Access to this full-text is provided by Springer Nature.
Content available from Obesity Surgery
This content is subject to copyright. Terms and conditions apply.
REVIEW ARTICLE
Bariatric Surgery or Non-surgical Weight Loss for Idiopathic
Intracranial Hypertension? A Systematic Review
and Comparison of Meta-analyses
James H. Manfield
1
&Kenny K-H. Yu
1
&Evangelos Efthimiou
2
&Ara Darzi
3
&
Thanos Athanasiou
3
&Hutan Ashrafian
2,3
Published online: 15 December 2016
#The Author(s) 2016. This article is published with open access at Springerlink.com
Abstract
Background Idiopathic intracranial hypertension (IIH) is as-
sociated with obesity and weight loss by any means is consid-
ered beneficial in this condition.
Objectives This study aims to appraise bariatric surgery vs.
non-surgical weight-loss (medical, behavioural and lifestyle)
interventions in IIH management.
Methods A systematic review and meta-analyses of surgical
and non-surgical studies.
Results Bariatric surgery achieved 100% papilloedema reso-
lution and a reduction in headache symptoms in 90.2%. Non-
surgical methods offered improvement in papilloedema in
66.7%, visual field defects in 75.4% and headache symptoms
in 23.2%. Surgical BMI decrease was 17.5 vs. 4.2 for non-
surgical methods.
Conclusions Whilst both bariatric surgery and non-surgical
weight loss offer significant beneficial effects on IIH symp-
tomatology, future studies should address the lack of prospec-
tive and randomised trials to establish the optimal role for
these interventions.
Keywords Idiopathic intracranial hypertension .
Pseudotumor cerebri .Benign intracranial hypertension .
Obesity .Bariatric surgery .Metabolic surgery .Weight loss
Introduction
The worldwide burden of idiopathic intracranial hypertension
(IIH) continues to rise with the current annual incidence esti-
mated at up to 21 per 100,000 per year in obese young women
[1]. This increase occurs in the context of a concomitant rise in
obesity rates; in the USA, more than a third of adults are now
obese, compared with around 11% worldwide, with a further
third overweight (body mass index (BMI) 25–30 kg/m
2
). In
2013, the American Medical Association declared obesity as a
genuine disease state [2].
IIH, also known as pseudotumour cerebri, is a clinical di-
agnosis defined by criteria that comprise symptoms and signs
of intracranial pressure (e.g. headache, papilloedema and vi-
sual loss), elevated intracranial pressure (e.g. on lumbar punc-
ture) with normal cerebrospinal fluid (CSF) composition and
without any other cause identified on neuroimaging or other
evaluations [3].
Although previously called benign intracranial hyperten-
sion, it is not a benign disorder with many patients suffering
intractable, disabling headaches with a significant risk of se-
vere and permanent visual loss [4]seeninupto30%[5].
The pathogenesis of IIH remains unclear, although several
risk factors have been identified [6]. IIH is most prevalent in
obese females of reproductive age [7]; at least 90% of patients
are female with obesity prevalence ranging from 70.5 to 94%
[8–10] and recent weight gain is a further significant factor for
its development [2].
Weight loss is traditionally advocated for all overweight
IIH patients and remains the cornerstone of management as
Electronic supplementary material The online version of this article
(doi:10.1007/s11695-016-2467-7) contains supplementary material,
which is available to authorized users.
*Hutan Ashrafian
h.ashrafian@imperial.ac.uk
1
Department of Neurosurgery, Royal Preston Hospital,
Preston, Lancashire, UK
2
Department of Bariatric Surgery, Chelsea and Westminster Hospital,
London, UK
3
Department of Surgery and Cancer, Imperial College London, 3rd
Floor Chelsea and Westminster Hospital Campus, 369 Fulham Road,
London SW10 9NH, UK
OBES SURG (2017) 27:513–521
DOI 10.1007/s11695-016-2467-7
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
it generally improves symptomology [11]. Although lifestyle
weight-loss interventions, comprising exercise promotion and
dietary modification are widely advised, long-term weight
control and accordingly IIH outcomes remain suboptimal [4].
Bariatric surgery is an alternate way of sustainably reduc-
ing both excess weight and IIH symptomology [12], whilst
also improving glycaemic control and cardiovascular and can-
cer risk [13,14]. A previous review of 65 patients demonstrat-
ed that following bariatric surgery 92% (60/65) had improve-
ment in IIH outcomes [15]. Although there is also evidence
suggesting that non-surgical interventions, including a recent
multicentre RCT of weight loss vs. weight loss with acetazol-
amide [16], may improve IIH outcomes via weight reduction
and possibly additional mechanisms, there are lack of studies
directly comparing these treatment strategies.
The aim of this paper was therefore to systematically re-
view the current evidence and concomitantly appraise both
bariatric surgery and non-surgical weight-loss interventions
in the management of IIH, via the assessment of visual out-
comes (papilloedema and visual field deficits), symptoms
(headache), intracranial pressure (via cerebrospinal fluid
opening pressure measurement) and BMI as summary out-
come parameters.
