J Neurol (2007) 254:676–677
DOI 10.1007/s00415-006-0386-6

A. Hiraga
M. Beppu
T. Uehara
T. Matsunaga

Dysarthria and
paresthesia of the
thumb caused by a
small cortical infarction
Received: 20 March 2006
Received in revised form: 28 May 2006
Accepted: 6 June 2006
Published online: 6 April 2007

Sirs: Based on a functional MRI
study, cortical representation of
the hand is reported to be in the
omega-shaped structure of the
precentral gyrus, the ‘‘precentral
knob’’ [7]. There have been many
recent reports that small cortical
infarctions in this precentral knob
cause isolated hand or finger palsy, but reports of cortical infarction presenting with pure
dysarthria or dysarthria with a
minimum of other neurological
signs are, however, rare [2]. We
describe a case of transient dysarthria with paresthesia of the
thumb caused by an acute, small
distinct cortical infarction in the
motor vocal area. The mechanism
of the close cortical association of
dysarthria and sensory symptoms
of the thumb is discussed.
A 62-year-old, right-handed
woman, with a history of hypertension, suffered dysarthria with
paresthesia of the left thumb while
A. Hiraga, MD (&) Æ M. Beppu, MD
T. Uehara, MD Æ T. Matsunaga, MD
Dept. of Neurology
Asahi General Hospital
I-1326 Asahi
Chiba 289-2511, Japan
Tel.: +81-479/63-8111
Fax: +81-479/63-8580
E-Mail: hiragaa@yahoo.co.jp

LETTER TO THE EDITORS

resting in the morning. The attack
ended within 5 minutes. After
10 minutes, twice she again suffered attacks of dysarthria without
paresthesia or limb weakness
which ended within 10 minutes.
Her husband also noticed her
transient dysarthria. On admission
to our hospital, her blood pressure
was 166/114 mmHg. She was alert
and cooperative and had no facial
paresis, dysarthria, or dysphagia.
There was no deviation of the
tongue on protrusion. Muscle
strength was normal. Tendon reflexes were all normal, and plantar
responses flexor bilaterally. Sensory examination results were
normal. Brain CT detected no
abnormalities. Brain MRI 4 days
after onset showed a hyperintense
lesion in the right precentral gyrus
on diffusion-weighted imaging
(DWI), T2-weighted imaging
(T2WI), and fluid-attenuated
inversion recovery (FLAIR) indicative of an acute stage infarction
(Figure 1). Brain MR angiography
was normal. She underwent oral
anti-platelet therapy and was discharged without neurological deficit 10 days after onset.
Our patient presented with
transient dysarthria without limb
weakness and MRI showed a lesion lateral to the precentral knob.
Her first attack of dysarthria
accompanied the paresthesia of
her thumb.
Most pure dysarthria caused by
cerebral infarction is reported to
be due to corona radiata or internal capsule lesions [1, 4, 6]. Kim
and colleagues reported 5 cases of
pure dysarthria or dysarthria with
minimum symptoms caused by
small cortical infarctions [2]. Two
of them were located lateral to the
precentral knob at the most lateral
part of the imaging, and 3 in the
most lateral cortical area at the
level of the lateral ventricle [2].
The lesions in those 5 cases were

only detectable on DWI, not on
T2WI. In our patient, FLAIR and
T2WI as well as DWI clearly
showed distinct small lesions in
the precentral gyrus lateral to the
precentral knob. Its location between the slice level of the lateral
ventricle and that of the precentral
knob was shown by MRI unlike in
previous cases.
Our patient had the unique
symptoms at onset of dysarthria
and development of ‘‘paresthesia
of the thumb’’ during the first attack. Similar phenomena were
found in 1 of 5 cases by Kim et al.
[2], but their patient had both
thumb and perioral sensory disturbance, and MRI showed more
diffuse lesions. In the human primary sensory cortex, thumb representation has been shown to be
located at the lateral shoulder of
the inverted omega-shape (precentral knob) by a functional MRI
study [3], and thumb sensory somatotopy near the face or tongue
motor cortex by a somatosensory
evoked potentials (SEPs) study
[5]. In this regard, cortical lesions
lateral to the precentral knob may
cause dysarthria due to dysfunction of the motor cortex, and
sensory disturbance of thumb
caused by dysfunction of the sensory cortex. Although sensory
symptoms occurred in our patient
only once in 3 attacks, the patient
had no sensory deficit on examination, and MRI detected no
postcentral gyrus lesions, her case
provides direct clinical evidence of
the closeness of the motor speech
and sensory thumb area locations
in humans and supports previous
findings of functional MRI and
SEPs studies. Dysarthria without
limb paresis rarely is caused by
cortical infarction, but if dysarthria with thumb sensory disturbance is detected, a small cortical
infarction lateral to the precentral
knob area should be suspected.

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Fig. 1 MRI performed four days after onset. (A) Diffusion-weighted image showing a small high signal intensity lesion in the right precentral gyrus. (B) Axial T2weighted image, (C) fluid-attenuated inversion recovery. MRI showing a high signal lesion in the same area

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