Open Journal of Mo dern Neurosurgery, 2011, 1, 10-16
doi:10.4236/ojmn.2011.12003 Published Online October 2011 (http://www.SciRP.org/journal/ojmn)
The Natural History and Treatment Guidelines of
Cerebellar Liponeurocytoma—A Case Report
Or Cohen-Inbar, Euvgeni Vlodavsky, Menashe Zaaroor
Department of N e urosurgery, Rambam Maimondes Health care campus, Haifa, Israel
Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel
Received August 16, 2011; revised September 5, 2011; accepted September 20, 2011
Abstract
Background and Importance: Lipomatous medulloblastoma (cerebellar liponeurocytoma) is a rare cerebellar
tumor, with only twenty-nine cases reported, considered a distinct variant of medulloblastoma. The few cases
described support an indolent nature for this tumor. We aim at defining the optimum treatment strategy and
long-term behavior for this tumor entity. Clinical presentation: A 74 years old male presented on September
2010 complaining of mild dizziness and headache slowly progressing over a few months. This gentleman
was operated on at our department some 18 years ago for a right cerebellar hemispheral lesion, defined as a
liponeurocytoma. This patient received no adjuvant treatment. Current magnetic resonance imaging (MRI)
studies disclosed a right hemispheral cerebellar mass, locally recurrent in the original surgical tumor bed.
Gross total resection of the tumor was accomplished through a suboccipital craniotomy, with complete re-
section of the lesion. The histopathological diagnosis was defined as cerebellar liponeurocytoma. No adju-
vant therapy was given as initially, after the first operation. Currently, the patient is alive, fully alert with
minimal neurological deficits, Barthel index 90, Kernofsky performance status of 90 and with no evidence of
disease on neuroimaging. Conclusion: This patient portrays this tumor’s natural history after surgical inter-
vention with no adjuvant treatment, being the longest reported follow-up and recurrence. This distinct variant
of medulloblastoma appears to have a uniquely favorable prognosis, even without adjuvant therapy. A com-
plete surgical resection with close follow-up seems both sufficient and prudent.
Keywords: Natural History, Cerebellar Liponeurocytoma, Recurrence in 18 Years
1. Introduction
Medulloblastoma rarely occurs in adults. Greater than
70% of medulloblastoma cases occur in children [1].
This tumor represents less than one percent of all adult
primary central nervous system (CNS) tumors. Most
adult medulloblastoma are located in the cerebellar
hemisphere, unlike the midline/vermis location most
prevalent in the pediatric patients [2]. Medulloblastoma
is well known as having multiple histopathological vari-
ants, including those displaying predominantly neuronal,
glial, and/or myoid differentiation [3]. Sarkar et al. stated
that the survival benefit in adults does not seem to be
related to the histological variant (classical versus des-
moplastic medulloblastoma variant), but rather to age [4].
The one exception to this statement is the lipomatous
medulloblastoma variant, occurring almost exclusively in
adults. The first lipomatous medulloblastoma (Cerebellar
liponeurocytoma) was reported in 1978 by Bechtel et al.
in a 44-year-old man [5]. Twenty-nine cases have been
reported so far, under different names, such as “lipoma-
tous medulloblastoma, lipidized medulloblastoma, neu-
rolipocytoma, medullocytoma and lipomatous glioneu-
rocytoma” [6] [Table 1]. Cerebellar liponeurocytoma has
been recognized by the 2000 World Health Organization
(WHO) classification of tumors of the central nervous
system as a distinct clinicopathologic entity. In the new
classification, this tumor subset is classified in the cate-
gory of glioneuronal tumors grade I or II due to its fa-
vorable clinical behavior [7], even with incomplete re-
section or multicentric appearance [3]. Cerebellar lipo-
neurocytoma is a neuroectodermal tumor consisting of
both neuronal and glial elements. Immunohistochemistry
for GFAP, synaptophysin and NSE are usually positive

O. COHEN-INBAR ET AL.11
Table 1. Treatment of liponeurocytoma with radiotherapy/
death cross-tabulation.
death
No Yes
Total
No 8 3 11
Radiotherapy
Yes 8 8 16
Total 16 11 27
indicating the mixed glial and neuronal elements [6,8,9].
