Tension Type Headache in Adolescence and Childhood:
Where Are We Now?
Teshamae S. Monteith & Till Sprenger
Published online: 7 October 2010
# The Author(s) 2010. This article is published with open access at Springerlink.com
Abstract Tension type headache (TTH) is a primary
headache disorder considered common in children and
adolescents. It remains debatable whether TTH and
migraine are separate biological entities. This review
summarizes the most recent literature of TTH with regards
to children and adolescents. Further studies of TTH are
needed to develop a biologically based classification system
that may be facilitated through understanding changes in
the developing brain during childhood and adolescence.
Keywords Tension-type headache.Migraine.Children.
Adolescents.Calcitonin gene receptor peptide.
Primary headaches are common in children and adoles-
cents. Tension-type headache (TTH) and migraine are
important sources of disability with several health-related
considerations. In comparison to migraine, little is known
about TTH in children; most of our knowledge has been
extrapolated from adult studies. Childhood and adolescence
mark periods of rapid growth, emotional maturation,
physiological perturbations, and hormonal changes, all
which may influence the expression of primary headache
disorders in those with a predisposition . For example,
the prevalence of migraine increases with age in both males
and females during preadolescence . With puberty, there
is a higher prevalence of migraine in girls than boys,
suggesting a role of female sex hormones in the expression
of headache. The prevalence of TTH also increases with
age in adolescents [3•]. It is important to better understand
TTH in this age group because these changes influence
headache phenotypes and may provide important points of
considerations when distinguishing TTH from migraine.
The diagnoses of TTH and migraine are typically based
on the second edition of the International Headache
Society’s International Classification of Headache Disor-
ders (ICHD-II) . According to the criteria, TTH lasts
from 30 min to 7 days and is classified as a bilateral
pressure, tightening or nonpulsating headache of mild to
moderate intensity, occurring without aggravation by
routine physical exertion and without nausea or vomiting,
but may have either photophobia or phonophobia but not
both (Table 1) . It may be argued that the classification
for TTH lacks sensitivity and specificity because the
diagnosis of TTH is essentially made by the lack of
associated symptoms diagnostic of migraine. The addition
of photophobia and phonophobia in TTH diagnosis may
lead to a diagnosis of TTH in quite a few cases that may be
better classified as migraine.
Diagnosis of TTH in children has obvious limitations.
There are difficulties related to the challenges in taking
histories in young children. In one retrospective study
testing the ICHD-II diagnoses of migraine and TTH in
children, many children were unclassifiable because chil-
dren were not able to communicate information regarding
pain quality, pain score, and aggravation by movement or
routine activities . Behavior may be a more useful
T. S. Monteith (*)
UCSF Headache Center,
1701 Divisadero Street, Suite 480,
San Francisco, CA 94115, USA
Neurologische Klinik und Poliklinik, Klinikum rechts der Isar,
Technische Universität München,
Ismaninger Strasse 22,
81675 Munich, Germany
Curr Pain Headache Rep (2010) 14:424–430
Clues to look for include a reduction in social interaction or
play, a child that once was active that later becomes sedentary
and requires more sleep, or perhaps a child that appears less
involved in school. Altogether, studies aimed at validating the
ICHD-II diagnostic criteria for TTH on a phenotypical–
biological basis are necessary to adequately interpret current
studies and begin to answer the pressing questions that exist
. This review aims to summarize the current studies
pertaining to TTH in the pediatric and adolescence age
groups, the applicability of the ICHD-II, and clinical and
Classification, Phenotype, and Diagnostic Challenges
The classification of TTH is based on its phenotype as
defined by the ICHD-II . According to ICHD-II, TTH
generally is defined as a bilateral headache with pressing or
band-like quality of low to moderate intensity. TTH can be
distinguished further in terms of frequency, which can vary
in individuals: the infrequent episodic subtype occurs less
than once monthly, the frequent episodic subtype occurs on
less than 15 days per month, and the chronic subtype occurs
15 days or more per month for over 3 months. The
distinctions based on frequencies are rather arbitrary and
the chosen terminology, such as the context in which the
word chronic is used, can be confusing. Moreover, the high
prevalence and the variance over time for infrequent and
frequent TTH make genetic studies harder to interpret and
distinguish from chance .
