Neurosurg Rev (2009) 32:171–179

DOI 10.1007/s10143-009-0185-5

ORIGINAL ARTICLE

Tumefactive demyelinating lesions: nine cases and a review

of the literature
Lei Xia & Song Lin & Zhong-cheng Wang & Shao-wu Li &
Li Xu & Jing Wu & Shu-yu Hao & Chuan-chuan Gao

Received: 18 April 2008 / Revised: 8 November 2008 / Accepted: 6 December 2008 / Published online: 27 January 2009
# Springer-Verlag 2009

Abstract Tumefactive demyelinating lesions (TDLs) are
misdiagnosed frequently. To investigate the characteristics
of TDLs, clinical and radiological data from nine cases with
TDLs were analyzed after admission. All cases underwent
surgery and pathological examination; some received
postoperative steroid therapy. Onsets were mostly within
3 weeks and main presentation included intracranial
hypertension, extremity weakness, epilepsy, and visual
disturbance. Symptoms in children were acute and severe,
frequently including headache, vomiting, and visual distur-
bance. Most intracephalic lesions were in cerebral hemi-
spheres. All intraspinal lesions were in cervical segments.
Radiological features included mass effect, perifocal edema
and enhancement (of which open-ring enhancement was
diagnostic), and decreased relative cerebral blood volume.
Intraoperative frozen section did not confirm the diagnosis,
while postoperative paraffin section did confirm it (by
evidence of macrophage infiltration). The patients responded
L. Xia : Z.-c. Wang : L. Xu : S.-y. Hao : C.-c. Gao
Beijing Neurosurgical Institute, Capital Medical University,
Beijing 100050, China
S. Lin
Neurosurgical Department, Beijing Tiantan Hospital,
Capital Medical University,
Beijing 100050, China
S.-w. Li : J. Wu
Image Center of Neuroscience, Beijing Tiantan Hospital,
Capital Medical University,
Beijing 100050, China
S. Lin (*)
Beijing Neurosurgical Institute, Beijing Tiantan Hospital,
Tiantan Xi li No. 6,
Beijing 100050, China
e-mail: linsong2005@126.com
well to steroid therapy and no relapse was found during
following up. Thus, intensive analysis of both clinical and
radiological data may provide some clues for diagnosis. For
suspected cases, it is advisable to take steroid therapy or
undergo advanced radiological examinations, such as serial
magnetic resonance spectroscopy. However, in difficult
cases, pathological evidence is beneficial to a final diagnosis.
Keywords Tumefactive demyelinating lesions .
Demyelinating pseudotumor . Demyelinating diseases .
Brain neoplasms
Introduction
The primary demyelinating diseases of the central nervous
system (CNS) encompass a series of entities, such as acute
disseminated encephalomyelitis, acute hemorrhagic leu-
koencephalopathy, and various types of multiple sclerosis
(MS). The latter entity includes chronic type (Charcot type),
acute type (Marburg type), myelinoclastic diffuse sclerosis
(Schilder type), concentric sclerosis, and optic neuromye-
litis (Devic type), of which Charcot type (classical MS) is
the most common and best known. But a rare demyelinat-
ing disease presenting as a large (>2 cm) focal area of
demyelination associated with mass effect can mimic brain
neoplasm or abscess. This disease have been called
“demyelinating pseudotumors,” “tumor-like demyelinating
lesions (TDLs),” “tumefactive demyelinating lesions,” and
“tumefactive multiple sclerosis lesions” in literature. Be-
cause of the tendency to mimic tumor or abscess clinically,
radiologically, and even pathologically and because of
important differences in treatment, it is critical to differen-
tiate among them in diagnosis. In this study, nine cases
pathologically diagnosed as having TDLs are presented. By
172
reviewing related reports, clinical, radiological, and patho-
logical characteristics of a TDL diagnosis are summarized.
Materials and methods
The criteria for patient enrollment included clinical
presentation mimicking neoplasm and biopsy confirming
the TDLs. After excluding one case of astrocytoblastoma
at repeat pathological investigation, nine patients were
included at Tiantan hospital (Beijing, China) from Jan.
2005 to Mar. 2007 (Table 1). Routine admission examina-