Methods
The review was performed according to guidelines from the
preferred reporting items for systematic reviews and meta-
analyses (PRISMA) [17]. A broad search of the electronic
literature was performed applying the following search terms:
surgical studies: ‘bariatr$ or obesity surg$ or gastr$ surg$’and
‘intracranial hypertension or pseudotumo$’and non-surgical
studies: ‘weight loss OR weight reduc$’and ‘intracranial hy-
pertension OR pseudotum$’.
The last date for this search was August 2016. The bibli-
ographies of articles accessed were also reviewed to identify
any relevant further literature. Studies included in the final
analysis are listed in Table 1(bariatric surgery) and Table 2
(non-surgical weight-loss management), and this includes
non-published data obtained from the corresponding author
to facilitate further analysis.
Inclusion and Exclusion Criteria
All case series and empirical studies that identified patients
diagnosed with IIH who underwent either bariatric surgery or
conventional weight management approaches were evaluated.
Individual case reports were excluded as were manuscripts not
reporting outcome data (either symptomatology or visual sta-
tus) and either BMI or absolute weight change data, as this
would preclude further appraisal.
Data Analysis
The following outcome data was extracted (based on clinical
relevance): types of surgery, body weight/BMI and data on
symptomatology and signs (visual fields, papilloedema and
CSF pressures). Standard deviations, if not explicitly reported,
were calculated where possible from available data. Where
articles reported multiple follow-up periods, the highest yield
interval with the most complete data was selected for
inclusion.
Meta-analysis was performed in line with recommenda-
tions from the Cochrane Collaboration and followed
PRISMA and (MOOSE) guidelines. Continuous data were
investigated using weighted mean difference (WMD) reported
with 95% confidence intervals (CI). Categorical variables
were analysed using risk ratio (RR) with 95% CI. The in-
verse-variance, random-effect model of DerSimonian and
Laird was used for both continuous and categorical outcomes.
Interstudy heterogeneity was explored using the χ
2
statistic
and the I
2
statistic. When I
2
was >65%, significant statistical
heterogeneity was considered to be present (I
2
30–65% mod-
erate heterogeneity, <30% low heterogeneity). Analysis was
performed by use of Stata 13 (StataCorp., College Station,
Texas, USA).
Several strategies were used to evaluate data validity and
quality:
Validity was assessed by (1) risk of bias assessments using
The Cochrane Collaboration’s tool, (2) funnel plots to assess
publication bias and (3) evaluation of publication bias using
Egger’s test for small-study effects. Quality scoring was per-
formed using the Newcastle-Ottawa Scale (NOS) [18]for
assessing the quality of studies in meta-analyses and the
Jadad Scale [19] for randomised trials (see Electronic
Supplementary Material for scoring) (Fig. 1).
Results
Surgical Group Seven studies [20–26] fulfilled the inclusion
criteria, generating a pooled data set of 65 patients with IIH
undergoing bariatric surgery (see Table 1). Four [20–22,25]
of these were non-randomised prospective observation stud-
ies, and three [23,24,26] were retrospective case series. One
study was subsequently excluded from quantitative synthesis
due to lack of standard deviation data precluding further
analysis.
Non-surgical Group Eight studies [16,27–33] met the inclu-
sion criteria, making a pooled data set of 277 patients with IIH
undergoing non-surgical management (see Table 2). Two [16,
31] of these were prospective randomised controlled trials,
four [28–30,32] non-randomised prospective observation
studies and two [27,33] retrospective case series.
514 OBES SURG (2017) 27:513–521
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Tab l e 2 Non-surgical weight-loss studies
Study
type
Subject
number
Average
age
Female/
male
Follow-up
(months)
Pre-
interventions
Mean BMI (kg/m
2
) Percentage of subjects with improvement in
Pre/post-
interventions
Headache Papilloedema Visual
fields
Visual
symptoms
Wall et al. [16]
a
RCT 79 30 77/2 6 39.9 39.9/38.6 19.3 38 68 n/a
Newborg [27] RCS 9 28 7/2 10 42.4 42.4/30.9 n/a 100 n/a 100
Johnson et al. [28] NRPOS 15 31 15/0 5.5 40.7 40.7/39.2 n/a 73.3 n/a n/a
Kupersmith et al. [29] NRPOS 38 n/a 38/0 21.6 n/a n/a/n/a
e
n/a 92 89 n/a
Glueck et al. [30]
c
NRPOS 9 35 9/0 10 37.2 37.2/35.7 87.5 88.9 57 n/a
Ball et al. [31]
a
RCT 25 33 24/1 12 34.1 34.1/32.9 10 35 n/a n/a
