B ritish Journal of N eurosurgery (1997);11(2):161± 163

S HORT REP ORT

C erebellar m utism with subsequent dysarthria in an adult: case
report
G. W. D UNW OOD Y, Z. S. ALSAGOFF & S. Y. YUAN

Br J Neurosurg 1997.11:161-163.
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D ivision of N eurosurg ery, N ational University Hospital, Singapore

A bstract
An adult case of mutism and subsequent dysarthria after posterior fossa surgery is presented. An EEG perform ed during
the mute phase showed widespread left hemisphere abnormality although the CT ® ndings were normal. The possible
m echanisms underlying this syndrome are discussed.
K ey w ords: EE G abnorm ality, m utism , posterior fossa surgery

Introduction
T ransient m utism has been reported in children
undergoing posterior fossa surgery for excision of
intrinsic tum ours. 1,2 T ypically, the child develops
m utism several hours to a few days after surgery,
and seem s apathetic and withdrawn. Gradually,
speech returns, but initially it is dysarth ric and
eventually recovers to norm al over 3± 8 weeks. T his
syndrom e is usually associated with surgery for excision of midline intrinsic tum ours, typically m edulloblastoma. 1 Mutism with subsequent dysarthria
(M SD ) has rarely been reported in adults. 3,4 W e
describe a case and discuss the possible m echanism s
underlying this syndrom e.

C ase report
A 53-year-o ld C hinese m ale presented with acute
onset of headache, vom iting and slurred speech. He
had a past history of hypertension. On admission he
had m ild right-sided cerebellar ataxia and som e
slight slurring of speech. CT performed on
adm ission and M RI subsequently (Fig. 1) showed
an intracerebellar haem atoma in the verm is and
bilateral paravermian region particularly on the
right. Angiograph y showed an arteriovenous m alform ation (AVM ) arising from a distal branch of the
superior cerebellar artery on the right (Fig. 2).
The patient required a VP shunt for hydrocephalus 4 days after adm ission, but was w ell
enough to undergo de® nitive excision of the AV M

on day 19 at w hich time speech was slurred, but
otherwise norm al. At operation an AVM involving
the superior third of the right side of the cerebellar
verm is w as excised without com plication. The procedure was prolonged and postoperatively the
patient was electively ventilated. After weaning from
the ventilator the next day he was noted to be m ute
although he understood com mands. In addition he
had severe weakness of the right arm .
The initial clinical im pression was of a left hemisphere cerebral vascular accident (CVA). However,
C T perform ed post operatively (Fig. 3) did not
show any evidence of infarction. W ithin 3 days the
arm began to recover and rapidly regained norm al
strength although it was very ataxic. However, he
rem ained m ute for 3 weeks and when his speech
returned it was very dysarth ric and staccato in
nature. This took som e weeks to recover but when
reviewed 2 months postoperatively it had returned
to norm al. He rem ained, how ever, m oderately
ataxic. An EEG perform ed during this prolonged
m ute phase showed widespread abnorm ality in the
left frontal and temporal region with w idespread left
hem isphere slow w aves (Fig. 4).
Postoperative angiography con® rm ed com plete
excision of the AVM .
D iscussion
T his patient displayed the clinical features of what
has been described as cerebellar m utism with subsequent dysarthria (M SD ) syndrom e.1± 5

Correspondence: Mr G. W . Dunwoody, Division of Neurosurgery, National U niversity Hospital, 5 Lower Kent Rd, Singapore
Received for publication 30th January 1996. Accepted 24th May 1996.
0268-869 7/97/020161± 03 $9.50

Ó

T he Neurosurgical Foundation

Br J Neurosurg 1997.11:161-163.
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162

G. W . Dunw oody et al.

F IG . 1. M RI scan showing haematoma in superior cerebellar vermis.

F IG . 3. Plain CT obtained during m ute phase.

F IG . 2 Angiography showing AVM of distal superior
cerebellar artery.

The m echanism of production of this syndrom e is
not clearly understood. T he role of the cerebellum
in speech has long been recognized; Gordon
H olmes described lesions of the cerebellar verm is
asso ciated with dysarth ria in 1922. 6 The superior
verm is has been particularly im plicated in the production of dysarthria. 7 However, mutism is also
described after surgical lesions of the pons 8 and of
the dentate nucleus after bilateral stereotactic
lesions. 9
A patient described by Silveri et al. 10 had a right
cerebellar infarct which was heralded at onset with
m utism for several hours followed by dysarth ria, but
asso ciated with agram matic speech suggesting a lesion m ore com monly asso ciated with Broca’ s area.
T his patient had a SPEC T scan showing decreased
perfusion throughout the w hole left hem isphere.
Previous reports of M SD have predom inantly been

F IG . 4. EEG performed during mute phase showing
widespread left hem isphere slow waves.

in childhood. Van Dongen et al. 1 describe ® ve cases
of M SD after excision of intrinsic posterior fossa
tum our and refer to 36 other cases in the literature.
Interestingly, all ® ve of their cases had severe cere-

Br J Neurosurg 1997.11:161-163.
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Cerebellar mutism
bellar and pyram idal signs in lim bs and trunk after
surgery, having been norm al beforehand. T hese
tum ours were all m edial in position and four of ® ve
w ere m edulloblastom as.
Van D ongen et al. suggested that a ventricular
location, presum ably the roof of the 4th ventricle,
and adherence to the dorsal brainstem were necessary for M SD to occur, that it occurs in asso ciation
w ith a spectrum of severe neurological de® cits and
that it m ay be due to bilateral dysfu nction of the
denticulothalamic ® bre bundles or their cells of
origin.
The time course of onset of this syndrom e is
described as a few hours to a few days after
surgery. 12 O ur patient was electively ventilated postoperatively, thus w e are unable to say if a period of
norm al speech intervened before the onset of
m utism. The EE G ® nding suggests that in our case
the syndrom e was produced not solely from local
injury to the cerebellum (although an anatom ical
site of injury in the superior vermis or along the
cerebellar dentothalam ocortical pathw ay m ay be a
prerequisite for production of the abnorm ality), but
from some distant hemispheric disturbance provoked by the injury. T he time course for developing
the syndrom e suggests an abnormality due to either
oedema or som e disturbance in cerebral blood ¯ ow
as m ight be seen in vaso spasm . T he condition,
however, is m uch m ore prolonged in its clinical
course than is seen in vasospasm after subarachnoid
haem orrhage and appears anatom ically con® ned to
one vascular territory.
W ith evidence of disturbed blood ¯ ows in the left
hemisphere after surgery to the superior cerebellum
it is interesting to speculate w hether pretreating
patients about to undergo surgery such as ours with
nim odopine m ight am eleriorate or prevent the
developm ent of the condition.
D iaschisis or transient contralateral hypo-

163

m etabolism of the cerebellum after lesions of the
cerebral hem isphere is well docum ented w ith PET
studies. 11 W hether this phenom enon occurs in
reverse, that is transient hypo m etabolism of the
contralateral cerebral hem isphere after lesions of the
cerebellum , is not known.

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