tions, including physical examination, laboratory investiga-
tion, electrocardiogram, and X-ray, were performed in all
cases. Preoperative scans (computed tomography (CT) or
magnetic resonance imaging (MRI)) were examined. All
patients underwent operations to biopsy or remove the lesions.
In some cases, intraoperative frozen sections were investigat-
ed. TDLs were confirmed by hematoxylin and eosin (H&E) or
immunohistochemical staining with glial fibrillary acidic
protein, neurofilament, synaptophysin, myelin basic protein,
N-ethylmaleimide sensitive fusion protein, Vimtin, CD68,
and CD34 in all cases. Some patients also received medical
treatment and postoperative follow-up scans.
Results
Clinical features were as follows:
Age
The age of the patients at onset ranged from 4 to 65 years.
Two patients were children aged 4 and 11 years. Three
patients were in their 30s. Two patients were older than 40.
The other patient was 65 years old.
Sex
Four of the patients were female. Of the six patients with
intracephalic lesions, three were females. Of the three
patients with intraspinal lesions, two were male.
Duration from onset to admission
The duration from onset of symptoms to admission to
hospital ranged from 1 week to about 1 year; it was less
than 10 days for both children and was about 1 to 2 months
in five of the adults.
Chief symptoms and signs
Headache and vomiting occurred only in the two children.
Six of the patients presented with weakness in the extremities,
and two patients had epilepsy. General numbness/loss of
sensation was only found in the three patients with intraspinal
lesions. One patient complained of decreased visual acuity.
Neurosurg Rev (2009) 32:171–179
Location and number of lesions (by CT/MRI scan)
Of the six intracephalic lesions, four were in cerebral
hemisphere; one was in pons and one was in the basal
ganglia. All three intraspinal lesions were found in the
cervical cord and involved multiple segments. Two addi-
tional intracephalic lesions were found in two cases on MRI
scans: one was a left frontoparietal mass (accompanying
lesions in left frontal lobe, corpus callosum, and cerebellar
hemisphere); the other was a left brachium pontis mass
accompanying a lesion in left frontal lobe.
Lesion appearance on imaging
All lesions appeared as hypodensities on CT, hypointen-
sities on T1-weighted MRI, and hyperintensities on T2-
weighted MRI. The lesions all occurred together with
perifocal edema. The edema was remarkable in the
cases that had shorter histories (less than 3 weeks).
Also, there were marked mass effects in the acute cases.
In all cases with intraspinal lesions, spinal cord
swellings were found on MRI. The intracephalic lesions
displayed patchy enhancement in the children, ring
enhancement in three adults, and nodular enhancement
in one adult (Figs. 1, 2, 3, and 4). The intraspinal lesions
were all irregularly enhanced (Figs. 5 and 6). Decreased
relative cerebral blood volume (rCBV) and prolonged
mean transit time (MTT) were seen in one intracephalic
lesion (Fig. 4).
Preoperative diagnosis
Eight were preoperatively diagnosed as gliomas and one
was metastasis.
Intraoperative findings
Of the nine total lesions, five appeared grayish red; three
were grayish yellow in three patients and one was
yellowish green (with a 1.5-cm cyst and yellowish-green
fluid). Eight of the lesions were soft and one was tough.
Eight of the lesions had obscure boundaries, while one had
a distinct boundary. Six lesions appeared to be moderately
vascularized; two were well vascularized and one had
minimal vascularity. Intracephalic lesions were completely
resected in one patient, almost completely resected in
another, mostly resected in three patients, and biopsied
only in the case of one patient with a pontile lesion.
Intraspinal lesions were partly resected in two patients and
biopsied in one patient.
Results of intraoperative frozen sectioning and postoperative
paraffin sectioning
Five lesions underwent intraoperative frozen sectioning.
Two of these lesions were gliosis; one was an astrocytoma;
Table 1 Summary of patients

