CME

Idiopathic intracranial hypertension

Elizabeth Boyter, MPA, PA-C

ABSTRACT Learning objectives

Idiopathic intracranial hypertension is a rare disorder of
elevated intracranial pressure with normal cerebrospinal
fluid composition and without intracranial pathology. This
condition primarily affects obese women of childbearing
age and frequently causes headaches, vision loss, diplopia,
tinnitus, and nausea. The incidence of idiopathic intracranial
hypertension is rising along with obesity rates. Primary care
and ED clinicians must recognize the signs and symptoms of
idiopathic intracranial hypertension and intervene promptly
to control symptoms and to preserve vision. This article
reviews the clinical presentation and management of patients
with idiopathic intracranial hypertension.
Keywords: idiopathic intracranial hypertension, obesity, head-
ache, vision loss, tinnitus, increased intracranial pressure
Identify patient populations most at risk for idiopathic
intracranial hypertension.
Describe the diagnostic criteria and appropriate work-up
for idiopathic intracranial hypertension.
Discuss definitive and symptomatic treatment options for
idiopathic intracranial hypertension.
intracranial hypertension also has been reported in chil-
dren as young as age 4 months old and adults up to age
88 years.3
Most cases are self-limited, but the condition may recur
and become chronic, requiring follow-up care for years.4,6
Healthcare providers must be prepared to identify the signs
and symptoms of increased intracranial pressure (ICP) and

I
diopathic intracranial hypertension occurs in 1 to 2 per
100,000 people per year.1 About 90% of patients
with this condition are female, and 94% are Cortical veins
Falx cerebri
obese.2 Obese women ages 15 to 44 years are at Superior
high risk for idiopathic intracranial hyperten- sagittal sinus Sigmoid sinus
sion, with a higher incidence rate of 19 to 21 Inferior Superior
petrosal sinus
per 100,000.3,4 Obese women in their 20s sagittal sinus
are most susceptible. In 1980, 12.7% of US Inferior
adults were obese, and in 2012, that num- Straight sinus petrosal
sinus
ber approached 35%.5 The incidence of
Confluence of
idiopathic intracranial hypertension sinuses
reflects this rise in obesity, doubling
between 1990 and 2014.5
Males account for 8% to 10% of Tentorium
cerebelli
patients with idiopathic intracranial
hypertension. At presentation, they are Transverse
© ASKLEPIOS MEDICAL ATLAS / SCIENCE SOURCE

more likely to be older and less likely to sinus

be obese.3,6,7 Men with idiopathic intracra-
nial hypertension experience fewer head-
aches, but are twice as likely as women to Great
cerebral vein
experience severe vision loss.6,7 Idiopathic

Elizabeth Boyter practices neurology with Laureate Medical Group

Cavernous sinus
at Northside in Atlanta, Ga. The author has disclosed no potential
conflicts of interest, financial or otherwise.
DOI:10.1097/01.JAA.0000554732.85914.91
FIGURE 1.
Copyright © 2019 American Academy of PAs Cerebral venous system

30 www.JAAPA.com Volume 32 • Number 5 • May 2019

Copyright © 2019 American Academy of Physician Assistants

 Idiopathic intracranial hypertension

Key points
Idiopathic intracranial hypertension is defined as elevated
ICP in a patient with normal CSF composition and no
intracranial pathology.
Patients typically are obese women of childbearing age;
symptoms include headaches, vision loss, diplopia,
FIGURE 2.
tinnitus, and nausea. Normal optic disk
Prompt intervention is key to controlling symptoms and
Reprinted with permission
preserving vision. from Palay DA, Krachmer JH.
Weight loss is considered the cornerstone of treatment, Ophthalmology for the Primary
Care Physician. St. Louis, MO:
but medications also can help lower ICP.
Mosby; 1997.

