Acta Neurochirurgica 73, 59--65 (1984)

ACTA
NEUROCHIRURGICA
9 by Springer-Verlag 1984

Department of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne,
Switzerland

Benign Outcome in Unoperated Large CerebeHar
Haemorrhage
Report of 2 Cases
By

J. Bogousslavsky, F. Regli, and X. Jeanrenaud
With 2 Figures

Summary
We studied two patients with large cerebellar haemorrhages, who were
conscious on admission and did not deteriorate during the following days. Surgical
decompression was not performed and the patients regained their former level of
activity, except for moderate persisting ataxia. We suggest that cerebellar
haemorrhage may have a benign spontaneous outcome, more often than
previously assumed from autopsy series. The main selection criteria for surgery is
an impaired state of consciousness and evidence of neurological worsening. Taken
alone, the size of the haemorrhage on computerized tomography is not a reliable
criterion for surgery.

Cerebellar haemorrhage usually bears a catastrophic outcome,
because the patients rapidly die from acute intracranial hypertension with brainstem compression 2,7,15. During the last 25 years,
early surgical decompression has been emphasized by most authors
in order to avoid this relentless evolution 1,2,4,11,13,14,16 However,
isolated cases with a small haemorrhage have also been reported
doing quite well without surgery 4,6,14.We now report two cases with
a large cerebellar haemorrhage, who were successfully managed
with a conservative approach.

60

J. Bogousslavsky etal.:
Case I

This 80-year-old hypertensive (untreated) man was in good health until two
years prior to admission, when he suffered a right hemiparesis that progressively
disappeared in three weeks. He took dicoumarol during four months at that time.
Two years later, he showed an increasing fatigue, with postural instability, and
disorientation, which progressively develop within a few days. Gait disturbances increased and the patient was admitted after he showed recurrent
vomiting.
The patient was afebrile, blood pressure was 180/110 mm/Hg, with a regular
pulse (80 rain). An aortic murmur (2/6) was present but auscultation of the carotid
arteries was normal. Optic fundi were normal. Visual acuity and visual fields were
preserved. Occular mobility was slowed in all directions, and optokinetic
nystagmus was absent to the left. No pupillary disturbances were present. Other
cranial nerves were normal. Strength and tonus appeared symmetrical and normal
in the four limbs, but a slight increase in the tendon reflexes was present on the
right side of the body, with a bilateral Babinski sign. Sensation was completely
preserved. A dysmetria and hypermetria were present in the right superior and
inferior limbs. Adiadochokinesia and the rebound phenomenon were present in
the right arm. The patient remained well-oriented, but was quickly fatigued during
the examination.
Standard blood and urine tests were normal. ECG showed atrial fibrillation
(60 rain) with a partial right bundle-branch block. A computerized tomographic
scan of the brain showed a large intraparenchymatous haemorrhage in the right
cerebellar hemisphere also involving the vermis and the left paravermis. Widening
of the cerebral sulci and enlargement of the lateral ventricles was also present.
The patient was not operated on because of the absence of signs of intracranial
hypertension. He remained stable for 10 days and was referred for convalescence
to another hospital, which he could leave after six weeks, being able to walk with a
stick. Alpha-methyldopa (250 mg/day) was introduced to control the hypertension.
Case 2

This 75-year-old non-insulin dependent diabetic man suffered an anterior
myocardial infarction with residual angina pectoris, three years prior to the
present admission. He was taking aspirin, dipyridamole, oxprenolol and
isosorbide dinitrate. The day before admission he suddenly complained of
rotatory vertigo without directional preponderance, with exacerbations on head
movements. A few hours later he experienced vertical diplopia, and vomited three
times.
On admission the following day, the patient was well-oriented and still
complained of vertical diplopia and dizziness, but without headache. No
meningitis was present. There was a skew deviation with the left eye being higher
than the right eye, with a gaze-paretic nystagmus to the left and no response on
optokinetic stimulation to the right. Other cranial nerves were normal. No
hemiparesis was present, but the patient showed a massive axial deviation to the
right in the sitting position, and walking was impossible. Tendon reflexes were
slightly hyperactive in the left limbs, with a left Babinski sign. Sensation was

