Comparison between the cranial magnetic resonance imaging features of neuromyelitis optica spectrum disorder versus multiple sclerosis in Taiwanese patients
Comparison between the cranial magnetic resonance imaging features of neuromyelitis optica spectrum disorder versus multiple sclerosis in Taiwanese patients
Ming-Feng Liao 1
Kuo-Hsuan Chang 0 1
Rong-Kuo Lyu 1
Chin-Chang Huang 1
Hong-Shiu Chang 1
Yih-Ru Wu 1
Chiung-Mei Chen 1
Chun-Che Chu 1
Hung-Chou Kuo 1
Long-Sun Ro 0 1
0 Department of Neurology, Chang Gung Memorial Hospital , 199, Tung Hwa North Road, Taipei , Taiwan
1 Department of Neurology, Chang Gung Memorial Hospital-Linkou Medical Center and Chang Gung University College of Medicine , Taipei , Taiwan
Background: Neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS) are inflammatory diseases of the central nervous system with different pathogenesis, brain lesion patterns, and treatment strategies. However, it is still difficult to distinguish these two disease entities by neuroimaging studies. Herein, we attempt to differentiate NMOSD from MS by comparing brain lesion patterns on magnetic resonance imaging (MRI). Methods: The medical records and cranial MRI studies of patients with NMOSD diagnosed according to the 2006 Wingerchuk criteria and the presence of anti-aquaporin 4 (anti-AQP4) antibodies, and patients with MS diagnosed according to the Poser criteria, were retrospectively reviewed. Results: Twenty-five NMOSD and 29 MS patients were recruited. The NMOSD patients became wheelchair dependent earlier than MS patients (log rank test; P = 0.036). Linear ependymal (28% vs. 0%, P = 0.003) and punctate lesions (64% vs. 28%, P = 0.013) were more frequently seen in NMOSD patients. Ten NMOSD patients (40%) had brain lesions that did not meet the Matthews criteria (MS were separated from NMOSD by the presence of at least 1 lesion adjacent to the body of the lateral ventricle and in the inferior temporal lobe; or the presence of a subcortical U-fiber lesion or a Dawson finger-type lesion). The different image patterns of NMOSD didn't correlate with the clinical prognosis. However, NMOSD patients with more (10) brain lesions at onset became wheelchair dependence earlier than those with fewer (<10) brain lesions (log rank test; P < 0.001). Conclusions: The diagnostic sensitivity of NMOSD criteria can be increased to 56% by combining the presence of linear ependymal lesions with unmet the Matthews criteria. The prognoses of NMOSD and MS are different. A specific imaging marker, the linear ependymal lesion, was present in some NMOSD patients. The diagnosis of NMOSD can be improved by following the evolution of this imaging feature when anti-AQP4 antibody test results are not available.
Neuromyelitis optica; Multiple sclerosis; Anti-aquaporin 4 antibody; Magnetic resonance imaging
Neuromyelitis optica (NMO) is an inflammatory disease
mainly characterized by optic neuritis (ON) and
longitudinally extensive spinal cord lesions (LESCLs) [1,2]. It
displayed relapsing and remitting disease course and central
nervous system (CNS) inflammation which is similar to
Asian or optico-spinal form multiple sclerosis (OSMS).
The discovery of NMO biomarker anti-aquaporin-4
(anti-AQP4) antibody clearly separates these two
diseases into different entities [1-3]. Anti-AQP4 antibody
plays an important role in the pathogenesis of NMO. It is
reported in around 61% ~ 90% of patients with NMO and
in only 0% ~ 9% of MS patients [4-7]. Typical LESCLs are
rarely seen in the patients with multiple sclerosis (MS).
This clear distinction suggests that NMO and MS could
be two different CNS inflammatory disorders with respect
to their immunopathogenesis [4,8].
