revue neurologique 169 (2013) 413–418

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Migraine

Migraine and obesity, is there a link?

Obésité et migraine, un lien existe-il ?

P. Giraud a,*, S. Chauvet a,b

a
Consultation céphalées et douleur, centre hospitalier de la région Annecienne, 1, avenue de l’Hôpital, Metz Tessy, BP 90074,
74374 Pringy, France
b
Consultation douleurs chroniques-céphalées, centre médical de Meyrin, hôpital de la Tour, 24, Promenade des Artisans,
1217 Meyrin/Genève, Switzerland

info article abstract

Article history: Obesity and migraine are two frequent conditions found in the general population. In the
Received 13 September 2012 past years, large-scale studies have established epidemiological links between the two
Received in revised form conditions. Migraine prevalence appears to be increased in the obese population, and some
31 October 2012 characteristics of migraine are affected in the overweight population. More recent but
Accepted 14 November 2012 limited data point out an improvement of migraine in the obese population after weight
Published on line 18 April 2013 loss. Obesity may facilitate migraine progression to chronic daily headache or chronic
migraine. Common physiological mechanisms that would be responsible for both condi-
Keywords : tions are not fully established. Several hypotheses suggest a common etiological factor for
Migraine obesity and migraine. This work proposes to review the epidemiological data and to
Obesity highlight the main hypotheses currently discussed.
Epidemiology # 2013 Elsevier Masson SAS. All rights reserved.
Review
r é s u m é
Pathogenic hypothesis

L’obésité et la migraine constituent deux pathologies fréquentes en population générale.

Mots clés :
Depuis quelques années, des travaux ont démontré des liens entre ces deux affections sur le
Migraine
plan épidémiologique. Ainsi, la prévalence de la migraine en population obèse semble
Obésité
accrue et les caractéristiques de la migraine modifiées par le surpoids. D’autres études
Épidémiologie
plus limitées et récentes ont mis l’accent sur une amélioration des migraines en cas de prise
Prise en charge du poids
en charge d’une obésité morbide avec perte de poids. L’obésité intervient également comme
Hypothèses physiopathologiques
un facteur facilitant du passage de la migraine peu fréquente vers une forme plus fréquente,
voire chronique. Les mécanismes physiopathologiques communs qui pourraient entraı̂ner
les deux affections ne sont pas élucidés. Plusieurs hypothèses d’un facteur étiologique
commun à l’obésité et la migraine sont avancées. Ce travail propose de revoir les données
épidémiologiques et de rappeler les principales hypothèses actuellement débattues.
# 2013 Elsevier Masson SAS. Tous droits réservés.