Sinclair et al. [32] NRPOS 20 34 20/0 9 38.2 38.2/32.8 45 n/a n/a 91
Pollak et al. [33]
d
RCS 82 30 73/9 61.3 31.6 31.6/26 n/a 84
b
84
b
n/a
a
Data from RCT control arm (i.e. weight reduction diet only)
Data also includes personal correspondence from Wall
b
Composite endpoint (papilloedema and visual fields)
c
Data from diet only group
d
Six per cent underwent bariatric surgery; 22% underwent salvage surgery (CSF diversion or optic nerve fenestration)
e
Data for absolute weight change (kg) available
Tab l e 1 Surgical weight-loss studies
Study Study type Subject
number
Average
age
Female/male Procedures performed Follow-up
(months)
Mean BMI (kg/m
2
) Percentage of subjects with improvement in
Pre/post-surgery Headache Papilloedema Visual fields
Sugerman et al. [20] NRPOS 8 33 8/0 8 RYGB 34 49/27.5 100 100 100
Sugerman et al. [21] NRPOS 6 32 6/0 5RYGB, 1LGB <6 45/n/a 83 n/a n/a
Sugerman et al. [22] NRPOS 24 34 24/0 23 RYGM, 1 LGB 12 47/30 96 100 n/a
Michaelides et al. [23] RCS 16 34 16/0 13 RYGB, 3GPs Various 45/28 81 100
a
n/a
Nadkarnietal.[24] RCS 2 42 2/0 1 RYBG, 1 LGB 12 47.9/26.3 100 100 n/a
Egan et al. [25] NRPOS 4 32 4/0 4 LGB 19.8 46.1/33.4 100 100 50
Sanmugalingam et al. [26] RCS 5 45 5/0 5 LSG 17 58/37 80 n/a n/a
Abbreviations: GP gastroplasty procedure, LGB laparoscopic gastric band, LSG laparoscopic sleeve gastrectomy, NA not available, RYGJB Roux-en-Y gastrojejunostomy bypass, NRPOS non-randomised
prospective observational study, RCS retrospectivecaseseries,RCT randomised controlled trial
a
Twelve out of twelve examined
OBES SURG (2017) 27:513–521 515
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Primary Outcomes
Papilloedema
Surgical Group Surgical interventions were associated with
100% post-operative resolution.
Non-surgical Group Non-surgical weight-loss intervention
was associated with a significant regression in 66.7% (95%
CI [45.6, 87.8], p= <0.005); interstudy heterogeneity was
significant (χ
2
=39.4,p=0.000,I
2
=84.8%).
Visual Field Defects
Surgical Group Only two studies reported these hence data
was insufficient for quantitative synthesis. In these two stud-
ies, resolution or significant improvement was reported in
100% and 50% of cases, respectively.
Non-surgical Group Non-surgical weight-loss intervention
was associated with significant improvement in 75.4% (95%
CI, 63.6, 87.2; p= <0.005); interstudy heterogeneity was not
significant (χ
2
=3.67,p=0.300,I
2
=18.2%).
Headache Symptoms
Surgical Group Bariatric surgery was associated with a clini-
cally significant post-operative reduction or resolution in 90.2%
(95% CI, 67.4, 113; p= <0.005) (Fig. 2a); interstudy heteroge-
neity was not significant (χ
2
= 0.48, p= 0.993, I
2
=0.0%).
Non-surgical Group Non-surgical weight-loss intervention
was associated with a reduction or resolution in 23.2% (95%
CI, 11.5, 34.9; p= <0.005) (Fig. 2b); interstudy heterogeneity
was significant (χ
2
=26.4,p=0.000,I
2
=88.6%).
Body Mass Index
Surgical Group Surgical intervention was associated with a
significant post-operative reduction in BMI of 17.5 kg/m
2
(95% CI, 14.2, 20.7; p= <0.005); interstudy heterogeneity
was moderate (χ
2
= 11.29, p=0.024,I
2
=64.6%).
Non-surgical Group Non-surgical weight-loss intervention
was associated with a significant reduction in BMI of
4.2 kg/m
2
(95% CI, 1.38, 7.03; p= 0.008); interstudy hetero-
geneity was significant (χ
2
= 11.8, p=0.019,I
2
=66.2%).
CSF Pressure
Surgical Group Only two studies reported these hence data
were insufficient for quantitative synthesis. In these two stud-
ies, CSF pressure decreased in both cases by clinically signif-
icant levels (a mean of 185 and 198 mm H
2
0 respectively).
Non-surgical Group Non-surgical weight-loss intervention
was associated with a significant reduction in CSF opening
pressure of 61.0 mmHg (95% CI, 35.9, 86.0, p= <0.005);
interstudy heterogeneity was moderate (χ
2
=2.12,
p=0.145,I
2
=52.8%).
Fig. 1 Search strategy flow diagrams for asurgical and bnon-surgical studies
516 OBES SURG (2017) 27:513–521
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Quality Scoring and Analysis
The overall quality of non-randomised studies is
summarised in the Electronic Supplementary Material
Tab les 1,2and 3.
Surgical Series All but one of the seven studies were consid-
ered to be of moderate quality scoring ≥the mean of 6.
Non-surgical Series Of the six studies, three were of moder-
ate quality (scoring 6) and three of high quality (scoring ≥7).
There were insufficient high-quality studies to warrant sepa-
rate subgroup analysis.
