Chronic Tension-type Headache
Jessica Ailani, MD
Corresponding author
Jessica Ailani, MD
Department of Neurology, Georgetown University
Hospital, 3800 Reservoir Road NW,
7-PHC, Washington, DC 20007, USA.
Current Pain & Headache Reports 2009, 13:479–483
Current Medicine Group LLC ISSN 1531-3433
Copyright © 2009 by Current Medicine Group LLC
Tension-type headache is the most common head-
ache type worldwide. Chronic tension-type headache
(CTTH) affects 2% to 3% of patients, yet it repre-
sents the least talked about subtype of chronic daily
headache. There is much debate in the headache com-
munity on whether CTTH exists as its own entity or
is a milder form of chronic migraine (CM), because
there are similarities and differences between the
two headache forms. This article reviews CTTH, as
well as the current pathophysiology and treatment,
and discusses controversial issues in the diagnosis of
CTTH and CM.
Introduction
Tension-type headache (TTH) is the most common head-
ache type worldwide, considered by most people to be a
“normal” headache [1]. Patients usually do not seek medical
attention for tension headaches. The headache is featureless;
the pain is described by patients as bilateral, pressure, or
tightening in type, and mild to moderate in severity. TTH
is occasionally associated with mild nausea, and resolves
with simple analgesics such as acetaminophen.
Chronic tension-type headache (CTTH) is defined as
having the pain qualities of TTH, but occurring on 15 or
more days of the month, for at least 6 months (Table 1) [2].
CTTH occurs in 2% to 3% of the population worldwide
[3–5]. Unlike migraine, CTTH is almost as common in
men as in women, with a 4:5 male-to-female ratio [6]. The
prevalence of CTTH decreases with increasing age [6].
CTTH is often associated with somatic complaints, such
as nausea, generalized myalgias and arthralgias, difficulty
falling asleep and staying asleep, chronic fatigue, decreased
libido, irritability, and disturbed memory and concentra-
tion [7]. The disability is considered to be greater than in
migraine, due to the large number of patients affected [8•].
Rasmussen et al. [6] reported that 5% of the employed
population from ages 25 to 64 were absent 4 days per year
due to headache, 2% were absent for 20 days per year due
to headache, and 59% of people with TTH felt that it inter-
fered with activity. Even with high prevalence and disability,
CTTH is the least studied subtype of headache [9••].
Psychiatric comorbidities are common in patients
with CTTH, not unlike patients who suffer from other
chronic pain syndromes. There is a 25% chance of devel-
oping secondary depression in patients with CTTH [7],
and higher rates of anxiety [9••]. Patients with CTTH
also have higher rates of catastrophizing and avoidance
[9••]. Depression and anxiety may contribute to the
already existing disorder in patients with CTTH, causing
a decreased threshold for pain and a higher frequency of
headache [10]. The severity of headache also increases sig-
nificantly with higher frequency [6].
Pathophysiology
The underlying mechanism of TTH is poorly understood,
although it is generally believed that patients who have epi-
sodic tension-type headache (ETTH) (less than 8 episodes
of tension headache a month) may have a different underly-
ing pathophysiology than patients with CTTH. The origin
of the term tension headache comes from older theories on
pathophysiology of the disease. It was believed that TTH
was caused by muscle contraction and ischemia of head and
neck muscles [9••]. This contraction was caused by excess
stress and tension, leading to a headache. This theory has
been refuted by normal electromyographic (EMG) stud-
ies in patients with TTH, and by studies that have shown
normal muscle lactate levels in patients with CTTH who
perform static muscle exercises [11,12]. Current theory sug-
gests that myofascial trigger points and central sensitization
play a big role in TTH. Chronic activation of peripheral
myofascial triggers may cause central sensitization of
second-order neurons at the level of the spinal dorsal
horn and trigeminal nucleus, sensitization of supraspinal
neurons, and decreased antinociceptive activity from supra-
spinal structures, leading to TTH [13]. Patients with
CTTH are hypersensitive to stimuli applied at cephalic and
extracephalic nonsymptomatic locations, indicating that
synaptic transmission of nociceptive input within the cen-
tral nervous system is increased [13].
Treatment Strategies
Treatment strategies need to address both chronic pain
faced by patients with frequent to daily headache, as well
as treatment of acute exacerbations of pain.
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I Tension-type Headache
Table 1. Comparison of ETTH with CTTH
ETTH
Pain features Bilateral
Pressure/tightening pain
Mild to moderate severity
Associated features Occasional nausea
Frequency 8 or less episodes a month
Acute treatment Acetaminophen
NSAIDs
Aspirin
CTTH—chronic tension-type headache; ETTH—episodic tension-type headache.
