Acta Neurochirurgica (2018) 160:1547–1553

https://doi.org/10.1007/s00701-018-3554-4

ORIGINAL ARTICLE - BRAIN TUMORS

Non-operative meningiomas: long-term follow-up of 136 patients

Rossana Romani 1 & George Ryan 2 & Christian Benner 3 & Jonathan Pollock 2

Received: 6 November 2017 / Accepted: 18 April 2018 / Published online: 6 June 2018
# Springer-Verlag GmbH Austria, part of Springer Nature 2018

Abstract
Background Improving access to neuroradiology investigations has led to an increased rate of diagnosis of incidental
meningiomas.
Method A cohort of 136 incidental meningioma patients collected by a single neurosurgeon in a single neurosurgical centre is
retrospectively analysed between 2002 and 2016. Demographic data, imaging and clinical features are presented. The radiolog-
ical factors associated with meningiomas progression are also presented.
Results The mean age at diagnosis was 65 (range, 33–94) years. Univariate analysis showed oedema was most strongly correlated
with progression (p = 0.010) followed by hyperintensity in T2-weighted (T2W) MRI (p = 0.029) and in Flair-T2W MRI (p = 0.017).
Isointensity in Flair-T2W MRI (0.004) was most strongly correlated with non-progression of the meningioma followed by calci-
fication (p = 0.007), older age (p = 0.087), hypointensity in Flair-T2W MRI (p = 0.014) sequences and in T2W MRI (p = 0.096). In
multivariate analysis, the strongest radiological factor predictive of progression was peritumoural oedema (p = 0.016) and that of
non-progression was calcification (p = 0.002). At the end of the median follow-up (FU) of 43 (range, 4–150) months, 109 (80%)
patients remained clinically stable, 13 (10%) became symptomatic and 14 (10%) showed clinical and radiological progression.
Conclusions One hundred and nine (80%) patients remained stable at the end of FU. Peritumoural oedema was predictive of
meningiomas progression. Further prospective study is needed to identify the combination of factors which can predict the
meningioma progression for an early surgery or early discharge.

Keywords Calcification . Incidental . Magnetic resonance imaging . Meningioma . Natural history . Oedema . Progression

Introduction follows: benign WHO grade I (> 90%); atypical/borderline,

Meningiomas account for around 20% of all intracranial tu-
mours in males and 38% in females [4]. These tumours orig-
inate from meningothelial cells, called arachnoid cap cells, of
the arachnoid granulations mainly concentrated at the venous
sinuses and major venous structures [4, 11].
The female preponderance of these tumours is correlated
with sex hormone influences previously described in the liter-
ature [1, 5, 13]. The majority of meningiomas are benign as
* Rossana Romani
romanirossana16@gmail.com
1
Department of Neurosurgery, Charing Cross Hospital, Imperial
College NHS Trust, Fulham Palace Rd, London W6 8RF, UK
2
Department of Neurosurgery, Essex Neuroscience Centre, Queen’s
Hospital, Romford RM7 0AG, UK
3
Department of Mathematics and Statistics, University of Helsinki,
2b, P.O. Box 68, FI-00014 Helsinki, Finland
grade II (5%); anaplastic/malignant, grade III (2–3%) [17].
Improving access to neuroradiology investigations has led
to an increased rate of diagnosis of incidental meningiomas
especially in the past two decades. Incidental meningiomas
are the most frequent incidental findings following diagnostic
brain imaging [3]. In the pre-CT/MRI imaging era, these tu-
mours were diagnosed when they were large and symptomat-
ic. They are frequently followed up by neurologists, general
practitioners and neurosurgeons. The surgical removal of
symptomatic or growing tumours compressing surrounding
brain or neurovascular structures is generally recognised as
best management.
However, the management of an incidentally discovered
meningioma is controversial and options include the follow-
ing: watch, wait and rescan (WWR), microsurgical removal
(MR), radiosurgery (RS) or fractionated radiotherapy (RT).
National or international guidelines regarding the modality
of follow-up (FU) of asymptomatic incidental meningiomas
are lacking. Furthermore, there is an absence of prospective
studies of large cohorts of WWR patients in order to detect
1548 Acta Neurochir (2018) 160:1547–1553