This tumor shares several features with the cerebellar
medulloblastoma, which may include an origin from the
periventricular matrix of the fourth ventricle or the ex-
ternal granular layer of the cerebellum. Recent work us-
ing cDNA expression array data suggests a relationship
to central neurocytomas [10]. Microscopically, the tumor
consists of small round to ovoid cells, with an eosino-
philic scanty cytoplasm, extending between interspersed
regions of lipidized cells that resemble mature adipocytes.
Mitoses, areas of vascular proliferation and necrosis are
all rare [1,6-9,11-16]. Mitotic activity is usually absent
and the growth fraction, as reflected by the MIB-1 label-
ing index, is in the range of 1% ~ 3% [1, 6-8,11-16].
The radiological appearance of this tumor on com-
puted tomography (CT) is characterized as a hypodense
mass with intermingled areas exhibiting the attenuation
values of fatty tissue. T1-weighted MR images feature
this tumor as hypointense with scattered foci of hyperin-
tense signal, displaying moderate contrast enhancement.
T2-weighted MR images feature this tumor as slightly
hyperintense relative to the cortex, with no edema pre-
sent. Areas of fat density as assessed on CT scans and on
MRI-T1WI help to distinguish this rare neoplasm from
the more common adult medulloblastomas or ependy-
momas [17]. The aim of surgery is a gross total resection
(GTR) of the tumor. In most of the cases reported there
was a reasonable border between the tumor and sur-
rounding tissue [17-19] and gross total removal of the
tumor was feasible.
2. Clinical Summery
A 74 years old male presented to our institute on Sep-
tember 2010 describing an indolent, subjective feeling of
dizziness and headache slowly progressing over the pre-
vious few months. Aside from a mild benign prostatic
hyperplasia and hypercholesterolemia controlled medi-
cally, he did not suffer any other chronic illnesses. This
gentleman was operated on at our institute some 18 years
ago, for a right cerebellar hemispheral lesion. A GTR
was achieved. The histopathological specimens were sent
for consultation to professor John J. Kepes, who de-
scribed it as “a tumor, whose neuroectodermal origin is
probably not in doubt, having cellular areas to suggest
differentiating medulloblastoma, elsewhere pilocytic
astrocytoma, oligodendroglioma like foci and perivascu-
lar rosettes as seen in ependymomas, and striking large
round spaces that I am sure were filled with fat”. It was
diagnosed as a medulloblastoma with lipoid differentia-
tion (termed later as a liponeurocytoma). The patient
received no adjuvant radiotherapy or chemotherapy and
returned to a fully independent, working and productive
life.
During the next few years the patient was followed as
an outpatient, but dropped out of follow-up at some point.
During the years 2004 and 2005 the patient presented to
the emergency room twice reporting of a mild dizziness.
A non-contrast enhanced computed tomography was
performed, interpreted as normal with minimal chronic
changes in the tumor bed. The patient was discharged
without a neurosurgical consult, and returned to be fully
active. A retrospective review of these scans raises sus-
picion of a local recurrence within the tumor bed, meas-
uring 13 mm in its largest diameter (Figure 1).
Neurological examination: Mild dysdiadochokinesis,
no ataxia, a negative Romberg sign.
Neuro-radiological findings: Current imaging as of
September 2010 showed a non-enhancing mass within
the tumor bed on tomography, measuring 43 mm in its
largest diameter (Figure 2). The MRI appearance was
described as a hypercellular partially cystic lesion, hav-
ing delayed diffusion and a pathological enhancement.
Signs of intralesional hemorrhage or calcifications were
suspected and a mild peritumoral edema and multiple
VRS described (Figure 3).
Surgical in tervention: A right paramedian suboccipital
craniotomy in the sitting position was performed. The
tumor was grossly gray-reddish in color, partially at-
tached to the surrounding tissue but well circumscribed.
It was easily detachable from adjacent brain tissue and a
GTR was achieved. The postoperative course was un-
eventful with the exception of an obstructive hydro-
cephalus secondary to peritumoral edema causing a nar-
Figure 1. A non contrast enhanced computed tomography,
2005.