Patient Age Sex Onset of clinical Neuroimaging features Intraoperative findings Intraoperative Postoperative Medical treatment and follow-up
symptoms and signs frozen events
sections

1 4 Male Headache and Well-defined right frontotemporal mass, Gray red, soft, fish-like, well Astrocytoma Fever for Receiving steroid and transported to pediatric
vomiting for hypodensity and hypointense T1 vascularity, obscure 8 days, department, doing well after steroids, the
1 week, hemiparesis hyperintense T2, vasogenic edema, marked boundary, largely resection hemiparesis lesion disappeared on MRI 22 months later
in left lower mass effect, patchy enhancement resolved
extremity for 2 days
2 11 Female Headache and Poorly defined left frontoparietal mass, Yellow green, soft, obscure Gliosis Visual acuity Transported to pediatric department and
Neurosurg Rev (2009) 32:171–179

vomiting for hypodensity, vasogenic edema, marked mass boundary, moderate progressively receiving steroid, doing well and visual acuity
10 days, visual effect, patching enhancement; left frontal, vascularity, with a 1.5-cm decreasing and decreasing resolved after steroids, remnant
acuity decreasing at corpus callosum and cerebellar hemisphere cyst with yellow green diagnosed as lesion shrunk on MRI 12 months later
the fifth day after abnormal enhancement fluid; largely resection optic neuritis
admission
3 27 Female Dizzy and ataxia, Poorly defined left brachium pontis lesion, Gray, soft, obscure Cerebellar Fever for Facial palsy maintained as usual
aphagia left facial hypointense T1 hyperintense T2, vasogenic boundary, moderate tissue 10 days
palsy for 5 years edema, minimal mass effect, irregular ring vascularity, biopsy
enhancement; left frontal lesion
(demyelination)
4 32 Female Right lower extremity Well-defined left parieto-occipital round Part gray red and part light Tumor tissue Fever for 6 days Doing well, lesion disappeared on MRI
weakness for lesion, hypointense T1 hyperintense T2, yellow, soft, obscure and 8 months later
20 days and seizure vasogenic edema, marked mass effect, ring boundary, moderate hemorrhagic
once enhancement vascularity, near total necrosis
resection
5 45 Male General seizure once Poorly defined right frontoparietal lesion, mix Dark yellow, soft, obscure The left upper Transport to neurological department to receive
2 weeks ago, left intense, marked vasogenic edema, marked boundary, well vascularity, extremity steroids for l month; the muscle strength
extremities mass effect, irregular nodular enhancement, total resection paralyzed, the recovered to grade 5, the lesion disappeared
weakness rCBV decreasing muscle on MRI 14 months later
strength was
grade 1
6 42 Female Left hemianesthesia Poorly defined C3–4 lesion, hypointense T1 Gray yellow, soft, distinct Gliosis General seizure Discharging and receiving antiepileptic
and right upper hyperintense T2, spinal swelling, moderate boundary, moderate one time treatment, no neurological deficit and the
extremity weakness patching enhancement vascularity, partly resection lesion disappeared on MRI 12 months later
for 20 days
7 44 Male Upper extremity Poorly defined C2–6 lesion, hypointense T1 Gray red, soft, obscure Fever for 7 days Receiving steroid and vitamin B1, B12, and
anesthesia for hyperintense T2, spinal swelling, moderate boundary, moderate transported to neurological department for
2 months and lower mixed strip-like enhancement vascularity, partly resection steroid treatment, anesthesia persists, no other
extremity for neurological deficit, the lesion disappear on
20 days MRI 32 months later
8 65 Male Lower extremity Poorly defined C1–7 lesion, hypointense T1 Gray, firm, minimal Smooth Receiving steroid and vitamin B1, B12; the
paraplegia and hyperintense T2, spinal swelling, irregular vascularity, obscure patient aggravated to quadriplegia for 2 years,
anesthesia for strip-like enhancement boundary, biopsy and the relatives gave up positive treatment
12 months
9 35 Male Right extremities Poorly defined left basal ganglia lesion, Gray red, soft, moderate Smooth Transported to neurological department and
weakness for hypointense T1 hyperintense T2, irregular vascularity, obscure doing well after steroids, died from
1 month open-ring enhancement boundary, largely resection pneumonia 1 year later
173
174 Neurosurg Rev (2009) 32:171–179

Fig. 1 a, b CT scan showed left

parietal lobe hypodense lesion
with perifocal edema (a). After
contrasting, the lesion displayed
open-ring enhancement

another was cerebellar tissue and the last one was tumor Follow-up
tissue with hemorrhagic necrosis.
Eight patients underwent follow-up examination up to
Postoperative paraffin pathological findings showed the
32 months following the surgical procedure (mean =
diffuse presence of infiltrating macrophages with finely
17 months). The lesion disappeared on MRI later in five
vacuolated cytoplasms. A final diagnosis of TDLs was
cases and shrank in one case. Overall, Six cases received
rendered in all cases (Fig. 7).
postoperative steroid therapy. Five patients responded well
to steroids and one progressed to quadriplegia.
Postoperative course

