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Cerebellar softening.

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Cerebellar Sofiening
G i u s e p p e Scotti, MD, H a n s Spinnler, MD, R o b e r t o Sterzi, MD, and G i u s e p p e Vallar, M D
Twenty-one adults w i t h acute cerebellar softening confirmed b y computerized tomography ( C T ) were divided i n t o
two groups according to clinical course, CT findings, a n d outcome. In the first g r o u p , consisting of 6 patients, the
condition ran a progressive course, w i t h deterioration of consciousness, signs of brainstem compression, a n d the
appearance of hydrocephalus o n CT scan. Three patients u n d e r w e n t surgery successfully, 2 died postoperatively,
a n d 1 recovered spontaneously. In t h e second g r o u p , comprising 15 patients, the course was benign: cerebellar
symptoms and signs improved w i t h o u t surgery, and only discrete cerebellar signs remained a month after onset.
Scotti G , Spinnler H , Srerzi R, Vallar G: Cerebellar softening. Ann Neurol 8:133-140, 1980
Case r e p o r t s o v e r t h e past 30 years have begun to
describe t h e clinical s y n d r o m e of cerebellar infarction [ 18, 291. Before t h e advent of computerized to-
gressive deterioration of consciousness; Group 2 consisted
of 15 patients who had n o deterioration of consciousness.
mography ( C T scanning), vertebral angiography, by
showing occlusion of a vertebral artery or of o n e
of its cerebellar branches, s o m e t i m e s provided
neuroradiological evidence of cerebellar infarction.
Ventriculography i n s o m e cerebellar s t r o k e s s h o w e d
hydrocephalus and obliteration of the fourth ventricle.
R e c e n t p a p e r s have analyzed the clinical a n d CT
features of cerebellar h e m o r r h a g e [20] and infarction
[12]. T h i s r e p o r t assesses t h e contribution of CT
scanning t o diagnosis a n d m a n a g e m e n t of such patients. Up to this time, CT scanning i n acute supratentorial s t r o k e has provided scant assistance i n
therapeutic management. The value of CT i n
providing an indication e i t h e r for cerebellar d e c o m pression and removal o f tissue or for following a conservative course in a patient with cerebellar
s t r o k e has n o t received extensive attention in the
clinical literature. Accordingly, we r e p o r t here our
experience with 2 1 patients having a c u t e cerebellar
Clinical Features and Results
All patients with a clinical diagnosis of stroke and CTdemonstrated softening limited to the cerebellum who
were admitted during the two and a half years before this
writing to the neurological, neurosurgical, or emergency
departments of Milan University were included in this
study. The mean age of the group was 57 years (range, 22
to 75). Fourteen of the patients were men and 7 were
The 21 patients were divided into two groups based o n
their level of consciousness: Group 1 included 6 patients
who were comatose from the beginning or developed proFrom the Department of Neurology, Universiti di Milano, Milan,
Received May 24, 1979, and in revised form Oct 4 and Dec 5.
Accepted for publication Jan 22, 1980.
T h e symptoms and signs at onser are summarized in Table
1. I n 2 0 cases the onset was abrupt and was not preceded
by premonitory symptoms. O n e Group 1 patient suffered
repeated brief episodes of vertigo and unsteadiness during
the two weeks preceding the stroke.
Two comatose patients showed brainstem signs at onset
consisting of contralateral ocular deviation, bilateral miosis,
and occasional nonspecific irregularities of respiratory
rhythm. Four initially noncomatose Group 1 patients
lacked signs of brainstem dysfunction. Among the Group 2
patients, 4 had a pupil smaller on the ipsilateral side, 2 had
ipsilareral sixth nerve palsy, 1 had an ipsilateral lateral gaze
palsy, 1 had ocular opsoclonous (a sign traceable to the
cerebellar lesion itself), and 8 had a peripheral seventh
nerve palsy ( 6 ipsilateral and 2 contralateral).
