Tension-type headache: the most common, but also the most

neglected, headache disorder

Lars Bendtsen and Rigmor Jensen

Purpose of review
Tension-type headache is the most common type of
headache and, in its chronic form, one of the most
neglected and difficult types of headache to treat. Recently
published data will be reviewed.
Recent findings
The prevalence of frequent tension-type headache
increased significantly from 1989 to 2001, and several risk
factors have been identified. The incidence decreases
markedly with age. The prognosis is fairly favorable for the
episodic forms. Chronic tension-type headache, coexisting
migraine, sleep problems and not being married were
identified as risk factors for a poor outcome. Previous
reports of sensitization of the central nervous system in
patients with chronic tension-type headache were
confirmed by the findings of generalized pain
hypersensitivity both in skin and in muscles, and of a
decrease in the volume of gray matter in brain structures. A
promising new animal model of tension-type headache has
been developed. In addition, the efficacy of a prophylactic
drug, mirtazapine, with fewer side-effects than the tricyclic
antidepressants has been demonstrated.
Summary
The new data on the prevalence, incidence and prognosis of
tension-type headache are valuable for health care planning
and in daily clinical practice. The increased knowledge
with regard to abnormal central pain modulation, together
with the development of an animal model, hold promise
for much-needed improvements in the understanding
of pathophysiological mechanisms and treatment.
Keywords
epidemiology, pathophysiology, tension-type headache,
treatment
Curr Opin Neurol 19:305309. 2006 Lippincott Williams & Wilkins.
Danish Headache Center, Department of Neurology, Glostrup Hospital, University
of Copenhagen, Denmark
Correspondence to Dr Lars Bendtsen, MD, PhD, Danish Headache Center,
Department of Neurology, Glostrup Hospital, University of Copenhagen, DK-2600
Glostrup, Copenhagen, Denmark
Tel: +45 4323 2063; fax: +45 4323 3839; e-mail: bendtsen@dadlnet.dk

Introduction
Tension-type headache (TTH) is the most common form
of headache, and what many people consider as their
normal headache, in contrast with migraine. The direct
costs due to medical services and medications are higher
for TTH than for migraine, due to the higher prevalence
[1], and decreased work effectiveness and a reduction in
social activities are reported by up to 60% of persons with
TTH [2]. A recent study [3] found overall increased
absence rates for subjects with frequent TTH, but not for
migraineurs. Therefore, even though this disease is not
the most visible type of headache, it is one of the most
costly to society. At the same time, it is the least studied
type of headache. Fortunately, scientific acceptance
and interest have increased over the last few decades.
Prevalence and socio-demographic impact have been
elucidated [1,2,4], and whereas TTH previously was
considered to be primarily psychogenic, a neurobiological
basis has now been demonstrated [57]. The most exciting recent findings on the epidemiology, pathophysiology
and treatment of this widespread disorder will be
reviewed.

Revision of diagnostic criteria

TTH is characterized by a bilateral, pressing, tightening
pain of mild to moderate intensity. The headache is not
associated with the typical migraine features such as
vomiting, aggravation by physical activity, or severe
photophobia and phonophobia. The vague characteristics
and the lack of proper diagnostic criteria and a biological
marker were for decades a major obstacle to research into
TTH. Therefore, the first and most important step
toward acceptance of and interest in TTH was the
introduction of the International Headache Classification
in 1988 [8], in which TTH was delineated and defined as
a separate primary headache disorder that deserved
focused research. The first International Headache
Classification distinguished between an episodic form
(ETTH) that occurs on fewer than half of all days, and
a chronic form (CTTH) that occurs on half of all days or
more [8].

