J Neurol (2007) 254:442–447
DOI 10.1007/s00415-006-0385-7

Yasuo Terao
Yoshikazu Ugawa
Tomotaka Yamamoto
Yasuhisa Sakurai
Tomohiko Masumoto
Osamu Abe
Yoshitaka Masutani
Shigeki Aoki
Shoji Tsuji

Received: 14 February 2006
Received in revised form: 31 May 2006
Accepted: 6 June 2006
Published online: 22 March 2007
Y. Terao, MD, PhD (&)
Y. Ugawa, MD, PhD
T. Yamamoto, MD, PhD
S. Tsuji, MD, PhD
Dept. of Neurology,
Division of Neuroscience
Graduate School of Medicine
University of Tokyo
7-3-1 Hongo
Bunkyo-ku113-8655
Tokyo, Japan
Tel.: +81-3-3815-5411 ext. 33784
Fax.: +81-3-5800-6548
E-Mail: yterao-tky@umin.ac.jp
Y. Sakurai, MD, PhD
Dept. of Neurology
Mitsui Memorial Hospital
Tokyo, Japan
T. Masumoto, MD, PhD
O. Abe, MD, PhD
Y. Masutani, MD, PhD Æ S. Aoki, MD, PhD
Dept. of Radiology and Bioengineering
Graduate School of Medicine
University of Tokyo
Tokyo, Japan

ORIGINAL COMMUNICATION

Primary face motor area as the motor
representation of articulation

j Abstract No clinical data have

yet been presented to show that a
lesion localized to the primary
motor area (M1) can cause severe
transient impairment of articulation, although a motor representation for articulation has been
suggested to exist within M1. Here
we describe three cases of patients
who developed severe dysarthria,
temporarily mimicking speech arrest or aphemia, due to a localized
brain lesion near the left face
representation of the human primary motor cortex (face-M1).
Speech was slow, effortful, lacking
normal prosody, and more affected
than expected from the degree of
facial or tongue palsy. There was a
mild deficit in tongue movements
in the sagittal plane that impaired
palatolingual contact and rapid
tongue movements. The speech
disturbance was limited to verbal
output, without aphasia or orofacial apraxia. Overlay of magnetic

Introduction
Human speech requires intricate planning and coordination of mouth and tongue muscles. The assumption of a left-hemisphere speech motor module [1]
comes from a multitude of observations that lesions in
the lower motor cortex of the dominant hemisphere
give rise to aphemia or severe impairment of articulation [2–7]. This module may well lie near the lower
motor area because pure dysarthria, a rare manifesta-

resonance images revealed a localized cortical region near face-M1,
which displayed high intensity on
diffusion weighted images, while
the main portion of the corticobulbar fibers arising from the lower
third of the motor cortex was
preserved. The cases suggest the
existence of a localized brain region
specialized for articulation near
face-M1. Cortico-cortical fibers
connecting face-M1 with the lower
premotor areas including Broca’s
area may also be important for
articulatory control.

j Key words face motor area Æ
articulation Æ speech arrest Æ
diffusion weighted image

tion of cortical stroke, is often accompanied by facial
palsy [8–10], involving the part of primary motor cortex lying just laterally to the precentral knob (face-M1).
Most of the lesions reported so far, however, are relatively large, with varying extensions into the premotor
cortex, frontal operculum, anterior insula and/or the
underlying white matter, precluding conclusions as to
the precise location of cortical region responsible for
such disorder [2–12]. Recent functional imaging studies [13–15] point to the existence of a speech module

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within M1 that is specialized for articulation. On the
other hand, transcranial magnetic stimulation over the
face-M1 has also been shown to interrupt overt production of prepositional speech [16] and to delay the
onset of vocalization [17]. Speech arrest can be induced
by direct electrical stimulation of the cerebral cortex
around the face motor area [18]. However, no clinical
data have yet been presented to show that a small lesion
near face-M1 can cause a severe transient impairment
of articulation, mimicking speech arrest or aphemia.
In this report, we show that a region specialized for
articulation exists within M1. Damage to this region
should temporarily present with an arrest of speech,
since the entire speech system would be deprived of
its output stage. Combining the findings of three
cases, we were able to delineate this region to a cortical area near face-M1.