Course, Surgical Treatment, and Outcome
I n 3 of the 4 initially noncomatose Group 1 patients, about
24 hours passed between the onset of stroke and the beginning of neurological deterioration, while in the fourth
case the interval was about 6 days. After an initially stable
course, these 4 patients over a relatively short period of a
few hours dereriorared and developed signs of brainstem
dysfunction, including ipsilateral gaze palsy, bilateral
miosis, and occasional irregularities of respiratory rhythm.
Five of the 6 Group 1 patients underwent emergency surgery for removal of softened cerebellar tissue; 3 survived.
Two patients died postoperatively; they had pinpoint
pupils, quadriplegia, and irregular breathing. No postmortem examination was possible. O n e patient, whose stroke
had occurred two weeks after a myocardial infarction, did
not undergo surgery: he regained consciousness spontaneously after 10 days, a right hemiparesis and mild cerebellar
signs being present. At l-month follow-up in the 4 surviving patients, only slight arm and gait ataxia were present.
Address reprint requests to H. Spinnler, MD, Department of
Neurology, Universiti di Milano, Via Francesco Sforza 35, 20122,
Mi'ano* Italy'
0 3 6 4 - 5 1 3 4 / 8 0 / 0 8 0 1 3 3 - 0 ~ ~ 0 1'E.l~ 51979 by Hans Spinnler
Table 2. CT Fiudings in 21 Cases of Cerebellar Sofrening
Table I . Symptom and Signs
in 21 Cases of Cerebellur Sojteizirig
No. of Patients
No. of Patients
Clinical Data
Symptoms at onset
N ausedvorniting
Slurred speech
Blurring of vision
Group 1
Group 2
( N = 15)
Signs at onset
Full alertness
Decreased consciousness
Stiff neck
Pupillary disorders
Ocular movement disorders
Seventh cranial nerve palsy
D y sarthriaa
Gaidtrunkal ataxiaa
Limb ataxiaa
Muscle hypotonus
Extensor plantar response
Location of softening
Left hemisphere
Right hemisphere
Triventricular hydrocephalus
Fourth ventricle
Cisterns obliterated
Contrast enhancementb
Group 1
( N = 6)
Group 2
( N = 15)
. . .a
. . .a
"In the 6 Group 1 patients the location, deep or superficial, of the
lesion was not definable.
Group 2, contrast examination was performed in only 4 patients.
911 5
Surgical procedures
Recovery (at 1 mo)
Previous cardiovascular disease
"In the noncomatose patients able to cooperate
Among the Group 2 patients, the neurological picture
improved i n a few days in all cases with disappearance of
brainstem signs. Surgery was never performed. At 1-month
follow-up the 15 patients complained only of varying mild
degrees of unsteadiness. I n all patients, ataxia of one arm
and of gait was elicited.
Two patients in Group 2 were reexamined at longer
intervals. A 29-year-old woman was examined 6 and 12
months after her stroke: at both examinations she had only
dysmerria and hypotonia of the left arm, and had been able
to resume her life as a housewife without limitations. A
69-year-old woman was reexamined at 6, 12, and 24
months. At 6 months she was dysmetric and hypotonic in
all four limbs and had gait ataxia as well as palatal and pharyngeal myoclonus; this was attributed to a deep-seated
cerebellar lesion 113, 15, 161, as no associated brainstem
signs were present. O n e year after her stroke she had gait
134 Annals of Neurology
Vol 8 No 2
August 1980
F i g 1 . C'l' paltern of cerebellar infarction with triventricular
hydrocephalus. (A) Scans i n a 25-year-old woman show arz
ill-defined area of decreased density i n the left cerebellar hemisphere with the fourth ventricle and cisterns obliteruted. ( B ) I n
a 52-year-old woman an area of decreased density i s seen i n the
left cerebellar hemisphere; the fourth veiitricle arid the ambient
and quadrigemiizal cisterns are obliterated
F i g 2. CT pattern in a 62-year-old man with a right cerebellar infarction who experienced spontaneous resolution of
triventricular hydrocephalus. (A) Supraten torial triven tricular
hydrocephalus i s visible on a scan performed 7 days after the
stroke. ( B ) After I month the fourth ventricle is better defined
and is not compvwsed;the third and lateral ventricles have
decreased in size.
ataxia, slight dysmetria of the left arm, and palatalpharyngeal myoclonus; two years after the stroke the picture remained unchanged.