Current Opinion in Neurology 2006, 19:305309

Abbreviations
CTTH
ETTH
TTH

chronic tension-type headache

episodic tension-type headache
tension-type headache

2006 Lippincott Williams & Wilkins

1350-7540

The recent, second version of the International Headache Classification [9] further subdivides ETTH into
infrequent episodic (fewer than 12 headache days per
year) and frequent episodic (between 12 and 180 days per
year) TTH. The infrequent episodic form has very little
impact on the individual; it is a normal phenomenon, not
305

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306 Headache

a disease, and can be regarded as trivial, without the need

for medical attention. Patients with frequent ETTH,
however, may encounter considerable disability and
warrant specific intervention. Pooling these extremes
together in an overall prevalence may therefore be highly
misleading when evaluating the impact of TTH. The
revised criteria allow more precise description of headache impact, and will probably lead to more consistent
findings in epidemiological studies, where there have
been considerable variations in prevalence rates for
ETTH, in contrast with CTTH [4,10].
CTTH differs from the episodic forms with respect to
pathophysiology, lack of effect of most treatment strategies, more medication overuse, more disability, and
higher personal and socioeconomic costs. Two important
subgroups have been clearly segregated from CTTH in
the revised classification. First, stricter criteria for separating the clinically extremely important entity medication-overuse headache from CTTH have been
provided. Second, the revised classification is more
specific with regard to the evolution of headache over
time, defining a new and probably pathophysiologically
distinct entity, new daily persistent headache, which has
an acute onset and is refractory to treatment. Thus the
revised classification enables more precise diagnosis with
regard to headache frequency and impact, medication
overuse, and evolution of headache over time [11].

Epidemiology
The lifetime prevalence of TTH has been reported to be
as high as 89% [4], but the vast majority of people suffer
from TTH on 1 day a month or less, and can now be
classified as having infrequent ETTH [9]. Nevertheless,
1837% of people have TTH several times a month, 10
25% have it weekly, and 23% of the population has
CTTH, usually lasting for the greater part of a lifetime [1].
All of the above-mentioned studies were cross-sectional,
and do not provide information on the important question
of what happens to prevalence rates over time. This was
recently investigated for the first time by Lyngberg and
colleagues [4], who replicated a cross-sectional study
among the young adult population from 1989 onwards.
The 1-year prevalence of TTH increased significantly
from 79% to 87% over a 12-year period, while the increase
in the frequent episodic sub-form was even more pronounced, from 29% to 37% [4]. These findings suggest
that the socioeconomic impact of TTH has increased
markedly in the last decade.
How can we explain this increase? To answer this question, it is necessary to clarify the risk factors in a longitudinal study. This was done recently for the first time
[10]. A total of 740 persons from the general population
were interviewed and examined in 1989, and again

12 years later in a follow-up study. Risk factors for the

development of TTH were poor self-related health, an
inability to relax after work, and sleep disturbances.
These findings are interesting, because they may lead
to new ways of preventing or treating TTH. In the same
study, incidence rates for TTH were calculated for the
first time in a longitudinal study. The annual incidence of
frequent TTH was 14.2 per 1000 persons, with a female/
male ratio of 2.6:1. The incidence decreased markedly
with age (Fig. 1), which is clinically important, for
example when considering the need for paraclinical
investigations in an elderly patient presenting with newly
developed frequent headaches.
The clinician is often asked by patients with TTH,
Doctor, how long do I have to suffer from frequent
headaches?. The spontaneous prognosis was examined
recently for the first time in a longitudinal study [12].
The headache status for the participants in a cross-sectional study performed in 1989 was re-evaluated in a
follow-up study in 2001. Among subjects with frequent
ETTH or CTTH in 1989, 45% had remission (that is,
they experienced infrequent or no headaches in 2001),
39% had unchanged frequent ETTH, and 16% had poor
outcome (experienced CTTH in 2001). Poor outcome
was associated with baseline CTTH, coexisting migraine,
not being married, and sleeping problems. Thus, patients
with frequent ETTH can be reassured that the prognosis
is fairly favorable, with an almost 50% chance that they
will not suffer from frequent headaches over a prolonged
period. Intervention studies with specific focus on the
identified risk factors in headache disorders have not yet
been published.

Pathophysiology
Headaches are generally reported to occur in relation to
emotional conflict and psychosocial stress, but as in

Figure 1 Annual incidence rates for frequent tension-type headache in a Danish general population, 19892001

Frequent
tension-type
headache
incidence per
1 000

40
Men
Women
Both genders

30

20

10

0
25--34

35--44

45--54

55--64
Age groups

Reproduced from [10], with permission from the American Journal of

Epidemiology.