* Corresponding author.
E-mail address: pgiraud@ch-annecy.fr (P. Giraud).
0035-3787/$ – see front matter # 2013 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.neurol.2012.11.009
414 revue neurologique 169 (2013) 413–418
1. Introduction
Migraine is one of the most prevalent painful conditions
worldwide it affects 11% of adults and almost the same
percentage in pediatric population (Stovner et al., 2007).
Clinical criteria of migraine, as defined by the International
Headache Classification (IHS, 2004), are essential to allow
research on epidemiologic aspects, comorbidities and evolu-
tion over life (Table 1).
Obesity affects over 35% of adults in United States (Flegal
et al., 2002, 2012) and its prevalence worldwide has risen
dramatically, becoming a major public health problem in most
part of the world. In industrialized countries 25% of the general
populations are considered to be obese or overweight. It
affects quality of life and general health status, because of
cardiac, rheumatologic, respiratory or endocrinology compli-
cations. World Health Organization (WHO) standards for total
obesity and abdominal obesity are widely accepted and
summarized in Table 2.
The question of a possible link between those two frequent
conditions has obviously been addressed (Bond et al., 2011a).
To date, epidemiological studies lead to opposite conclusions
about the possible impact of obesity on migraine prevalence
and the frequency or severity of attacks (Keith et al., 2008).
However, a link between both diseases is generally recognized.
A recent study reporting migraine improvement after impor-
tant weight loss reinforces the hypothesis that both diseases
would have an impact on each other (Bond et al., 2011b).
Therefore, physiological mechanisms implicated in obesity
and migraine could be a key to understand and treat both
diseases.
In this paper, we first review epidemiologic data on obesity
and migraine, we Secondly summarize how weight loss may
influence migraine, and finally try and analyze possible
mechanisms that may link Migraine and Obesity.
2. Migraine and obesity, what did we learn
from epidemiological studies?
There are two different ways to address the question of a
possible link between migraine and obesity. The first way is to
consider the prevalence and characteristics of both migraine
Table 2 – WHO Criteria for total body obesity (TBO) and abdominal obesity (AO).
BMI (TBO, BMI = T in centimeters/weight in kg2)
< 18,5
18,5–24,9
25–29,9
30–39
 40
AO based on waist circumference in centimeters (WC)
Men WC
Normal weight’
Overweight
AO
Table 1 – Criteria for migraine without aura (IHS, 2004).
A. At least 5 attacks fulfilling 2–4
B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully
treated)
C. Headache has at least two of the following four characteristics
Unilateral location
Pulsating quality
Moderate or severe intensity which inhibits or prohibits
daily activities
Aggravated by walking stairs or similar routine physical activity
D. During headache at least one of the two following symptoms occur
Nausea and/or vomiting
Photophobia and phonophobia
E. At least one of the following three characteristics is present
History and physical and neurological examinations do not
suggest one of the disorders listed in 5–11
History and/or physical and/or neurological examinations do
suggest such a disorder, but it is ruled out by appropriate
investigations
Such a disorder is present, but migraine attacks do not occur
for the first time in close temporal relation to the disorder
and obesity in the general population, in order to establish a
correlation. A second way is to examine migraine prevalence
in overweight or obese population and also to evaluate the
impact of weight loss on migraine in these selected groups.
Both approaches have been used in some large epidemiolo-
gical studies, which we try to summarize.
Large studies have explored the correlation between BMI
(Body Mass Index) and headache or migraine prevalence in the
general population but they lead to opposite results. Most of
them define Obesity according to Body Mass Index (BMI). A
review from Evans et al. (2012) explored these data which we
summarize in two groups whether obesity influence migraine
prevalence or migraine profile (Table 3). Four main studies
conclude that high BMI is responsible for increased migraine
prevalence.
In the first one, Ford et al. (2008) studied 7601 persons, aged
20 to 85, from the National Health and Nutrition Examination
Survey (NHANES) population. Obesity was associated with
37% increased risk for severe headache and migraine. The
mechanism of the increased prevalence was unexplained.
However this was a self-reported evaluation, and as criticized
by Evans et al., 2012 the method may not be suitable for
qualifying migraine.
Underweight
Normal
Obesity Grade I
Obesity Grade II
Obesity Grade III
Women WC
< 94 < 80
94–102 80–88
 102  88
 revue neurologique 169 (2013) 413–418
Table 3 – General population-based studies on obesity and migraine: main conclusions.
Reference
Obesity increase migraine prevalence
Ford et al. (2008)
Peterlin et al. (2010a)
Vo et al. (2011)
Yu et al. (2012)
Obesity modify migraine profile but not its prevalence
Bigal and Lipton (2006b)
Bigal et al. (2007)
Keith et al. (2008)
Winter et al. (2009)
Peterlin et al. (2010a, b) confirm this increased migraine
prevalence but also explore the role of sex, age and localization
of adiposity. Twenty-one thousand seven hundred and eighty-
three participants were questioned and classified according to
age sex and fat localization at inclusion. Abdominal obesity
(AO) was distinguished from total body obesity (TBO)
according to WHO standards (Table 2) and using Standard
anthropometric measures. They conclude that age, sex and
