Journal of Neurology, Neurosurgery, and Psychiatry 1984;47:1342-1344

Short report

Mutism following left hemisphere infarction
AS DAVID,* I BONE
From the Department of Neurology, Institute of Neurological Sciences, Southern General Hospital,
Glasgow, UK

SUMMARY A case of mutism due to left hemisphere infarction is described. Recovery revealed
mild motor dysphasia. Review of the literature showed that the case resembles aphemia but is
unique by virtue of its duration, and the absence of associated apraxia and paresis.
any limb. Reflexes were symmetrical and the plantar
responses flexor. Indirect laryngoscopy showed normal
larynx and vocal chord movement.
CT scanning without contrast showed a very small area
of reduced density in relation to the left sylvian fissure. A
contrast revealed a large area of
repeat scan inwith
enhancement the left fronto-parietal region extending to

Mutism is a rare clinical entity. It may occur transiently in lesions of Broca's area,' or the inferior
rolandic region.2 We describe a case of total mutism
following left common carotid artery occlusion in
the absence of hemiparesis and oro-bucco-lingual
apraxia which we believe to be due to a highly
specific apraxia of speech.
Case report
A 51-year-old, right-handed housewife, with a history of
controlled hypertension, was on holiday abroad when she
awoke, unable to speak. A relative noticed right sided
facial weakness. On her return, the patient was admitted to
her local hospital and on the 12th day after the onset of her
illness was transferred to this Institute for further investiga-

_

tion.
On admission she was alert and undistressed. Blood
pressure was 140/90 mm Hg. Slight upper motor neuron
facial weakness was detected on the right. She was unable
to speak or indeed utter any sound though she could cough
to command. The patient could not whisper, hum or mouth
words either spontaneously or in imitation. Her comprehension appeared to be good in that she could follow
simple written and verbal instructions. Questions were
answered by nodding "yes" or "no". Writing was printed
initially with some paraphasic errors but was adequate for
day-to-day communication. The patient could perform a
range of buccal, lingual, and facial movements on request.
Such manoeuvres as licking lips and rolling the tongue
were carried out with ease, as were chewing and swallowing. General neurological examination was entirely normal, in particular there was no weakness or dyspraxia of

l

*Present address and address for reprint requests: Dr AS David,
Department of Psychiatry, The Bethlem Royal and Maudsley Hospitals, Monks Orchard Road, Beckenham, Kent BR3 3BX, UK.

Received 2 December 1983 and in revised form 1 June 1984.
Accepted 11 June 1984

Fig CT scan with contrast enhancement showing large
lesion in left fronto-parietal region.

1342

Mutism following left hemisphere infarction
the brain surface (fig). An isotope brain scan showed an
irregular area of increased uptake in the left inferior frontal region. Angiography was performed and though technically difficult showed absent filling of the left common and
internal carotid arteries. There was no evidence of
arterio-venous malformation.
The diagnosis was made of cerebral infarction secondary
to common carotid artery occulsion. Assessment on the
Boston Diagnostic Aphasia Examination one day after
admission showed some auditory comprehension failure on
complex sequential commands and abstract reasoning
material. Reading comprehension and narrative writing
also showed slight impairment. Verbal expression was of
course absent. Follow-up assessment 12 days later showed
substantial improvement to virtually normal in reading,
writing, and comprehension. The patient could write longhand with only a few paraphasic errors. Screening parietal
tests showed no abnormalities. Nevertheless, she was still
mute and remained so for a further 5 weeks, until speech
returned abruptly. Examination at that time revealed
non-fluent, laboured speech with dysprosody, articulation
errors and some phoneme substitutions ("I have
difficult... in finding right words"). Transient word blocking was evident, though repetition reduced errors. Verbal
expression was however functional and easily understood.

Discussion

Mutism is a rare clinical entity. It may occur in
patients with gross dementia, bilateral basal ganglia
lesions,3 pseudo-bulbar palsy,4 or in the syndrome of
akinetic mutism.5 In these instances, the underlying
cause is usually self-evident. Other causes include
psychotic illness,6 elective mutism, relatively common in children,7 and hysteria.8 The above case is
remarkable in that for 7 weeks the patient remained
totally mute in the absence of significant receptive
dysphasia, dysgraphia, dyspraxia or hemiparesis.
Recovery was sudden with only residual language
impairment. The inability to speak with retained
capacity to read, write and understand has been
called pure motor aphasia9 where recovery uncovers
agrammatism and paraphasia. A second pattern of
recovery exists whereby speech, when it returns,
though laboured is not aphasic.23 Terms such as
aphemia,'"01 cortical dysarthria,'2 and pure word
dumbness,'3 have been used to describe this. Many
modern authors regard it as an apraxia of
speech.'4-'6

Recent clinico-pathological studies of lesions in

Broca's area (3rd inferior frontal convolution),''7

showed that many patients were nearly mute at the
onset of their illness but made good recoveries. Most
could utter some sounds or words or were mute for a
few days only. They all had some degree of right
sided motor weakness with one exception,'8 and
prominent oro-bucco-lingual dyspraxia. Our patient
differed in the sustained and absolute nature of her

1343
mutism and the absence of obvious motor or dyspraxic signs. LeCours2 described a case of mutism
without apraxia who recovered without dysphasia
due to a lesion in the inferior rolandic region, sparing Broca's area. Mutism is seen in lesions of the
supplementary motor area,'9 but dysgraphia and
hemiparesis are outstanding. Subcortical lesions give
rise to a variety of language and motor deficits20-22
but not mutism.
Critchley23 stated that even severe aphasics can
say something and that "total speechlessness" usually lies outwith "organic neurology". An appealingly eclectic alternative explanation to our patient' s
mute state was that it was a hysterical reaction to
genuine aphasia. The ability to cough despite apparent aphonia is a classic sign of hysteria though such
patients usually whisper.8
The varieties of emotional response are as
numerous as there are patients, yet common reactions are either frustration, the so-called catastrophic reaction,24 or withdrawal. However, in the
latter, the patient is too embarrassed or depressed to
speak abnormally so withdraws, but in more total
way than just keeping silent, from interpersonnal

communication.6

We postulate that this case of mutism was due to
an apraxia, so localised that it only affected those

movements directly subserving the execution of
speech and voice production. The centre of the
causative lesion probably lies in the inferior part of
the pre-central gyrus,2 overlapping Broca's area yet
not impinging upon the motor area. We wish to
draw attention to this syndrome firstly because it
demonstrates the discreteness of certain language
functions in the brain each of which may be put out
of action by localised infarctions, and secondly
because it may be mistaken for hysteria.
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