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Tension-type headache Bendtsen and Jensen 307

migraine the causeeffect relationship is not clear. Stress

and mental tension are the most frequently reported
precipitating factors, but they occur with similar frequency in TTH and migraine [13]. These findings are
in correspondence with the findings of widely normal
personality profiles in subjects with ETTH [13], whereas
studies of subjects with the chronic form often reveal a
higher frequency of depression and anxiety [14]. As in
other chronic pain disorders, psychological abnormalities
in TTH may be viewed as secondary rather than primary.
It was recently demonstrated, however, that depression
increases vulnerability to TTH in patients with frequent
headaches during and following a laboratory stress test,
and that the induced headache was associated with
elevated pericranial muscle tenderness [15]. The authors
suggested that depression may aggravate existing central
sensitization (see below) in patients with frequent headaches [15]. Thus there may be a bidirectional relationship
between depression and frequent TTH.
Peripheral factors have traditionally been considered of
major importance in TTH, and numerous studies have
reported increased tenderness and hardness of pericranial
myofascial tissues in these patients [16,17]. Moreover, it
was recently reported [18] that TTH patients are more
liable to develop shoulder and neck pain in response to
static exercise than healthy controls. The increased myofascial pain sensitivity in TTH could be due to the release
of inflammatory mediators, resulting in excitation and
sensitization of peripheral sensory afferents [16,17]. This
hypothesis was challenged in a recent study demonstrating
normal in-vivo interstitial concentrations of inflammatory
mediators and metabolites in a tender point of patients
with CTTH [19]. The same group [20] demonstrated
that release of glutamate from myofascial nociceptors is
not involved in experimentally induced muscle pain
and tenderness. Mork et al. [21] infused a combination
of endogenous substances into the trapezius muscle and
reported that patients with frequent ETTH developed
more pain than healthy controls. Concomitant psychophysical measures indicated that a peripheral sensitization of myofascial sensory afferents was responsible for
the muscular hypersensitivity in these patients. To summarize, pericranial myofascial pain sensitivity is increased
in patients with TTH. Peripheral sensitization of myofascial nociceptors could play a role in the increased pain
sensitivity, but firm evidence is still lacking.
Central factors play an important role in CTTH. Thus,
pain thresholds are normal in patients with ETTH, while
patients with CTTH have decreased pain thresholds
to pressure, electrical and thermal stimuli [16,17,22].
These findings were confirmed and extended in a recent
study [23] that convincingly demonstrated increased
suprathreshold pain sensitivity both in skin and in
muscle, and in both cephalic and extracephalic regions,

in patients with CTTH. The fact that the hyperalgesia is

generalized (found in all tissues examined) and of comparable degree in all examined locations, together with the
fact that the locus of pain in patients with CTTH is in the
cephalic region and not in the extremities, makes it highly
unlikely that the hyperalgesia is caused by peripheral
sensitization of nociceptors in muscle and skin. The
hyperalgesia is best explained by abnormal pain modulation in the central nervous system. This could be caused
by prolonged nociceptive input from tender pericranial
myofascial tissues resulting in segmental central sensitization at the level of the upper cervical spinal dorsal
horn/trigeminal nucleus, with secondary sensitization of
supraspinal neurons, for example in the thalamus or somatosensory cortex [24]. This hypothesis was further supported by a recent study [25] demonstrating a decrease in
the volume of gray matter brain structures involved in pain
processing in patients with CTTH. This decrease was
positively correlated with duration of headache, and the
authors interpreted the data as being the consequence of
central sensitization generated by prolonged input from
pericranial myofascial structures. Decreased anti-nociceptive activity from supraspinal structures, that is deficient descending inhibition, may also contribute to the
increased pain sensitivity in CTTH [26,27]. Impaired
descending inhibition could be the primary abnormality, or
it could contribute to or be a consequence of central
sensitization [6]. Longitudinal studies are needed to clarify
this. Thus, present knowledge strongly suggest that the
central nervous system is sensitized both at the level of the
spinal dorsal horn/trigeminal nucleus and supraspinally in
patients with CTTH, while central pain processing seems
to be normal in patients with ETTH. An animal model of
TTH has recently been developed [28]. This model
allows investigation of the important interactions between
peripheral myofascial factors and central sensitization, and
may prove to be of major importance for investigations
of pathophysiology [29] and drug development [30,31]
in TTH.