distribution of adiposity influence the migraine prevalence.
Under 55 years old, migraine prevalence was increased by
obesity, and AO was a main key factor at this age. Surprisingly,
after 55 years old, migraine prevalence was not influenced by
obesity in men nor in women. In this same group, after 55
years old, migraine prevalence was actually lower in case of
AO, but not influenced by TBO. Authors recommend stratify-
ing obese population depending on age and localization of
adiposity. They also suggest to separate pre menopausal and
post-menopausal women.
Vo et al. (2012) confirmed these previous works, reporting
that migraine in pregravid women is more frequent in obese
women than in normal weight women (OR: 1.48). Moreover,
they demonstrated that the risk of migraine increases with
the level of obesity. In fact, severely obese (BMI: 35–39.9 kg/
m2) or morbidly obese (BMI  40 kg/m2) had a higher risk of
suffering from migraine than normal weight women. Authors
open the discussion on the age at migraine diagnosis: they
indicate increased odds of adult weight gain among migrai-
neurs diagnosed with the condition prior to age of 18 years.
Women who have been diagnosed as migraineurs in
childhood had a higher risk of weight gain (over 10 kg) later
in life compared to others (OR: 1.67). This significant result
would suggest paying special attention to the prevention of
obesity among children diagnosed with migraine. However,
we need larger epidemiological multicentric studies to
confirm these findings.
Another study conducted by Yu et al. (2012) confirms the
association between migraine and obesity in across-sectional
secondary analysis from a general population Chinese cohort,
Among 5029 cases, they found that having a BMI over 30 kg/m2
increases significantly the odds of migraine (8.6% vs. 11.8%,
P = 0.0001). In contrast, no association was observed between
obesity and migraine severity, frequency nor disability. They
conclude that morbid obesity was associated with twofold
increase odds of migraine in the cohort of men and women
mainly at reproductive age.
As a conclusion after these four previous studies, obesity
tends to increases the prevalence of migraine, particularly in
415
n Comments
7601
21683
3763
5029
30125 Increase in pain and headache frequency
162276 Increase in headache frequency
220370 Increase prevalence of CDH
63467 Increase prevalence of CDH
women, at reproductive age. Findings are similar within
studies concerning European or Chinese populations, adults or
children groups. An early diagnosis of migraine during
childhood seems to increase the risk of obesity in adulthood
but this last conclusion should be verified.
In contrast, five more studies, summarized by Bond et al.
(2011a), failed to demonstrate that obesity would increase
significantly the migraine prevalence. In these works, obesity
did not change the prevalence of migraine, but only influenced
the frequency and the intensity of migraine attacks.
Keith et al. (2008) reviewed 11 epidemiologic datasets in
order to evaluate the association between BMI and headache
in women. In total 220,370 US women, aged 18 years old or
older had self-declared migraine or headache, the condition
not being confirmed by a physician. High BMI was positively
associated with headache in general but not with migraine.
Authors suggest that the absence of a definite link with
migraine could be due to several bias: the type of analysis
(mixing cross sectional and longitudinal studies), the hetero-
geneity of the population tested, and the fact that migraine
would be underestimated because poorly known.
Bigal et al., 2006a, 2007; Bigal and Lipton (2008) have
conducted several, large, population-based studies. Their
work, usually considered as a reference on this subject, does
not conclude that Obesity is a proper risk factor for migraine
but only that obesity is associated with higher frequency of
attacks (more than 10–15 days a month) and increased
severity. In Bigal and Lipton (2006b) report, among the
30,125 participants, 3091 suffered from episodic migraine,
and there was no significant difference between the odds in
non-obese population (31.1%) and in overweight group (27.7%).
Winter et al. (2009) studied 63467 women from a Women’s
Health Study to identify the relationship between obesity and
migraine prevalence after the age of 45 years old. If migraine
prevalence was associated with BMI over 35, this association
was not confirmed after correction for post-menopausal
status and cardiovascular factors. In contrast, the presence
of overweight was correlated with an increase in headache
frequency and severity.
To conclude from these epidemiologic studies, it is
established that Obesity modifies frequency and intensity of
migraine attacks. But an increased prevalence of migraine
within obese population remains controversial. The discor-
dant results might be due to variations in the methodologies,
the populations, migraine definitions or obesity criterias.
Further studies are necessary, especially in overweight or mild
obesity population.
416 revue neurologique 169 (2013) 413–418
3. Migraine and obesity: what is the impact of
weight loss on migraine?
Because obesity is implicated in migraine disability, recent
trials have addressed the question of a possible influence of
weight loss on migraine, particularly in Chronic Migraine (CM)
(Katsarava et al., 2004). CM belongs to the group of Chronic
Daily Headache (CDH) defined by the presence of primary
headaches, lasting at least 4 hours per day, on at least 15 days
per month, for three months or over. The estimated
prevalence of CM is about 3 to 5%. CM is associated with
altered quality of life.
Bond et al. (2011b) conducted a prospective trial in a
population of severely obese patients. Twenty-nine migrai-