those factors which predict meningioma progression. Some were classified into four groups: (1) stable clinical condi-
meningiomas have an aggressive growth pattern and some tion and size of tumour; (2) stable clinical condition and
remain stable for the patients’ lifetime. increasing tumour size; (3) progressive clinical condition
The understanding of predictive factors regarding progres- and stable size of tumour; (4) progressive clinical condi-
sion can permit the selection of patients who may benefit from tion and size.
early surgery avoiding the cost and inconvenience of long-
term FU and also allows selection of those patients who will
Statistical analysis
not progress permitting early discharge. An understanding of
the predictive factors for meningioma progression could im-
Univariate linear regression implemented in the lm() function
prove clinical practice with substantial economic savings for
in R was applied with growth of the meningioma as the re-
the UK National Health Service.
sponse variable and a factor of meningiomas progression as
We present a cohort of 136 incidental meningioma patients
the predictor variable. Age at first FU and sex were controlled
who were retrospectively analysed between 2002 and 2016 at
for by including them as covariates in each model.
the Department of Neurosurgery, Essex Neurosciences
Association between a predictor and the response variable
Centre, Queen’s Hospital, Romford, UK. The purpose is to
was tested by using robust standard error estimation imple-
understand predictive factors of clinical and radiological pro-
mented in the sandwich package in R and declared statistically
gression. This is a pilot report with the aim of promoting the
significant at the 5% significance level. Multiple linear regres-
establishment of a national UK meningioma database.
sion was applied to test for associations between growth of the
meningioma and univariate significant predictors. All calcu-
lations were performed in the R statistical environment (R
Methods and materials
Development Core Team, Vienna).
Patients and imaging

A cohort of 136 patients with a radiological diagnosis of in- Results

tracranial meningioma were followed up by the senior author
(JRP) at the Department of Neurosurgery of Queen’s Hospital Age and sex
between March 2002 and June 2016.
Sex, age and comorbidities were correlated with tumour Mean age at diagnosis was 65 (range, 33–94) years. There was
progression. Clinical performance at diagnosis was scored statistically significant correlation between the age of the pa-
with the Karnofsky score [14]. tients and progression (p = 0.087). Older patients demonstrat-
An extra-axial lesion with a broad-based dural attachment ed a less marked tendency to progress (Fig. 1).
and uniform enhancement after gadolinium was considered
radiological criterion for the diagnosis of meningioma.
The location of the meningioma: supratentorial, infratentorial
and skull base was correlated with progression.
According to the maximum tumour diameter, the meningi-
omas were divided into three groups: small (< 2 cm), medium
(2–4 cm) and large (> 4 cm) sizes [23, 24].
The surrounding vasogenic oedema was calculated consid-
ering the volume of the oedema and of the tumour, which were
calculated by the maximum diameter in the three dimensions.
Imaging (CT and MRI) was reviewed. Calcification and, T1-,
T2- and, Flair-(T2)-weighted sequences when available were
correlated with progression. MRI and CT were not available in
five patients but outpatient clinical data was sufficient to exclude
clinical or radiological progression of the meningioma.

Clinical and radiological progression

Growth of the meningioma was defined by an increase in

the maximum intracranial diameter of the tumour by a
minimum of 3 mm [10]. During FU, meningioma patients Fig. 1 Relationship between age and progression
Acta Neurochir (2018) 160:1547–1553 1549