Migraine can commonly present as a bilateral, short-
lasting headache, with episode-to-episode differences in
associated features resembling TTH. Another problem is
that the phenotype may not be fully developed with age
because the phenotype of migraine without aura can evolve
Migraine without aura (code 1.1)
A. At least five attacks fulfilling criteria B–D
B. Attacks lasting 1–72 h (untreated or successfully treated)
C. Two of the following characteristics:
1. Migraine headache commonly is bilateral; occipital headache in children is rare
2. Pulsating quality
3. Moderate to severe intensity
4. Aggravated by, or causing avoidance of, routine physical activity
D. At least one of the following associated symptoms:
1. Nausea and/or vomiting
2. Photophobia and phonophobia (photophobia may be inferred from behavior in young children)
Subtypes: Episodic (<15 days/mo) and chronic (≥15 days/mo on average for >3 mo)
Tension-type headache (code 2)
A. At least 10 episodes occurring on <1 day/mo on average (12 days/y) and fulfilling criteria B–D
B. Headache lasting 30 min to 7 days
C. Two of the following characteristics:
1. Bilateral location
2. Pressing/tightening (nonpulsating) quality
3. Mild to moderate intensity
4. Not aggravated by routine activity
D. At least one of the following associated symptoms:
1. No nausea or vomiting
2. Photophobia or phonophobia
A. May occur with or without pericranial muscle tenderness
a. At least 10 episodes occurring on <1 day/mo on average (<12 days/y) and fulfilling criteria B–D
a. At least 10 episodes occurring on ≥1 but <l5 day/mo for at least 3 months
A. ≥15 days/mo on average for >3 mo
Table 1 ICHD-II Criteria for
migraine without aura and
tension-type headache for
ICHD-II The International
Classification of Headache
Disorders, second edition
(Data from the Headache
Classification Subcommittee of
the International Headache
Curr Pain Headache Rep (2010) 14:424–430425
in adolescence or early adulthood from a bilateral to
unilateral headache . Ultimately, the variability in
phenomenology raises the possibility that, at least in some
patients, we may be speaking of the same disorder with
both typical and atypical attacks of migraine [6, 7].
In clinical practice, it is not always easy to distinguish
between the two entities (Fig. 1). Altogether, it has been
debated whether such distinctions need to be made because
there seem to be more similarities than differences . Due
to several considerations, a significant number of patients
cannot be diagnosed, remain unclassifiable, or carry the
diagnosis of probable migraine or probable TTH . For
migraine in children, the ICHD-II recognizes that attacks
may be of shorter duration, lasting from 1 to 72 h, with
bilateral location and pain intensities that may be inferred
from their behavior. According to one study analyzing the
ICHD-II diagnosis of migraine and TTH in children, the
criteria classify TTH and migraine well, although many
patients were left unclassifiable with a reduction in duration
not making a significant difference . The authors
suggested that the duration criteria be eliminated for TTH
and migraine because a significant increase in duration has
been shown to occur with age. Mixed phenotypes propose
yet another diagnostic issue. In one study, the prevalence of
coexisting TTH and migraine was 6% based on a
population-based study in Swedish schoolchildren .
This certainly can be supported by Lipton et al. , who
showed that TTH in patients with migraine responds to
sumatriptan whereas patients with TTH alone do not,
supporting the continuum theory at least in patients with
For chronic forms, problems also exist when children
can be diagnosed with both chronic TTH (CTTH) and
chronic migraine. It has been argued that these patients’
ailments could be diagnosed as chronic migraine based on
the new appendix criteria for a broader concept of chronic
migraine . A retrospective chart review of chronic daily
headache in French children and adolescents supports the
use of detailed histories and diaries along with the
Silberstein-Lipton criteria for chronic daily headache,
which encompasses transformed migraine, CTTH, and
new daily-persistent headache. The ICHD-II revised criteria
also were found useful and allowed for the diagnosis of
chronic migraine, new daily-persistent headache, CTTH,
CTTH and migraine without aura, CTTH and migraine with
and without aura, probable CTTH, and CTTH with
probable migraine without aura.