neurs were evaluated before and after bariatric surgery.
Patients were middle aged, mainly women (88%), with morbid
obesity (BMI  46.6) at baseline. The mean number of heada-
che days at post-surgery evaluation was reduced almost by
fifty percent (11.1 + –10.3 days versus 6.7 + –8.2, P < 0.05)
independently of the type of the surgery or the percentage
of weight loss. There was a reduction in intensity and severity
of pain, as assessed with the Migraine Disability Assessment
Scale (MIDAS) six months after surgery. Other factors than
weight loss may be responsible for these positive results, such
as a great expectation in the surgical procedure especially
among severe migraineurs and the global psychological
impact of the procedure. The absence of control group might
also be a possible bias. Therefore, further works would be
needed.
Verrotti et al., 2012 reported almost the same data in obese
adolescent migraineurs. In this group, they demonstrate that
the association of specific diet, physical training program and
behavioral therapies improve not only the weight but also the
migraine evolution after 12 months. Frequency, intensity and
duration of attacks, as well as MIDAS scores (adapted for
pediatric population: pedMIDAS) significantly improved with
the multidisciplinary medical program.
These recent studies acknowledge that weight loss changes
migraine and evolution to CDH in severely obese population.
However, the available studies were conducted with severely
obese persons and not with low-grade obese or overweight. In
these groups of patients, the impact of weight loss on migraine
needs to be evaluated. To date, recommendations for weight
loss in migraine patients should only be founded on the
generally admitted benefit of having a normal BMI on general
health status.
4. Is obesity a real factor for migraine
transformation?
The link between CDH and obesity was firstly identified and
explored by Scher et al. (2002). In their case control
longitudinal study, they analyze the evolution at 1 year of
episodic headache sufferers. At one year, 3% of the 1932 cases
had progressed to CDH. The transformation into CDH was
significantly correlated with weight: the risk to suffer from
CDH at one year was 5 times higher in obese group than in
control population. Even in overweight patient, the risk to
become a CDH sufferer was increased 3 times. Some more
studies also confirm this result. Bigal and Lipton (2006b) and
Bigal et al. (2007) conclude a direct link between obesity and
CDH. While others end up indirectly to this conclusion,
demonstrating that obesity is associated with increased
attack frequency (Keith et al., 2008; Winter et al., 2009). As
suggested by Evans et al. (2012) obesity influences migraine
frequency itself a well-known factor for the transformation of
episodic migraine into CM. Indeed, several factors are
responsible for migraine progression and CM. Classically,
these factors are divided into modifiable factors or not (Scher
et al., 2002). Non-modifiable factors include old age, low
education or low socio economic status, past history of head
injury. In contrast, excessive consumption of analgesics or
caffeine overuse, depression, anxiety, snoring, sleep apnea,
high frequency of migraine, as well as obesity, can be
modified by medical intervention and thus are considered
as modifiable factors.
In conclusion, obesity is now considered as a modifiable
factor for CM and needs to be identified and systematically
treated, especially as, given the tendency for obesity pre-
valence itself to increase decade after decade, the prevalence
of CM might actually increase in future epidemiological
studies. This hypothesis needs to be verified in the future.
5. What are the possible mechanisms to
explain the possible influence of obesity on
migraine profile?
Several hypotheses have been proposed to explain the link
between migraine and obesity (Bigal et al., 2007). Some are
based on clinical grounds, whereas others examine patho-
physiological aspects implicated in both diseases, such as the
role of neurotransmitters including serotonin and pro-
inflammatory mediators, the role of hypothalamus in
Migraine and Obesity, especially via the orexinergic system,
or the possible role of raised intracranial pressure found in a
proportion of obese patients as well as in some migraineurs.
We will review some of these hypotheses.
With regards to clinical evidences, one current hypothesis
suggests the frequent association of Migraine and Obesity is
fortuitous. This frequent association may only be due to the
high prevalence of both conditions. Furthermore, these
patients may tend to visit their physician more frequently,
leading to overestimate the association in clinical practice.
This hypothesis makes sense in theory, but epidemiological
data described above contradict this view.
Another possibility is the direct influence of obesity and
migraine on each other, due to the treatments as well as to the
behavioral changes or quality of life impairments. Indeed,
most first line prophylactic treatment of migraine can be
responsible for weight gain. As a consequence an increased
number of obese individuals is expected in severe headache
population. Frequent migraine is often responsible for
significant reduction of physical activities and increasing rest
time, which facilitate obesity. Obesity itself is often associated
with low physical activity, excessive food intake, anxiety and
depression, all well known trigger factors for migraine attacks
(Robbins, 1994). As illustrated by these examples, a direct
 revue neurologique 169 (2013) 413–418
influence between both conditions is possible, however it
remains insufficient to explain epidemiological data.
Another concept as developed by Bigal and Lipton (2008)