For all patients with CTTH, keeping a diary of head-
aches and treatment is important. This helps identify
triggers in the patient’s life that may aggravate headaches,
such as increased stress, poor sleep, missed meals, excess
caffeine, or psychosocial problems. Diaries also help track
medication use, helping to identify overuse of medication
that can cause or aggravate headaches.
Many nonpharmacological treatments are an impor-
tant part of the overall treatment plan for patients who
suffer from daily or near daily headaches. Biofeedback
with EMG is an effective form of behavioral therapy that
allows patients to learn to develop control over pericra-
nial muscle tension [14]. Cognitive behavioral therapy has
been shown to be an effective adjuvant treatment when
added to a tricyclic antidepressant in patients who suf-
fer from low severity CTTH [15••]. Physical therapy and
exercise programs, both effective in reducing headache
frequency and severity in patients with ETTH, have insuf-
ficient evidence to support or refute their effectiveness in
patients with CTTH [16•]. Massage therapy and hot and
cold packs are often helpful in the day-to-day manage-
ment of CTTH.
Acute treatment
Most patients with CTTH suffer from mild to moderate
headache daily, allowing them to function with some level
of pain, but there are patients who have episodes of more
severe pain, causing missed work days and activities.
Many analgesic medications are moderately effective in
ETTH, but are incompletely effective in CTTH.
NSAIDs currently have the best evidence in treating
acute episodes of TTH, such as ibuprofen (800 mg) and
naproxen sodium [17••]. Some evidence supports the use
of acetaminophen (1000 mg) [18] and aspirin (500 to 1000
CTTH
Same as ETTH
Nausea
Myalgias
Sleep disturbances
Concentration problems
Fatigue
Decreased libido
Depression
≥ 15 days a month for ≥ 6 months
None proven effective thus far
mg) during acute attacks [19]. Based on gastrointestinal
safety profi le, 1000 mg of acetaminophen should be tried
fi rst, followed by ibuprofen and then naproxen sodium
[20]. Combined analgesics, such as caffeine- or butalbital-
containing compounds, may be helpful in patients with
CTTH who experience exacerbations of pain. Patients
can overuse these medications due to their ineffectiveness
at remitting headache, placing them at risk for medication
overuse headache, which may cause or compound TTH.
A discussion between the physician and patient about
limits on analgesic medication use is important to try to
mitigate this problem (Table 2).
Triptans (5-HT1 receptor antagonists), one of the
most successful medications in treating acute attacks
of migraine headache, are not as successful in treat-
ing patients with pure TTH. Cady et al. [21] examined
a group of 76 patients with a history of migraine who
had treated one headache attack that fit the description
of TTH with sumatriptan, and found that headache
resolved in 73 of the patients. Likely, triptans are effec-
tive in patients with a primary diagnosis of migraine
who suffer from occasional TTH, but are ineffective in
patients with primary TTH. The reason for this may be
due to a slight difference in the basic pathophysiology
between the two headache subtypes. The same difference
may explain why migraine has more associated features
and occasional aura, whereas in TTH there is an absence
of these two.
Preventive treatment
For patients suffering from CTTH, preventive therapy
helps reduce the frequency and severity of headaches.
Unlike in migraine, very few agents have proven efficacy
in CTTH. Amitriptyline, a tricyclic antidepressant, was
 Chronic Tension-type Headache
I Ailani
I 481

Table 2. Medication overuse headache: signs and symptoms

Patients using almost any medication to treat acute headache more than 2 to 3 days a week, or between 8 to 15 days a
month are at risk for MOH
Medications at high risk for causing MOH:
Opioids
Butalbital-containing compounds
Caffeine-containing compounds
Triptans
Ergots
Medications at low, if any, risk for causing MOH:
Dihydroergotamine
Acetaminophen
Aspirin
Antiemetics
COX-2 inhibitors
NSAIDs: debate over whether or not NSAIDs cause MOH vs the chronic use of NSAIDs may provide some protection
against headache in patients with CDH
The features of headache associated with MOH may not differ from the patient’s usual headache:
May be migrainous or tension-type, depending on the type of headache usually experienced by patient
Unable to distinguish an “MOH headache” or “rebound headache” from a typical TTH or migraine
Diagnosis is often “probable MOH,” and discontinuation of frequently used medication is necessary to see if reduction in
headache frequency follows
Patient may not respond to preventive medication until MOH is stopped
Patients need to be educated about MOH by their physicians:
Keep headache diary documenting use of medication
Instruct patients with CDH to reserve medication use for more severe headaches
Train patient in relaxation techniques and biofeedback for mild to moderate headaches
CDH—chronic daily headache; COX—cyclooxygenase; MOH—medication overuse headache; TTH—tension-type headache.