Case reports
j Case 1
A hypertensive right-handed woman had conducted a normal life
until the age of 65, when after noting a hot choking sensation
around the neck and tingling dysesthesia on the right side of the
body, she suddenly developed weakness of the right upper and
lower limbs and became unable to talk. The paresis resolved
quickly as she became ambulatory within a few hours, but the
speech disturbance persisted. When she was admitted to our hospital, her utterances had become confined to grunts like ‘‘uuh’’ or
‘‘aah’’. Meanwhile, higher functions including comprehension of
verbal and written language and handwriting remained completely
normal, without any signs of aphasia. A slight facial droop with a
shallow nasolabial groove was noted on the right side, but there was
no orofacial apraxia. Sensory function of the oral cavity was normal. No deviation was noted on tongue protrusion, and she could
wiggle or elevate the tongue to order. The palatal and pharyngeal
movements were unimpaired, and there was no apparent dysphagia. A mild right hemiparesis was noted, but there was no objective
sensory disturbance in the limbs.
One week later, she began to form words, although these were
limited mostly to single word utterances. By two weeks, she was able
to speak short sentences, but speech was remarkably slow and
slurred with distorted phonemes and altered prosody, assuming a
foreign accent. There was no semantic or literal paraphasia. After one
month of onset, weakness of the limb had disappeared and speech
had improved to a near normal level without any inconvenience in
daily conversation. However, after six months of follow up, she
sometimes feels the tongue ‘‘thick’’ and has been aware of omitting
lingual consonants when she speaks quickly. Otolaryngologic studies
disclosed normal motility of the pharyngeal and laryngeal muscles.
Magnetic resonance imaging (MRI) of the brain taken on the
day of onset showed a discrete lesion at the depth of the central
sulcus, partly extending into the precentral gyrus (left figure in
Fig. 1). The same area exhibited high intensity in the diffusionweighted image (DWI), pointing to the recent emergence of the
lesion (right figure in Fig. 1). MR angiography was normal.
j Case 2
A right-handed 80-year-old man with diabetes mellitus and
esophageal varices, suddenly developed right facial paresis without

Fig. 1 T2 weighted and DW images of Case 1. Transverse scans for the
T2 weighted (left figure) and DWI image (right figure) are shown. The lesion
was noted at the depth of central sulcus, partly extending to the precentral
gyrus. The same region displayed high intensity in the DWI
involvement of the limbs, and was admitted to our hospital. He also
exhibited a marked reduction in the amount of speech. On the next
day, he began to form words very slowly, mostly utterance of single
words with a breathy and slightly hoarse voice. Facial palsy became
confined to the right mouth angle within 3 days. Even one week
after onset, however, his speech still demanded enormous effort
and remained extremely slow with a distorted prosody and
imprecise articulation.
Neurological examination showed a mild facial palsy of upper
motor neuron type. No deviation was noted on tongue protrusion,
and wiggling and elevation of the tongue could be performed
normally. Sensory function of the oral cavity was normal. Palatal
and pharyngeal movements were normal without dysphagia as was
also demonstrated by larygoscopy. There was no indication of
orofacial apraxia, nor were there any signs suggestive of other
cranial nerve involvement. Motor or sensory functions of all four
limbs were normal.
Speech was characterized by a prolongation of sounds, distorted
phonemes, and monotonous pitch, but without paraphasia. The
changes were so dramatic that it was difficult for his friends and
family members to recognize the man by his voice alone. Handwriting and verbal comprehension was perfect.
MRI taken on the next day after admission disclosed a small
subcortical infarction confined to the depth of the central sulcus,
extending partially to the precentral and postcentral gyri (Fig. 2).
DWI showed a high intensity area at the same region, indicating
that this lesion emerged recently and was responsible for the dysarthria and facial palsy.
By one month, speech was still slow but had largely recovered.
Iteration of syllables (/pa/, /ta/, /ka/) was difficult and irregular,
especially when production of these sounds in rapid sequence was
required (such as articulating /tatata..../, or /pataka/, /pataka/, ....).
The patient could repeat /pa/ at a rate of 4 Hz, while repetition of /
ta/ and /ka/ could be achieved at a maximal rate of 2–3 Hz with
some hesitation. This was due to impairment in lifting the root of
tongue against the posterior part of upper palate and, to a lesser
extent, in thrusting the tip of tongue against the back of the upper
teeth, resulting in defective palatolingual closure not only at the soft
palate but also at the hard palate.
j Case 3
A 27-year-old left-handed man was referred to our hospital on 29
November, 1984, because of repeated attacks of weakness involving
the right upper and lower limbs, difficulty in handwriting for small
letters, and a severe dysarthria mimicking speech arrest, which all
cleared within several minutes.