One hundred and two patients were female and 34 male. Clinical features
Sex did not correlate with progression of the meningioma
(Table 1). Asymptomatic incidental meningiomas were 49, of which 14
progressed during FU (p = 0.057). The majority of the patients
presented at diagnosis with minor or stable symptoms which
Table 1 Demographic, clinical and radiological features of 136 patients are listed in the Table 1. One hundred and nine patients had
with intracranial meningiomas comorbidities (Table 1) and 29 of these patients progressed.
Age (year) 65 (range, 33–94)
Sex
Female 102 (75%)
Location of the meningiomas
Male 34 (25%)
The Karnofsky (mean) 85 (range, 30–100) Ninety-two (68%) meningiomas were supratentorial and 80
Incidental 49 (36%) (59%) were in a skull base location (Table 1). Skull base
The Karnofsky (mean) 87 (range 50–100)
Symptomatic 87 (64%) location of the meningiomas was at tuberculum sellae, olfac-
The Karnofsky (mean) 84 (range, 30–100) tory groove, anterior clinoidal process, planum sphenoidale,
Symptoms jugular foramen, medial sphenoid wing, cavernous sinus, or-
Seizures 22
Visual impairment 19 bital roof with intraorbital extension, petroclival, hypoglossal
Headache 17 foramen and middle cranial fossa. The location of the menin-
Gait impairment 8 gioma did not correlate with progression.
Dizziness 8
Hearing loss 7
Proptosis 4 Size of the meningiomas
Memory loss 2
Haemiparesis 1
Anosmia 1 Twenty-nine meningiomas were small, of which eight
Trigeminal neuralgia 1 progressed during FU. The majority (76) of meningiomas at
Comorbidities 109
Severe
diagnosis were of medium size, of which 21 increased during
Cancer 17 FU. Thirty-one were large and eight of these progressed dur-
Ischemic heart disease 11 ing FU (Table 1). We dichotomized different tumour size and
Atrial fibrillation 9
correlated with progression. We considered two groups: < 2
Dementia 7
Chronic kidney disease 4 and > 2 cm; they did not correlate with progression. We also
COPD 4 verified two groups: < 3 and > 3 cm; there was no statistical
Metastatic cancer 3 correlation with tumour progression. We wished to keep the
Angina 3
Severe aortic stenosis 2 three subgroups as the size was not statistically significant.
Schizophrenia 1 Statistical analysis indicated no significant association be-
Multiple sclerosis 1 tween the size of the meningioma and progression during FU.
Minor
Hypertension 50
Diabetes type 2 20 Radiological findings indicative of progression
Hypercholesterolemia 20
Transitory ischemic attack 8
Obesity 8 Oedema was present in 35 patients and there was a statistically
Migraine 7 significant association between this finding and progression
Asthma 7
Depression 6
(p = 0.010). Hyperintensity in T2-weighted (T2W) MRI (p =
Others 44 0.029) and Flair-T2-weighted (T2W) MRI (p = 0.017) se-
Radiological features quences was also associated with meningioma progression.
Supratentorial 92 (68%)
Infratentorial 44 (32%)
Skull Base 80 (59%) Radiological findings indicative of non-progression
Side
Left 69 (51%)
Right 48 (35%) Calcifications were associated with non-progression or a
Bilateral 19 (14%) decrease in size of the meningioma during FU (p =
Size
0.007). Hypointensity in T2W MRI (p = 0.096) and Flair-
Small < 2 cm 29 (21%)
Medium 2–4 cm 76 (56%) T2W MRI (p = 0.014) sequences was associated with non-
Large > 4 cm 31 (23%) progression of the meningioma. Isointensity in Flair-T2W
Oedema 35 (26%) MRI sequences was the radiological finding most strongly
Calcifications 34 (25%)
No CT 26 (19%) correlated with non-progression of the meningioma (p =
0.004).
1550
Multivariate analysis and progression
In multivariate analysis, we considered those variables with a
significant p value regarding non-progression of the meningi-
oma. The strongest radiological factor predictive of non-
progression remained calcifications (p = 0.002), predictive of
progression was peritumoural oedema (p = 0.016).
Outcome at the end of the FU and long-term survival
At the end of the median FU of 43 (range, 4–150) months, 86
(63%) patients remained stable clinically and radiologically, 23
(17%) remained clinically stable but had radiological progres-
sion, 13 (10%) presented clinical progression but remained
radiologically stable and 14 (10%) showed evidence of both
clinical and radiological progression (Table 2). Figure 2 shows
the Kaplan-Meier survival curves for the time of neurosurgical
follow-up until radiological progression. The final outcome is
reported in Table 3. The patients discharged and those with
non-progression who are still under FU are 91 (67%).
At the end of the neurosurgical FU, only one patient died
for causes not related to meningioma: an 80-year-old man with
an incidental 38-mm convexity meningioma still under obser-
vation died for a posterior circulation aneurysm rupture. At the
end of the clinical FU, eight patients died for causes not related
to meningioma, seven of them were previously discharged and
one required the surgical removal of the meningioma.
Discussion
Ready and improving access to neuroradiological investiga-
tions has resulted to the diagnosis of an increasing number of
incidental intracranial meningiomas. These may be associated
with no symptoms at all, or they may present with symptoms
which are minimal and stable and do not warrant early surgical
treatment. An example of this is the elderly patient with a late
diagnosis of a visual deficit which proves to be stable. Such
patients, especially those with associated comorbidities, may be
better treated with non-operative management in the first
Table 2 Outcome at the end of a median follow-up of 43 (range, 4–150)
months
Outcome Number of patients (%)
Clinically and radiologically stable 86 (63%)
Clinically stable, radiological progression 23 (17%)
Clinical progression, radiologically stable 13 (10%)
Clinical and radiological progression 14 (10%)
Total 136 (100%)
Acta Neurochir (2018) 160:1547–1553
instance. There are currently no clear guidelines regarding
how often to follow-up such patients and for how long FU
should be continued. There is a lack of knowledge regarding
the factors determining progression of incidental meningiomas.
Table 4 reports the literature review on incidental meningioma
with initial conservative management. A review of factors
predicting progression yielded similar findings to the present
study [26].
Age, sex and neurological deficit
Older age was associated with non-progression [10, 18, 21,
28]. In our study, there was a statistical correlation between
age and non-progression in patients over 65 years. Other au-
thors did not find an association between age and tumour
growth [6, 8].
Lee et al. in the largest series reported that older age and
male sex are associated with rapid progression of the menin-
giomas; however, the data were only statistically significant in
univariate analysis [16]. Other authors did not find an associ-
ation between age, sex and tumour progression [8, 15] or
between sex and tumour progression [10, 18, 28]. A larger
number of patients may clarify the correlation between sex
and meningioma progression.
Neurological deficit at presentation may also correlate with
a tendency to growth [16]. We did not find this association in
our report.
Location
Location of the meningioma did not seem to be predictive of
progression. We did not find a statistically significant correla-
tion between supra-infratentorial or skull base location. Bindal
et al. reported a series of 40 patients with skull base meningi-
oma followed up for a mean of 83 (range, 10–312) months.
The authors did not report factors which predict tumour pro-
gression [2]. Herscovici et al. reported an association between
non-growing tumour and sphenoid ridge location [10].
Size of the meningioma
We did not find an association between the size of the tumour
and progression. Nakamura et al. reported as well that the size of
the tumour cannot be considered a predictive factor of progres-
sion in a small number of 41patients [18]. Similar conclusion is
reported by Kuratsu et al. in a 109 meningioma patients conser-
vatively treated [15]. Herscovici reported an association between
small size and non-progression [10]. Only a few series report an
association between larger size of tumour and progression [20,
28]. Jadid et al. affirmed that small size meningiomas (< 2 cm)
progressed during FU but the authors did not report a statistically
significant correlation [12]. A recent report of a series of 232
patients found an association of larger size and progression in
Acta Neurochir (2018) 160:1547–1553 1551