The overall results of assessments for each study are also
summarised in the Electronic Supplementary Material
Tables 3and 4; most studies were deemed to be at moderate
risk of bias with none at critical risk of bias (which would
otherwise have warranted exclusion from further analysis).
Fig. 2 Headache symptom forest
plots for asurgical and bnon-
surgical studies
OBES SURG (2017) 27:513–521 517
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Heterogeneity Assessment: Bias Exploration
Funnel plots were employed to detect publication bias
(Electronic Supplementary Material Fig. 2). Visual inspection
showed no asymmetry, and Egger’s test did not detect a signif-
icant small-study effect (Electronic Supplementary Material
Fig. 1).
Discussion
In 65 patients with a mean pre-interventional BMI of 48.3,
bariatric surgery gave a weighted mean decrease of BMI by
17.5 kg/m
2
, associated with complete resolution of
papilloedema in all documented cases (indicative of relief of
raised intracranial pressure) and a significant reduction in head-
ache symptoms. Studies of subjects undergoing non-surgical
weight reduction therapies found 277 individuals with a mean
pre-intervention BMI of 37.7, which decreased by a weighted
mean of 4.2 kg/m
2
. This more modest weight loss was also
associated with significant improvements in papilloedema, vi-
sual fields and headache symptoms, although excepting visual
fields, these were all associated with significant interstudy het-
erogeneity that was generally not noted in the surgical studies.
This study provides the first available means to systemati-
cally and concurrently appraise the effects of surgical and non-
surgical weight-loss interventions on BMI and measures of
IIH severity. Although surgical and non-surgical patient
groups differed in their baseline characteristics, both outcomes
of weight loss and the clinical improvement in IIH symptom-
atology were found to be superior in surgical studies. The
quality of non-surgical studies was however higher, compris-
ing class 1 as opposed to class 3 or 4 evidence, such that there
is now stronger evidence corroborating the clinical consensus
that obesity-associated IIH improves with weight loss. There
is also class 1a evidence [34,35] in the literature that bariatric
surgery leads to greater weight loss and higher remission rates
of metabolic sequelae compared with non-surgical manage-
ment, and it is now established as the most effective treatment
for morbid obesity and obesity-associated co-morbidities
(such as type 2 diabetes mellitus, obstructive sleep apnoea,
cardiovascular outcomes, renal dysfunction and cancer),
hence more than 340,000 metabolic operations are performed
annually worldwide [36–38].
There is now an increasingly accepted view that obesity
plays a central role in the development of IIH, although precise
pathophysiological mechanisms are not yet fully elucidated [2].
With the largest quantifiable series to date assessing the
role of weight loss on IIH, we can confirm that bariatric sur-
gical studies demonstrate a greater effect size on IIH outcomes
when relating their results to non-surgical interventions.
Although these studies were not comparative trials, and there-
fore cannot be utilised to convey directly comparative results
between bariatric and non-surgical weight-loss interventions,
our analysis alludes to the mechanistic effects of sustained
weight less in resolving the pathology of IIH.
Current pathogenic theories linking obesity and IIH center
on alterations of CSF homeostasis, cerebral venous
haemodynamics and other hormonal and metabolic factors
[2]. The main hypotheses of IIH aetiology comprise (i) in-
creased cerebral venous pressure, (ii) reduced CSF outflow
conductance (both of which result in reduced CSF absorption)
and (iii) increased CSF secretion, all of which may be ulti-
mately impacted by obesity [2,6,39]. These are summarised
in Table 2.
Although metabolic surgery is unlikely to fully replace all
measures to manage IIH, as approximately 6–30% of IIH
patients are not obese and bariatric operations also pose some
operative risk, it offers many advantages compared with other
surgical treatment options such as CSF diversion procedures
Tabl e 3 Some current hypotheses linking obesity and IIH
Hypothesised factor Proposed mechanisms Final common pathway leading
to increased CSF pressure and IIH
Increased intra-abdominal pressure (via central obesity). 1. Leads to increased pleural pressure, cardiac
filling pressure, and central venous pressure
and may lead to increased intracranial venous
pressure and IIH [21].
1. Reduced CSF absorption via
increased cerebral venous
pressure.
2. Reduced CSF compliance via limited expansion
of spinal canal CSF spaces [2].
2. Altered CSF homeostasis.
Hypercoagulable state (obesity is a well-recognised
risk factor, which may be at least in party mediated
via pro-coagulant adipokines, e.g. leptin [44–46]
and sex steroids, e.g. oestrogen [47,48])
Occult cerebral venous sinus microthrombosis
leading to increased cerebral venous pressure
and reduced CSF outflow conductance [2,39].
Reduced CSF absorption
Neuroendocrine adiposopathy (endocrinologically
active secretions from adipose tissue include
mineralocorticoid releasing factors in addition
to the aformentioned adipokines/ sex steroids).
Increased CSF secretion and altered dynamics
results from mineralocorticoid receptor
activation [5].