Some patients with anti-AQP4 antibody had recurrent
optic neuritis, recurrent myelitis, optic neuritis and
myelitis associated with systemic autoimmune disease or the
brain lesions, rather than the typical features of optic
neuritis and LESCLs. Those patients are regarded as
having NMO spectrum disorder (NMOSD) [8,9]. The
reported frequency of brain involvement in NMO patients
ranges from 5% to 89% [10-25]. The brain lesions of
NMOSD also become temporally and spatially
disseminated, as do those of MS. Around 5.6% ~ 42% of brain
lesions in NMOSD fulfill the Barkhof magnetic
resonance imaging (MRI) criteria [11,13,16,19,20,26]. Although
Matthews et al. have proposed criteria to distinguish
NMOSD from MS by identifying characteristic cerebral
lesions for NMOSD in the hypothalamus and
periaqueductal area [10-16,20,26-30], validation, especially in Asians, is
still required [27,31,32]. Given that the pathogenesis and
treatment of NMOSD and MS are different, the standard
immunomodulation therapy for MS, such as interferon,
may be ineffective to control relapses or disease progression
of NMO [8,33-35]. Specific imaging markers are needed to
distinguish NMOSD from MS particularly in the early
stage. By comparing the cranial magnetic resonance
imaging (MRI) characteristics of NMOSD with those of MS,
we found linear ependymal and punctate lesions specifically
occurring in patients with NMOSD, whereas corpus
callosum lesions are frequently seen in patients with MS. This
clear difference in imaging features will be helpful in
distinguishing NMOSD from MS in clinical practice.
We retrospectively reviewed the medical records of all
NMO or MS patients with one or more episodes of CNS
inflammatory disease treated between January 2009 and
January 2014 at Chang Gung Memorial Hospital-Linkou
Medical Center, a tertiary referral medical center in the
northern Taiwan. A CNS inflammatory episode was defined
as the presence of patient-reported symptoms or objectively
observed typical signs of an acute inflammatory event
including optic neuritis and myelitis in the CNS, with
duration of at least 24 hours . Patients with optic neuritis is
diagnosed as having typical clinical symptoms of blurred
vision and visual-field defect with evidence of a relative
afferent pupillary defect (by neurological examination or
prolonged p100 wave of visual evoke potential study) ,
or by the diagnosis of ophthalmologists. At the time of the
attack, all patients were tested for anti-AQP4 antibodies to
confirm the diagnosis. The protocol of this study was
approved by the Institutional Review Board of Chang Gung
Memorial Hospital and University (License no. 101-3410B).
Diagnosis of NMOSD and MS
The diagnoses of NMO and MS were according to the
revised 2006 Wingerchuk criteria  and Poser criteria
, respectively. The NMO patients who also had brain
lesions were diagnosed as NMOSD . All NMOSD
patients had both optic neuritis and myelitis during the
follow-up periods. The serum anti-AQP4 antibodies were
detected using an enzyme-linked immunosorbent assay
(ELISA) system according to the manufacturers
instructions (RSR/Kronus, Cardiff, UK) , and a level greater
than 5 U/mL was considered seropositive. There are
reports of combined autoimmune disease (myasthenia gravis
or Sjgrens syndrome) with NMOSD [40-43]. To simplify
the study population, patients with Sjgrens syndrome,
systemic lupus erythematosus, rheumatoid arthritis,
vasculitis, myasthenia gravis or underlying malignancies were
excluded in our study.
Collection of clinical and imaging data
We retrospectively reviewed patients clinical data
including gender, age of onset, clinical symptoms, results
of cerebrospinal fluid (CSF) analysis, and auto-antibody
profiles (antinuclear antibody [ANA], rheumatoid factor
[RF], and anti-Sjgrens syndrome A [SSA]/ Sjgren
syndrome B [SSB] antibodies). Cranial MRIs were taken
during the clinical relapse; the protocols included T1
(repetition time [TR] = 250 ~ 760 ms, echo time [TE] =
1.8 ~ 20 ms), T1-enhanced, T2-weighted (TR = 2830 ~
6400 ms, TE = 70 ~ 120 ms), and fluid-attenuated
inversion recovery (FLAIR) sequencing images (TR = 7000 ~
9800 ms, TE = 70 ~ 150 ms). The sections were obtained
at 4 or 5 mm slice thickness. Several cranial MRI studies
were carried out during the follow-up periods, and any
abnormality in a series of MRI images was noted. The same
MRI abnormalities detected by repeated MRI studies in
the same patient were not counted again (no double
counting). We used the term linear ependymal lesions
(Figure 1A-C) to describe the symmetric and continuous
Figure 1 Brain MRI findings of three NMOSD patients and three MS patients. FLAIR MRI shows a (A) continuous linear ependymal lesion
along the ventricle in a 29-year-old woman with NMOSD; (B) symmetrical hypothalamic lesion in an 18-year-old girl with NMOSD; and (C) typical
symmetrical and continuous ependymal lesion around the periaqueductal area in a 17-year-old girl with NMOSD. T2-weighted image shows
(D) ependymal dot lesions beside the ventricle in a 32-year-old woman with MS. FLAIR MRI shows (E) an asymmetric hypothalamic lesion in a
26-year-old woman with MS and (F) asymmetric ependymal dot lesions along the periaqueductal gray in a 37-year-old woman with MS. NMOSD:
neuromyelitis optica spectrum disorder; MS: multiple sclerosis; FLAIR: fluid attenuated inversion recovery; MRI: magnetic resonance imaging.