Fig. 2 The Kaplan-Meier

1.0
survival curves for the time of
neurosurgical follow-up until
radiological progression. Dashed
lines represent 95% confidence
intervals for event-free survival

0.8
Radiological progression-free survival

0.6
0.4
0.2
0.0

0 2 4 6 8 10 12

Follow-up time in days

univariate analysis [16]. An older report neither found associa- meningiomas [16]. Hyperintensity in T2W imaging has been
tion between size and growth of the meningioma [6]. previously reported by Niiro et al. [20], Nakamura et al. [18]
and Yano and Kuratsyu [27] to be a statistically significant
factor for meningiomas progression.
Imaging Hashiba et al. suggested peritumoural oedema, loss of
peritumoural rim and irregular shape of the meningioma to
Standard MRI sequences correlate with progression of the be correlated with tumour growth [9]. Our series found that
meningiomas. In a univariate analysis, T2W imaging and oe- non-progression of the meningioma was statistically signifi-
dema were associated with meningioma progression. Both cant associated with calcifications, hypointensity in T2W and
factors were found predictive of the progression by Lee et al. Flair-T2W sequences. Hypointensity in T2W MRI sequences
in their retrospective review of 232 patients of asymptomatic was associated with non-progression in a series of 109 asymp-
tomatic meningiomas reported by Kuratsu et al. [15]. In our
series, isointensity in Flair-T2 MRI sequences seems to be the
Table 3 Final outcome at the end of a median follow-up of 43 (range, strongest imaging finding associated with non-progression of
4–150) months the meningioma. Jadid et al. did not find a statistically signif-
icant association between calcifications and meningioma pro-
Outcome Number of patients (%)
gression [12]. Previous reports confirm the association be-
Discharge 44 (32%) tween calcification and non-progression [7, 9, 10, 15, 16,
Continue observation 47 (34%) 18–20, 25, 27].
Surgery 23 (17%)
Radiotherapy 12 (9%) Histology and DNA methylation
Refused surgery 5 (4%)
Biopsy + radiotherapy 1 (1%) Twenty-three patients of the present report required surgical
Lost at FU 4 (3%) intervention for clinical and radiological progression of the
Total 136 (100%) meningioma and one patient had biopsy and radiotherapy.
The histology of this surgical cohort with progression of the
1552 Acta Neurochir (2018) 160:1547–1553