When the phenotype is unclassifiable, it may be helpful
to ascertain further information to determine a diagnosis.
Parents usually accompany their children and make it
plausible to obtain a detailed family history of headache.
Classically, TTH lacks the circadian rhythmicity seen in
other primary headache disorders such as migraine or
cluster headache. Ice cream headaches and motion sickness
in the childhood history of the patient may be useful
markers for migraine in unclear diagnostic circumstances.
A history of cyclical vomiting or recurrent abdominal pain
in an unclassifiable patient is suggestive of an evolution to
migraine. Recurrence may be reassuring in confirming the
benign nature of a headache disorder. On the other hand,
the number of episodes in young children is limited by a
short lifespan, and therefore, it has been suggested to
eliminate the number of episodes in young children. This
also may be reasonable keeping in mind headache
transformation in this age group.
High rates of headache transformation between TTH and
migraine create diagnostic challenges. For example, a 4-year
annual follow up study in 12- to 17-year-old patients with
headache showed that headache diagnosis changed in 20.69%
of patients on follow-up . Specifically, there was
transformation of headache type in 4 of 50 patients with
migraine (8%), 10 of 24 patients with TTH (41%), and 4 of
13 patients with other headache types (30.8%). Headache
transformation suggests the possibility of a common under-
lying biology or coinheritance of TTH and migraine.
The evidence for the existence of TTH as a separate
biological disorder needs further validation. Nitric oxide
(NO) appears to be an important molecule involved in
regulation of cerebral and extracerebral blood flow, regula-
tion or arterial diameter, and nociceptive signaling possibly
linked to release of calcitonin gene–related peptide (CGRP).
Nitroglycerin infusion has been shown to trigger immediate
and delayed headaches in patients with either migraine or
CTTH, and the authors suggested that NO-related central
sensitization may be an important common denominator in
pain mechanisms of TTH and migraine . While
nociception from myofascial tissues is considered important
in TTH, the role of a peripheral mechanism as an inciting
Fig. 1 Diagnostic ambiguity of current criteria for migraine and TTH
in pediatric and adolescent populations. Difficulties in diagnosing
TTH in children from migraine include 1) frequent headache
transformations; 2) changes in phenotype with age and sex; 3)
coexisting migraine and TTH; 4) communication barriers; 5) not
fulfilling the prior episode or duration requirement; 6) methodological
variability in epidemiological studies; and 7) lack of a biological-
based classification system for TTH and migraine
426 Curr Pain Headache Rep (2010) 14:424–430
factor is not clearly known, and certainly central factors are
important for CTTH because general hypersensitivity to
pain stimuli has been demonstrated . It has been
suggested that peripheral inputs also are important in
migraine pathophysiology, although the presences of aura,
premonitory symptoms, and functional imaging studies
support central activation as a primary mechanism [16,
17]. In a magnetic resonance imaging voxel-based mor-
phometry study comparing 20 patients with CTTH and 20
patients with medication overuse headache with 40 controls
patients, only patients with CTTH demonstrated significant
gray matter decreases in areas of the brain involved in
nociceptive transmission . Such changes seem to be
reversible, as shown in other chronic pain conditions .
Further subclassification for the episodic and chronic
subtypes of TTH can be made for children with or without
pericranial tenderness, caused from excessive contraction of
the jaw or scalp muscles . In a blinded study, restricted
neck mobility was significant in children with CTTH with
pericranial tenderness for flexion, extension, and right–left
lateral rotation . Another study showed increased
pericranial muscle tenderness at palpation in children with
migraine, but failed to find an association in the neck–
shoulder regions of children with TTH . The study found
no differences in mean pressure pain thresholds between
children in the TTH, migraine, and nonheadache groups.