NMOSD: neuromyelitis optica spectrum disorder.
sub-ependymal lesions extending in parallel to the
ventricular surface including the periaqueductal gray matter
surface, which is different from the ependymal irregularity
known as the dot-dash sign previously described in MS
patients [44,45]. The term ependymal dot indicated the
asymmetric and non-continuous demyelinated lesions in
the ependymal layer covering the periaqueductal and
ventricular surface (Figure 1D-F). The MRI presentations of
NMOSD patients were variable [14,27]. After reviewing
brain images of those patients, we divided the MRI into
three subtypes as follows: (1) linear ependymal type
(Figure 1A-C); (2) punctate type (Figure 2A); (3)
demyelination type (including dawson finger like lesions and
large tumefactive demyelination lesions) (Figure 2B-D).
All different image subtypes of MRI may show multiple
brain lesions. We counted the brain lesions number
(either small punctate lesions or large demyelination
lesions) on the first MRI of NMOSD patients and
evaluated its correlation with prognosis.
Criteria for the evaluation of diagnostic accuracy
To distinguish MS from NMOSD on cranial MRIs,
Matthews et al. proposed the presence of at least 1
lesion adjacent to the body of the lateral ventricle and in
the inferior temporal lobe; or the presence of a
subcortical U-fiber lesion or periventricular Dawsons finger
lesion . The sensitivity, specificity, positive
predictive value, and negative predictive value of using unmet
the Matthews criteria and the presence of linear
ependymal lesions to distinguish NMOSD from MS
were tested in our patients.
Statistical analyses were performed using Statistical
Program for Social Sciences (SPSS) statistical software
(version 13.0; Chicago, IL, USA). Fisher exact test was used
to compare clinical symptoms and imaging features of
NMOSD with those of MS. Non-categorical variables
are expressed as the means standard deviation (SD)
and compared by two-sample t-tests. Survival curves
were estimated by the KaplanMeier method. Time zero
for the survival analysis was taken as the date of the first
CNS inflammatory episode. The primary end-point was
the time when patients became wheelchair dependent
(EDSS = 7). For patients who remained ambulatory, the
follow-up period ended on the date of the last visit. All
P values were two-tailed, and a P value less than 0.05
was considered statistically significant.
Of the 31 patients with NMO fulfilling the Wingerchuk
2006 criteria, 25 (81%) had brain lesions and were
diagnosed as having NMOSD. All above patients had
longsegment cervical or thoracic myelitis (3 segments)
confirmed by MRI studies during follow-up periods. Of
the 29 patients with MS meeting the Poser criteria, all
fitted the clinical presentations of MS and had negative
anti-AQP4 antibody tests. The age of onset in NMOSD
patients (37.8 13.6 years old) was similar to that in MS
Figure 2 Different brain magnetic resonance imaging characters of NMOSD. Fluid attenuated inversion recovery (FLAIR) magnetic
resonance imaging (MRI) shows a (A) punctate lesion (white arrow) on subcortical region in a 71-year-old woman with NMOSD; (B) right
temporal (white arrow head) and left mid brain lesion (white arrow) in a 44-year-old girl with NMOSD; and (C) dawson finger like lesion around
the bilateral subcortical and peri-ventricular region area in a 56-year-old girl with NMOSD; (D) tumefactive lesions on the left thalamus and
posterior limb of internal capsule in a 34-year-old woman with NMOSD. NMOSD: neuromyelitis optica spectrum disorder.
patients (33.7 9.2 years old, Table 1). The follow-up
period was longer in NMOSD patients (129.0
69.5 months) than in MS patients (77.6 64.2 months,
P = 0.007). Sensory disturbances were the most
common symptoms occurring during the follow-up period
in both NMOSD patients (100%) and MS (79%)
patients. Symptoms of weakness (100% vs. 69%, P =
0.002), sensory disturbance (100% vs. 79%, P = 0.025),
blurred vision (100% vs. 66%, P = 0.001), and urine/
stool retention (48% vs. 10%, P = 0.003) were more
frequently seen in NMOSD patients. On the other
hand, diplopia (34% vs. 8%, P = 0.025) and dysphagia/
dysarthria (24% vs. 0%, P = 0.012) were more
frequently seen in MS patients. Common
endocrinopathies (diabetes mellitus, and thyroid dysfunction),
polyuria (8% vs. 0%, P = 0.210), and hiccup (8% vs.