Benign Outcome

61

Fig. 1. Case 1: CT scan on admission. Large vermian and right hemispheric
haemorrhage in the cerebellum

normal, except a moderate distal tactile hypaesthesia in the inferior limbs. Blood
pressure was 190/110 mmHg, pulsations were 100 rain and regular, general
examination was normal.
Standard blood and urine tests were normal. CSF (lumbar puncture) was
bloody, with 10,000 red cells/ml and three white cells/ml (1 polymorphonuclear, 2
lymphocytes); protein content was 1,530 mg/1. A C T scan performed on the same
day showed a vermian and left hemispherical haemorrhage in the cerebellum (Fig.
2 a) and diffuse cortical atrophy.
Because of clear consciousness and absence of acute intracranial hypertension
the patient was not referred for surgery. He remained stable during the following
days, except that some cerebellar dysmetria and adiadochokinesia developed in
the superior limbs, with visual hallucinations (animals). Dexamethasone, which
had been introduced on admission (20 rag/day i.v.) was discontinued after one
week. A control of the CT scan showed a progressive resolution of the
haemorrhage (Fig. 2 b).
The patient was discharged four weeks after admission. He was able to walk

62

J. Bogousslavsky et al.:

Fig. 2 a. Case 2: CT scan on admission. Large vermian and left hemispheric
haemorrhage in the cerebellum
alone and showed oniy a slight axial instability. A moderate dysmetria was still
present in the left superior limb, with bilateral postural tremor. The tendon
reflexes were still hyperactive in the left limbs, with a Babinski sign.
Discussion
The rate ofintracerebellar haemorrhage has been found to be 513 per cent of intracerebral haemorrhages 8,12,14. In most published
series, the natural evolution o f spontaneous cerebellar haemorrhage has been fatal, because of the quick development of
intracranial hypertension and brainstem compression1,2,4,11,14,15
Thus, surgical decompression has been suggested, being imperative
as soon as the diagnosis has been made 1,2,4,1t,13,14,16. However, it
should be emphasized that most of the large published data deal
with autopsy series, and may not include some more benign
cases 4,14. In fact, a few recent studies reported that isolated
unoperated cases might survive, when the haemorrhage is limited
and the mass effect minor 3,4,6,9,14. This finding is partially related to

Benign Outcome

63

Fig. 2 b. Case 2: CT scan after two weeks. Partial resolution of the cerebellar
haemorrhage
the development of computed tomography (CT), which allowed
clinicians to make an earlier diagnosis, because the signs and
symptoms of cerebellar haemorrhage are usually non-focalizing or
may suggest pontine haemorrhage 2,4,1~ However, even if the
patient spontaneously survives, the evolution may not be "benign",
because of persisting and disabling neurological sequelae 5,9.
In our two cases with a large intracerebellar haemorrhage we
were able to avoid surgical treatment, because the patients'
conditions remained stable and no coma developed. It is probable
that both our patients benefited from the cerebral (and probably
cerebellar) atrophy demonstrated by CT, which attenuated the
mass effect of the haemorrhage and its consequences on the
brainstem. The most important point that incited us to medically
treat our patients was the well-preserved state of consciousness on
admission, without further deterioration. Some authors suggested
that all patients suffering a spontaneous cerebellar haemorrhage
should be rapidly operated on 2,11,13,16. However, other reports
suggested that in stable and conscious patients, a conservative