O. COHEN-INBAR ET AL. 12
Figure 2. Computed tomography findings, both enahnced
and not-enhanced by contrast, 2010.
(a) (b)
(c) (d)
Figure 3. 2010 MRI, A. axial FLAIR, B. Coronal T1 with
gadolinium, C. Axial T2, D. Sagittal T2.
rowing of the forth ventricle. This was managed with a
ventricular drain for a few days after which the edema
subsided and the hydrocephalus resolved. The patient
was discharged shortly after.
Pathological findings: On histopathological sections,
small round to oval cells characteristic of medulloblas-
toma were found in eosinophilic neuropil matrix, inter-
spread with groups of lipocytes. Sections stained strongly
positive for Neurontin, synaptophysin, only minimally
positive for the proliferation marker Ki-67, estimated as
less than 5% of the cells (Figure 4).
3. Discussion
Lipomatous differentiation of central nervous system
(a) (b)
(c) (d)
Figure 4. Microscopic and immunohistochemical features of
lipomatous medulloblastoma. (a) small round and oval cells
of medulloblastoma in eosinophilic neuropil matrix and the
group of lipocytes; Hematoxylin and eosin, x100; (b)
strongly positive immunostain for NeuN; immunoperoxi-
dase, x100; (c) positive immunostaining for synaptophysin;
immunoperoxidase, x100; (d) only few cells are positive for
proliferation marker Ki-67, immunoperoxidase, x200.
tumors is rare. Among astrocytic neoplasias, lipomatous
differentiation is best known to be present in pleomor-
phic xanthoastrocytoma [20]. Multivacuoler lipidization
is also observed in glioblastoma multiforme, ependy-
moma and primitive neuroectodermal cerebral tumors
[21-24]. Cerebellar liponeurocytoma is a rare cerebellar
tumor, with only 29 cases reported under many different
names [Table 2]. Although the few cases described sup-
port the relatively benign nature of this lesion, the opti-
mum treatment strategy and long-term follow-up and
prognosis still has to be defined [8]. Reviews published
in the literature report a 5-year survival rate of 81% [6,
19], with recurrence appearing as late as 15 years after
surgery, although most appear sooner [1,7,8-13,13-14,
25-30]. A caveat to this figure stems from the low num-
ber of patients per report (most are case reports) and the
inconsistency in pathological classification prior to 2000.
Furthermore, since these patients were treated using dif-
ferent protocols, this figure seems misleading. Some,
more aggressively behaving relapsing lesions have also
been described [29]. The patient described in this paper
is, to the best of our knowledge, the longest follow-up
reported presenting with radiographic progression at 13
years and a clinical progression at 18 years.
Current day guidelines as to the treatment of adult
medulloblastoma define surgical resection of the lesion
as the first line treatment. According to Brandes et al.,
low-risk patients with no resiual disease should receive d

O. COHEN-INBAR ET AL. 13
Table 2. Review of the literature , pre sumptive case s of liponeurocytoma: The clinical, histo-pathological and follow-up data.
Immunostaining Tx. Reference
No Age Sex Site Adi Tc Pi %SRT Follow-up Year Authors
1 44 M Cerebellar
hemisphere - - - +- D 18 hours after surgery 1978 Bechtel et al. [5]
2 42 M Lt.Cerebellar
hemisphere
GFAP(+),
Vim(+), S100(+)
GFAP(+), NSE(+)
S100(+) - +- A at 5 years 1991 Chimelli et al. [12]
3 49 F Vermis NA Syn(+), Leu-7(+),
GFAP(−), NF(−)- +- A at 5 years 1993 Davis et al. [13]
4 53 M Vermis, bilateral
extension NA Syn(+) ,Leu-7(+), GFAP(−), NF(−)- +54 GyD at 6 monthes 1993 Davis et al. [13]
5 50 F Cerebellar
hemisphere GFAP(+)
Syn(+), NSE(+),
PGP-9.5(+),
DES(+)F
<1 +- A at 4 years 1993 Ellison et al.
[27]
6 37 M Lt. Cerebellar
hemisphere GFAP(+) Syn(+), NF(−), GFAP(+)F <1 +-
R at 10 years,
Reop. at R, D 1
year post-op.