take action to control disabling headaches and avoid tension or explain why the condition occurs in patients
significant vision loss. who are not overweight or obese. Furthermore, pregnancy
does not confer a higher risk of idiopathic intracranial
PATHOPHYSIOLOGY hypertension.3 Cerebrospinal fluid (CSF) homeostasis may
The cause of idiopathic intracranial hypertension remains be disturbed by reduced CSF absorption, increased CSF
unknown, but it has been closely correlated with obesity. secretion, or abnormal water and sodium metabolism
Recent weight gain, even in patients who are not obese, is related to endocrinologically active adipose tissue.1-3
a significant risk factor for developing idiopathic intracra- ICP may rise because of cerebral venous outflow abnor-
nial hypertension. Weight gain often triggers recurrent malities, such as dural venous hypertension and dural venous
symptoms in patients with idiopathic intracranial hyper- sinus stenosis (Figure 1). Whether venous sinus stenosis is
tension.2,3,6,8,9 A higher BMI is associated with worse visual a cause or a consequence of intracranial hypertension is
outcomes; for every 10-unit increase in BMI, the odds of controversial, and studies suggest it may be both.3,12 A
severe vision loss increases by 1.4 times.2,10 As obesity positive feedback mechanism may fuel both venous sinus
increases in the general population, reports of idiopathic stenosis and intracranial hypertension. Under the stress of
intracranial hypertension in children and males are grow- elevated ICP, the walls of the transverse sinuses may remodel,
ing in number.11 Obesity, rather than sex or age, may be triggering fibrosis and stenosis. The stenosis aggravates
the primary causative factor.11 venous hypertension, which reduces CSF absorption. As a
The medical literature offers several theories to explain result, ICP continues to rise and venous stenosis worsens.1
the pathogenesis of increased ICP that causes symptoms Several other conditions may be associated with idiopathic
of idiopathic intracranial hypertension in obese patients. intracranial hypertension, including hypervitaminosis A;
For example, central obesity may increase intra-abdominal, use of retinoids; and exposure to exogenous growth hor-
pleural, cardiac filling, and central venous pressures, and mone, tetracyclines, or fluoroquinolones.3 Idiopathic intra-
ICP may rise as a result. However, this theory does not cranial hypertension related to medications tends to be
explain the sex disparity in idiopathic intracranial hyper- self-limited and often resolves when the medication is
discontinued.6 Other conditions
associated with idiopathic intracra-
FIGURE 3. Bilateral papilledema
nial hypertension are Addison dis-
Reprinted with permission from Palay DA, Krachmer JH. Ophthalmology for the Primary Care Physician. St. Louis, MO: Mosby; 1997.
ease, hypoparathyroidism, severe
anemia, systemic lupus erythemato-
sus, Behçet disease, sleep apnea,
uremia, and coagulation disorders.3
Polycystic ovarian syndrome is twice
as prevalent among women with
idiopathic intracranial hypertension
(15.5%) as in the general population
(8.7%).13 Treating these disorders
should improve idiopathic intracra-
nial hypertension.3

CLINICAL MANIFESTATIONS
Patients with idiopathic intracranial
hypertension present with symptoms

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Copyright © 2019 American Academy of Physician Assistants

