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Pediair Neurosurg 1990-91:16:25-31

Cerebellar Mutism after Posterior Fossa Surgery
Donald D. Dietze, Jr., J. Parker Mickle
Department of Neurosurgery, University of Florida, Gainesville, Fla., USA

Key Words. Mutism • Cerebellum • Posterior fossa surgery, complications • Tumor •
Arteriovenous malformation
Abstract. A large midline posterior fossa medulluloblastoma and a cerebellar arteriovenous malformation with
associated clot were moved with postoperative mutism. Mutism was immediate and resolved into an ataxic dys­
arthria with residual mild dysarthria at 3 months. The literature is reviewed, and theclinicopathological and neu­
rophysiological data of cerebellar function in speech are discussed. Acute injury to the midportion of the cerebellum
with or without dentate nuclear involvement can cause a spectrum of speech disturbances. The more widespread the
injury to the midportion of the cerebellum with dentate nuclei involvement the greater the risk of developing
postoperative mutism.

The cerebellum has been associated with a wide range
of speech dysarthrias. These dysarthrias range from a
monotonous, scanning speech to an explosive, hesitant
outburst of speech [1, 2]. Degenerative disorders of the
cerebellum have most commonly been associated with
speech abnormalities, but diffuse or widespread injury
by hemorrhage, infection, or tumor have also been as­
sociated with speech abnormalities.
Mutism can be defined as the inability to produce
verbal output in a cognitively alert patient with the abili­
ty to read and write with intact comprehension and no
evidence of oral apraxia. Posterior fossa lesions causing
speech abnormalities have been attributed to brain
stem, cranial nerve, and cerebellar pathologies. Brain
stem and cranial nerve pathologies causing mutism are
usually associated with other neurologic signs, i.e., longtract deficits or decreased level of consciousness, and
respiratory compromise, respectively.
Transient mutism was recently observed in 2 of our
patients after posterior fossa surgery. Our 2nd case in­
volving an arteriovenous malformation is unique be­
cause all cases reported have involved tumors in the

posterior fossa. This rare phenomenon after posterior
fossa surgery is a dramatic deficit and should be includ­
ed in the preoperative discussion with the patient and
family. We propose a hypothesis for mutism as a result
of cerebellar pathology based on our experience with
these 2 cases.
Case Reports
Case 1
A 7-year-old presented with a chief complaint of severe frontal
headaches associated with intermittent right-arm pain for a duration
of approximately 2 months. His physical examination was pertinent
for mild truncal ataxia and normal speech production.
Preoperative magnetic resonance imaging (MRI) of the head
revealed a large midline posterior fossa tumor with moderate obstruc­
tive hydrocephalus (fig. I, 2). The patient underwent a suboccipital
craniectomy and C l-2 laminectomies in a left-sided modified park
bench position. Intraoperative findings revealed chronic tonsillar
herniation and a widened, thickened vermis. Just beneath the vermian cortex, a soft, greyish tumor was encountered. The tumor was fol­
lowed laterally into both cerebellar hemispheres and anteriorly until
the floor of the fourth ventricle was encountered. The tumor was re­
moved except for a small attachment to the floor of the fourth ventri­
cle. The pathological diagnosis was medulloblastoma.
The patient tolerated the procedure well and was placed in the

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Introduction

26

Dietze/Mickle

a
Fig. 1. Transaxial MRI sections with T2-weighted images demonstrating a large midline posterior fossa tumor, a Entire midportion of the
vermis involved with obliteration of the fourth ventricle, b Tumor encroaching on the tentorial incisura with left superior paravermal involve­
ment.

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pediatric intensive care unit. He was bright, awake and alert, and neurologically intact with moderate truncal ataxia and mild right-arm
ataxia. He was mute with rare incomprehensible sounds, but was able
to read and write with good comprehension and had no evidence of
oral apraxia.
He was treated with spinal and cranial external-beam radiation.

Routine clinic follow-up at 6 weeks revealed resolution of his appen­
dicular ataxia, but with persistence of truncal ataxia and moderate
dysarthria. His dysarthria was characterized by a sparse, slow, and
monotonous speech associated with intermittent explosive-hesitant
outbursts and exaggerated facial grimacing. At 3 months of follow'ttp the patient had almost complete resolution of his dysarthria. MRI

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Fig. 2. Midsagittal (a) and coronal (b) MRI sections with Tl-weighted images demonstrating obliteration of the fourth ventricle by a large
tumor extending superiorly, involving lingula, central lobule, and culmen, and posteriorly, involving declive, folium, and tuber of the vermis.

