Intracranial Lipoma
Case Report
S. YA.LCIN, M . D . , AND S. FRAGOYANNIS, M . D .

Department of Pathology, The Allentown Hospital Association, Allentown, Pennsylvania
T h e l i p o m a is one of t h e m o s t f r e q u e n t b e n i g n
t u m o r s in t h e h u m a n b e i n g ; it occurs in a l m o s t
every o r g a n of t h e b o d y , b u t it is e x t r e m e l y r a r e
inside t h e skull ( i n t r a c r a n i a l space). M o s t of t h e
r e p o r t e d cases arise f r o m t h e c o r p u s c a l l o s u m 2
Since t h e first d e s c r i p t i o n b y R o k i t a n s k y in 1856,
only 110 cases h a d b e e n r e p o r t e d u p t o 19583
W e h a v e h a d a n o p p o r t u n i t y t o observe a n d
s t u d y a case of i n t r a c r a n i a l l i p o m a w h i c h presented some peculiarities.

Case Report
A 91-year-old white woman was admitted ou March
~5, 1963. The night before admission, her daughter had
found her, unable to talk or move her right side, but
able to "moan and groan." She also seemed to be very
short of breath.
History. The patient had been deaf for ~0 years. The
uterus had been removed several years before.
Examination. She was an obese woman, lying motionless in bed; she did not respond to verbal orders,
but constantly moaned. The pupils were small, but reactive, and she had bilateral cataracts. The general
physical examination was normal for her age. The
clinical impression was t h a t she had suffered a cerebral
vascular accident.
EKG showed auricular fibrillation consistent with
left ventricular enlargement and strain. The chest x-ray
showed increased density at the left base. There were
19,900 white blood cells with 80% segmented and 16%
band forms. The hemoglobin was 1~.s gln. The blood
urea nitrogeu was 24 rag. %, the alkaline phosphatase
o~.6 units, the blood sugar ~09 mg. %, the serum glutamic oxalaeetic transaminase 180 units, and the lactic
acid dehydrogenase 1400 units.
During the next few days the patient developed increased weakness of the legs; the left lower leg became
cool and bluish-purple. The posterior tibial and pedal
pulses were weaker on the left side, but palpable. She
given vaso-dilators and anti-coagulants. There was
clinical evidence of pulmonary edema. She died on
April 7.
Postmortem Examination. Autopsy was performed 12
hours after death. The significant general findings were
arteriosclerosis, multiple pulmonary infarcts, acute
fibrinous pericarditis, nephrosclerosis, pyelonephritis
and gangrene of the left leg.
The brain weighed 1300 gm. The gyri were slightly
atrophic. The vessels of the circle of Willis were patent;
there was only moderate arteriosclerosis. Coronal sections through the brain revealed a well-encapsulated
yellowish tumor near the right insula and compressing
the adjacent cortex and the region of the basal ganglia
Received for publication M a y 14, 1965.

FIG. 1. Yellow mass of the lipoma was found underneath the middle cerebral artery after retraction of the
temporal lobe.
(Fig. 1). This lipomatous mass was outside the pia
mater but beneath the branches of the middle cerebral
artery; it measured 3)<1 cm. Microscopic sections of
the mass showed well-encapsulated, m a t u r e fat tissue
with small areas of calcification in the capsule and adjacent brain cortex (Fig. 2).
There was also a small focus of hemorrhage, ~.5 cm.
in diameter, over the anterior left parietal region.
Microscopic section showed ischemic necrosis and recent hemorrhages. There was advanced arteriosclerosis.