Five cases presented with postoperative fever which lasted Discussion

for 5–10 days. One patient presented with progressively
decreasing visual acuity, which was diagnosed as optic
neuritis and was treated with steroid therapy. (Visual acuity
remarkably improved 10 days later.) One patient had a
general seizure and was given an antiepileptic agent. One
patient suffered from facial palsy and another’s hemi-
paralysis was relieved.
TDLs are rare disease of the CNS. It has been documented that
TDLs are most commonly seen in the initial background of MS
[4, 9, 11, 14, 20, 23, 28, 30, 36, 37, 40, 45]. Other primary
demyelinating diseases, such as myelinoclastic diffuse sclero-
sis (Schilder’s disease) [1, 44] and acute disseminated
encephalomyelitis [26], can also manifest as tumefactive

Fig. 2 a, b Postcontrast T1-

weighted image showed left
basal ganglia lesion with
irregular open-ring enhancement
Neurosurg Rev (2009) 32:171–179 175

Fig. 3 MRI showed that the lesion was in the left brachium pontis and hypointense in T1 (a), hyperintense in T2 (b), with irregular ring
enhancement (c)

lesions. It has been suggested that TDLs may represent either
a variant of MS [38] or a unique form of isolated
demyelinating disease [26]. Some patients were found to have
developmentally immature myelin basic protein, pointing to a
genetic predisposition to more severe demyelination [46].
Others have antecedent vaccination or infection, suggesting
the involvement of an autoimmune mechanism [26]. The
clinical, radiological, and pathological presentations of TDLs
resemble brain tumors, leading to unnecessary biopsy, surgery,
or even radiotherapy which usually causes aggravation.
TDLs have no specific clinical presentation and lesions
can occur at any age (a range of 2 to 71 years has been