Increased CSF secretion
518 OBES SURG (2017) 27:513–521
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
including shunt surgery. These non-bariatric approaches are
limited by a high failure which includes symptom recurrence
in 48% by 36 months [40] and typical revision rates of at least
30–60% [41–43]. Bariatric surgery has the advantage of di-
rectly targeting obesity and its associated metabolic dysfunc-
tion as well as mitigating other obesity-related co-morbidities.
Further work is however necessary to clarify whether bar-
iatric surgery offers an equivalence in the rapidity of treatment
outcome in the context of acute or rapidly progressive visual
loss, given the time required for both multidisciplinary pre-
operative workup and resolution of symptoms [12].
We suggest that IIH can be regarded both as significant, and
as a condition convincingly demonstrated to respond to weight
loss, and as such it is reasonable for bariatric surgery to be
offered to patients in this group. As such we explicitly advocate
that IIH should be considered as a co-morbidity of obesity that
should be added to the criteria for bariatric surgery worldwide (it
is principally listed only in clinical practice guidelines in the
USA for patients with IIH and BMI > =35 kg/m
2
[15]).
It is also noteworthy that multiple studies have associated
more severe obesity with worse visual outcomes in IIH [5]
which further supports the rationale for aggressive treatment
in morbidly obese individuals. Recently, an RCT has been
commenced comparing bariatric surgery vs. a community
weight-loss programme for the sustained treatment of IIH
(NCT02124486). This will likely clarify some factors regard-
ing patient selection for bariatric surgery in IIH; however,
remaining questions in this field include: (a) Whether bariatric
procedures should be a first line option for a selected obese
patients, (b) which bariatric procedure is most preferable in
these patients and (c) the most appropriate BMI cutoff where
the benefits of surgery outweigh possible risks (0.08% mor-
tality within 30 days and a reoperation rate of 7% [13]).
Strengths and Limitations
This meta-analysis statistically appraises pooled data from 65
patients in 7 surgical studies and 277 patients receiving non-
surgical management in 8 studies, which is the largest synthe-
sis to date. There are nevertheless several limitations within
which context these results should be interpreted. Most of the
constituent studies are intrinsically limited by their design
with no surgical studies and two non-surgical studies being
randomised controlled trials. Surgical studies are further lim-
ited to uncontrolled series although we have omitted the mul-
tiple case reports as these are inherently biased towards
favourable outcomes. Nonetheless, the effect size of surgical
intervention was marked and without significant heterogene-
ity, in contrast to that seen in non-surgical interventions which
are indicative of several potential confounding variables.
Despite this heterogeneity in the non-surgical group, we per-
formed an analysis based on the aggregation of interventions
as this reflects clinic practice where lifestyle approaches (e.g.
diet and exercise programs) are typically practised concurrent-
ly. Furthermore, other studies have utilised this approach as an
established methodology [37].
Our study aimed to clarify the impact of weight loss
on IIH outcomes, rather than the method by which the
weight loss is achieved; hence, we have included stud-
ies where this is quantified. Of the seven non-surgical
studies included the primary intervention was a speci-
fied low-energy diet in four [16,27,30,32] as opposed
to weight loss via unspecified means in the other three.
In the three [16,30,31] studies with multiple arms,
data from the weight-loss-only arm was used for analy-
sis. Overall, co-interventions were adequately appraised
with clinical or statistical controls.
Studies in both arms differed in demographics, follow-up
period and spanned a 40-year time period. This could mean
our analysis may not capture the difference between contem-
porary and historic weight-loss modalities or the develop-
ments in IIH diagnostic workup (particularly higher resolution
neuroimaging which can exclude differential diagnoses). For
instance, bariatric surgical techniques have evolved, yet the
newer technique of sleeve gastrectomy is under-represented in
these studies and some of our analysed data comes from
gastroplasty, which is no longer routinely performed. Similar
inconsistencies are present in non-surgical studies, and both
arms also included patients that had undergone cerebrospinal
fluid diversion therapies or optic nerve sheath fenestration
(another salvage procedure for deteriorating visual function).
Patients in both the surgical and non-surgical trials (exclud-
ing the two non-surgical RCTs who used a placebo) received
the diuretic acetazolamide which has been shown to have a
modest effect on IIH symptoms [16]. Other non-surgical
weight-loss interventions were non-standardised between tri-
als, reflecting real world variation in practice. A small number
of non-surgical patients also underwent bariatric surgery in
one included study.
Studies in both arms also showed variation in reported
outcome measures, which restricted the extent of analysis;
notably in the case of visual field status and CSF opening
pressure following bariatric surgery. In comparing the two
meta-analytical groups, both the mean pre-intervention BMI
and the prevalence of IIH symptoms and signs were materially
higher in the surgical group, which could impact the overall
reduction in BMI and degree of decrease in symptoms (al-
though absolute improvements were still considerably greater
than in non-surgical patients).