Table 4 Literature review and factors associated with progression and non-progression of intracranial meningiomas

Author Year Cases FU, months (range) Factors for progression Factors for non-progression

Firsching et al. [6] 1990 17 22 (2–89) NR NR

Olivero et al. [21] 1995 57 32 (6–180) NR NR
Go et al. [7] 1998 35 74 (5–182) NR Calcification
Kuratsu et al. [15] 2000 109 28 (12–87) NR Calcification, hypointense in
T2W MRI
Niiro et al. [20] 2000 40 (> 70 year) 38 (6–97) Hyperintense in T2W MRI, sex, Calcification
tumour size (> 3.5 cm)
Yoneoka et al. [27] 2000 37 Younger age (<58 years) NR
Volume (>4 cm)
Bindal et al. [2] 2002 40 (skull base) 83 (10–312) NR NR
Nakamura et al. [18] 2003 41 43 (6–105) Age (< 60 years) Calcification, hypointense/isointense
in T2W MRI
Herscovici et al. [10] 2004 43 67 Age (< 60 years), Calcification, size (< 2 cm), sphenoid
ridge location
Yano and Kuratsu [26] 2006 67 94(62–155) Hyperintense in T2W MRI Calcification
Hashiba et al. [9] 2009 70 39 (12–123) Oedema Calcification
Oya et al. [22] 2011 161 35 (4–202) NR
Jadid et al. [12] 2015 65 48 (6–240) NR NR
Lee et al. [16] 2017 232 47 (6–151) Size, oedema, hyperintense in T2W Calcification
MRI, isointense in T2W MRI
Present report 2017 136 43 (4–150) Oedema, hyperintense in T2W and Older age (> 65 years), calcification,
Flair-T2W MRI hypointense in T2W MRI and
Flair-T2W MRI, isointense in
Flair-T2W MRI

NR: not reported

disease will be analysed in a different report. A recent large Conclusions

multicentre retrospective study showed that high resolution of
DNA methylation pattern can be associated with the menin-
gioma recurrence after surgery [25]. It will be interesting to
analyse the methylation pattern of our patients who progressed
during FU.
Study limitations
The current study is a retrospective collection of data from a
single surgeon and a single neurosurgical centre. The number
of the patients is small. The MRI sequences reviewed are only
the basic ones. Larger prospective multicentre study enrolling
patients with incidental or minimal symptomatic meningio-
mas is necessary.
Advanced MRI with diffusion tensor sequences should be
considered for the prospective long-term study. Volume, shape
and signs of invasion of the meningioma should be prospec-
tively studied. Comorbidities of the patient and epidemiolog-
ical factors like smoke should also be considered.
This is only a pilot study to justify a further prospective UK
study with the aim to identify the combination of factors
which can predict the meningioma progression for an early
surgery or early discharge.
Oedema remains the strongest factor predictive of menin-
gioma progression. Calcification is confirmed to be asso-
ciated with non-progression. Clinical and radiological fea-
tures require larger number of patients to be statistically
significant predictive of meningioma progression.
The knowledge of prediction of meningioma progres-
sion will clarify the modality of follow-up and early
surgical management of those asymptomatic meningio-
mas. The majority of patients remain clinically stable
during FU and therefore could have been benefited from
an early discharge with significant economic impact on
NHS.
Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.
Ethical approval All procedures of this study were in accordance with
the ethical standards of the institutional and/or national research commit-
tee and with the 1964 Helsinki declaration and its later amendments or
comparable ethical standards. For this type of study, formal consent is not
required.
Acta Neurochir (2018) 160:1547–1553
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