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Fig 3 T2 weighted images of Case 3. Transverse (upper two figures), coronal
(lower left) and sagittal (lower right) scans are shown. Arrows indicate the
location of the lesion
Fig 2 T2 weighted and DW images of Case 2. Transverse (upper left figure),
coronal (lower left) and sagittal (lower right) scans for T2 weighted images and
transverse scan (upper right) for the DWI image. Arrows indicate the location of
the lesion
There was no apparent facial palsy or tongue deviation on
protrusion, and the palatal and pharyngeal movements were normal without dysphagia. Gross muscular power of the limbs was
normal, but diadochokinesis and finger tapping was slower for the
right upper limb than for the left. He also perceived slight difficulty
in handwriting.
One month later, he suddenly developed speech arrest after
ingesting alcohol, which lasted for only 4–5 minutes. Handwriting
was normal. On 2 May 1986 (age 29), he noted a tingling sensation
at the tip of right thumb and index finger as well as at the right
mouth angle. Two weeks later, he perceived tremendous difficulty
in handwriting, which now apparently deteriorated. He was
admitted to our department for detailed clinical examination and
possible treatment.
On admission, there was no overt palsy of the facial, palatal,
pharyngeal or tongue muscles. Sensation in the face and the oral
cavity was normal, and there was no sign of other cranial nerve
involvement. Swallowing was normal without dysphagia. Gross
muscular power was preserved proximally in the upper and lower
limbs, but a slight weakness was noted for thumb adduction and
abduction. Dysesthesia was noted around the right mouth angle
and also at the tips of all five fingers of the right hand.
Despite normal motility of the facial, palatal, pharyngeal and
tongue muscles, he found it difficulty to produce sounds like /pa/, /
ta/ and /ka/. Articulation of these sounds in repetitive sequence was
dysrhythmic with hesitation. Comprehension of spoken and written
language was normal, and the deficit was confined to that of verbal
output, especially that of articulation.
Brain MRI disclosed atrophy of the left lateral convexity most
pronounced around the central sulcus. Small T2 weighted high
intensity spots were scattered throughout the white matter, the
most prominent of which was situated at the depth of the lower
central sulcus near the face area of the motor cortex (Fig. 3).
Carotid angiography demonstrated complete occlusion of the left
internal carotid artery at a site where the anterior choroidal artery

branches from its supraclinoid portion. Retrograde filling was noted from the left anterior and posterior cerebral arteries into
branches of the middle cerebral artery.
Since then, he has experienced several episodes of central facial
weakness combined with dysarthria till the age of 43, either with or
without impairment in handwriting. All episodes have cleared
within several minutes.

Methods
The study including the imaging procedure as described below was
approved by the ethical committee of Tokyo University and all
patients gave their written informed consent prior to enrollment.
MRI was acquired with echoplanar imaging (EPI) using the 1.5T
Signa Horizon Lx (General Electric Company, Milwaukee, USA).
Conventional T1 and T2 weighted images of MRI were also obtained in contiguous transverse, coronal and sagittal sections. In
cases 1 and 2, DWIs were also taken within 48 hours of the onset to
disclose any lesion that emerged recently. DWIs were acquired
using a spin-echo sequence, with an echo planar imaging acquisition window. Each slice was interleaved gapless with a slice thickness of 5 mm. The DWI parameters were set at SE-EPI, TR
5000 ms, TE 78 ms, Matrix 128x128, FOV 24 cm, NEX 4,
b = 1000 s/mm2 [19]. The extent of lesions in each case was
overlaid onto a schematically drawn coronal, transverse, and sagittal slices of the brain at the corresponding anterior-to-posterior
coordinate of the brain (Fig. 4A).

Results
The lesions in all three cases involved a region at the
depth of the central sulcus and lateral to the precentral ‘‘knob’’ where the hand motor area is localized

445

Fig 4 A. The extent of lesions in the three cases was overlaid onto a
schematically drawn coronal (upper figure), transverse (middle figure) and
sagittal (lower figure) slices of the brain, gray-scaled according to the degree of
overlap, with darker tints representing more overlap. The region common to all
three cases (shown in black) is located at the depth of the central sulcus, which
is near the face representation of the primary sensorimotor cortex. B. The same
region coincides with the mouth region of human primary sensorimotor cortex
[7] (blue circle) as well as with the activated region during the articulatory/
phonetic production of polysyllables as the produced sequence becomes
complex [15] (yellow zone). This region also lies near the generator of the
magnetic field and cortical activation related to tongue protrusion [22, 29] (red
circle). The activated area in Riecker et al (yellow zone) was not shown on the
sagittal scan because it was not given in the original paper

[20]. This region is near the area generally considered
as the face-M1 [21] and immediately medial to the
tongue motor area [22]. Superimposition of the defined regions again indicated that a region near faceM1 was responsible for dysarthria (Fig. 4A). In all
cases, the extent of lesion spared the main part of the
corticobulbar tract arising from the lower third of M1;
involvement, if anything, was limited to its upper
portion.