Fig. 4 MRI T2-weighted image

showed the right parietal hyper-
intense lesion with perifocal
edema (a). Postcontrast T1-
weighted image showed that the
lesion displayed heterogeneous
nodular enhancement (b).
Perfusion-weighted image
showed decreased rCBV (c) and
prolonged MTT (d) within
lesions and perifocal tissue as
compared with that within the
contralateral normal-appearing
white matter
176
Fig. 5 MRI showed that the lesion was in the cervical cord and hypointense in T1 (a), hyperintense in T2 (b), with irregular enhancement (c)
reported [26, 34, 48]). A history of relapsing–remitting MS
symptoms or preceding vaccination or viral infection may
provide the diagnostic clue of demyelinating diseases.
TDLs have a relatively acute onset (mostly less than
3 weeks in the present study) with a progressive aggrava-
tion in symptoms. Onset time for children is typically
within 1 week [34, 48]. In children, symptoms are acute
and severe and usually include headache and vomiting
resulting from intracranial hypertension [34, 48]. Moreover,
it is notable that pediatric cases frequently present with
symptoms of optic neuritis, such as visual acuity and field
changes [2, 34]. In this study, one child developed
decreased visual acuity 1 week after admission. Having
gone unnoticed, the child’s visual acuity decreased abruptly
thereafter, resulting in an examination of the optic fundi and
a diagnosis of optic neuritis.
There are several important radiological hallmarks that
favor the detection of demyelination. TDLs are mainly
localized in the subcortical hemispheric white matter [12,
26] and may also be found in the corpus callosum [25, 39]
Fig. 6 MRI showed another intraspinal lesion which involved multiple cervical segments and caused spinal swelling
Neurosurg Rev (2009) 32:171–179
or pons. In cases with spinal lesions, multiple cervical
segments appear to be most often involved [5, 6, 18, 29].
Indeed, in this study, the lesions of all three intraspinal
cases were confined in cervical segments. This observation
is helpful in diagnosis. The presence of other demyelinating
changes in the CNS, especially in periventricular areas or
spinal cord, may be indicative of further demyelinating
lesions [12, 34]. In two cases in this study, multiple lesions
were found in the frontal lobe, corpus callosum, and
cerebellum on MRI. An additional characteristic of TDLs
is their relative lack of mass effect and less substantial
perifocal edema compared to brain neoplasm [12]. The
pattern of enhancement in the lesions is an important
identifying feature. It consists of “open-ring” enhancement,
as compared to the complete ring of enhancement seen in
abscesses and tumors. The open-ring sign was present in
70% of cases with demyelinating disease [33]. In some
cases, the open portion of the partial ring abuts the cortical
gray matter or basal ganglia and the area of enhancement
sweeps through the white matter [32]. The area of
Neurosurg Rev (2009) 32:171–179
Fig. 7 H&E staining showed the diffuse presence of infiltrating
macrophages with finely vacuolated cytoplasm. Original magnifica-
tion ×400
enhancement is regarded as the border of demyelination
and therefore localized at the site of whiter matter [22],
while the nonenhancing center of the lesion represents
chronic inflammation.
Some advanced radiological techniques have been
applied to TDLs. It was noted from several MRI perfusion
studies that dilated veins drain toward distended subepen-
dymal veins, running centrally within TDLs on T2 images
[8]. It was reported that the mean rCBV within TDLs was
lower than that within the contralateral normal-appearing
white matter and substantially less than that found in high-
grade gliomas [8, 17]. In this study, decreased rCBV was
found in a case which was misdiagnosed as glioma.
Therefore, decreased rCBV is an important clue. Apparent
diffusion coefficients within TDLs are mildly increased,
which is helpful in differentiating ring-enhancing TDLs
from cerebral abscesses—the latter being associated with
restricted diffusion centrally within the lesions. Neoplasms
with central necrosis may also display increased diffusion
coefficients centrally within the lesion, which make it less
helpful in differentiating from neoplasms [21]. Proton
magnetic resonance spectroscopy (MRS) is a powerful
noninvasive tool. Although several nonneoplastic brain
lesions (including TDLs) may produce an magnetic
resonance spectrum mimicking a neoplastic process [17,
41], the mean central-region NAA to Cr ratio in gliomas
was significantly lower than that of TDLs [41]. Also, the
size of the glutamate/glutamine peaks, which are typically
not seen in aggressive intra-axial neoplastic processes, may
be useful [10]. It should be mentioned, however, that MRS
findings in patients with TDLs vary with disease stage.
Acute demyelinating plaques show an MRS spectrum
similar to that of low-grade gliomas, with reduction in
NAA and an increase in choline. Therefore, the use of serial
proton MRS has proven to be beneficial in distinguishing
177
these lesions. If serial proton MRS shows no obvious
changes, which is inconsistent with the course of acute
demyelinating plaque, it supports the diagnosis of neo-
plasms [7]. Decreased magnetization transfer value (MTV)
has been shown in MS plaques. A similar decline in MTV
within TDLs was also observed [17], with MTV decline
around or below 30% in the chronic TDLs [15, 35].
Positron emission tomography shows a low or no uptake of
glucose, methionine, or choline [27] and a marked increase
in the uptake of tyrosine, which is nonspecific [19].
Diagnostic therapy is critical for the final diagnosis of
TDLs. In whom the diagnosis of TDLs is suspected, repeat
MRI may be performed during or shortly after completion of
corticosteroid therapy [34]. Although perifocal edema asso-
ciated with tumor or abscess may respond to corticosteroids,
a rapid reduction in the size of the lesion associated with
significant clinical improvement favors demyelination.
Noteworthy is the fact that MS can coexist with gliomas
and lymphomas [13, 42]. The concurrence of MS and
gliomas could be purely coincidental or the result of
neoplastic transformation of reactive glial cells in the areas
of demyelination. A nonenhancing tumefactive lesion in a
patient with MS is highly suspicious for the presence of
low-grade glioma since TDLs typically display contrast