0%, P = 0.210) occurred with similar frequency in both
groups. Five NMOSD patients but no MS patient had
respiratory failure (20% vs. 0%, P = 0.017) and two of
these five died from pneumonia and sepsis. Eleven of
25 (44%) NMOSD patients and 1 of 29 (3.4%) MS
patients became wheelchair dependent during the
follow-up periods (log rank test; P = 0.036) (Figure 3).
There were 40 brain MRI studies in 25 NMOSD patients
and 54 brain MRI studies in 29 MS patients at relapses.
Thirty (75%) relapsing episodes in NMOSD group received
high dose (500 ~ 1000 mg methylprednisolone/day)
intravenous steroid therapies, while 29 (54%) relapsing episodes
in MS group received the same treatment. Ten (25%)
NMOSD patients had optic neuritis at their first disease
attack and five patients received pulse therapy. On the other
hand, only five (17.2%) MS patients had optic neuritis as
their first clinical attack and three of them received pulse
therapy during attack. For the long-standing immunological
treatment, twenty-two (88%) NMOSD patients received
oral steroid, and five (20%) took oral steroid and
azathioprine concurrently. Only eight (27.6%) MS patients received
oral steroid treatment. Ten (34.5%) MS patients received
interferon beta, one (3.4%) had copaxone, and nine (31%)
took fingolimod. Some NMOSD patients were diagnosed
as OSMS before testing anti-AQP4 antibody and three
patients still received treatment with interferon beta and
copaxone (Table 1).
Linear ependymal lesions were present in 7 of 25
(28%, Figure 4) NMOSD patients but absent in MS
patients (0%, P = 0.003, Table 2). Punctate lesions were
Table 1 Demographic data of evaluable NMOSD and MS
patients during the follow-up period
Age at 1st attack (years old)
Symptoms during the study period
Consciousness change (%) 8(32)
Polyuria >3000 ml/day (%) 2(8)
Follow-up duration (months)
Annual relapse rate (%)
Long term steroid, IST and DMT
NMOSD: neuromyelitis optica spectrum disorder; MS: multiple sclerosis; IST:
immunosuppressant therapy; DMT: disease modifying therapy.
*Statistically significant difference between NMOSD and MS.
Conscious change due to sepsis, epilepsy, shock, or other brain structure lesions.
more frequently seen in NMOSD than in MS patients
(64% vs. 28%, P = 0.013). More MS patients (34%)
demonstrated corpus callosum lesions than NMOSD patients
(4%, P = 0.007). The spatial pattern of
dissemination-inspace (DIS) pattern defined by the 2010 McDonald
criteria  can be seen in 76% and 60% patients with MS
and NMOSD, respectively (P = 0.449). The Mathews
brain MRI pattern was seen in 79% of patients with MS
and 60% of patients with NMOSD (P = 0.145). The
frequencies of lesions located in the juxtacortical area,
subcortical area, basal ganglion, periventricular area, temporal
area, infratentorium, central/dorsal medulla,
hypothalamus, and periaqueductal area (unilateral/bilateral) and
the frequencies of juxtacortical U fibers, Dawsons fingers,
tumefactive, and ependymal dot lesions were similar on
cranial MRIs of both groups.
Figure 3 Wheelchair dependence occurred earlier in NMOSD
patients than MS patients (log rank test; P = 0.036). NMOSD:
neuromyelitis optica spectrum disorder; MS: multiple sclerosis.
The specificity and sensitivity of using linear
ependymal lesions to distinguish NMOSD from MS were
high (100%) and low (24%), respectively (Table 3). The
MRI findings in 10 NMOSD patients and 6 MS patients
did not meet the Matthews criteria (sensitivity: 40%;
specificity: 79%) for separating MS from NMOSD. The
diagnostic sensitivity of these criteria for detecting NMOSD
can be increased to 56% by combining the presence of
linear ependymal lesions with unmet the Matthews criteria.
