Copyright I Munksgaard 1999
ACTA NEUROLOGICA
SCANDINAVICA
ISSN 0001-6314

Acta Nerirol Scund 1999: 99: 77-79
Printed in U K - uN rights reserved

Case report

Right parietal infarction with concomitant
rnutisrn
Chaudhuri JR, Anand J, Shivshankar N, Jaykumar PN, Suvarna A, Murali T,
Taly AB. Right parietal infarction with concomitant mutism.
Acta Neurol Scand 1999: 99: 77-79. C Munksgaard 1999.

Right brain damage results in a variety of cognitive and behavioural
dysfunctions. Mutism however, has been described only with left or
bihemispheric lesions involving the parietal lobe. We report an elderly man
who had left faciobrachial monoparesis and concomitant mutism. His
auditory-verbal comprehension was intact. MRI revealed a right parietal
infarct involving the cortical and subcortical regions. Recovery from mutism
during the course of treatment was abrupt and complete with no residual
dysarthria. A possibility of diaschisis or impaired modulation of left
hemispheric function due to right cerebral infarct, presenting as conversion
reaction, is proposed for this rare association.

Right brain damage results in a variety of cognitive
dysfunctions that include disturbance in spatial
behaviour, anosognosia, confusion, flat affect
and abulia (1). Conversion disorder is frequently
associated with comorbid neurological diseases;
however, conversion symptom as a manifestation of
stroke is rare (2). A variety of language and
communication problems could be due to conversion reaction but mutism presenting as a conversion
reaction is exceptional. We report an elderly man
who acquired left faciobrachial monoparesis following a right parietal infarct and developed
mutism concomitantly. The pathophysiology of
this association is discussed.

Case report

A 50-year-old gentleman presented with sudden
onset of inability to talk and non-progressive
weakness of the left upper limb of 2 days’ duration.
He denied having hypertension, diabetes, ischemic
heart disease or past history of any neurological or
psychiatric illness. He was a smoker and a social
drinker. He was a right-handed, monolingual
(Kannada, a south Indian language) agriculturist

J. R. Chaudhuri’, J. Anand’,
N. Shivshankar4, P. N. Jaykumar3,
A. SuvarnaZ,T. Murali’, A. B. Taly’
Departments of ’Psychiatric & Neurological
Rehabilitation. ‘Neurology, 3Neurorad~ology.and
4Speech Pathology, National Institute of Mental
Health and Neuro Sciences. Bangalore 560029, India

Key words right parietal infarct. rnutism. diaschisis
Dr Arun B Taly. Additional professor,
Department of Neurology, Nimhans, Hosur Road,
Bangalore-560029, India
Accepted for publication September 9. 1998

with no formal education. He did have a family
history of left handedness in his paternal uncle.
Neurological examination revealed a conscious
alert patient with normal attention span. His
auditory and verbal comprehension was intact
with a score of 10/10 on Western Aphasia Battery
(Kannada version) but he was unable to verbalize or
vocalize and was totally mute. He could cough and
the palatal and gag reflexes were normal. He had no
orofacial apraxias and other fronto-parietal lobe
functions were normal. Visual memory was intact.
He had left-sided facial weakness and left brachial
monoparesis (2/5 MRC grade) with decreased
sensory perception in the same limb. Cardia was
clinically normal and there was no carotid bruit. Non
contrast CT scan showed hypodensity in the right
parietal region suggestive of infarct in the right
middle cerebral artery territory. Right parietal
infarct could not explain the mutism in the patient
and hence an MRI was done on the 14th day of
illness which showed a recent infarct in the right
parietal region (Figs. 1, 4) involving the cortical and
subcortical regions, an old lacunae in the left frontal
periventricular region (Fig. 2) due to the occlusion
of the terminal branches of the left lenticulo striate
arteries along with an old right cerebellar infarct
77

Chaudhuri et al.

Fig. 1. An acute infarct in the right parietal lobe with
effacement of the sulci (arrow). T, weighted image.

(Fig. 3 ) . Electrocardiogram and echocardiogram
revealed an old anterolateral wall ischemia and
aortic sclerosis respectively.
The patient was neurologically stable for 4 days
and was then transferred to a rehabilitation unit.
He communicated through gestures. He was
amotivated and reluctant to participate in any of
the rehabilitation programmes. In view of the
atypical presentation, mutism as a conversion
reaction was considered. During one of the
speech training sessions, the patient was asked to
initiate sounds which he was able to do. Soon after,
he produced bilabial sounds like Pa, Papa later Ba
and PaBa then to Ma. Subsequently word level and
sentence repetition were tried and the patient did it
with ease after which a spontaneous conversation
was held between the patient and the therapist
without any dysarthria, dysprosody or dysphonia.
Complete speech recovery occurred during the
same session. He had depressed but reactive affect
without psychotic features. His cognitive functions
were intact. He had significant stress regarding
financial and family matters.

Fig. 3. T, weighted transverse section through the posterior
fossa shows an old infarct in the right cerebellum.