CME

of increased ICP. They may experience throbbing frontal cranial nerve VI that causes diplopia.6,14 Patients often hear
or retro-orbital headaches, nausea, vomiting, tinnitus, and pulsatile, “whooshing” tinnitus related to high-pressure,
visual loss.1,6,12,14 Actions that increase ICP, including the turbulent blood flow in the cerebral venous sinuses.11 Neck
Valsalva maneuver, bending forward, and lying supine, stiffness and back pain also are common complaints.14
14
commonly aggravate these symptoms. Resuming an
upright position often relieves them. DIAGNOSIS
At diagnosis, 93% of patients with idiopathic intracranial Idiopathic intracranial hypertension is a diagnosis of exclu-
hypertension complain of headache.11 Headache is one of sion.19 If increased ICP is suspected, MRI and magnetic
the most common reasons for primary care visits and ranks resonance venography of the brain are recommended to
among the top 10 disabling conditions worldwide, accord- exclude secondary causes of increased ICP, including dural
ing to the World Health Organization.15 In women, headache venous sinus thrombosis, mass lesion, aneurysm, subarach-
ranks among the top five causes of disability.15 Patients with noid hemorrhage, meningitis, subdural hematoma, and
idiopathic intracranial hypertension often present with stroke. A few imaging findings suggest intracranial hyper-
typical symptoms of migraine, such as photophobia, pho- tension, but they are not diagnostic of idiopathic intracra-
nophobia, nausea, and vomiting. In fact, migraine frequently nial hypertension, nor does their absence exclude idiopathic
coexists with idiopathic intracranial hypertension.12 Increased intracranial hypertension. These findings include bilateral
ICP may exacerbate the primary headache disorder. or unilateral dural venous sinus stenosis, flattening of the
Patients with idiopathic intracranial hypertension often posterior sclera, an empty sella turcica, and distension of
describe transient visual dimming, visual blackout, or the optic nerve sheaths (Figure 4).6,12,14
“tunnel vision” occurring with postural changes.14,6,12 High If brain imaging does not reveal a structural cause for elevated
CSF pressure compresses the optic nerves and causes isch- ICP, the next step is high-volume lumbar puncture, which
emia, which may lead to optic disk edema or papilledema obtains 30 to 40 mL of CSF compared with 8 to 15 mL for
(Figures 2 and 3).12 With prolonged pap-
illedema, optic nerve damage progresses, FIGURE 4. MRI findings in patients with idiopathic intracranial hypertension: empty sella (A),
and the visual fields gradually constrict.6 distended optic nerve sheaths (B), transverse sinus stenosis (C), and flattened posterior sclera (D)
Bedside fundoscopy is the first step in
Reprinted with permission from Markey KA, Mollan SP, Jensen RH, Sinclair AJ. Understanding idiopathic intracranial
identifying unilateral or bilateral papill- hypertension: mechanisms, management, and future directions. Lancet Neurol. 2016;15(1):78-91.
edema.11 Confrontational visual fields
testing may detect restricted visual
fields.14 Perimetry, or visual field testing A B
performed by an ophthalmologist or
neuro-ophthalmologist, involves flashing
lights in different locations in the visual
field. The patient responds when she or
he sees the light.16,17
Perimetry identifies visual loss in about
95% of patients with idiopathic intracra-
nial hypertension, but only one-third of
patients recognize the loss.18 The most
common visual field abnormalities are an
enlarged blind spot and peripheral vision
loss. Central vision loss is a late find-
ing.6,11,14,16 About 25% of patients have C D
some irreversible visual loss, and 5% to
10% may progress to blindness.6,18 Serial
perimetry is essential to monitor the disease
and guide treatment.6,11,14,18 Only about
6% of patients with idiopathic intracranial
hypertension do not have papilledema.12
These patients do not experience typical
transient vision disturbances and are not
at risk for permanent visual loss.6
The cranial nerve examination is usu-
ally normal, but may reveal an ocular
motility defect, such as a palsy involving

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Copyright © 2019 American Academy of Physician Assistants