Cerebellar Mutism

27

Fig. 3. Postoperative MR1 sections demonstrating encephalomalacia of inferior and middle vermis and paravermis. aTransaxialTl-weighted image, b midsagittal Tl-weighted image.

6 months postopcratively showed encephalomalacia in the posterior
fossa around the fourth ventricle and no tumor (fig. 3).

Fig. 4. Transaxial CT section with intravenous contrast enhance­
ment showing irregular enhancement of the midvermis and blotchy
areas of lucency bilateral in the paravermal zones.

The patient was sent for inpatient rehabilitation. At 3 months she
was able to produce all sounds, but had a monotonous, slightly la­
bored, and bradykinetic dysarthria. Her appendicular ataxia had
almost completely resolved, but she persisted to have moderate trun­
cal ataxia requiring mild assistance for ambulation.

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Case 2
A 15-year-old awakened at 0.400 It with an acute severe headache.
Her headache was associated with photophobia and bilateral car
pain. She deteriorated rapidly with loss of consciousness and respira­
tory compromise. At a nearby hospital an emergent computerized
tomography (CT) scan showed acute posterior fossa bleed and acute
obstructive hydrocephalus. An emergent suboccipital craniectomy
and hematoma evacuation with placement of a ventriculostomy was
performed. She awakened slowly over several days. Examination re­
vealed diffuse hypotonia, bilateral appendicular ataxia with marked
truncal ataxia, and mutism. Placement of a right frontal ven­
triculoperitoneal shunt was performed, and she was transferred to the
Shands Hospital at the University of Florida.
A CT scan showed inhomogeneous areas of lucency within both
cerebellar hemispheres adjacent and posterior to the fourth ventricle
(fig. 4). No substantial mass effect was noted. Cerebral angiography
revealed a superior vermian arteriovenous malformation principally
fed by the left superior cerebellar and the right posterior inferior cere­
bellar arteries and minimally by the right superior cerebellar artery
(fig. 5). The patient underwent exploration of the suboccipital defect
in a left modified park bench position. The right posterior inferior
cerebellar artery and the left superior cerebellar artery were identified
and followed to the superior vermal and paravermal nidus. The nidus
was posterior to the fourth ventricle and extended into the area of the
deep cerebellar nuclei. A complete resection of the arteriovenous
malformation was performed without complications. Her postoper­
ative course was unremarkable with no new neurologic deficits. The
postoperative CT scan showed cerebellar encephalomalacia of the
bilateral paravermal hemispheres and the middle superior vermis
(fig. 6). The ventricular size was normal.

Dietze/Mickle

28

r

Fig. 5. Lateral vertebral angiography demonstrating a posterosuperior vermian arteriovenous malformation nidus principal­
ly led by the left superior cerebellar and the right posterior inferior
cerebellar arteries, extending intraparenchymally adjacent to the den­
tate nuclei.

Discussion
A review of the literature disclosed 19 cases of tran­
sient mutism after surgical removal of posterior fossa
tumors. Rekate el al. [3] reported 6 cases of children with
mutism which lasted 1-3 months. All of the children
were severely dysarthric during recovery. Volcan et al. [4]
reported a case of transient mutism after surgical
removal of a posterior fossa tumor. Humphreys [5]
reported 5 cases of postoperative cerebellar mutism in
children recovering from posterior fossa surgery. This
author comments that 3 of his cases had delayed onset
of mutism. These delayed cases were associated with
postoperative neurologic decline, except 1 case who had
documented residual hydrocephalus requiring shunting
2 weeks later. These cases still had resolution into a cere­
bellar dysarthria with complete or near complete recov­
ery. Humphreys [5] also comments on 4 cases reported
by Yonemasu with ‘giant’ fourth ventricular tumors.
These patients developed postoperative mutism which
occurred after a brief interval of normal speech perfor­
mance. The mutism resolved into a cerebellar dysarthria
within 1-3 months and continued to complete or near
complete resolution. Ferrante et al. [6] most recently
reported 3 cases of transient mutism after surgical
removal of large midline cerebellar pilocytic astrocyto­
mas. The mutism in their cases evolved after a ’clear’
interval of speech production of 36-48 h. The cases
reported of transient mutism with a clear interval
involve a secondary insult such as meningitis or
hydrocephalus. A synopsis of the pertinent clinical
characteristics of these cases and our 2 cases are listed in
table 1.
Postoperative evaluation of this complication in­
cluded speech therapy, clinical psychology, CT, elec-

Fig. 6. Postoperative transaxial CT section demonstrating cncephalomalacia of the posterosuperior vermis and the adjacent
paraverntal zones.