1996 Giangaspero
et al. [28]
7 36 F Lt. Cerebellar
hemisphere GFAP(+) Syn(+), NF(−) GFAP(+)F, <1 +-
R at 10 years,
Reop, 2nd R at
5years, Reop. A.
1996 Giangaspero et
al. [28]
8 57 F Vermis GFAP(+) Syn(+), NF(−),
GFAP(+)F <1 +60 GyAAW after 2 years 1996 Giangaspero et al. [28]
9 48 F Rt. Cerebellar
hemisphere
Syn(+), NSE(+),
MAB-2(+)
Syn(+), GFAP(+),
NSE(+), S100(+),
MAP-2(+), P53(−)
<1 +50 GyA at 3.5 years 1996 Söylemezoğlu
et al. [15]
10 53 M Lt. CPA Syn(+), NSE(+),
MAB-2(+)
Syn(+), GFAP(+),
S100(+),P53(−),M
AP-2(+), NF(−),
NSE(+),
<5 +- R at 12 years,
Reop., A. 1996 Söylemezoğlu et al. [15]
11 59 F Lt. CPA Syn(+), NSE(+),
MAB-2(+)
Syn(+), GFAP(+),
S100(+), P53(−),
MAP-2(+), NF(−),
NSE(+),
<3 +55 Gy
24 GyAAW at 5 years. 1996 Söylemezoğlu et al. [15]
12 55 M
Vermis and Rt.
Cerebellar
hemisphere
S100(+)F,
Vim(+)
Syn(+), S100(+),
NSE(+), GFAP(+)<1+- A at 8 months 1997 Orlandi et al. [16]
13 67 F Vermis
Syn(+),
GFAP(+),
S100(+)
Syn(+), S100(+),
NSE(+), GFAP(+)<1+- D post-op. 1998 Compora et al.
14 28 F Vermis D at 4 years
15 23 M Hemisphere D at 7 years
16 30 M Vermis D at post-op.
17 9 M Vermis D at 5 years
18 11 M Vermis D at 2 years
19 4 F Hemisphere
Vim(+),
KO-1(+),
CR3/43(+)
NF/MAP-2(+) 19.5~
40.5 ++
D at post-op.
2000 Giordana
et al. [14]
20 38 M Rt.hemisphere NA Syn(+), GFAP (−)low +- A at 15 months 2001 Alkadhi
et al. [17]
21 66 M Lt.hemisphere NA NA 3 +36 Gy*A at 6 months 2001 Jackson
et al. [19]
22 61 M Rt.hemisphere NA
Syn(+), NSE(+),
GFAP(+), P53(+),
NF(+)
F +- NA 2001 Taddei
et al. [9]

O. COHEN-INBAR ET AL. 14
23 6 F Vermis Syn(+), S100(+),
GFAP(-) Syn(+), S100(+) 33.3 ++
Chemotherapy tx.
As well, A at 6
months
2002 Sharma
et al.
24 53 F Rt. hemisphere GFAP(+),
Vim(+), NSE(+)Syn(+), NSE(+) <5 ++ A at 1 year 2002 Montagna et al.
25 49 F Vermis,
Intra-ventricular Syn(+) weak Syn(+), S100(+), GFAP(+), P53(−)<1 ++ D at 19 months 2003 Aker et al. [6]
26 45 F Rt. hemisphere NA GFAP(+), NSE(+),
CEA(−) <2.5+3.6 Gy**
Chemotherapy tx.,
AAW at 3 years. 2003 Elshihabi et al. [3]
27 38 F Lt. hemisphere NA NA NA+NA NA 2003 Amina
et al. [7]
28 64 M Rt. hemisphere NSE(+), NF(+),
GFAP(+)
NSE(+), NF(+),
GFAP(−) 20 +15.4 Gy
R at 3.5 years,
Reop. A at 5
months
2005 Buccoliero
et al. [30]
29 39 M Vermis,
Intra-ventricular NA NSE(+), Syn(+), GFAP(−), NFP(−)<1 +- A at 45 days 2006 Bayar et al. [8]
M/F – male / female, Adi – adipocytes, Tc – Tumor cell, S – surgery, RT – radiotherapy, F - Focal, Pi – Proliferation index, D – Deceased, A – alive, AAW –
alive and well, R – recurrence, NA – not available, GFAP – Glial fibrillar acid protein, NSE – neural specific enolase, Syn – synaptophysin, Vim – vimentin.