suggest that common factors could facilitate both conditions,
migraine and obesity. In this conception, the common keys
would be possibly biological The implication of numerous
biological substances implicated in both obesity and migraine
have been reviewed by Bigal and Lipton (2008), Peterlin et al.
(2010b), and Bond et al. (2010a). These authors insist on the
role of adipose tissue which functions as an endocrine organ
and produces the release of pro-inflammatory cytokines,
such as Tumor Necrosis Factor alpha or interleukine 6. Most
of these substances are actually found elevated during a
migraine attack (Sarchielli et al., 2006). The inflammatory
state that exists with obesity is implicated in pain transmis-
sion, can influence the trigeminal pathways and contribute
actively to increase migraine frequency. For example leptin
and adiponectin secreted by adipose tissue and implicated in
the pro-inflammatory state may be of importance. Their role
in migraine transformation is suggested by Bigal and Lipton
(2008) but need to be confirmed. Another substance possibly
implicated in both condition is the Calcitonin gene-related
peptide (CGRP). CGRP plays a pivotal role in the pathophy-
siology of migraine, its implication has been accurately
documented (Goadsby, 2006). High levels of CGRP had also
been observed in obese patients by Zelissen et al. (1991),
suggesting its active responsibility in migraine. CGRP can be
therefore considered as a pivotal factor in migraine in the
context of obesity (Recober and Goadsby, 2010). Nevertheless,
the authors suggest continuing the research to confirm its
implication. The role of other neurotransmitters implicated
in food intake and satiety had also been suspected to play a
rule because in obesity modification of numerous neuropep-
tides are well known at the hypothalamus level. As an
illustration, serotonin or orexins A or B could influence the
food intake as well as the feeling of satiety. Kajiyama et al.
(2005), had demonstrated the implication of orexins A in the
modulation of nociceptive message. Holland and Goadsby
(2007) propose to considerate the importance of the orexi-
nergic system in pain and in primary headaches. As illustrate
in their paper, the orexinergic system is particularly impor-
tant because it modulate several system implicated in
feeding, sleeping, cardiologic function or even pain modula-
tion. This paper gave a new possibility of the link between
obesity and migraine. Because of the complexity of the
neuroendocrin interactions in the central nervous system at
the hypothalamus level, further studies are necessary to
understand fully the relationship between obesity and
migraine in this area.
Recently, another hypothesis to explain the link between
migraine and obesity have been suggested by the implication
of idiopathic intracranial hypertension. Obesity is a well-
known risk factor for Idiopathic Intracranial Hypertension
(IIH) (Biousse et al., 2012). The criteria of this diagnosis are well
described in the IHS classification and the presence of
papilledema is an easy signs that allows in clinical practice
to detect its presence. Nevertheless, some observations have
suggested that papilledema can miss during the IIH, and thus
does not allow to suspect the disease. The absence of
papilledema in IIH is not fully understood but authors have
417
suggested that a bilateral transverse sinus stenosis can be
implicated. In a prospective study Bono et al. (2006) compared
724 migraineurs to control subjects and found 6.7% of these
migraineurs had bilateral transverse sinus stenosis, 67.8% of
which had IIH without papilledema (IIH-WOP). Authors
suggest that obesity and IIH with bilateral transverse sinus
stenosis can contribute to transform episodic headache to
chronic headache and in particular chronic migraine. In the
same way, IIH-WOP is considered by De Simone et al. (2010) as
a possible factor for transformation of headache. As conclu-
sion, the concept of IIH-WOP as well as its limits remains
under debate but the possibility of its rule in migraine
transformation is possible even if the further studies are
necessary.
As illustrated in this section, numerous explanations and
hypotheses are suggested to explain the association of
headache, migraine and obesity. A fortuitous, unidirectional
link does not seem valuable but the implication of biological
substances and their regulation in migraine and obesity could
be relevant. However, further experimental studies are needed
to identify the level and the type of biological dysregulation.
Better understand of the common pathophysiological mecha-
nisms between migraine and obesity might help the mana-
gement of both conditions.
6. Conclusion: in the end, what is relevant in
clinical practice?
Obesity is a well-known factor for the alteration of health
status. Its influence in chronic headache, in particular in CDH
and CM, is now well established and it is recognized as a
modifiable factor. The above data indicate clinicians should
pay special attention to obesity when observed in headache
population and migraineurs. Obese migraineurs should be
followed and managed more closely. In addition, when
clinicians introduce prophylactic treatment for migraine, they
must warn their patient about potential weight gain and its
possible consequence on migraine progression. When weight
gain is observed, treatment must be reevaluated and a diet
program suggested. Whatever the age of occurrence of obesity
and migraine, these advices apply but they are of a particular
importance in pediatric population with migraine, as demons-
trated in Vo et al. (2011).
Disclosure of interest
The authors declare that they have no conflicts of interest
concerning this article.
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