enhancement. Some cases of TDLs preceding the appear-
ance of primary cerebral lymphoma have been reported [3].
Many MS patients receive corticosteroids and other
immunosuppressant medications and develop an immuno-
compromised state; this might contribute to the occurrence
of a primary CNS lymphoma [47] and an elevated risk of
infection and abscess [34].
Overall, when differentiation cannot be confidently
established, a biopsy is advisable—especially paraffin-
embedded tissue sections followed by staining. However,
the histologic features observed on intraoperative frozen-
section preparations can be deceptive and difficult to
interpret, especially when neoplasms have been previously
diagnosed by neurosurgeons or radiologists. As seen in this
study, no frozen sections suggested a diagnosis of TDLs.
The histologic tableau consisting of astrocytosis, atypical-
appearing reactive astrocytes with mitotic figures, and
lymphocytic infiltrates can closely mimic gliomas. The
key to avoiding misdiagnosis of demyelinating disease is to
identify the macrophage infiltrate. But macrophages in
brain tissue are frequently mistaken for infiltrating neoplas-
tic astrocytes or oligodendroglia. The immunohistochemi-
cal staining for histiocytes (anti-HAM 56 and CD68
antibody) is helpful [16].
Most patients with TDLs usually respond well to high
doses of corticosteroids [26], especially children (as seen in
this study and others), while a poor response to such
therapy occurs mainly in adults when associated with MS.
It has been reported that these steroid-unresponsive cases
178
can be successfully treated with plasma exchange and
mitoxantrone [24, 31].
Most patients with TDLs have a single acute clinical
attack and generally do not undergo recurrence. However,
some of these patients may evolve to MS [43].
Conclusions
The diagnosis of TDLs is a challenge for neurosurgeons,
neuroradiologists, and neuropathologists. First of all, neuro-
surgeons should be aware of the existence of nonneoplastic
masses in CNS and should be rid of traditional ideas, which
may help to avoid the thought processes leading to
misdiagnosis. Comprehensive information from the
patient’s history and results of steroid therapy may provide
clues for the final diagnosis. Open-ring enhancement is
relatively characteristic and mild mass effect and perifocal
edema is also useful. Decreased rCBV in the lesion should
be noticed and emphasized. While it is advisable to observe
suspected cases dynamically by serial MRS, pathological
data are still beneficial to the final diagnosis in difficult
cases, especially paraffin sections and special staining.
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Comments
Chang Jin Kim, Seoul, Korea
The authors reported on a pathologically proven series of
tumefactive demyelinating lesions with nine cases, and conducted a
comprehensive review on clinical, radiological, and therapeutic
consideration. Awareness of demyelinating lesions mimicking brain
neoplasm is important for neurosurgeons in that they can be
179
appropriately managed simply by medication. Actually, unnecessary
biopsy or even resective surgery has been applied by the authors based
on preoperative misdiagnosis, although pathologic diagnosis may be
required only on limited occasions. Considering the clinical similar-
ities, utmost care should be taken interpreting the neuroradiologic data
to differentiate neoplastic conditions from this kind of nonneoplastic
inflammatory disease. Further investigation using advanced magnetic
resonance (MR) techniques such as MR diffusion and perfusion
sequences and, especially, MR spectroscopy together with analysis of
the cerebrospinal fluid may obviate the need for brain biopsy in many
circumstances.
Jin-song Wu, Liang-fu Zhou, Shanghai, China
Primary central nervous system (CNS) demyelinating lesions,
including multiple sclerosis, are a group of disorders with unknown
etiology. Classical CNS primary demyelination is often made on
clinical ground. Histological diagnosis is uncommon except when
atypical clinical or imaging features are present. Tumefactive
demyelinating lesions (TDLs) pose a diagnostic challenge as they
simulate neoplasm. Dr. Xia et al. reported nine cases of tumefactive
demyelinating lesions mimicking CNS malignant neoplasm and a nice
review of the literature. When a single large or multiple small
tumefactive demyelinating lesions are present, the correct presurgical
diagnosis is often difficult, as the MRI appearance, comprising
enhanced T1-weighted images, T2-weighted images, and even proton
MR spectroscopy, is not specific for these lesions. The diffusion
imaging of MRI was proven to be a useful tool in differentiating ring-
enhancing tumefactive demyelinating lesions from cerebral abscesses,
while the perfusion imaging of MRI was reported to be showing
decreased perfusion within tumefactive demyelinating lesions, as
compared with high-grade gliomas and lymphomas (1). However,
these imaging features are not specific, given that the degree of
overlap is most likely with other pathological processes. Therefore, an
image-guided biopsy is recommended for suspected patients. The
initial frozen-section specimen should be sent to neuropathologist. In
our opinion, it is still feasible for the experienced neuropathologist to
differentiate this lesion from malignant gliomas. In short, the neuro-
surgeons should be aware of the broad and heterogeneous spectrums
of TDLs in clinical, imaging, and pathological manifestations. The
exact perioperative diagnosis is essential to avoid unnecessary
resection and improper adjunctive therapy.
References
1. Given CA 2nd, Stevens BS, Lee C (2004) The MRI appearance
of tumefactive demyelinating lesions. AJR Am J Roentgenol
182:195–199
Takamasa Kayama, Yamagata, Japan
The authors described a pathologically proven series of tumefac-
tive demyelinating lesions with nine cases. It is important that
clinician be of aware demyelinating lesions mimicking brain neo-
plasm. Actually, radiological findings including rCBV are very useful,
but they are not able to replace pathological diagnosis so far. It is
noteworthy that intraoperative frozen section did not confirm the
diagnosis. We must avoid unnecessary respective surgery. This report
makes an important contribution for the differential diagnosis and the
preoperative planning of the lesions mimicking brain neoplasm.