Though this analysis elucidates the comparison of surgical
and non-surgical studies by combining results from both treat-
ment strategies, it does not formally quantify the difference in
their effects. As result of the selection criteria requiring the
inclusion of both BMI and visual status findings pre and post-
intervention, several studies were excluded meaning that our
OBES SURG (2017) 27:513–521 519
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
analysis may not be fully representative of all interventions in
the literature to date.
Conclusion
We demonstrate that both bariatric surgery and non-surgical
weight loss may benefit IIH patients to improve papilloedema
and headache symptoms. Bariatric surgery offers a materially
greater treatment effect, in addition to the health benefits of
significant sustained weight loss and metabolic improvement.
The current evidence base is limited by a lack of randomised
controlled surgical trials and comparative studies between sur-
gical and non-surgical treatment strategies. Nevertheless, there
is broad consensus that obesity plays a central role in the path-
ogenesis of IIH and weight loss remains the essential corner-
stone of management. Bariatric surgery is the most effective
method achieving sustainable weight loss in obese patients.
Other treatment strategies, such as CSF diversion and optic
nerve sheath fenestration, are limited by a high incidence of
complications and they do not treat the most significant and
modifiable underlying risk factor, i.e. obesity.
Based on the best evidence available, a compelling case can
be made to regard IIH as obesity co-morbidity and thus bariatric
surgery should be offered at similar BMI thresholds to other
obesity co-morbidities in line with internationally endorsed
guidelines.
Further research is needed to determine the precise BMI
threshold where the benefits of bariatric surgery outweigh its
short- and long-term operative risks, as well as cost effective-
ness. This requires a holistic consideration of all the conse-
quences of obesity of the patient rather than only IIH in iso-
lation. More and better-designed trials are now required to
evaluate post-intervention periods, effects on visual loss and
underlying mechanistic factors to establish the precise rela-
tionship between bariatric surgery and non-surgical weight-
loss management in IIH resolution.
Compliance with Ethical Standards
Conflict of Interest The authors have no commercial associations that
might be a conflict of interest in relation to this article.
Ethical Approval This articledoes not contain any studies with human
participants or animals performed by any of the authors.
Informed Consent Does not apply.
Open Access This article is distributed under the terms of the Creative
Commons Attribution 4.0 International License (http://
creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
distribution, and reproduction in any medium, provided you give
appropriate credit to the original author(s) and the source, provide a link
to the Creative Commons license, and indicate if changes were made.
References
1. Radhakrishnan K, Ahlskog JE, Garrity JA, et al., editors. Idiopathic
intracranial hypertension. Mayo Clin Proc. 1994; Elsevier.
2. Banik R. Obesity and the role of nonsurgical and surgical weight
reduction in idiopathic intracranial hypertension. Int Ophthalmol
Clin. 2014;54(1):27–41.
3. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic in-
tracranial hypertension. Neurology. 2002;59(10):1492–5.
4. Yri HM, Wegener M, Sander B, et al. Idiopathic intracranial hyper-
tension is not benign: a long-term outcome study. J Neurol.
2011;259(5):886–94.
5. Andrews LE, Liu GT, Ko MW. Idiopathic intracranial hypertension
and obesity. Horm Res Paediatr. 2014;81(4):217–25.
6. Wakerley BR, Tan MH, Ting EY. Idiopathic intracranial hyperten-
sion. Cephalalgia. 2015;35(3):248–61.
7. Wall M. Idiopathic intracranial hypertension (pseudotumor cerebri).
Curr Neurol Neurosci Rep. 2008;8(2):87–93.
8. Wall M. Idiopathic intracranial hypertension and the idiopathic in-
tracranial hypertension treatment trial. J Neuroophthalmol.
2013;33(1):1–3.
9. Wall M, George D. Idiopathic intracranial hypertension. A prospec-
tive study of 50 patients. Brain. 1991;114(Pt 1A):155–80.
10. Rowe FJ, Sarkies NJ. The relationship between obesity and idio-
pathic intracranial hypertension. Int J Obes Relat Metab Disord.
1999;23(1):54–9.
11. Biousse V, Bruce BB, Newman NJ. Update on the pathophysiology
and management of idiopathic intracranial hypertension. J Neurol.
2012;83(5):488–94.
12. Fridley J, Foroozan R, Sherman V, et al. Bariatric surgery for the
treatment of idiopathic intracranial hypertension: a review. J
Neurosurg. 2011;114(1):34–9.
13. Ashrafian H, Darzi A, Athanasiou T. Bariatric surgery: can we
afford to do it or deny doing it? Frontline Gastroenterol.
2011;2(2):82–9.
14. Ashrafian H, Ahmed K, Rowland SP, et al. Metabolic surgery and
cancer: protective effects of bariatric procedures. Cancer.
2011;117(9):1788–99.
15. Handley JD, Baruah BP, Williams DM, et al. Bariatric sur-
gery as a treatment for idiopathic intracranial hypertension:
a systematic review. Surg Obes Relat Dis. 2015;11(6):
1396–403.
16. Wall M, McDermott MP, Kieburtz KD, et al. Effect of acetazol-
amide on visual function in patients with idiopathic intracranial
hypertension and mild visual loss: the idiopathic intracranial hyper-
tension treatment trial. JAMA. 2014;311(16):1641–51.