Age, years
Range
2-15
Mean
7.5
Diagnoses
Large midline 4th ventricle tumors
Medulloblastomas
11
4
Ependymomas
5
Cystic astrocytomas
20
Total
1
Vascular malformation with hemorrhage
Duration o f mutism
Range from
3 weeks to 7 months
3 months
Mean

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Table 1. Synopsis of the reported cases (including our 2)

Cerebellar Mutism

29

troencephalography, indirect laryngoscopy, brain stem
evoked response potentials, carotid ultrasound, and spi­
nal myelography. Speech evaluation and indirect laryn­
goscopy showed no evidence of oropharyngeal or laryn­
geal musculature abnormalities or vocal cord abnor­
malities. Clinical psychology could not support a diag­
nosis of depression and conversion reaction. Evoked
potential responses revealed no brain stem abnormali­
ties, and electroencephalography revealed no seizure ac­
tivity. Spinal myelogram and carotid Doppler studies
were normal, and a CT scan revealed expected postoper­
ative changes. Thus, the conclusion of the extensive
evaluations was that the mutism was of cerebellar
origin.
The association between cerebellar lesions and
defects of speech production has long been recognized
and reported with a multitude of cerebellar diseases. In
1823 Flourens described the tremor, staggering gait, and
slurred speech accompanying cerebellar disease. In 1917
Holmes [7] reported that speech associated with gun­
shot wounds to the cerebellum was slow, drawling, and
monotonous with an unnatural separation of the sylla­
bles and a jerky, often explosive articulation. This
author concluded that speech production was more seri­
ously affected when vermis and mesial hemispheres of
the lateral lobes of the cerebellum were injured. Speech
in bilateral cerebellar lesions in 2 patients was so in­
distinct that it was scarcely intelligible [7]. Homes [8] in
his classic article for the Croonian Lectures in 1922
reiterated these observations, but also commented that
disease limited to one lateral lobe could affect speech
production.
Amici et al. [9] reviewed 250 patients with cerebellar
tumors prior to surgery and found the highest incidence
of dysarthria with lesions in paravcrmal and lateral ele­
ments of the hemispheres. Multiple studies reporting on
cerebellar hemorrhages implicate unilateral left-sided
lesions associated with speech disturbances [10-14], Gil­
man and Lechtenberg [12] and Lechtenberg and Gilman

[15] present good evidence in nondegenerative diseases
of the cerebellum that damage to t he superior portion of
the left paravermal cerebellar hemisphere is associated
with disturbance of speech production (fig. 7). Neu­
rophysiologic studies with auditory and laryngeal nerve
stimulation show inputs into this superior paravermal
segment of the left hemisphere [16-18].
The clinicopathological and neurophysiological data
localize speech modulation to the midportion of the left
paravermal area. Kent and Netsell [1] have described the
role of the cerebellum in speech as to supplement and re­
vise as necessary the basic cortically generated motor
program by monitoring the positions of the speech or­
gans and generating appropriate motor instructions to
realize the articulatory targets. With respect to the lon­
gitudinal-zonal organization of the cerebellum, the
paravermal zone is involved in a closed sensorimotorcerebellar-sensorimotor loop capable of updating the
cortically generated programmed movement based on
the integration of central and peripheral inputs [19],
In this extensive investigation of disturbances in cere­
bellar lesions mutism is not described. However, mutism
of cerebellar origin cannot be discarded. Fraioli and
Guidetti [20] in their report on the effects of stereotactic
lesions of the dentate nucleus for dyskinetic syndromes
report 2 cases of transient mutism as a complication (for
1 and 3 months, respectively). Tolbert et al. [21] present­
ed evidence that the dentate nucleus has nucleocortical
projections over large areas of the ipsilateral cerebellar
cortex, including the vermis, and that the dentatonucleocortical projection to the mesial cerebellar
hemispheres was large as compared with the nucleo­
cortical projections from the interposed and fastigial
nuclei. The implication of this evidence is that the
higher primate cerebellum functionally may not con­
form to the longitudinal-zonal organization and that
the dentate efferent output would be expected to affect
cerebellar cortical integration not only in the neocere­
bellum but also in the paleocerebellum. Morphological­

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Fig. 7. Schematic illustration showing the posterosuperior
surfaces of the cerebellum. The stippled area in the left palaver
mal region of simple lobule and superior and inferior semilunar
lobules is the proposed area involved in speech disturbances
from cerebellar pathology and with extension into the dentate
nucleus possibly in cerebellar mutism.