Discussion
L i p o m a s in t h e c r a n i a l c a v i t y h a v e b e e n k n o w n
for a b o u t 100 years. R o k i t a n s k y d e s c r i b e d t h e
first case, a l i p o m a of t h e c o r p u s c a l l o s u m , i n 1856.
Ewing mentioned that Virchow had observed 6
l i p o m a s of t h e d u r a a n d v e n t r i c u l a r e p e n d y m a . 5
C a s c i n o et al. f o u n d o n l y 110 i n t r a c r a n i a l l i p o m a s
in t h e l i t e r a t u r e u p t o 1958.1 C o o p e r a n d V o n
H a g e n i n d i c a t e d t h a t t h e r e p o r t e d c a s e s of l i p o m a
of t h e corpus e a l l o s u m t o t a l l e d 65 i n 196~. 2
L i p o m a s of t h e b r a i n h a v e b e e n o b s e r v e d i n
v a r i o u s locations, b u t chiefly o n t h e s u r f a c e of t h e
corpus callosum2 Other locations have been the
b a s e of t h e c e r e b r u m , t h e b r a i n s t e m a n d c e r e b e l lum, t h e roots of t h e c r a n i a l n e r v e s 2 t h e v e n t r a l
a s p e c t of t h e d i e n c e p h a l i c s t r u c t u r e s , t h e e h o r o i d
plexus of t h e lateral ventricles, a n d t h e d o r s a l
a s p e c t of t h e m i d - b r a i n . ~
M a n y of t h e t u m o r s a r e s m a l l 2 n o b i g g e r t h a n

895

896

S. Yalcin and S. Fragoyannis
A n t t i n e n have outlined the radiologic criteria for
the diagnosis of lipoma of the corpus callosum, 9 as
follows:
1. A midline lesion lying just above the corpus
eallosum.
~2. A radiolucent area at the site of the tumor,
especially in the lateral view.
3. Symmetrical parenthesis-shaped calcifications in posterior-anterior projections.

Fro. 2. The tumor consists of well differentiated
adipose tissue with very minimal amount of fibrous
stroma. There is definite encapsulation. )<100.

Our patient had a left-sided hemiplegia and
later paraplegia. The autopsy findings showed
ischemic and hemorrhagic necrosis due to arteriosclerotic vascular disease in the left parietal region of the anterior portion. The lipoma was
located over the right insula and was compressing
the adjacent cortex. We therefore assume that the
paraplegia was caused b y both tile lipoma and the
arteriosclerotic vascular disease. The compression
exerted by the lipoma m a y have been precipitated
by the increased intIacranial pressure originating
from the hemorrhage on the left side.
There were some interesting laboratory findings. The serum transaminase was 180 units and
the lactic acid dehydrogenase (LDH) was 1400
units. L D H activity has been shown to have
diagnostic value in tissue necrosis and neoplasia. TM
Our patient had had multiple pulmonary infarcts.
The elevation of L D H and bilirubin in the serum
arc important findings of pulmonary embolism. 4,n,12 The acute fibrinous pericarditis may
have played a secondary role in the elevation of
the serum LDYI.

cm. in diameter. ~ The histologic pattern is mainly
m a t u r e adipose tissue, with variable amounts of
collagen. Infrequently they may contain muscle
fibers and fibro-osseous tissue. Russell and RubinSummary
stein observed small patches of leukopoiesis. 1~
Some lipomas have a b u n d a n t vascularization.3
We have reported the case of a 91-year-old
T h e origin of intracranial lipomas is controver- woman with an asymptomatic lipoma of the
sial. Accoiding to Ewing, s they always arise from insular region.
the pia. Some 9 say that they are not tumors at all,
References
b u t the general belief is that they are tumorsJ
1. CASCINO, J. P., LAKE, F., JACKSON, C., and
Cooper and Von Hagen suggested that intraKAPLAN, A. Lipoma of the corpus callosum. J.
cranial lipomas, especially the lipomas of the
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corpus callosum, are congenital or developmental
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lesions.2
of the corpus callosum. Report of a case. Bull. Los
There is no particular age or sex incidence.
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According to Cascino et al., the youngest known
3. EHNI, G., and LovE, J. G. Intraspinal lipomas.
case was a 3-day-old child and the oldest was 75.1
Report of cases; review of the literature, and clinZ e t t n e r and Netsky found that just over half of
ical and pathologic study. Arch. Neurol. Psychiat.,
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seems to be the oldest case of intracranial lipoma
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T h e main symptoms of intracranial lipoma
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Pathology, 1952, Section 10, Fasc. 35 (See p. 96).
evidence m a y help considerably. Roukkula and

Intracranial Lipoma
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897

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