17. Moher D, Liberati A, Tetzlaff J, et al. Preferred reporting items for
systematic reviews and meta-analyses: the PRISMA statement.
Ann Intern Med. 2009;151(4):264–9.
18. Wells G, Shea B, O’connell D, et al. The Newcastle-Ottawa Scale
(NOS) for assessing the quality of nonrandomised studies in meta-
analyses. 2000.
19. Jadad AR, Moore RA, Carroll D, et al. Assessing the quality of
reports of randomized clinical trials: is blinding necessary?
Control Clin Trials. 1996;17(1):1–12.
20. Sugerman HJ, Felton WL, Salvant JB, et al. Effects of surgically
induced weight loss on idiopathic intracranial hypertension in mor-
bid obesity. Neurology. 1995;45(9):1655–9.
21. Sugerman H, DeMaria E, Felton W, et al. Increased intra-abdominal
pressure and cardiac filling pressures in obesity-associated
pseudotumor cerebri. Neurology. 1997;49(2):507–11.
22. Sugerman HJ, Felton 3rd WL, Sismanis A, et al. Gastric surgery for
pseudotumor cerebri associated with severe obesity. Ann Surg.
1999;229(5):634–40. discussion 40-2
520 OBES SURG (2017) 27:513–521
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
23. Michaelides EM, Sismanis A, Sugerman HJ, et al. Pulsatile tinnitus
in patients with morbid obesity: the effectiveness of weight reduc-
tion surgery. Otol Neurotol. 2000;21(5):682–5.
24. Nadkarni T, Rekate HL, Wallace D. Resolution of pseudotumor
cerebri after bariatric surgery for related obesity: case report. J
Neurosurg. 2004;101(5):878–80.
25. Egan RJ, Meredith HE, Coulston JE, et al. The effects of laparo-
scopic adjustable gastric banding on idiopathic intracranial hyper-
tension. Obes Surg. 2011;21(2):161–6.
26. Sanmugalingam N, Khan O, Bond A, et al. The impact of bariatric
surgery on idiopathic intracranial hypertensive patients. Obes Surg.
2013;23:1142.
27. Newborg B. Pseudotumor cerebri treated: by rice-reduction diet.
Arch Intern Med. 1974;133(5):802–7.
28. Johnson LN, Krohel GB, Madsen RW, et al.The role of weight loss
and acetazolamide in the treatment of idiopathic intracranial hyper-
tension (pseudotumor cerebri). Ophthalmology. 1998;105(12):
2313–7.
29. Kupersmith M, Gamell L, Turbin R, et al. Effects of weight loss on
the course of idiopathic intracranial hypertension in women.
Neurology. 1998;50(4):1094–8.
30. Glueck CJ, Golnik KC, Aregawi D, et al. Changes in weight,
papilledema, headache, visual field, and life status in response to
diet and metformin in women with idiopathic intracranial hyperten-
sion with and without concurrent polycystic ovary syndrome or
hyperinsulinemia. Transl Res. 2006;148(5):215–22.
31. Ball AK, Howman A, Wheatley K, et al. A randomised controlled
trial of treatment for idiopathic intracranial hypertension. J Neurol.
2011;258(5):874–81.
32. Sinclair AJ, Burdon MA, Nightingale PG, et al. Low energy diet
and intracranial pressure in women with idiopathic intracranial hy-
pertension: prospective cohort study. BMJ. 2010;341:c2701.
33. Pollak L, Zohar E, Glovinsky Y, et al. Reevaluation of presentation
and course of idiopathic intracranial hypertension—alargecohort
comprehensive study. Acta Neurol Scand. 2013;127(6):406–12.
34. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabe-
tes after bariatric surgery: systematic review and meta-analysis. Am
J Med. 2009;122(3):248–56.
35. Gloy VL, Briel M, Bhatt DL, et al. Bariatric surgery versus non-
surgical treatment for obesity: a systematic review and meta-
analysis of randomised controlled trials. BMJ. 2013;347:5934.
36. Buchwald H, Oien DM. Metabolic/bariatric surgery worldwide
2011. Obes Surg. 2013;23(4):427–36.
37. Ashrafian H, Toma T, Rowland SP, et al. Bariatric surgery or non-
surgical weight loss for obstructive sleep apnoea? A systematic
review and comparison of meta-analyses. Obes Surg. 2014;1-12
38. Bower G, Toma T, Harling L, et al. Bariatric surgery and non-
alcoholic fatty liver disease: a systematic review of liver biochem-
istry and histology. Obes Surg. 2015;1-10
39. Fraser C, Plant GT. The syndrome of pseudotumour cerebri and
idiopathic intracranial hypertension. Curr Opin Neurol.
2011;24(1):12–7.
40. Mcgirt MJ, Woodworth G, Thomas G, et al. Cerebrospinal fluid
shunt placement for pseudotumor cerebri-associated intractable
headache: predictors of treatment response and an analysis of
long-term outcomes. J Neurosurg. 2004;101(4):627–32.
