Case Report
Cerebrovasc Dis 2000;10:155–157

Received: December 18, 1998
Accepted: June 15, 1999

Diffusion-Weighted MRI in
Acute Mutism
K. Blanc-Lasserre a N. Nighoghossian a, c L. Derex a P. Lucain b
F. Turjman b, c Y. Berthezene b, c J.C. Froment b, c P. Trouillas a
a Cerebrovascular Disease and Ataxia Research Center, Lyon and b Department of Radiology,
c Creatis UMR CNRS 5515, Lyon, France

Abstract
Mutism defined as a complete loss of speech may be
related to psychiatric or neurologic disorders. The ischemic stroke origins of mutism are often difficult to assess
at the acute stage. Accordingly, the search for the underlying mechanism as the localization of the damages
may be difficult by conventional radiological techniques.
Diffusion-weighted (DWI) MRI may accurately identify
patients with acute ischemic stroke and distinguish them
from those who mimic acute stroke better than clinical
and conventional neuroradiological methods. This report aims to demonstrate the utility of DWI-MRI in the
diagnosis of acute mutism.
Copyright © 2000 S. Karger AG, Basel

Acute mutism, defined as a complete loss of vocalization and speech has been related to psychiatric or neurologic disorders [1]. Diffusion-weighted MRI (DWI-MRI)
may be more useful to accurately identify patients with
acute ischemic stroke and distinguish them from those
who mimic acute stroke than clinical and conventional
neuroradiological methods [2].
The present report aims to demonstrate the utility of
DWI-MRI in the diagnosis of this equivocal clinical syndrome.

ABC

© 2000 S. Karger AG, Basel
1015–9770/00/0102–0155$17.50/0

Fax + 41 61 306 12 34
E-Mail karger@karger.ch
www.karger.com

Accessible online at:
www.karger.com/journals/ced

MRI Studies
MRI was performed on a 1.5-tesla unit (Siemens AG, Erlangen,
Germany) with a circularly polarized head coil. In addition to diffusion-weighted echo-planar imaging (DWI-EPI), a T2-weighted Turbo
spin echo (T2-TSE) and a three-dimensional time-of-flight (3D TOF)
Turbo MRA were acquired. The technical parameters were as followed:
T2-TSE: TR 3,000 ms; TE 98 ms; flip angle 180°; matrix 200 !
512; field of view 250 mm; excitation 2; 20 axial slices; slice thickness
5 mm; acquisition time 4 min 7 s.
3D TOF Turbo MRA: TR 35 ms; TE 6.4 ms; flip angle 20°;
matrix 160 ! 512; field of view 230 mm; excitation 1; acquisition
time 6 min 14 s. Three axial slabs (thickness 31.9 mm, partition 24;
distance factor –0.38) were placed over the entire circle of Willis.
MIP reconstruction was used for postprocessing.
EPI isotropic diffusion: TR 4,700 ms; TE 118 ms; 20 axial slices;
thickness 5 mm; matrix 96 ! 128; field of view 230 mm; excitation
1; acquisition time 23 s. On vision system two b values were used
(0 and 1,000 s/mm2). The MR diffusion sequence at b = 1,000 s/mm2
was run three times with diffusion gradients applied in each of the x,
y and z directions.

Case Reports
Case 1
A 28-year-old right-handed obese woman who smoked and was
under an oral contraceptive presented with a sudden complete loss of
speech associated with severe anxiety. Six hours later, she was alert
and fully oriented, she had a nonfluent aphasia characterized by
sparse verbal output and considerable effort to produce words. Naming and repetition were mildly impaired, the comprehension of spoken and written language, and writing were spared. Speech was mildly
dysarthric. No paraphasia, apraxia or motor deficit were observed.

Dr. N. Nighoghossian
Service d’Urgences Cérébrovasculaires
Hôpital Neurologique, 59, bd Pinel
F–69003 Lyon (France)
Fax +33 72 35 73 29

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Key Words
Diffusion-weighted MRI W Acute mutism W Stroke

a

b
Fig. 1. a Conventional T2-weighted MRI showing a doubtful abnormality on a single slice within the left premotor
cortex. b DWI-MRI showing an obvious ischemic lesion within the left frontal operculum.

a

Fig. 2. a Conventional T2-weighted MRI:
ischemic lesion involving the left caudate
nucleus and the insula. b DWI-MRI showing
a larger lesion through the left middle cerebral artery territory and an additional contralateral ischemia within the right primary
motor cortex.

Cerebrovasc Dis 2000;10:155–157

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b

Case 2
A 41-year-old right-handed woman developed a left-sided weakness 2 h after a road accident with whiplash injury. On admission 3 h
later, she was mute, while comprehension was normal. Neurological
examination showed a severe facial diplegia, affecting the mouth
more than the eyes. The jaw reflex was brisk, and an invincible trismus was present. The patient was unable to swallow. A right gaze
palsy and a prominent left upper limb weakness with a left Babinski
sign were noted. Monitored blood pressure was below 160/80 mm
Hg. Body temperature was 37 ° C. Cardiovascular examination,
ECG, chest X-ray, serum electrolytes, blood sugar levels and routine
coagulation studies were normal. A brain CT scan performed 3 h
after the onset showed early ischemic changes limited to the left sylvian area. Conventional T2-weighted MRI performed 6 h after stroke
(fig. 2a) depicted an ischemic lesion located exclusively within left
hemisphere and involving the caudate nucleus and the insula. DWIMRI (fig. 2b) showed a larger lesion through the left middle cerebral
artery territory and additional contralateral ischemic damage within
the right primary motor cortex. MRA showed bilateral cervical internal carotid artery dissection.

References

DWI-MRI in Acute Mutism

Discussion

These data first draw attention to the potential of
DWI-MRI as a sensitive detector of ischemic brain injury
[3]. In our cases, brain CT scans performed 4 and 3 h after
onset and conventional T2-MRI performed after 6 and
20 h, respectively, lacked sensitivity to detect ischemia
and explain the cause of acute mutism. These findings are
consistent with recent data [4, 5] indicating that with CT
scan, 30–60% of the ischemic lesions are missed in the
acute stage, and that T2-weighted MRI have 20–30%
false-negative results during the first 24 h [6].
The 2 cases had different mechanisms although both
were ischemic. The first case is consistent with the diagnosis of motor aphasia [7]. This acute loss of speech, extending to delayed initiation of language, usually occurs after a
lesion of the left frontal operculum.
In the second case, mutism was related to an acute
pseudobulbar palsy. This syndrome is usually explained
by acute damage to the corticonuclear tract on one side
when contralateral fibers have previously been interrupted or by recent acute lesions. DWI-MRI disclosed a
contralateral insult to the corticonuclear fibers. This acute
combination is rare, but it could be expected, as the stroke
was related to a bilateral internal carotid artery dissection.

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Monitored blood pressure was below 130/70 mm Hg. Body temperature was 37 ° C. Cardiovascular examination, ECT, chest X-ray, complete blood count, chemistries, coagulation studies and brain CT performed 4 h after the onset were normal. Twenty hours after the onset,
while the symptoms persisted, Conventional T2-weighted MRI
showed a questionable left premotor cortex hypersignal (fig. 1a)
whereas DWI-MRI definitively demonstrated ischemic damage
within the frontal operculum (fig. 1b). MRA was normal, transesophageal echocardiography revealed a patent foramen ovale and an
atrial septal aneurysm.