78

Fig. 2. A lacunae is seen in the left-paraventricular region
(arrow head). T, weighted image.

Discussion

This patient had left-sided faciobrachial monoparesis due to right parietal infarct with concomitant
mutism.. A diagnosis of conversion disorder was
suspected when cranial CT and MRI failed to
disclose any recent left hemispheric lesion (Fig. 1Fig. 4). Recovery on the 9th day was rather abrupt
and complete. Subsequent interview revealed stress
factors and depression.
The majority of patients with conversion disorder usually have a well-documented medical or
neurological comorbid condition and typically
there is an elaboration of symptoms stemming
from the original organic lesion. Aphonia is one of
the common motor symptoms of conversion disorder (2). Alexia, agraphia and aphemia are the
other language dysfunctions that present as conversion disorder but mutism presenting as a
conversion disorder is very rare. The anatomical
substrate of conversion disorder is not precisely
known. The preponderance of left-sided, unilateral

Fig. 4. Dark fluid attenuated inversion recovery (coronal
image) shows a distinct wedge shaped hyper intense infarcted
lesion in the right parietal lobe.

Right parietal infarct with mutism
symptoms seen in conversion disorder and the
strong association of depressive disorders with it
point to non-dominant right hemispheric vulnerability.
Anatomic basis of mutism has not been defined
precisely. Mutism can be produced by lesions
affecting the dominant inferior frontal motor and
underlying white matter but sparing Broca’s area.
Patients recover from these lesions with slow
hypophonic dysarthric speech ( 3 ) . Lesions in the
supplementary motor area of the dominant hemisphere can also cause mutism (4). In pseudobulbar
state, mutism can occur in lesions involving the
limbic brain stem pathways (5). Akinctic mutism
has been reported with lesions in bilateral frontal
lobe, cingulate, orbital gyri and septa1 areas (6).
Acute bilateral cerebellar lesions damaging the
deep dentate nuclei can cause temporary speech
loss with a severely dysarthric recovery (7).
Catatonic depression, schizophrenia and rarely
psychogenic illness are the psychiatric causes of
mutism (5).
This patient had normal comprehension with
mutism and right parietal lesion. Though the MRI
showed an old lacunar infarct in the left periventricular region (Fig. 2), it could not explain the
present episode of mutism with abrupt recovery.
The comorbid association of left faciobrachial
weakness and mutism thus could not be explained.
Atypical symptoms with comorbid neurological
disease, not explained by appropriate investigations can be a conversion disorder.
Right hemisphere modulates left hemispheric
functions through interhemispheric white matter
projections. Sudden right hemispheric insult can
suppress left hemispheric functions, albeit transiently, a phenomenon referred to as diaschisis.
Hemispheric infarctions can produce reduction of
cerebral blood flow and metabolic rate in the

contralateral hemisphere and contralateral cerebellum (8,9). Mutism in our patient may be a result
of right parietal infarction leading to suppression of
left hemispheric function. Thus, the sensory and
motor symptoms of conversion suggest defect in
the processing and analysis of sensorimotor signals
and failure in integrating endogenous somatic
signals (2). It remains to be established whether
mutism in this patient indicated a dependent sick
role to avoid the stressors temporarily or was it due
to the right hemispheric lesion which compromised
the function of the homologous left brain and
evolved as a conversion reaction in the form of
mutism?

References
1. CALVANIO
R, LEVINF
D, PETRONE
P. Elements of cognitive
rehabilitation after right hemispheric stroke. In: BRUNBACK
KA, ed. Behavioural Neurology, Neurologic Clinics. Philadelphia. WB Saunders 1993:25-54.
FG, SMITHGK. Somatisation disorders. In:
2. GUGGENHEIM
KAPLAN
M, SADOCK
BJ, eds. Comprehensive textbook of
psychiatry. 6th ed. Philadelphia. Williams and Wilkins
19951251-70.
3. SCHIFF
MR, NAESER
MA, GALABURDA
AM.
HB, ALEXANDER
Aphemia: Clinical anatomical correlations. Arch Neurol
1983;4O:720-7.
JC, SCHOENE
WC, FUNKENSTEIN
4. MASDEU
H. Aphasia following
left supplementary motor area. Neurology 1978;28:1220-3.
5. DEVINSKY
0. Behaviour Neurology. New Delhi: BI Publications 1994:100-3.
6. Ross ED. The Aprosodias: Functional-anatomic organisation of the affective components of language in right
hemisphere. Arch Neurol 1981;38:561.
7. KEKATE
HL, GRUBB
RL, ARAMDM, HAHNJF, RATCHESON
RA. Muteness of cerebellar origin. Arch Neurol
1985;42:697-8.
WJ, RAICHLE
8. POWER
ME. Positron emission tomography and
its application to the study of cerebrovascular diseases in
man. Stroke 1985;16:361-76.
9. FEENAY
DM, BARON
JC. Diaschisis. Stroke 198617817-30.

79