41. Jusué-Torres I, Hoffberger JB, Rigamonti D. Complications of
lumboperitoneal shunts for idiopathic intracranial hypertension.
Cureus. 2014;6(7):e188.
42. Abubaker K, Ali Z, Raza K, et al. Idiopathic intracranial hy-
pertension: lumboperitoneal shunts versus ventriculoperitoneal
shunts–case series and literature review. Br J Neurosurg.
2011;25(1):94–9.
43. Tarnaris A, Toma AK, Watkins LD, et al. Is there a difference in
outcomes of patients with idiopathic intracranial hypertension with
the choice of cerebrospinal fluid diversion site: a single centre ex-
perience. Clin Neurol Neurosurg. 2011;113(6):477–9.
44. Lampl Y, Eshel Y, Kessler A, et al. Serum leptin level in women
with idiopathic intracranial hypertension. J Neurol Neurosurg
Psychiatry. 2002;72(5):642–3.
45. Dellas C, Schäfer K, Rohm I, et al. Absence of leptin resistance in
platelets from morbidly obese individuals may contribute to the
increased thrombosis risk in obesity. Thromb Haemost.
2008;100(6):1123–9.
46. Konstantinides S, Schäfer K, Neels JG, et al. Inhibition of endoge-
nous leptin protects mice from arterial and venous thrombosis.
Arterioscler Thromb Vasc Biol. 2004;24(11):2196–201.
47. Nelson LR, Bulun SE. Estrogen production and action. J Am Acad
Dermatol. 2001;45(3):S116–S24.
48. Tchaikovski SN, Rosing J. Mechanisms of estrogen-induced ve-
nous thromboembolism. Thromb Res. 2010;126(1):5–11.
OBES SURG (2017) 27:513–521 521
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
1.
2.
3.
4.
5.
6.
Terms and Conditions
Springer Nature journal content, brought to you courtesy of Springer Nature Customer Service Center GmbH (“Springer Nature”).
Springer Nature supports a reasonable amount of sharing of research papers by authors, subscribers and authorised users (“Users”), for small-
scale personal, non-commercial use provided that all copyright, trade and service marks and other proprietary notices are maintained. By
accessing, sharing, receiving or otherwise using the Springer Nature journal content you agree to these terms of use (“Terms”). For these
purposes, Springer Nature considers academic use (by researchers and students) to be non-commercial.
These Terms are supplementary and will apply in addition to any applicable website terms and conditions, a relevant site licence or a personal
subscription. These Terms will prevail over any conflict or ambiguity with regards to the relevant terms, a site licence or a personal subscription
(to the extent of the conflict or ambiguity only). For Creative Commons-licensed articles, the terms of the Creative Commons license used will
apply.
We collect and use personal data to provide access to the Springer Nature journal content. We may also use these personal data internally within
ResearchGate and Springer Nature and as agreed share it, in an anonymised way, for purposes of tracking, analysis and reporting. We will not
otherwise disclose your personal data outside the ResearchGate or the Springer Nature group of companies unless we have your permission as
detailed in the Privacy Policy.
While Users may use the Springer Nature journal content for small scale, personal non-commercial use, it is important to note that Users may
not:
use such content for the purpose of providing other users with access on a regular or large scale basis or as a means to circumvent access
control;
use such content where to do so would be considered a criminal or statutory offence in any jurisdiction, or gives rise to civil liability, or is
otherwise unlawful;
falsely or misleadingly imply or suggest endorsement, approval , sponsorship, or association unless explicitly agreed to by Springer Nature in
writing;
use bots or other automated methods to access the content or redirect messages
override any security feature or exclusionary protocol; or
share the content in order to create substitute for Springer Nature products or services or a systematic database of Springer Nature journal
content.
In line with the restriction against commercial use, Springer Nature does not permit the creation of a product or service that creates revenue,
royalties, rent or income from our content or its inclusion as part of a paid for service or for other commercial gain. Springer Nature journal
content cannot be used for inter-library loans and librarians may not upload Springer Nature journal content on a large scale into their, or any
other, institutional repository.
These terms of use are reviewed regularly and may be amended at any time. Springer Nature is not obligated to publish any information or
content on this website and may remove it or features or functionality at our sole discretion, at any time with or without notice. Springer Nature
may revoke this licence to you at any time and remove access to any copies of the Springer Nature journal content which have been saved.
To the fullest extent permitted by law, Springer Nature makes no warranties, representations or guarantees to Users, either express or implied
with respect to the Springer nature journal content and all parties disclaim and waive any implied warranties or warranties imposed by law,
including merchantability or fitness for any particular purpose.
Please note that these rights do not automatically extend to content, data or other material published by Springer Nature that may be licensed
from third parties.
If you would like to use or distribute our Springer Nature journal content to a wider audience or on a regular basis or in any other manner not
expressly permitted by these Terms, please contact Springer Nature at
onlineservice@springernature.com
Available via license: CC BY 4.0
Content may be subject to copyright.