CT Findings
The two groups of patients presented contrasting CT patterns. The C T findings are summarized in Table 2.
The 6 Group 1 patients had large, hemispheric cerebellar
infarctions that appeared as ill-defined areas of decreased
density. In 3 of the 4 patients who were noncomatose at the
onset, CT examination was performed shortly after neurological deterioration was noticed; 1 patient had already
undergone an earlier CT examination during the first hours
after stroke (see Fig 3). In all 6 cases, triventricular hydrocephalus was shown; the fourth ventricle and the quadrigeminal and ambient cisterns were obliterated (Fig 1).
The CT pattern was not specific and simulated that observed with other space-occupying lesions of the posterior
fossa such as medulloblastornas or metastases. In the patient who did not undergo surgery, the hydrocephalus regressed over a few days (Fig 2). In the single patient with a
precoma CT scan (Fig 3), the initial scan performed 2 hours
after stroke was negative; no areas of abnormal density
could be detected in the posterior fossa, although the
fourth ventricle was barely visible. After 24 hours the CT
picture had changed: almost all of the right cerebellar
hemisphere had become hypodense, the fourth ventricle
and posterior fossa cisterns were obliterated, and supratentorial hydrocephalus had developed.
In the 15 patients of Group 2, no mass effect causing
occlusion of the cerebrospinal fluid pathways or triventricular hydrocephalus was detected. The fourth ventricle
was usually only moderately deformed or displaced. The
infarction was small and had a well-defined outline; the location of the lesion varied from deep to cortical but the
vascular territory involved was not well defined (Fig 4). In
1 case contrast enhancement was observed (Fig 5). Angiography was performed in only 1 patient and showed stenosis
of the left vertebral artery at the level of the sixth cervical
vertebra, accompanied by a hypoplastic right vertebral artery.
In all patients the density of the CT shadow varied with
time, becoming more hypodense, with more clearly definable margins, as demonstrated by follow-up examinations
performed from 13 days to two years after the first C T examination in 7 of the 21 patients.
Scotti e t al: Cerebellar Softening
Fig 3. Modijcation of the CT image of a cerebellar softening
i n a 42-year-old man during the first 24 hours after stroke.
(A)Thefirst CT scans, performed 2 hours after the stroke,
show only posstble obliteration of the fourth ventricle but no
definite areas of decreased density i n the posteriorfossa; the
quadrigeminal and ambient cisterns are not obliterated and the
ventricles are of normal size. ( B ) Twenty-four hours later a
large area of decreased density is seen i n the right cerebellar
hemisphere; upward transtentorial herniation of the superior
vemis is vhible; the quadrigeminal and ambient cisterns are
obliterated and the lateral ventricles have enlarged.
F i g 4 . CT pattern of cerebellar infarction without triventricular hydrocephalus. Scans in (A)a 29-year-old woman
and (B) a 69-year-old woman each show a deep area of decreased density in the lef hemisphere, including the middle
peduncle. (C) In a 63-year-old man a superficial area of decreased density is seen in the left hemisphere.
136 Annals of Neurology Vol 8 No
August 1980
Fig 5 . CT pattern in a case of infarction involving the left
cerebellar convexity in a 46-year-old m n . (A) Five days after
stroke the infarcted area is barely recognizable. ( B ) Contrastenhanced scan a t 5 days. (C) Afrer 10 months there is a clearly
recognizable area of decreased density with well-defined margins.
Clinical Features and Prognojis
The clinical findings in these 21 patients most often
included cerebellar signs at onset. In the noncomatose patients the most important differential
diagnosis was from cerebellar hemorrhage. The ciinical patterns at onset of hemorrhagic and ischemic
stroke are summarized in Table 3 , compiled from the
most informative reports in the literature. According
to our analysis, no symptom or clinical sign differentiates cerebellar infarction from hemorrhage with
certainty except perhaps headache, which occurs in
83% of hemorrhages and only 29% of infarcts.
When the onset of stroke is marked only by sudden
coma, as in 2 patients in Group 1, the neurological
picture can be nearly indistinguishable from that of
pontine hemorrhage [9, 281 or some cases of basilar
thrombosis 111.