CPA – cerebellopontine angle, Reop –reoperation, *36 Gy for the entire brain, 56 Gy boost to posterior fossa; **3.6 Gy to the spine and whole brain, 1,800
cGy boost dose to the posterior fossa. The patient also received chemotherapy for 12 months, consisting of cisplatin, PCNU, and vincristine.
craniospinal radiation of 36 Gy and a boost to the poste-
rior fossa of about 18 Gy. High-risk patients with resid-
ual or metastatic disease should receive additional che-
motherapy with cisplatin, etoposide, and cyclophospha-
mide [2,31]. Out of the twenty-nine patient described,
four pediatric patients operated on underwent a GTR.
Proliferation index was >3% in all children, all received
radiotherapy following different protocols, one patient
received chemotherapy. Prognosis was dismal, with most
children deceased during the follow-up (3 out of 4 pa-
tients). Of the remaining 25 patients described, 12 re-
ceived radiotherapy following the operation (described
as GTR for all) following different protocols. Prolifera-
tion index in this group was >3% in 7 patients (58%), as
compared to 15% in those not receiving radiotherapy.
Only a single recurrence is described in the irradiated
group (as compared to 3 in those not receiving radio-
therapy), although a significantly higher mortality rate
was noted in those patients receiving radiotherapy (8
patients versus 3 in those not irradiated). This can be
attributed to iatrogenic irradiation induced pathology,
concurrent illnesses, a more aggressive tumor behavior
or a combination of all of the above [Table 2]. Trying to
construct a Kaplan-Meier (KM) survival curve is some-
what problematic, still supporting the same conclusions
[Table 1, Figure 5]. The main weakness of the KM
curve stems from the small sample size, inherent to this
tumor. Of the eleven patients not receiving radiotherapy,
three died during the follow-up. Of the sixteen patients
irradiated, eight died during the follow-up. Incomplete
data required for the KM curve construction exist for two
patients [no. #22 and #27 in Table 2]. The KM curve,
under the caveats mentioned, supports the argument that
radiotherapy and accompanying morbidity is not proven
in the liponeurocytoma patient, actually resulting in
shorter survival.
The indolent clinical behavior and suspected natural
history of the cerebellar liponeurocytoma, manifesting as
a slowly growing lesion only locally recurrent, raises
doubts about the appropriateness of adjuvant radiothe-
rapy and/or chemotherapy. Such an aggressive treatment
approach, having a high biological toil and horrible
iatrogenic side effects [8] has not been proven effective
enough to our opinion, given any outcome parameter as
an indicator. According to Kleihues [1], the prognosis is
favorable if the MIB-1 index is in the range of 1% ~ 3%
and aggressive adjuvant therapy is not mandatory. There
have been no reports of spinal drop metastases in the
literature and it is therefore reasonable to avoid spinal
radiation [8]. In our patient, after reviewing current
literature, a joint multidisciplinary staff comprising of
neurosurgeons, neuro-oncologists, neuroradiologists and
neuropathologists has recommended pursuing a conser-
vative treatment approach with close clinical and radio-
logical follow-up.
4. Conclusions
The small number of patients reported with this type of
lesion, limits our understanding of this tumor's natural
history. Most of the information available from case re-
ports indicates that this tumor has a benign biological
behavior and prognosis in adults. Thus, expectant treat-
ment with close follow-up seems both prudent and suffi-
cient. We suggest that a patient with established liponeu-
rocytoma, who underwent aGTR, and in which the tu-

O. COHEN-INBAR ET AL.15
Figure 5. Kaplan-Meier survival curve by months, as influenced by treatment with radiotherapy.
mor shows a low proliferation index, can undergo a
yearly MRI and follow-up with no additional adjuvant
care. The patient presented underwent a GTR in both
operations, received no adjuvant treatment during the last
18 years, hence presenting the natural history of this tu-
mor after a surgical intervention and spared the side-
effects of un-necessary radiotherapy or chemotherapy.
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