a routine lumbar puncture.12,14,20 High-volume lumbar punc-
ture aids in diagnosis and often provides temporary headache
relief.6,12,14 The opening pressure must be documented accu-
rately because it is critical to making a diagnosis. In patients
with idiopathic intracranial hypertension, the opening pressure
is elevated above the normal level of 20 to 25 cm H2O. CSF
also is collected in sterile tubes to be sent for analysis. The
CSF analysis includes a cell count with differential, protein,
and glucose, which are usually normal. If clinically indicated,
the CSF may be analyzed for cytology and bacterial, viral,
fungal, and mycobacterial pathogens.14,20
The Modifi ed Dandy Criteria can be used to aid
providers in the diagnosis of intracranial hypertension.
• Symptoms and signs of increased ICP: headache, transient
visual obscuration, pulse-synchronous tinnitus, papilledema,
visual loss
• No other neurologic abnormality (except unilateral or
bilateral cranial nerve VI palsy) or impaired level of con-
sciousness
• Elevated ICP with normal CSF composition
• Neuroimaging showing no secondary cause of intracra-
nial hypertension
• No other apparent cause of intracranial hypertension.6,14
TREATMENT
The goals of treatment for patients with idiopathic intra-
cranial hypertension are to alleviate symptoms and preserve
vision.6,8 Refer the patient to a neurologist for ongoing
management of headaches and other symptoms.6 Because
the condition may lead to severe and permanent vision
loss, the patient should be followed by an ophthalmologist
or neuro-ophthalmologist to monitor papilledema and
perform serial perimetry.1,12,14
Weight loss Educate patients about the effect of excess
weight on idiopathic intracranial hypertension and the
critical role of weight loss in controlling the condition.6
Weight loss is considered the cornerstone of manage-
ment.2,6,9,12 Patients should receive counseling on regular
exercise and diet modification.2
Some patients may be candidates for bariatric surgery.
Compared with nonsurgical weight loss techniques, bar-
iatric surgery produces greater weight loss and higher
remission rates of the metabolic consequences of obesity.2
A 2017 systematic review appraised the effects of bariat-
ric surgery and nonsurgical weight loss methods on signs
and symptoms of idiopathic intracranial hypertension.2
Bariatric surgery provided superior outcomes: BMI dropped
by 17.5 kg/m2, compared with 4.2 kg/m2 for patients who
used nonsurgical weight loss techniques.2 Bariatric surgery
reduced or resolved headache in 90.2% of patients, but
only 23.2% of patients got headache relief from nonsur-
gical weight loss.2 Papilledema resolved in 100% of surgi-
cal patients and 66.7% of nonsurgical patients.2
The Idiopathic Intracranial Hypertension Weight Trial
(IIH:WT) is in progress.21 This randomized controlled
JAAPA Journal of the American Academy of PAs
Copyright © 2019 American Academy of Physician Assistants
Idiopathic intracranial hypertension
prospective trial will assess the effect of bariatric surgery
compared with a community weight loss program for the
long-term treatment of idiopathic intracranial hypertension
in patients with BMIs over 35 kg/m2. The study will
monitor ICP, idiopathic intracranial hypertension symp-
toms, headache, papilledema, visual function, quality of
life, and cost-effectiveness over 5 years. The investigators
aim to determine whether bariatric surgery provides supe-
rior sustained weight loss and idiopathic intracranial
hypertension symptom relief.21
Medications Although weight loss is considered the
cornerstone of treatment for idiopathic intracranial hyper-
tension, medications also can help lower ICP. The carbonic
anhydrase inhibitors acetazolamide and methazolamide
may reduce CSF production and CSF pressure.8 Acetazol-
amide may improve idiopathic intracranial hypertension
symptoms, visual field measurements, and papilledema.
The usual starting dose of acetazolamide is 500 mg twice
daily, titrating as needed and tolerated to 2 to 4 g/day.8
Patients taking acetazolamide often experience acral par-
esthesias. Monitor electrolytes periodically, as patients may
experience a mild metabolic acidosis.8,12
The antiseizure medication topiramate also inhibits car-
bonic anhydrase. Like acetazolamide, topiramate may
relieve some symptoms of idiopathic intracranial hyperten-
sion and improve vision impairment.8 Often used for
migraine headache prophylaxis, topiramate 100 to 150 mg/
day may provide dual benefit for patients with idiopathic
intracranial hypertension who also suffer from migraines.12
In addition, topiramate may suppress the appetite and boost
weight loss efforts.6,8,12 Adverse reactions, including cogni-
tive slowing, memory impairment, alteration of taste, acral
paresthesias, metabolic acidosis, acute angle-closure glau-
coma (rare), and kidney stones, may limit the titration of
topiramate.8,22 Topiramate use during pregnancy has been
associated with an increased risk of birth defects such as
oral clefts.23,24 Before prescribing topiramate to women of
childbearing age, advise them to use effective birth control.24
A loop diuretic, such as furosemide, can be used in
combination with acetazolamide to reduce CSF pressure
and treat papilledema. Labwork should be drawn regularly
to monitor renal function and electrolytes.8
Controlling headaches is often challenging for patients
with idiopathic intracranial hypertension. Headache
abortive treatments, such as triptans and butalbital-APAP-
caffeine, relieve pain but may elevate BP. Counsel patients
about judicious use of analgesics to avoid the common
problem of analgesic rebound headache.8,25 Preventive