From the clinical course of our patients, two main
patterns can be distinguished. In Group 1 the course
was that of progressive worsening of a posterior fossa
compression syndrome or of coma from onset. It
Scotti et al: Cerebellar Softening
Table 3. Symptoms and Signs in Cerebellar
Hemorrhage and Infarction"
No. of Patients
(N = 46)
(N = 41)
Symptoms at onset
Slurred speech
Signs at onset
Full alertness
Decreased consciousness
Pupillary disorders
Ocular movement
Seventh cranial nerve
Gaidtrunkal ataxiab
Limb ataxia'
Extensor plantar
16 (35%)
20/33 (61%)
15/30 (50%)
20/32 (62%)
15 (33%)
(5 1%)
15/33 (45%:)
21/33 (64%)
18/33 (54%)
16 (39%)
*The table has been constructed from the following series: cerebellar hemorrhage: kttle et al [201, 10 cases; Brennan and Bergland [2], 12 cases; Muller er al [221, 4 cases; and Rosenberg and
Kaufman [26], 20 cases; cerebellar infarction: Lehrich et al [18], 4
cases; Sypert and Alvord [29], 28 cases; Greenberg et al [12], 6
cases; and Rosenberg and Kaufman [261, 3 cases.
"In the noncomatose patients able to cooperate.
should be noted, however, that brainstem damage
with cerebellar infarction is not always due to compression by a swollen cerebellum: arterial occlusion
producing an associated infarction of the brainstem
is found in more than 50% of the cases occurring
outside the cerebellum [27]. Recently Greenberg
et al [12] have suggested that with cerebellar infarction or hemorrhage, impaired function of supratentorial structures is more important than brainstem
compression in producing neurological deterioration.
In the present series, brainstem signs were present
in all comatose or deteriorating patients, and the
observed bilateral miosis could have been due to
either hydrocephalus C121 or pontine compression.
Our study confirms the frequent association of cerebellar infarction with brainstem involvement but
neither supports nor refutes a role for hydrocephalus
itself in producing the symptoms. In Group 2 the
138 Annals of Neurology Vol 8 No 2 August 1980
neurological status improved spontaneously in a few
days, and residual signs at l-month follow-up were
surprisingly few. Brainstem signs, initially absent in
the 4 noncomatose patients in Group 1, were present
in half of the Group 2 patients, whose disease took a
benign course. Thus the presence or absence of
brainstem signs at onset does not permit a forecast of
the course of the disease.
Nineteen patients in the present series lived, an
overall 90% survival rate. However, when discussing
the mortality of cerebellar infarctions, a distinction
should be drawn between the two groups. In our
small Group 1, who had deterioration of consciousness, 3 of the 5 operated patients and the 1 nonoperated patient lived, a two-thirds survival rate. In their
autopsy series of 24 old cerebellar infarcts and 28
cases of acute massive cerebellar softenings causing
death by compressing the brainstem, Sypert and Alvord [27] speculated a mortality rate of 50%.
Moreover, since a history of brainstem compression
was elicited from the records of only 6 of their 24
patients with old softenings, the mortality rate for
severe softenings was calculated to exceed 80%.
However, this retrospective autopsy study did not give
information about the efficacy of treatment, as surviving patients were not included; only 3 of the 2 8
patients in Sypert and Alvord's series were treated
The 15 patients without deterioration of consciousness all survived. Greenberg et a1 [ 121 have described 4 similar patients. From these cases it can be
inferred that discrete cerebellar infarctions have a
benign outcome, like that of small cerebellar hemorrhages [20]. Prior to these contributions and CT
scanning, the existence of such infarcts was documented only indirectly by the postmortem
finding of old softenings in the absence of a past
medical history of brainstem compression [29].