Treatment
Non-pharmacological treatment is widely used for TTH,
but the evidence for the effectiveness of the various
treatment modalities is, at best, scarce. Physical therapy
is the most common of these therapies, but two recent
independent reviews [32,33] concluded that further studies of improved quality are necessary to either support or
refute the effectiveness of physical modalities in TTH. A
recent study reported no effect of greater occipital nerve
block in CTTH [34], while a large trial found acupuncture better than no treatment, but not superior to minimal
acupuncture [35].
Simple analgesics are effective in ETTH [36,37], but
have to be used with caution to avoid medication-overuse
headache [38], and are often ineffective in CTTH. The

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308 Headache
Figure 2 Efficacy of a multidisciplinary headache clinic: treatment results for all patients discharged within 1 year

Days/month 30

25

***

20

**

15

Visit 1
Final visit

*** P < 0.001

10

** P < 0.01
*P < 0.05

5
***

***

***

0
Frequent
episode tensiontype headache
(N = 51)

Chronic
tension-type
headache
(N = 87)

Migraine
(N = 136)

Cluster
headache
(N = 21)

Posttraumatic
headache
(N = 10)

Other headaches
(N = 22)

Headache frequency in days per month at first visit (filled bars) and at discharge (open bars) is shown. Significance of differences:

P < 0.01. Reproduced from [43], with permission from Blackwell Publishing.

prophylactic efficacy of the tricyclic antidepressant amitriptyline in CTTH is well documented, while the selective serotonin re-uptake inhibitors have no effect in the
absence of depression [39,40]. It was recently demonstrated [41] that the analgesic effect of amitriptyline in
CTTH is not due solely to serotonin re-uptake inhibition, and that other mechanisms must be involved.
In agreement with this, the noradrenergic and specific
serotonergic antidepressant mirtazapine was reported to
be equally effective and better tolerated than amitriptyline [42]. Amitriptyline and mirtazapine are far from
being effective or tolerated in all patients, however,
and improved treatment modalities are much needed.
It is therefore reassuring that the first study that has
evaluated the efficacy of a multidisciplinary headache
clinic reports positive results [43]. Treatment results for
all patients discharged within 1 year were evaluated
(Fig. 2). Patients suffering from frequent ETTH,
CTTH, migraine, cluster headache, medication-overuse
headache and other headaches all had a significant
positive treatment outcome, as defined by reduced
headache frequency; only patients with post-traumatic
headache showed no effect. Patients with ETTH
demonstrated a 50% reduction in frequency, 75%
reduction in intensity, and 33% reduction in absence
rate, whereas CTTH patients responded with 32%,



P < 0.001;

30% and 40% reductions respectively [43]. Future

studies should also examine the relative efficacy of
the various treatment modalities, for example, physical,
psychological and pharmacological, and clarify how treatment programs should be optimized to best suit the
individual patient.

Conclusion
Within the review period, there have been improvements
in classification criteria and increased knowledge with
regard to socioeconomic impact, prognosis, risk factors
and abnormal central pain modulation. An animal model
has been developed, a new prophylactic drug has been
reported to be effective, and the efficacy of multidisciplinary treatment has been demonstrated. The increased
scientific activity in the area of TTH in recent years is
highly positive, and provides hope for more effective and
focused treatment of this prevalent disorder in the future.

References and recommended reading

Papers of particular interest, published within the annual period of review, have
been highlighted as:

of special interest
 of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 330).
1

Jensen R, Symon D. Epidemiology of tension-type headaches. In: Olesen J,

Goadsby PJ, Ramadan N, et al., editors. The Headaches, 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2005. pp. 621624.

Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Tension-type headache Bendtsen and Jensen 309

Schwartz BS, Stewart WF, Lipton RB. Lost workdays and decreased work
effectiveness associated with headache in the workplace. J Occup Environ
Med 1997; 39:320327.

24 Bendtsen L, Schoenen J. Synthesis of tension-type headache mechanisms.

In: Olesen J, Goadsby PJ, Ramadan N, et al., editors. The Headaches, 3rd
edn. Philadelphia: Lippincott Williams & Wilkins; 2005. pp. 677681.

