her speech and writing difficulties. In the acute phase,
formation of letters (for example, ‘h’ and ‘m’) was laborious and inaccurate,
and ‘little’ became ‘littlee’. By 2 months, her writing had regained its former
accuracy and fluency.

© 2000 Harcourt Publishers Ltd

Expressive language disorder after infarction of left lentiform nucleus 457

Fig. 2 T1-weighted axial MRI brain slice 24 h after onset of the deficit,
showing ischaemic infarction of the left posterior lentiform nucleus.

predicted 10). Free recall and recognition of a learned list of 15
everyday words at 5 and 30 min on the Rey Auditory Verbal
Learning Test9 was average for age. There was no evidence of a
recency effect. Although the effect of word length was not
assessed systematically, in recall of spoken sentences (12 to 30
syllables long) she made errors affecting short (monosyllabic) as
well as longer (trisyllabic) words. Visual short-term memory for
the Rey-Osterreith Figure9 was above average for age. Recall of
factual information and ability to draw inferences from a short
spoken or written passage were normal.
Tests of arithmetic, frontal executive and motor functions, and
visuo-spatial construction were performed normally.9 Oro-facial
and limb praxis were assessed using Western Aphasia Battery
subtests. She pantomimed hand positions and sequential actions
correctly. To verbal command, she was able to whistle, sniff, blow a
kiss, wave goodbye and mime the use of everyday tools and utensils,
as well as complex actions (such as pretending to drive a car), with
complete accuracy. She also manipulated real objects normally.
Visual fields were normal, there was no facial weakness and the
remainder of the cranial nerves were intact. Limb strength and
sensation were normal, tendon reflexes were symmetrical and
plantar responses flexor bilaterally. Fine finger movements of
the right hand were normal, two point discrimination, graphaesthesia and stereognosis were intact and there was no evidence of
sensory inattention. She was in sinus rhythm and blood pressure was
170/90.
MRI of the brain (Fig. 2), 24 h after the onset of the speech
disturbance, revealed an ischaemic infarct of the left posterior
lentiform nucleus. When reviewed 2 months later, her writing had
returned to normal (Fig. 1, bottom) and she made only occasional
articulatory errors.

The spontaneous speech of our patient had many features in
common with the cases described by Dronkers,2 including articulatory errors approximating the target word, dysprosody and
slowness of speech output. The features were not those of
the dysarthria described in lesions of the corticolingual
pathways.12 In addition, she presented a unique opportunity
to examine the effects of a subcortical lesion of the dominant
hemisphere in a bilingual patient. Her speech errors were
very similar in different languages, and accompanied by a
severe reduction in verbal fluency. Errors were also similar
whether signing her name (a familiar motor programme) or
writing a spontaneous sentence (a novel task). These observations suggest that a lesion of the left lentiform nucleus may
disrupt a final common pathway mediating fine motor control of
language output, both spoken and written, and complement
recent PET evidence that the left pallidum is involved in speech
articulation.3
However, language difficulties in the present case were not
restricted to articulation. It is known that speech articulation and
retrieval of words from semantic memory share components of
similar neural networks in the dominant hemisphere.13 An ‘articulatory loop’ is thought to mediate short-term verbal memory,
and may be involved in particular language tasks such as
sentence comprehension, new word acquisition and word repetition.14,15 The loop has two anatomically distinct subcomponents:14,15 a phonological store (left supramarginal gyrus and
inferior parietal lobe) and a subvocal rehearsal system (Broca’s
area, left premotor cortex, insula, supplementary motor area and
right cerebellum). Interference with the function of this loop
might explain our patient’s difficulties in immediate recall of
verbal stimuli, auditory repetition, discrimination of complex
semantic relationships, definitions, similarities and construction
of sentences using particular content words. Tasks of this type
probably require an intact articulatory loop to permit comparison and selection of possible responses prior to generation of
the final response. The types of articulatory errors made by our
patient, her reduced verbal fluency and digit span and the lack of
normal recency and word length effects are similar to the
deficits described after lesions of the articulatory loop.15
However, the pattern does not suggest preferential involvement
of either subcomponent of the loop. The present case provides
circumstantial evidence that a lesion in a basal ganglia structure
(the left lentiform nucleus) may disrupt motor planning of
speech, word retrieval and verbal short-term memory, perhaps
by interfering with the function of the articulatory loop. This
accords well with emerging concepts of the broad role of the
basal ganglia in cognition,9 and the distributed nature of expressive language processing.1
REFERENCES