Role of Surgery
To evaluate properly the place of surgery in treatment of the disease and its influence on mortality,
one must consider clinical studies of patients selected
for having cerebellar softening associated with rapid
worsening of signs of brainstem compression. Accordingly, we reviewed 51 cases of cerebellar softening [3-8, 10-12, 17-19, 21, 24, 27, 301" published after the influential paper of Fairburn and
Oliver [71, which introduced surgical decompression
of the posterior fossa, with or without resection of
infarcted tissue, as a treatment of the disease. Four patients who were alert were operated on [ 5 , 7 , 171because ventriculography showed a pseudotumor of the
+Case 1 of Duncan, Parker, and Fisher [6] was not included as n o
signs of brainstem compression were reported.
cerebellum. The data must be evaluated cautiously,
as no controlled study concerning treatment of cerebellar infarction is presently available.
Twenty-nine of the 5 1 patients lived, an overall
survival rate of 57%. Dividing the 51 cases into operated and nonoperated groups, we find that 28 of 37
(76%) operated patients survived while 13 of 14
(93%) nonoperated patients died, a figure akin to
Sypert and Alvord’s prediction of 80% [29]. Since
the main indication for surgery was deterioration of
consciousness [24], this mortality rate can be regarded as that of the severely ill nonoperated patients. In terms of preoperative level of consciousness, 14 of 20 comatose patients, 11 of 13 stuporous
patients, and 3 of 4 alert patients survived. Taking
into account only stuporous and comatose patients,
the data suggest that to be effective, intervention
must be initiated as soon as possible when consciousness begins to deteriorate. Ott et al [231 drew a similar conclusion for the treatment of cerebellar hemorrhages. Inasmuch as Sypert and Alvord [29] found
that the mean interval between onset of stupor and
onset of coma was about 6 hours, one has only a short
time to make the decision to operate.
Among the 37 patients operated on for cerebellar
softenings most were treated by craniectomy and removal of the softened tissue, with 23 out of 31 surviving. Ventricular drainage alone [ l o , 121 and drainage followed by craniectomy [8, 101 were performed
in 3 patients each. As more than 80% of the patients
underwent craniectomy, its value in comparison with
alternative approaches cannot be inferred from the
present data. Richardson [251 and Heros [141 emphasized the potential danger of ventricular drainage
alone, as upward herniation of the brainstem can
occur. However, ventricular drainage has been successfully performed by Giraud et al ([lo], Case 3 )
and Greenberg et a1 ([12], Cases 1 and 2), who
stressed the less traumatic nature of this technique.
Postmortem findings in 18 of the 22 deceased patients showed that in half, cerebellar infarction was
not associated with a brainstem stroke. These data
are in line with Sypert and Alvord’s pathological
study [29], in which the brainstem was normal in 18
out of 28 cases. These results also suggest that in
about half of the cases, brainstem functions are impaired because of compression by a swollen cerebellum, thus strengthening the rationale for posterior
fossa decompression. As shown by 1 case in the
present series, the posterior fossa syndrome can
spontaneously remit; this benign course is unusual,
however, as only 1 case of spontaneous resolution of
a coma has been reported ([71, Case 1).
The bulk of evidence thus favors a role for
emergency surgery in the treatment of cerebellar
stroke producing impaired consciousness. Although
a controlled study on a large unselected series might
seem scientifically desirable, it is hardly ethical in
view of the analysis presented here.
Role of CT Scanning
Within the limits of this small but reasonably unselected series of CT-confirmed cerebellar infarcts,
we conclude that emergency C T scanning in posterior
fossa stroke serves to locate the lesion, to exclude
subdural or cerebellar bleeding, and to reveal the
presence of triventricular hydrocephalus. Because
hypodensity in the cerebellum may be delayed by a
few hours to a few days and brainstem lesions are
poorly detected by present apparatus, the initial C T
examination may be diagnostically inconclusive.
Even when a negative scan is obtained, it is advisable
to perform contrast enhancement and serial CT examinations as soon as possible following the ictus.
Despite a negative early CT examination, if the clinical pattern suggests cerebellar infarction, close
clinical monitoring is needed to detect potential
neurological deterioration. The decision to treat
CT-documented cerebellar softening surgically
should depend on the appearance of the CT scan,
on any worsening of consciousness, and on the development of signs of brainstem dysfunction. No signs
predicted severe postischemic swelling in the cerebellum in this series, although development of hydrocephalus was associated with large lesions.
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