3


Lyngberg AC, Rasmussen BK, Jorgensen T, Jensen R. Secular changes in

health care utilization and work absence for migraine and tension-type headache: a population based study. Eur J Epidemiol 2005; 20:10071014.
This study presents the first evaluation of secular changes in health care utilization
and work absence rates for TTH.

25 Schmidt-Wilcke T, Leinisch E, Straube A, et al. Gray matter decrease in

 patients with chronic tension type headache. Neurology 2005; 65:1483
1486.
The first study to demonstrate structural changes in the brain in patients with
CTTH.

Lyngberg AC, Rasmussen BK, Jorgensen T, Jensen R. Has the prevalence of

migraine and tension-type headache changed over a 12-year period?
A Danish population survey. Eur J Epidemiol 2005; 20:243249.
This was the first study to investigate changes in the prevalence rates of TTH over
an extended period.

26 Langemark M, Bach FW, Jensen TS, Olesen J. Decreased nociceptive flexion

reflex threshold in chronic tension-type headache. Arch Neurol 1993; 50:
10611064.

4


Jensen R. Pathophysiological mechanisms of tension-type headache: a review

of epidemiological and experimental studies. Cephalalgia 1999; 19: 602621.

Bendtsen L. Central sensitization in tension-type headache possible

pathophysiological mechanisms. Cephalalgia 2000; 20:486508.

Ashina M. Neurobiology of chronic tension-type headache. Cephalalgia

2004; 24:161172.

Headache Classification Committee of the International Headache Society.

Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988; 8 (Suppl. 7):196.

The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004; 24 (Suppl. 1):9160.

10 Lyngberg AC, Rasmussen BK, Jorgensen T, Jensen R. Incidence of primary


headache: a Danish epidemiologic follow-up study. Am J Epidemiol 2005;
161:10661073.
The first reliable estimate of incidence rates for TTH and identification of important
risk factors for the development of TTH.
11 Bendtsen L, Jensen R. Tension-type headache what are the news in the 2nd
edition of The International Classification of Headache Disorders? In: Olesen
J, editor. The classification and diagnosis of headache disorders. New York:
Oxford University Press; 2005. pp. 101108.
12 Lyngberg AC, Rasmussen BK, Jorgensen T, Jensen R. Prognosis of migraine

and tension-type headache: a population-based follow-up study. Neurology
2005; 65:580585.
This paper provides highly important information on the prognosis of TTH for the
clinician.
13 Jensen R, Becker WJ. Symptomatology of tension-type headaches. In:
Olesen J, Goadsby PJ, Ramadan N, et al., editors. The Headaches, 3rd
edn. Philadelphia: Lippincott Williams & Wilkins; 2005. pp. 685692.
14 Peatfield RC, Edmeads JG. General approach to treatment of tension-type
headaches. In: Olesen J, Goadsby PJ, Ramadan N, et al., editors. The
Headaches, 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2005 .
pp. 707710.
15 Janke EA, Holroyd KA, Romanek K. Depression increases onset of tensiontype headache following laboratory stress. Pain 2004; 111:230238.
16 Bendtsen L, Treede RD. Sensitization of myofascial pain pathways in tensiontype headaches. In: Olesen J, Goadsby PJ, Ramadan N, et al., editors.
The Headaches, 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2005.
pp. 635639.
17 Ashina S, Bendtsen L, Ashina M. Pathophysiology of tension-type headache.

Curr Pain Headache Rep 2005; 9:415422.
An up-to-date review on the pathophysiology of TTH.
18 Christensen M, Bendtsen L, Ashina M, Jensen R. Experimental induction
of muscle tenderness and headache in tension-type headache patients.
Cephalalgia 2005; 25:10611067.
19 Ashina M, Stallknecht B, Bendtsen L, et al. Tender points are not sites of
ongoing inflammation in vivo evidence in patients with chronic tension-type
headache. Cephalalgia 2003; 23:109116.
20 Ashina M, Jorgensen M, Stallknecht B, et al. No release of interstitial
glutamate in experimental human model of muscle pain. Eur J Pain 2005;
9:337343.
21 Mork H, Ashina M, Bendtsen L, et al. Possible mechanisms of pain perception
in patients with episodic tension-type headache. A new experimental model of
myofascial pain. Cephalalgia 2004; 24:466475.
22 Ashina S, Babenko L, Jensen R, et al. Increased muscular and cutaneous pain
sensitivity in cephalic region in patients with chronic tension-type headache.
Eur J Neurol 2005; 12:543549.
23 Ashina S, Bendtsen L, Ashina M, et al. Generalized hyperalgesia in patients
with chronic tension-type headache. Cephalalgia 2006; (in press).