Certainly, neck pain is a common finding in migraine,
associated with activation of the trigeminocervical complex.
Altogether, muscle factors may be more important in the
pathogenesis of TTH than migraine, but they are certainly
seen in both disorders, and are not of diagnostic utility .
Migraine is considered a neurobiological disorder with a
susceptibility to attacks based on external and internal
triggers. Some studies have indicated that the triggering
factors for migraine are greater than for TTH in this
population [3•, 23]. Stress and peripheral factors such as
posture are considered important in TTH. In an epidemio-
logically based population study, precipitation by sleepless-
ness, sunlight, hunger, exercise, and watching TV were
more common in the migraine group than children with
TTH. The reduced triggerability of TTH has been argued as
a way to distinguish the two entities, and it has been
suggested that lack of triggerability of TTH should become
a part of the ICHD-III criteria . Although helpful in some
cases, this would be an arbitrary distinction.
CGRP levels are not significantly elevated during TTH
in adults , unlike migraine, where CGRP levels were
predictive of pediatric migraine when compared to the
nonmigraine group . The CGRP levels were signifi-
cantly elevated when comparing levels during an attack
versus out of an attack. CGRP has been implicated in the
pathophysiology of migraine. CGRP is a neuropeptide
produced by alternative RNA splicing of the calcitonin
gene. CGRP receptors are found on meningeal blood
vessels, trigeminal ganglion and sensory afferents, in the
periaqueductal gray, and in other areas of the brain
associated with migraine pathogenesis . Stimulation of
the trigeminal ganglion can result in elevations of CGRP
and substance P [27, 28]; however, only CGRP was
significantly elevated in the external jugular veins in
patients during an acute attack of migraine. Elevated CGRP
levels are associated with severe and prolonged headaches,
and the headache can be normalized with sumatriptan
treatment [28, 29]. Therefore, one caution in interpreting
these results is that CGRP elevation is associated with
headache severity, so that it may be an artifact of our
classification system and, in line with the continuum theory,
that nonmigraine or TTH is not associated with significant-
ly elevated levels during acute attacks . There is a
relative over-representation of CGRP-enriched afferents
related to dural innervation, which may explain the
importance of CGRP in migraine and the trigeminal
autonomic cephalgias . It is arguable whether this is at
all important for TTH because headache perception in TTH
may be explained by referred pain from trigger points in the
craniocervical muscles . Further work that aims to
identify biomarkers that may distinguish migraine from
TTH is necessary to add biological validity to our
The variability in the prevalence estimates of TTH has been
attributed to environmental and genetic factors. According
to estimates based on several prevalence studies, TTH
affects about 31% (10%–72%) of children . In one
study, a family history of headache was found in 40% of
patients with TTH, and first-degree relatives had a 2.1- to
3.9-fold increased risk of CTTH compared to the general
population [33, 34]. In another study, 46% of patients with
migraine were found to have a family history of migraine as
compared to 18% of patients with migraine having a family
history of TTH . On the other hand, one study, a
population-based study of 33,764 adolescent and adult
twins, showed that the risk and frequency of TTH was
found to be higher in patients with migraine, perhaps
because they carry a single diagnosis of migraine .
Altogether, family histories are limited in that these
disorders have not been fully defined.
Age is a risk factor for TTH in children and adolescents
similar to migraine. According to a study of Swedish
schoolchildren between the ages of 7 and 15 years, both
TTH and migraine increased with age, especially in girls
. The influence of age also was seen in one study,
conducted in a pediatric specialty care center, where age
Curr Pain Headache Rep (2010) 14:424–430 427
accounted for more variance than sex in headache severity,
duration, frequency, and disability . In a 6-year
epidemiological follow-up study in children, headache
was reported in 909 of 1,155 adolescents and commonly
changed; 57.5% of headaches were diagnosed as TTH,
18.6% were diagnosed as migraine, and 2.6% were
unspecified [3•]. The most important variation was the
increase in TTH with medication overuse occurring
frequently in 8.7% of adolescents with TTH.