64

J. Bogousslavsky etal.:

approach could be tried (unless delayed deterioration develops) 3,4,6,9, but this situation is not common in the literature.
Heiman and Satya-Murti 4 recently reported two patients with a
spontaneously benign outcome, but on CT scan the cerebellar
haemorrhage was rather small, as it was in 4 cases reported by
Labauge et al. 9 Chin et al. 3 also reported cases with rather benign
outcome, but CT features were not described. Our cases, especially
Case 1, show that the indication for surgery does not depend on the
extent of the haemorrhage on CT, but rather on clinical features.
We agree with an early surgical decompression when the
patients are stuporous on admission or when they show a rapid
deterioration, and it should be pointed out that delayed and sudden
worsening may occur as late as one week after the initial event 7,14.
However, we think that in conscious patients who do not
deteriorate, a conservative therapy should be tried, with permanent
and careful neurological controls to detect any worsening.
"Benign" cerebellar haemorrhages may be more frequent than
previously assumed, because in older patients with non-specific
clinical findings, CT may not be routinely performed.

References
I. Aronson, H., Shafey, S., Gargano, F., Intracerebellar haematoma. J. Neurol.
Neurosurg. Psychiat. 28 (1965), 442-444.
2. Brennan, R. W., Bergland, R. M., Acute cerebellar haemorrhage. Analysis of
clinical findings and outcome in 12 cases. Neurology 27 (1977), 5 2 7 - 532.
3. Chin, D., Carney, P., Acute cerebellar haemorrhage with brainstem
compression in contrast with benign cerebellar haemorrhage. Surg. Neurol. 19
(1983), 406-409.
4. Fisher, C. M., Picard, E. H., Polak, A., Dalal, P., Ojemann, R. G., Acute
hypertensive cerebellar haemorrhage: Diagnosis and surgical treatment. J.
Nerv. Ment. Dis. 140 (1965), 38-57.
5. Freeman, J. W., Kennedy, R. M., Petty, S. S., Prognosis of nonoperated
cerebellar haemorrhage. Ann. Neurol. 4 (1978), 389-390.
6. Heiman, T. D., Satya-Murti, S., Benign cerebellar haemorrhages. Ann.
Neurol. 3 (1978), 366-368.
7. Heros, R. C., Cerebellar haemorrhage and infarction. Stroke 13 (1982),
106 - 109.
8. Hyland, H. H., Levy, D., Spontaneous cerebellar haemorrhage. Can. Med.
Assoc. J. 71 (1954), 315-323.
9. Labauge, R., Boukobza, M., Zinszer, J., Blard, J. M., Pages, M., Salvaing, P.,
H~matomes spontan+s du cervelet. Vingt-huit observations personnelles. Rev.
Neurol. 139 (1983), 193-204.

Benign Outcome

65

10. Little, J. R., Tubman, D. E., Etheir, R., Cerebellar haemorrhage in adults.
Diagnosis by computerized tomography. J. Neurosurg. 48 (1978), 575-579.
11. McKissock, W., Richardson, A., Walsh, L., Spontaneous cerebellar
haemorrhage. A Study of 34 consecutive cases treated surgically. Brain 83
(1960), 1 - 9 .
12. Mitchell, N., Angrist, A., Spontaneous cerebellar haemorrhage. Reportof 15
cases. Amer. J. Pathol. 18 (1942), 235-253.
13. Norris, J. W., Eisen, A. A., Branch, C. L., Problems in cerebellar haemorrhage
and infarction. Neurology 19 (1969), 1043-1050.
14. Ott, K. H., Kase, C. S., Ojemann, R. G., Mohn, J. P., Cerebellar haemorrhage:
Diagnosis and treatment. Arch. Neurol. 31 (1974), 160-167.
15. Rey-Bellet, J., Cerebellar haemorrhage. A clinico pathologic study.
Neurology 10 (1960), 217-222.
16. Siris, H., Beller, J., Spontaneous intracerebellar haemorrhage: surgical
treatment. Surg. Clin. North. Amer. 28 (1948), 412-415.
Authors' address: Dr. J. Bogousslavsky, Prof. Dr. F. Regli, and Dr. X.
Jeanrenaud, Department of Neurology, Centre Hospitalier Universitaire
Vaudois, CH-1011 Lausanne, Switzerland.

5

Acta Neurochirurgica,Vol. 73, Fasc. 1--2