30

Dietze/Mickle

Conclusion
Mutism as an apparent result of cerebellar injury has
been documented in 19 cases plus our 2 cases. This
mutism is not restricted to tumor pathology, but may
be associated with any acute pathological insult to the
midportion of the cerebellum. Mutism is a failure to
produce comprehensible sounds in a cognitively alert
patient with apparent normal functional ability of lips,
tongue, and laryngeal musculature, though there may be
an associated dysphagia. The mutism resolves com­
pletely or to a mild cerebellar dysarthria over a 3-month
period. The failure to produce speech appears associat­
ed with the inability to coordinate articulatory postures
in order to produce enough subglottic pressure for the
production of sound.
The midportion of the cerebellum is at risk of injury
in midline fourth ventricular tumors, especially midline
medulloblastomas. Review of the microsurgical anato­
my shows the close relationships of the superior medul­
lary velum, the cerebellar peduncles, and the midpor­
tion of the vermis (declive, folium, and tuber) [26], The
adjacent paravermis consists of the simple lobule and
the superior and inferior semilunar lobules. The mid­
portion of the cerebellum is generally involved in fourth

ventricular tumors, and if the vector force of tumor
growth extends to the inferior part of the roof of the
fourth ventricle, the dentate nucleus may be involved.
Dandy [27] warns to carefully avoid the dentate nuclei
upon splitting the vermis. The dentate nuclei are located
just rostral to the superior pole of the tonsils and are
wrapped around the superolateral recess of the ventricle
near the inferior medullary velum.
Acute injury to the midportion of the cerebellum
with or without dentate nuclei involvement can be
responsible for a spectrum of speech disturbances. The
more widespread the injury to the midportion of the
cerebellum with dentate nuclei involvement, the greater
the risk of developing postoperative mutism. Mutism is
such an overwhelming deficit that this possible compli­
cation after posterior fossa surgery should be discussed
as part of the preoperative planning.

Acknowledgments
The authors would like to thank David A. Peace, MS. for the con­
tribution of his superb illustration and Robert T. Watson, MD,
Professor of Neurology, for his critique of and his excellent advice on
the organization of this manuscript.
An abstract of this manuscript was submitted to the 42nd Annual
Meeting of the Southern Neurosurgical Society and accepted for
presentation as part of the scientific program on March 30, 1990. at
the Casa Marina Resort, Key West, Fla., USA.
An audiocassette recording of ‘Cerebellar Mutism as a Result of
Posterior Fossa Surgery’ was made for the Topics of Neurosurgery
Audio Cassette Journal on April 1, 1990.

References
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ly, the demate can be divided into a ventrolateral region,
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Brown [22], with reference to the paper by Snider and
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ments by the motor system [24, 25].

31

Cerebellar Mutism

Editorial Comment
With the recent reports o f the uncommon problem o f
mutism appearing after posterior fossa surgery, neuro­
surgeons fee! somewhat relieved that the disorder is
recognized (even though its explanation is still lacking)
and, most o f all, that recovery can be anticipated.
The 2 cases reported here are in the first instance typi­
cal o f those documented earlier in that a targe midline
posterior fossa tumor was responsible fo r the patient’s
postoperative complication. The second case is more in­
triguing to me as this is the first to my knowledge in
which a ruptured cerebellar arteriovenous malformation

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27 Dandy WE: The Brain. Hagerstown, Prior publishing, 1966, pp
452-458.

Donald D. Dietze, Jr., MD
Department of Neurosurgery
University of Florida
Box J-265
J. Hillis Miller Health Center
Gainesville, FL 32610 (USA)

has allegedly caused the mutism which in turn was de­
tected prior to any operative intervention. In neither in­
stance was there another parallel complication (infec­
tion, hydrocephalus, postoperative hematoma) which
must in all o f these cases be sought and remedied.
This second case provides a convincing argument for
disruption o f paravermian tissues as being the anatomic
substrate fo r the ‘cerebellar mutism’. The authors have
explored that matter in detail. Yet consider all o f the
pathological processes and surgical incursions in the
cerebellar midline, and just how infrequent mutism actu­
ally is. Why?
Robin R Humphreys, MD

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