Several large headache global initiatives are underway to
determine the prevalence and impact of headache disorders.
The “Lifting the Burden” campaign is a World Health
Organization global initiative to assess the prevalence and
burden of headache. Based on the initiative, the prevalence
data on pediatric TTH is relatively sparse, with estimates
for Norway, Sweden, and Brazil of 23.2%, 11.8%, and
72.3%, respectively . Winkler et al. [37•] studied the
prevalence of headache in rural Tanzania through a door-to-
door survey and found an exceedingly low prevalence rate
for TTH. The average 1-year prevalence of TTH in the age
group of 0 to 10 years was 0.04% based on the ICHD-II
criteria. Between the ages of 11 and 20 years, the average
1-year prevalence was only 1.3%. Further efforts that
uncover the scale, the impact, and the factors associated
with population differences of TTH in younger generations
need to be made on the local, national, and global levels.
The discrepancies in prevalence have been attributed to
differences in methodology including prevalence estimates,
usage of the ICHD-II versus other diagnostic criteria, and
interview types. While multiple headache diagnoses can be
appreciated in a clinic setting through a clinical interview,
questionnaire studies may be sensitive to more severe
phenotypes, resulting in single diagnoses of migraine.
Other considerations that may account for population
differences are psychosocial and cultural factors of pain
reporting. The Eurolight project is an initiative with the
objective of gathering updated reliable comparable infor-
mation regarding migraine, TTH, and chronic headache in
selected European countries . Both systematic and
consistent methodological approaches are necessary to
determine the true prevalence of TTH worldwide.
Recently, epidemiological studies have focused on
determining the population dynamics of headache based
on frequencies. A transitional model of TTH shows that
low-frequency TTH may remit or transition to high-
frequency TTH, which may in turn remit or transition to
CTTH . This may be an overly simplified approach, as
there is a substantial rate of transformation between
migraine and TTH in follow-up studies. Even so, epidemi-
ological studies assessing headache frequency have the
advantage of estimating primary headache without the
limitations of ICHD-II, such as those subjects that are
unable to be diagnosed. In a population-based study of
preadolescent school children in Brazil, the prevalences of
high-frequency headache and chronic daily headache were
2.5% and 1.6%, respectively . High frequency is an
important risk factor for chronic daily headache in adults
and is important to consider in children.
Chronic daily headache is important to study in this age
group, as in one clinic based study, early onset disease was
associated with a worst outcome . CTTH was more
common in adolescents than in adults, but medication
overuse was not seen.
Headache can have a significant impact on the lives of
children and parents; however, there may be too much
attention to psychosocial variables, which are more consis-
tent with the older terminology of tension headache as
opposed to TTH. For example, TTH is associated with
fewer close friends and had a higher rate of divorced
parents . Anotherstudyassessingthecognitiveprofilesof
children with headache when compared to control patients,
showed a significant negative correlation between total
intelligence quotient, performance intelligence quotient, and
thefrequencyofattacks. This indicates that children with
frequent headache perform not as well as they potentially
could in terms of cognition because of the headaches. This is
a strong argument for treatment. Perhaps these studies should
be approached agnostically to avoid errors of attribution,
especially for a disorder that is so common.
A recent population-based cross-section study of psy-
chopathological symptoms, such as emotional symptoms,
conduct problems, hyperactivity/inattention, and peer prob-
lems, in adolescents with headache did not find a
significantly increased risk in patients with TTH; however,
if psychological factors are present, they should be
appropriately managed in parallel .
Morecontrolledstudiesare neededtoassessthe efficacyof
nonpharmacological approaches. In an uncontrolled study,
electromyographic biofeedback–assisted relaxation techni-
ques appeared effective in reducing headaches in a 3-year
juvenileTTHfollow-up study . More studies for physical
therapy are needed; a study to determine the effects of
specific strength training versus lifestyle counseling in
children with TTH currently is underway (NCT01155557)
. A study of diet and lifestyle in high school students
suggests different habits in regular intake of breakfast,
physical activity, and consumption of alcohol in adolescents
with any type of headache may be important .
