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Editorial
Intracranial hypertension, headacheand obesity: Insights from magneticresonance venography
Deborah l Friedman
Idiopathic intracranial hypertension without papilloe-
dema (IIHWOP) is uncommon, accounting for, at
most, 5% of patients with IIH evaluated by neuro-
ophthalmologists (1). In contrast to patients with IIH
and papilloedema, patients with IIHWOP are less
obese, have lower cerebrospinal fluid pressures, and
are more likely to have non-organic visual loss (1).
This entity is perhaps more readily diagnosed among
headache specialists than neuro-ophthalmologists and
is suspected in obese women with intractable or chronic
daily headaches (2).
The integral relationship between the central venous
system and intracranial pressure has been emphasised
over the past several years with the discovery of venous
sinus abnormalities in patients with IIH (3). Morpho-
logical irregularities and abnormal pressure gradients
within the transverse sinuses are well described. In
most cases, transverse venous sinus stenosis appearsto be a result of high intracranial pressure rather than
its cause (4). The transverse sinuses are asymmetric in
most individuals and a unilateral hypoplastic sinus is
considered a normal variant. However, bilateral trans-
verse sinus stenosis (BTSS) may be associated with
intracranial hypertension.
In this issue of Cephalalgia, Bono and colleagues
studied 98 patients with chronic migraine and chronic
tension type headache using magnetic resonance venog-
raphy and 1-h continuous lumbar CSF pressure moni-
toring (5). Their findings are notable in several respects.
Strikingly, their patients were obese, regardless of
CSF pressure status. Patients with normal CSF pres-
sure (Group 1) were less overweight than in the groups
with either intermittently (Group 2) or consistently
(Group 3) elevated CSF pressure, and some patients
in Group 1 had a normal body mass index (BMI),
but overall this cohort was overweight. There was no
different in BMI between subjects in Groups 2 and 3.
Obesity is a risk factor for both IIH and the develop-
ment of chronic daily headache (6).
Although there was a statistically significant differ-
ence in both mean CSF pressure and opening pressure
between the three groups, only some of the patients in
Group 3 met criteria for the diagnosis of IIH by current
standards (7). Pressures between 201249 mm CSF are
non-diagnostic (8).
BTSS has been noted in a majority of patients with
IIH by various investigators. It is less commonly
encountered in a typical practice setting, even in
patients with papilloedema. The high prevalence of
BTSS in this cohort is perhaps attributable to the imag-
ing technique used, which the investigators previously
found to have a very high detection rate of transverse
sinus stenosis (three dimensional phase contrast images
with 15 cm/s velocity encoding). Conventional MR
venography is often performed using two dimensional
time of flight, and the images are likely subjected to less
scrutiny in the practice setting than the research setting.
All subjects in Groups 2 and 3 had BTSS, whereas only
four of 54 patients in group 1 had BTSS. As previouslynoted, unilateral transverse sinus stenosis was not asso-
ciated with abnormal intracranial pressure.
One-hour monitoring showed mean pressures that
were consistently higher than the opening pressure in
all groups. The importance of this finding cannot be
overemphasised. An isolated CSF pressure measure-
ment is but a snapshot in time and may be spuriously
high or low, depending on the situation and technique
employed. Prolonged monitoring also revealed B-waves
in Groups 2 and 3; B-waves are frequently recorded
with increased intracranial pressure of various aetiolo-
gies, although there is far greater experience defining
pressure wave abnormalities with intracranial pressure
monitoring systems than with lumbar recording
methods.
Digre and colleagues (1) found that treatment of
patients with IIHWOP with agents conventionally
University of Rochester, USA.
Corresponding author:
Dr Deborah l Friedman. University of Rochester, New York, USA
Email: [email protected]
Cephalalgia
30(12) 14151416
! International Headache Society 2010
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DOI: 10.1177/0333102410370872
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used for IIH was less than satisfactory than in patients
having IIH with papilloedema, and shunting was not
always beneficial. The patients of Bono et al. were trea-
ted with a low dose of acetazolamide and topiramate
which improved the headache in most subjects.
However, the response to acetazolamide and topira-
mate is not specific, as both medications have a symp-tomatic effect on headache. Interestingly, some of the
patients had been previously treated with topiramate
for headaches without improvement (personal commu-
nication with Professor Bono); it is a bit surprising that
adding a relatively low dose of acetazolamide would
dramatically increase their therapeutic response.
These patients were not re-imaged after treatment; par-
adoxically, another study by these investigators showed
that the BTSS persisted in IIH patients who were suc-
cessfully treated with medications rendering them
asymptomatic with normal CSF pressures (9). These
findings contrast with other reports demonstrating
reversal of venous sinus stenosis acutely after measures
to lower CSF pressure (4,10).
In summary, this paper raises intriguing questions
about the pathophysiology of IIH, the contribution of
both obesity and intracranial pressure to chronic head-
aches, and the possibility of a continuum of chronic
daily headache to IIH. It underscores the involvement
of the cerebral venous sinuses in the hydrodynamics of
CSF pressure. BTSS may be a marker of increased
intracranial pressure but it is not a consistent finding
in patients with IIH and papilloedema in clinical prac-
tice. Whether BTSS is the cause or the effect of intra-
cranial hypertension, its detection by magneticresonance venography in patients with chronic head-
aches may provide important information into the
nature of their headache disorder and subsequent man-
agement. Lumbar puncture, currently the gold
standard for diagnosing IIH and other disorders affect-
ing intracranial pressure, may demonstrate misleading
results at times but it is widely available and more
practical than prolonged monitoring in the clinical set-
ting. A high opening CSF pressure in and of itself is
neither specific nor diagnostic and must to be used in
context with other data from the history, examination,
neuroimaging and laboratory to arrive at the correct
diagnosis.
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