There were six (24%) and nineteen (76%) NMOSD
patients had abnormal MRI studies at the first clinical attacks
and during the follow-up periods, respectively. The annual
relapse rate (0.614 0.455 vs. 0.661 0.526, P = 0.846) and
the possibility of wheelchair dependent during the follow-up
periods are similar between them (log rank test; P = 0.401).
We found that 6 (24%), 7 (28%), and 12 (48%)
NMOSD patients demonstrated brain images fitting the
characteristics of punctate lesion, linear ependymal
lesion, and demyelination like lesion, respectively. The
different image patterns did not significantly correlate with
their clinical prognosis. The time to become wheelchair
dependent were similar among those three groups (log
rank test; P = 0.271). The annual relapse rate of linear
ependymal group was possibly higher than
demyelination group (0.93 0.61 vs. 0.46 0.40, P = 0.060).
Eight (32%) NMOSD patients had 10 or more (10)
brain lesions on their first MRI, These patients had
higher wheelchair dependent rate than the NMOSD
patients with fewer brain lesions (<10) during the
followup periods (log rank test; P < 0.001). The annual relapse
rate was possibly higher in the patients with more (10)
than those with fewer (<10) brain lesions (0.92 0.69 vs.
0.52 0.34, P = 0.068) (Figure 5).
Figure 4 Imaging characteristics of NMOSD and MS. NMOSD: neuromyelitis optica spectrum disorder; MS: multiple sclerosis.
Table 2 Brain magnetic resonance imaging findings of evaluable NMOSD and MS patients
NMOSD (n = 25) MS (n = 29)
Table 3 Diagnosis of NMOSD using different MRI criteria
1. Linear ependymal lesions
2. Unmet Matthews criteria* 3. 1 and 2 Sensitivity 24% (6/25)
*The Matthews criteria used to separate MS from NMOSD: at least 1 lesion adjacent to the body of the lateral ventricle and in the inferior temporal lobe; or the
presence of a subcortical U-fiber lesion or a Dawsons finger-type lesion.
NMOSD: neuromyelitis optica spectrum disorder.
In our series, brain lesions became apparent in 81% of
NMOSD patients during the follow-up periods.
Symmetric linear ependymal lesions were an imaging feature in
about one fourth (7/25) of NMOSD patients with brain
lesions but in none of the MS patients. This MRI feature
could therefore be used to distinguish NMOSD from MS
with a high specificity (100%) but a low sensitivity (24%).
We proposed that combining the presence of ependymal
lesions with unmet the Matthews criteria would increase
the sensitivity of the criteria to differentiate NMOSD from
MS (56%), while maintaining their high specificity (100%),
high positive predictive value (100%), and high negative
predictive value (73%).
The frequency of brain involvement in NMO differs
between Eastern and Western countries [10-25]. Brain
lesions developed in more than 60% of NMO patients in
studies from Japan [21,22] and Korea [13,14] and in less
than 30% of NMO patients in studies from France ,
Italy , and the Caribbean . Moreover, the
distribution of brain lesions in NMOSD differs as well. In a
study from the UK , few NMO patients had brains
Figure 5 NMOSD patients with more (10) brain lesions at
onset became wheelchair dependence earlier than those with
fewer (<10) brain lesions (log rank test; P < 0.001). NMOSD:
neuromyelitis optica spectrum disorder. 10 brain lesions: 10 or
more brain lesions on patients first MRI studies. <10 brain lesions:
<10 brain lesions on patients first MRI studies.
with Dawsons finger-type lesions (0%), subcortical
Ufiber lesions (0%), inferior temporal lobe lesions (19%),
and periventricular lesions (23%), whereas Korean and
Japanese NMOSD patients had brains with more
periventricular lesions (40%) and ovoid shaped brain lesions
(31.6%), respectively [14,16]. Similar to findings in other
Asian countries, our results showed Dawsons finger type
(ovoid) lesions (44%), U-fiber shaped lesions (48%),
inferior temporal lesions (36%), and periventricular lesions
(60%) were frequently present in NMOSD [14,16].
Although Matthews et al. showed that periventricular,
inferior temporal lobe, and U-fiber or Dawsons
fingertype lesions could be very sensitive (>90%) markers for
distinguishing MS from NMOSD in UK populations, we
showed that they were less sensitive in Taiwanese
patients. However, by combining the presence of linear
ependymal lesions with unmet the Matthews criteria, we
could increase the sensitivity of these criteria from 40% to
56%. It is still uncertain whether genetic or environmental
factors contribute to differences in brain lesion distribution.