Behavioral approaches have the benefit of minimizing the
need for pharmaceuticals and their potential side effects;
however, trigger management and lifestyle modifications
may be challenging due to issues of adherence.
428 Curr Pain Headache Rep (2010) 14:424–430
The European Federation of Neurological Societies
guidelines for treatment of TTH make general recommen-
dations, which can be applied to children . Simple
analgesics and NSAIDs are first-line agents considered
effective. The evidence for the efficacy of prophylaxis is
limited; amitriptyline often is used, as in migraine, although
more randomized controlled trials are needed . Drugs
blocking NO production may be effective for CTTH and
deserve further exploration . Ultimately, one important
aspect of studies in this age group is the issue of
expectation or high placebo rates, which can be accounted
for with a crossover design. On the other hand, the high
placebo rate may be used therapeutically.
To date, little is understood about the biological nature of
TTH in children and adolescents. Growth and develop-
ment with age are associated with many changes
influencing the phenotypic expression of headache.
Headache transformation in young children and adoles-
cents is common, suggesting the possibility of similar
biology at least in some patients. Prevalence estimates
are limited by differences in methodological approaches
including variability in diagnostic criteria. Studies based
on identifying risk factors for frequent headache may
better to identify at risk populations for TTH and
migraine. Altogether, face-to-face structured interviews
are optimal because longer histories of migraines over
time or ‘”chronicity” may trend to more featureless
CTTH [50, 51].
Future research is necessary to validate upcoming
classifications of migraine and TTH, especially in
children and adolescents. Ultimately, we await the point
in our scientific understanding where TTH can be
diagnosed beyond its clinical phenotype because the
current classification leaves many children unclassifiable.
It also is with great anticipation that models of head pain,
identifications of biomarkers, or advances in imaging
pave the way to a more biologically accurate diagnostic
classification system. With these goals in mind, we will
be on our way to ascertain the true impact of the
disorder, develop the best treatments, and effectively
Goadsby and Dr. Neil Raskin for their teaching and thoughts on
migraine and tension-type headache.
The authors would like to thank Dr. Peter J.
No potential conflicts of interest related to this article
Creative Commons Attribution Noncommercial License which per-
mits any noncommercial use, distribution, and reproduction in any
medium, provided the original author(s) and source are credited.
This article is distributed under the terms of the
Papers of particular interest, published recently, have been
• Of importance
1. Aegidius KL, Zwart JA, Hagen K, et al.: Increased headache
prevalence in female adolescents and adult women with early
menarche. The Head-HUNT Studies. Eur J Neurol 2010 Jul 15
(Epub ahead of print).
2. Lipton RB, Bigal ME, Diamond M, et al.: Migraine prevalence,
disease burden, and the need for preventive therapy. Neurology
3. • Ozge A, Sasmaz T, Cakmak SE, et al.: Epidemiological-based
childhood headache natural history study: After an interval of
six years. Cephalalgia 2010, 30:703–712. The authors propose
that there are significant changes in headache phenotypes in
4. Headache Classification Subcommittee of the International
Headache Society: The International Classification of Head-
ache Disorders: 2nd edition. Cephalalgia 2004, 24(Suppl 1):9–
5. Rossi LN, Cortinovis I, Menegazzo L, et al.: Classification criteria
and distinction between migraine and tension-type headache in
children. Dev Med Child Neurol 2001, 43:45–51.
6. Goadsby P: Chronic tension-type headache. Clin Evid 2002,
7. Russell MB, Levi N, Saltyte-Benth J, Fenger K: Tension-type
headache in adolescents and adults: a population based study of
33,764 twins. Eur J Epidemiol 2006, 21:153–160.
8. Cady R, Schreiber C, Farmer K, Sheftell F: Primary headaches: a
convergence hypothesis. Headache 2002, 42:204–216.
9. Rossi LN, Vajani S, Cortinovis I, et al.: Analysis of the
International Classification of Headache Disorders for diagnosis
of migraine and tension-type headache in children. Dev Med
Child Neurol 2008, 50:305–310.