DISCUSSION
Human speech requires complex planning and coordination of lip,
tongue, palatal, pharyngeal, laryngeal, respiratory and other accessory muscles. Apraxia of speech has been characterised as a
disorder of the programming of speech to preserve the correct
sound and sequence of words with appropriate timing.2,3,11
Composite lesion studies in stroke patients2 and functional
imaging data3 indicate that the left anterior insula plays a key role
in speech articulation. The left posterior pallidum participates in
several motor loops within the dominant hemisphere and is activated particularly in word repetition tasks.3 In contrast to earlier
studies of speech and oro-facial apraxia in stroke patients,4–9 nonverbal functions of the dominant hemisphere, including motor
praxis, were intact in the present case.
© 2000 Harcourt Publishers Ltd

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Asymptomatic
schwannoma of the
oculomotor nerve: case
report

CASE REPORT
A 66 year old woman with diabetes mellitus was referred to our
department due to an intracranial mass which was incidentally
found by magnetic resonance imaging (MRI).
Examination
The subject was alert, with normal higher cortical function. The
visual fields were intact; pupils were equal, with a normal light
reflex; and ocular movement were full and smooth, without
nystagmus. Sensation over the face was intact, and both corneal
reflexes were present. All other cranial nerves were normal and all
other neurological functions were intact. T1-weighted MRI
revealed an iso-intensity mass in the upper wall of the right
cavernous sinus, partially within the cavernous sinus and
extending to the interpeduncular cistern (Fig. 1). An injection of
contrast media homogeneously enhanced the mass. We predicted
that the tumour would be removed successfully without severe
functional deficit before growing too large for uneventful surgical
treatment. The patient underwent surgical removal of the tumour
with a preoperative diagnosis of meningioma or trigeminal
schwannoma.
Surgery

1

1

Masahito Katoh MD, Takashi Kawamoto MD, Kousuke
Ohnishi1 MD, Yutaka Sawamura2 MD, Hiroshi Abe2 MD
1

Department of Neurosurgery, Tomakomai City General Hospital,
Tomakomai, Japan 2Department of Neurosurgery, Hokkaido University
School of Medicine, Sapporo, Japan

Summary Intracranial oculomotor schwannoma without
neurofibromatosis is rare and is usually symptomatic. Only one
case of asymptomatic oculomotor schwannoma has been
previously reported. We present a case of intracranial oculomotor
schwannoma which caused no signs or symptoms. Microsurgical
resection of this tumour resulted in oculomotor palsy. We
reviewed 7 reported cases and the findings indicated that radical
removal of the tumour invariably caused or worsened the
oculomotor palsy. The reason why the tumour caused no
symptoms in this case was unclear. However, improvements in
diagnostic methods such as magnetic resonance imaging (MRI)
may increase the detection of such asymptomatic cases.
Indications for surgical treatment should be established. © 2000
Harcourt Publishers Ltd

Through the right pterional route, the tumour was found in the
basal cistern, extending into the superoposterior wall of the
cavernous sinus. Dissection of the tumour margin and intraoperative microscopic observation suggested schwannoma. After
removal of a small part of the tumour, the oculomotor nerve was
identified in the cistern; however, it had been partially injured
because it was contiguous with the tumour, with no clear border
(Fig. 2). The tumour mass attached to the nerve was left intact.
More than 90% of the tumour was removed.
Histologically, the tumour was a typical schwannoma without
evidence of malignancy (Fig. 3). The postoperative course was

A

Journal of Clinical Neuroscience (2000) 7 (5), 458–460 © 2000 Harcourt Publishers Ltd
DOI: 10.1054/ jocn.1999.0240, available online at http://www.idealibrary.com on

Keywords: oculomotor nerve, schwannoma
Received 7 April 1998
Accepted 8 December 1999
Correspondence to: Masahito Katoh MD, Department of Neurosurgery,
Tomakomai City General Hospital, Honkocho-1, Tomakomai, 053–8567,
Japan. Tel.: +81–144–33–3131; Fax: +81–144–34–7511; E-mail:
masasama@coral.ocn.ne.jp

INTRODUCTION
Schwannomas of the oculomotor nerve may be associated with
neurofibromatosis type 2; however sporadic intracranial oculomotor schwannomas are very rare and are usually symptomatic
mass lesions.1–15 We report a patient with intracranial oculomotor schwannoma who exhibited no signs or symptoms.
Journal of Clinical Neuroscience (2000) 7(5), 452–464

Fig. 1 MR images showing a mass in the right suprasellar cistern and
homogeneous enhancement after intravenous administration of Gd-DTPA. A:
axial view, B: coronal view, C: sagittal view.

© 2000 Harcourt Publishers Ltd