27 Pielsticker A, Haag G, Zaudig M, Lautenbacher S. Impairment of pain


inhibition in chronic tension-type headache. Pain 2005; 118:215
223.
This paper provides additional support for abnormal central pain modulation in
CTTH.
28 Makowska A, Panfil C, Ellrich J. Long-term potentiation of orofacial sensor
imotor processing by noxious input from the semispinal neck muscle in mice.
Cephalalgia 2005; 25:109116.
Describes the development of a promising animal model of TTH.
29 Makowska A, Panfil C, Ellrich J. Nerve growth factor injection into semispinal
neck muscle evokes sustained facilitation of the jaw-opening reflex in
anesthetized mice possible implications for tension-type headache. Exp
Neurol 2005; 191:301309.
30 Makowska A, Panfil C, Ellrich J. ATP induces sustained facilitation of craniofacial nociception through P2X receptors on neck muscle nociceptors in
mice. Cephalalgia 2006; (in press).
31 Panfil C, Makowska A, Ellrich J. Brainstem and cervical spinal cord Fos
immunoreactivity evoked by nerve growth factor injection into neck muscles in
mice. Cephalalgia 2006; 26:128135.
32 Biondi DM. Physical treatments for headache: a structured review. Headache
2005; 45:738746.
33 Lenssinck ML, Damen L, Verhagen AP, et al. The effectiveness of physiotherapy and manipulation in patients with tension-type headache: a systematic
review. Pain 2004; 112:381388.
34 Leinisch-Dahlke E, Jurgens T, Bogdahn U, et al. Greater occipital nerve block
is ineffective in chronic tension type headache. Cephalalgia 2005; 25:704
708.
35 Melchart D, Streng A, Hoppe A, et al. Acupuncture in patients with

tension-type headache: randomised controlled trial. Br Med J 2005;
331:376382.
A large study on acupuncture for the treatment of TTH.
36 Diener HC, Pfaffenrath V, Pageler L, et al. The fixed combination of acetylsalicylic acid, paracetamol and caffeine is more effective than single substances and dual combination for the treatment of headache: a multicentre,
randomized, double-blind, single-dose, placebo-controlled parallel group
study. Cephalalgia 2005; 25:776787.
37 Packman E, Packman B, Thurston H, Tseng L. Lumiracoxib is effective in the
treatment of episodic tension-type headache. Headache 2005; 45:1163
1170.
38 Katsarava Z, Muessig M, Dzagnidze A, et al. Medication overuse headache:

rates and predictors for relapse in a 4-year prospective study. Cephalalgia
2005; 25:1215.
Important study regarding the problems with medication overuse in TTH.
39 Bendtsen L, Mathew NT. Prophylactic pharmacotherapy of tension-type

headache. In: Olesen J, Goadsby PJ, Ramadan N, et al., editors. The
Headaches, 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2005 .
pp. 735741.
Up-to date review on prophylactic therapy for TTH.
40 Lenaerts ME. Pharmacoprophylaxis of tension-type headache. Curr Pain

Headache Rep 2005; 9:442447.
Another up-to date review on prophylactic therapy.
41 Ashina S, Bendtsen L, Jensen R. Analgesic effect of amitriptyline in chronic
tension-type headache is not directly related to serotonin reuptake inhibition.
Pain 2004; 108:108114.
42 Bendtsen L, Jensen R. Mirtazapine is effective in the prophylactic treatment of
chronic tension-type headache. Neurology 2004; 62:17061711.
43 Zeeberg P, Olesen J, Jensen R. Efficacy of multidisciplinary treatment in a

tertiary referral headache centre. Cephalalgia 2005; 25:11591167.
This paper contains the first data regarding the efficacy of the multidisciplinary
treatment of primary headaches in a tertiary headache center.

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