10. Laurell K, Larsson B, Eeg-Olofsson O: Prevalence of headache in
Swedish schoolchildren, with a focus on tension-type headache.
Cephalalgia 2004, 24:380–388.
11. Lipton RB, Stewart WF, Cady R, et al.: 2000 Wolfe Award.
Sumatriptan for the range of headaches in migraine sufferers:
results of the Spectrum Study. Headache 2000, 40:783–791.
12. Olesen J, Bousser MG, Diener HC, et al.: New appendix criteria
open for a broader concept of chronic migraine. Cephalalgia 2006,
13. Karli N, Bican A, Zarifoğlu M: Course of adolescent headache:
4-year annual face-to-face follow-up study. J Headache Pain
14. Ashina M, Bendtsen L, Jensen R, Olesen J: Nitric oxide-induced
headache in patients with chronic tension-type headache. Brain
15. Bendtsen L, Jensen R, Olesen J: Decreased pain detection and
tolerance thresholds in chronic tension-type headache. Arch
Neurol 1996, 53:373–376.
16. Afridi SK, Matharu MS, Lee L, et al.: A PET study exploring the
laterality of brainstem activation in migraine using glyceryl
trinitrate. Brain 2005, 128:932–939.
Curr Pain Headache Rep (2010) 14:424–430429
17. Weiller C, May A, Limmroth V, et al.: Brain stem activation in
spontaneous human migraine attacks. Nat Med 1995, 1:658–660.
18. Schmidt-Wilcke T, Leinisch E, Straube A, et al.: Gray matter
decrease in patients with chronic tension type headache. Neurology
19. Rodriguez-Raecke R, Niemeier A, Ihle K, et al.: Brain gray matter
decrease in chronic pain is the consequence and not the cause of
pain. J Neurosci 2009, 29:13746–13750.
20. Fernández-Mayoralas DM, Fernández-de-Las-Peñas C, Palacios-
Ceña D, et al.: Restricted neck mobility in children with chronic
tension type headache: a blinded, controlled study. J Headache
Pain 2010 May 28 (Epub ahead of print).
21. Attila P, Metsähonkala L, Mikkelsson M, et al.: Muscle tenderness
in pericranial and neck-shoulder region in children with headache.
A controlled study. Cephalalgia 2002, 22:340–344.
22. Oksanen A, Pöyhönen T, Metsähonkala L, et al.: Neck flexor
muscle fatigue in adolescents with headache: an electromyographic
study. Eur J Pain 2007, 11:764–772.
23. deGrauw TJ, Hershey AD, Powers SW, Bentti AL: Diagnosis of
migraine in children attending a pediatric headache clinic.
Headache 1999, 39:481–485.
24. Ashina M: Calcitonin gene-related peptide in tension-type
headache. ScientificWorldJournal 2002, 2:1527–1531.
25. Fan PC, Kuo PH, Chang SH, et al.: Plasma calcitonin gene-related
peptide in diagnosing and predicting paediatric migraine. Cepha-
lalgia 2009, 29:883–890.
26. Arulmani U, Maassenvandenbrink A, Villalón CM, Saxena PR:
Calcitonin gene-related peptide and its role in migraine patho-
physiology. Eur J Pharmacol 2004, 500:315–330.
27. Goadsby PJ, Edvinsson L, Ekman R: Vasoactive peptide release in
the extracerebral circulation of humans during migraine headache.
Ann Neurol 1990, 28:183–187.
28. Goadsby PJ, Edvinsson L: The trigeminovascular system and
migraine: studies characterizing cerebrovascular and neuropeptide
changes seen in humans and cats. Ann Neurol 1993, 33:48–56.
29. Goadsby PJ: Calcitonin gene-related peptide antagonists as treat-
ments of migraine and other primary headaches. Drugs 2005,
30. O’Connor TP, van der Kooy D: Enrichment of a vasoactive
neuropeptide (calcitonin gene related peptide) in the trigeminal
sensory projection to the intracranial arteries. J Neurosci 1988,
31. Fernández-de-las-Peñas C, Schoenen J: Chronic tension-type
headache: what is new? Curr Opin Neurol 2009, 22:254–261.