Discussion
The three cases showed that even a localized unilateral cortical damage to an area near to the face-M1
can cause severe disturbance of articulation tempo-

rarily mimicking aphemia or speech arrest, although a
generalized perfusion defect in the left hemisphere
could have contributed to the speech problem in case
3. This suggests that a brain region exists near faceM1 for coordinating speech. The discrete lesions in
our cases were remarkably consistent across cases and
located more deep into the central sulcus than those
described by Kim et al. [23]. Thus, the locations rather than the sizes of the lesions were more important
in producing the severe dysarthria in our cases, and
probably represent a ‘‘bottle-neck’’ region for controlling articulation. In case 3, the progression of
symptoms from impaired handwriting to facial palsy
is compatible with cortical ischemia initially affecting
the hand motor area but subsequently extending into
the adjacent face motor area. The preponderance of
left hemispheric lesions in Kim’s and our cases suggest predominant involvement of the left hemisphere
in articulation, although Kim’s cases included some
with right hemispheric lesions. The importance of the
face motor area in articulation may have escaped
recognition because cases with face-M1 lesions show
relatively good recovery from dysarthria within a
short period, possibly because nearby or contralateral
brain regions can take over the impaired function.
Indeed, resection of a relatively large area of the lower
motor cortex seldom leads to persistent dysarthria
[24].
The impairment was clearly limited to the motor
aspect of speech output, while verbal comprehension
and handwriting remained normal, without any signs
of aphasia or pseudobulbar palsy. The clinical features were distinct from those caused by lesions in
Broca’s area, anterior insula [12], or the anterior
operculum [25], or from apraxia of speech associated
with agraphia resulting from a lesion slightly more
anteriorly in the precentral gyrus [5, 26, 27]. Foreign
accent syndrome without aphasia has been reported
to occur in a patient with a lesion localized to the
convexity of the left posterolateral M1 [28], who
showed abnormal prosody but did not present with a
severe loss of speech. Japanese is quite different from
English with segmentation into morae and pitch accent as important features, and it is important that in
case 1 the subject also presented with foreign accent.
The lesion in case 1 therefore may have disrupted this
segmented structure, a feature specific to Japanese
articulation.
Why should such severe dysarthria occur due to a
lesion near the face-M1? Facial palsy does not provide
a sufficient explanation because dysarthria was significantly worse than expected, outlasting the facial
palsy, and articulation of lingual consonants was
affected more than that of labial consonants. On the
other hand, overt tongue palsy as well as palsy of the
laryngeal or pharyngeal muscles was excluded by

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neurological and otolaryngologic studies. However,
impairment of tongue movements in the sagittal plane,
not apparent on routine neurological examinations,
may play an important role in cortical dysarthria [29].
Defective palatolingual contact due to impairment of
tongue movements was observed in patients of aphemia [4] and one of our patients (case 2).
Together with recent functional imaging studies [7,
15, 22, 30], it is plausible to consider that articulation
is heavily represented in the upper tongue motor area
at a site contiguous to face-M1, especially on the left
side. Interestingly, tongue protrusion and production
of the lingual sound /ta/ activates wide regions over
the bilateral bulbar motor cortices, including both the
tongue and lip (face) motor areas. Articulating /ka/
produces a largely asymmetrical activation centered
around the lip area of the motor cortex in the left
hemisphere and the entire tongue motor representation in the right hemisphere [13, 31]. During the
production of polysyllables, the activation gets more
focused to a region near the left face-M1 as the sequence becomes more complex [15], which coincides
strikingly with the overlaid extent of lesions in our
patients (Fig. 4B). Both in humans and primates, regions within M1 where intracortical microstimulation
evokes movements at the mouth angle adjoin those
eliciting movements at the root or tip of tongue [32]
and those active during the masticatory sequence, i.e.

jaw movements [33] and swallowing [34, 35, 36] that
require muscle activation in common with that for
articulation.
Severe dysarthria may also result from functional
isolation of inferior frontal cortex from more
peripheral motor structures in the left and right M1
[2]. In macaque monkeys, face-M1 receives corticocortical inputs from the ventral division of the premotor cortex, whose counterpart cortical regions in
humans are implicated in speech [37]. In patients
with persistent developmental stuttering, the white
matter of speech-relevant brain regions in the left
motor and premotor regions display abnormal fractional anisotropy values, indicating functional disconnection between speech-relevant brain areas [38].
Meanwhile, a tighter cortico-cortical link between the
inferior frontal and primary motor cortices for the
lip/mouth emerges during reading than during tongue
movements [39]. Taking all the above arguments into
consideration, we conclude that a region near to the
face-M1 in the precentral sulcus is responsible for the
control of articulation in humans.
j Acknowledgement We are grateful to Professor John Rothwell
for his skillful editing and useful suggestions regarding the manuscript.

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