medications, including topiramate and beta-blockers, may
reduce headache burden. In the emergency setting, severe
headache may respond to a combination of IV antiemetics
(such as promethazine) or dopamine receptor blockers
(such as metoclopramide, prochlorperazine, or
chlorpromazine); and ketorolac, diphenhydramine, and
dexamethasone.25
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CME
Lumbar puncture This procedure may relieve escalating
headache or symptoms of increased ICP.6,8 However, serial
lumbar puncture is an undesirable long-term solution. CSF
reforms within 6 hours. The procedure itself may be tech-
nically challenging in obese patients. CSF infection, CSF
leak, and low-pressure headache are potential complications
of lumbar puncture.8
Surgery In patients with refractory intractable headache
or continued vision loss unresponsive to maximum medi-
cal therapy, surgical intervention is the next step.1,8,12 A
patient may require surgery if she is unable to participate
appropriately in care and follow-up because of noncompli-
ance or impaired cognition.8
Current surgical options include optic nerve sheath
fenestration, CSF diversion with ventriculoperitoneal
(VP) or lumboperitoneal (LP) shunt, and venous sinus
stenting.8 Optic nerve sheath fenestration is indicated for
papilledema-related vision loss and is performed by an
ophthalmologist or neuro-ophthalmologist.1,8,12,26 The
procedure involves making a slit or rectangular window
in the optic nerve sheath to decompress the nerve.26 The
procedure improves or stabilizes visual acuity and visual
fields and relieves papilledema.8,12,26 Optic nerve sheath
fenestration makes little effect on overall ICP, but there
is some evidence that it reduces headache.8,12 Patients
undergoing optic nerve sheath fenestration may experi-
ence temporary diplopia or pupillary dysfunction. Tran-
sient or permanent vision loss may occur. The benefit of
the procedure may wane over time, and patients may
require repeat surgery.8
The most common surgical intervention for idiopathic
intracranial hypertension is CSF diversion using VP or LP
shunt. CSF diversion is indicated for patients who experi-
ence refractory headache or progressive vision loss despite
maximal medical therapy.1,6,8,12 To implant a VP shunt, a
neurosurgeon passes a catheter through the skull into a
lateral ventricle and tunnels the catheter under the skin
and into the peritoneal cavity.27 Less common than VP
shunting, LP shunting involves inserting a catheter into
the lumbar subarachnoid space, then threading it under
the skin into the peritoneal cavity. In both types of shunt,
a programmable or nonprogrammable one-way valve is
used to control CSF flow.27
These procedures can stabilize or improve headache,
papilledema, vision loss, and diplopia.8,12 Headache burden
decreases in almost all patients soon after shunting, but
nearly half of patients have recurrent severe headaches
within 3 years.8 Shunts are associated with several common
complications, including shunt infection, CSF leak, and
abdominal or back pain.8 Shunts sometimes malfunction
and often need revision.8
Patients with dural venous sinus stenosis who do not
benefit from medical therapy may get relief from venous
sinus stenting, a relatively new intervention for idiopathic
intracranial hypertension.1,8,12 Stenting results in significant
34 www.JAAPA.com
Copyright © 2019 American Academy of Physician Assistants
reductions in headache, visual symptoms, papilledema,
and pulsatile tinnitus. Complications of the procedure
include ipsilateral headache, intracranial hemorrhage,
proximal stent stenosis, in-stent thrombosis, and stent
migration.1,6,8,12 To prevent thrombosis, the patient must
start antiplatelet therapy before the procedure and continue
therapy for 3 to 6 months after stenting.1,12 If vision loss
progresses, an alternative surgical procedure such as optic
nerve sheath fenestration or CSF diversion may have to
be delayed until after the patient has discontinued anti-
platelet therapy. More studies are needed to determine
the role of venous sinus stenting in managing patients
with idiopathic intracranial hypertension.6,8
CONCLUSION
Idiopathic intracranial hypertension is a diagnosis of
exclusion, and the diagnosis is often difficult to make.
Although idiopathic intracranial hypertension is most
common among obese women in their 20s, it also may
occur in children, males, and older adults. The US popu-
lation of obese patients continues to increase, and with
it, the burden of idiopathic intracranial hypertension.
Clinicians should consider idiopathic intracranial hyper-
tension in obese patients presenting with headache. Rec-
ognizing this serious disorder and promptly taking action
may make a tremendous effect on a patient’s vision and
quality of life.
Despite adequate medical or surgical therapy for idio-
pathic intracranial hypertension, many patients continue
to experience some degree of headache, elevated ICP,
papilledema, or vision loss. The road to recovery may be
long and frustrating, but patients can get better. Until they
stabilize, patients require regular follow-up with their care
team and monitoring for recurrent disease. JAAPA
Earn Category I CME Credit by reading both CME articles in this issue,
reviewing the post-test, then taking the online test at http://cme.aapa.
org. Successful completion is defined as a cumulative score of at least
70% correct. This material has been reviewed and is approved for 1
hour of clinical Category I (Preapproved) CME credit by the AAPA. The
term of approval is for 1 year from the publication date of May 2019.
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