32. Stovner LJ, Hagen K, Jensen R, et al.: The global burden of
headache: a documentation of headache prevalence and disability
worldwide. Cephalalgia 2007, 27:193–210.
33. Russell MB, Ostergaard S, Bendtsen L, Olesen J: Familial
occurrence of chronic tension-type headache. Cephalalgia 1999,
34. Friedman AP, von Storch TJ, Merritt HH: Migraine and tension
headaches: a clinical study of two thousand cases. Neurology
35. Lance JW, Anthony M: Some clinical aspects of migraine. A
prospective survey of 500 patients. Arch Neurol 1966, 15:356–361.
36. Slater S, Crawford MJ, Kabbouche MA, et al.: Effects of gender
and age on paediatric headache. Cephalalgia 2009, 29:969–973.
37. • Winkler A, Stelzhammer B, Kerschbaumsteiner K, et al.: The
prevalence of headache with emphasis on tension-type headache
in rural Tanzania: a community-based study. Cephalalgia 2009,
29:1317–1325. According to the authors, age is an important
factor associated with the phenotype of pediatric headache.
38. Stovner LJ, Andree C: Prevalence of headache in Europe: a
review for the Eurolight project. J Headache Pain 2010, 11:289–
39. Arruda MA, Guidetti V, Galli F, et al.: Frequent headaches in the
preadolescent pediatric population: a population-based study.
Neurology 2010, 74:903–908.
40. Bigal ME, Lipton RB, Tepper SJ, et al.: Primary chronic daily
headache and its subtypes in adolescents and adults. Neurology
41. Karwautz A, Wöber C, Lang T, et al.: Psychosocial factors in
children and adolescents with migraine and tension-type head-
ache: a controlled study and review of the literature. Cephalalgia
42. Parisi P, Verrotti A, Paolino MC, et al.: Headache and cognitive
profile in children: a cross-sectional controlled study. J Headache
Pain 2010, 11:45–51.
43. Milde-Busch A, Boneberger A, Heinrich S, et al.: Higher
prevalence of psychopathological symptoms in adolescents with
headache. A population-based cross-sectional study. Headache
44. Grazzi L, Andrasik F, D’Amico D, et al.: Electromyographic
biofeedback-assisted relaxation training in juvenile episodic
tension-type headache: clinical outcome at three-year follow-up.
Cephalalgia 2001, 21:798–803.
45. ClinicalTrials.gov: The Effect of Specific Strength-Training on
Tension-Type Headache in Children 9–17 Years. Available athttp://
clinicaltrials.gov/ct2/show/NCT01155557. Accessed September
46. Milde-Busch A, von Kries R, Thomas S, et al.: The association
between use of electronic media and prevalence of headache in
adolescents: results from a population-based cross-sectional study.
BMC Neurol 2010, 10:12.
47. Bendtsen L, Evers S, Linde M, et al.: EFNS guideline on the
treatment of tension-type headache: report of an EFNS task force.
Eur J Neurol 2010 May 11 (Epub ahead of print).
48. Lance JW, Curran DA: Treatment of chronic tension headache.
Lancet 1964, 1:1236–1239.
49. Olesen J: The role of nitric oxide (NO) in migraine, tension-type
headache and cluster headache. Pharmacol Ther 2008, 120:157–
50. Cuvellier JC, Couttenier F, Auvin S, Vallée L: The classification
of chronic daily headache in French children and adolescents: A
comparison between the second edition of the International
Classification of Headache Disorders and Silberstein-Lipton
criteria. Neuropsychiatr Dis Treat 2008, 4:263–267.
51. Silberstein SD, Lipton RB, Sliwinski M: Classification of daily
and near-daily headaches: field trial of revised IHS criteria.
Neurology 1996, 47:871–875.
430Curr Pain Headache Rep (2010) 14:424–430