The characteristic linear ependymal lesions of NMOSD
in this study may be explained by the spatial pattern of
AQP4, which is mainly expressed in astrocytes in the optic
nerve, spinal cord, hypothalamus, and periependymal area
in contact with CSF [34,46]. In a pathological study of rats,
the AQP4 protein was abundant in glial cells bordering
the subarachnoid space and ventricles , which is
consistent with the distribution of brain lesions in our NMO
patients. Moreover, in support of this speculation, Pittock
et al. noted that the locations of NMO brain lesions are
associated with structures expressing high levels of AQP4
. Other studies also reported similar periependymal
brain lesions in NMOSD patients [10,11,14,15,26,29].
Anti-AQP4 antibodies may penetrate the bloodbrain
barrier, bind to these AQP4-rich regions, and then
initiate downstream immunopathological cascades
responsible for the development of linear inflammatory lesions
in the periependymal tissue of NMOSD patients. Thus,
the identification of linear ependymal lesions on
cranial MRI could be a useful imaging characteristic for
The number of brain MRI lesions in the patients with
clinically isolated syndromes (CIS) may predict the
development of MS and correlate with disability status
after 20 years . Our study also shows the number of
brain lesions at onset is an important prognostic factor
for NMOSD. NMOSD patients that had 10 or more
(10) brain lesions on their first MRI may be bound to
wheelchairs more rapidly than those with fewer (<10)
brain lesions, indicating the application of high potency
immunosuppression on this group of patients.
In the present study, a few clinical features were found
to distinguish between these two diseases. NMOSD
patients with brain lesions more frequently had symptoms of
optic neuritis and severe myelitis including blurred vision,
sensory disturbance, weakness, and urine/stool retention,
while MS patients more frequently had diplopia and
dysphagia/dysarthria. Hiccup is reported to be a unique
clinical presentation of NMO in patients with periaqueductal
lesions . Both of our two patients with hiccup also had
linear ependymal lesions in the periaqueductal region.
One study also shows that endocrinopathies like
amenorrhea, diabetes insipidus, and hypothyroidism develop in
patients with recurrent optic neuromyelitis . In this
study, hiccup and polyuria (>3000 ml/d) were only seen in
NMOSD patients, but because the patient number was
too small, this difference between NMOSD patients and
MS patients was not statistically significant. The natural
history of untreated NMO is significantly worse than that
of MS [8,33]. The 5-year survival rate of NMO patients
was only 68% in an earlier study . Similarly in our
study, five NMOSD patients had respiratory failure during
the follow-up periods and two of them died from
pneumonia and sepsis around 8 years and 23 years after the
first symptoms onset, whereas none of our MS patients
had these serious complications. The greater likelihood of
wheelchair dependence in NMOSD patients is probably
due to longitudinally extensive and greater spinal cord
This retrospective study may suffer from recruitment
bias as a result of the small study population, and the
treatment and follow-up durations were inconsistent in
both groups. Nevertheless, in our study, prognosis was
poorer in NMOSD patients than MS patients. A
characteristic imaging marker, linear ependymal lesions, was
only present in NMOSD patients but not MS patients.
Thus, the differentiation of NMOSD from MS can be
improved by closely monitoring the evolution of this
In summary, NMOSD patients became wheelchair
dependence earlier than MS patients. Furthermore, NMOSD
patients who had more (10) brain lesions on their first
MRI had a worse prognosis than those with fewer (<10)
brain lesions. A specific imaging marker, the linear
ependymal lesion, was present in some NMOSD patients. The
diagnostic sensitivity of NMOSD criteria can be increased
by combining the presence of linear ependymal lesions
with unmet the Matthews criteria.
The Institutional Review Boards of the Chang Gung
Memorial Hospital waived the need for individual
informed consent because all data were anonymized and
de-identified prior to analysis.
MFL: reviewing and evaluating cranial images, analysis and interpretation of
data, drafting the manuscript. RKL, CCH, HSC, YRW, CMC, CCC, and HCK:
collect of the patients, analysis and interpretation of patients image and
clinical data. KHC and LSR: analysis and interpretation of data, drafting the
manuscript, revising manuscript critically for important intellectual content
and contributions to conception and design. All authors read and approved
the final manuscript.
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