the fi rst medication shown to be effective in TTH and
remains fi rst-line therapy in treating CTTH, even though
recent studies have shown mixed results [17••]. Other
tricyclic antidepressants, such as clomipramine and nor-
triptyline, can also be used, with doxepin, maprotiline,
or mianserin as second-line therapy. Mirtazapine, an
antidepressant with both noradrenergic and serotonergic
effects, has been found to be effective at 30 mg per day,
even in patients who did not respond to amitriptyline
[22]. It is useful in those patients who failed fi rst-line
treatment. Venlafaxine, a serotonin–norepinephrine
reuptake inhibitor (SNRI) antidepressant, was shown to
have moderate effect in patients with ETTH and con-
comitant depression, but not in CTTH [23]. Duloxetine,
another SNRI antidepressant, significantly improved
headaches during an open-label trial in patients with
chronic migraine (CM) or CTTH who had major depres-
sion [24]. Another open-label study on topiramate, an
antiepilepsy drug effective in treating migraine, CM,
and chronic daily headache (CDH), found reduction in
headache frequency and severity in CTTH patients on
100 mg daily [25].
Valproic acid, although effective in treating migraine
headache, has had mixed results in the treatment of
CTTH, and cannot be recommended [26,27]. Selective
serotonin reuptake inhibitors and tizanidine are also not
effective treatments of TTH [28]. Botulinum toxin type
A (BTX-A) has mixed results in the treatment of CTTH,
with a recent pilot study showing a reduction in headache
frequency when BTX-A was injected into myofascial
trigger points, but results dissipated after 12 weeks [29].
Memantine, an N-methyl-d-aspartate receptor antago-
nist, had limited benefit in lowering headache intensity in
women with CTTH [30] (Table 3).
Conclusions
The TTH component of CDH is one of the largest
debated areas in headache medicine. On one side is the
idea that the smaller level headaches experienced daily by
patients with CDH are a milder form of migraine, and all
migrainous features of headache tend to become reduced
or disappear in patients with high frequency migraines.
Patients with CTTH are those patients who do not expe-
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I Tension-type Headache
Table 3. Effective preventive medications for the treatment of CTTH
Drug Study type
Amitriptyline Randomized, double-blind,
placebo-controlled; multiple trials
have been conducted
Mirtazapine Randomized, double-blind,
placebo-controlled
Topiramate Open-label
Duloxetine Open-label
Memantine Randomized, double-blind,
placebo-controlled
CM—chronic migraine; CTTH—chronic tension-type headache; ETTH—episodic tension-type headache.
rience severe exacerbations in their headache, who never
had associated symptoms with their headache, and who
live day to day with mild to moderate level pain that is
relatively stable. On the other side is the thought that
CTTH is an entity on its own, with different pathophysi-
ology and a different response to treatment, and patients
who have CTTH are equally, if not more, disabled by
their headaches.
Likely, TTH and migraine headache lay in a spectrum
of disease, with patients experiencing both types of head-
ache forms during their lifetime. The pathophysiology of
both headache subtypes remains somewhat of a mystery,
although they do share some aspects. For example, cen-
tral sensitization plays a role in reducing pain threshold in
patients with CTTH and CM. Similar to chronic migraine,
CTTH studies have found that by inhibiting nitric oxide,
headache pain is reduced possibly due to a decrease in
central sensitization [31]. Studies on neuropeptides, such
as calcitonin gene–related peptide (CGRP), have found
mixed results in CTTH. Most studies have shown no
elevation in serum CGRP in patients with CTTH [32,33],
but a post hoc subanalysis of eight patients with pulsa-
tile CTTH did fi nd elevations in serum CGRP [33]. It is
unclear if this fi nding implies that there is a smaller group
of patients with CTTH that have a similar pathophysi-
ology to migraine. Larger prospective studies of patients
with pulsatile CTTH are needed to determine the validity
of these fi ndings.
Disclosure
No potential confl ict of interest relevant to this article
was reported.
Notes
First-line treatment for both ETTH and CTTH
Mixed results
May also use nortriptyline or clomipramine for first-line
treatment (both with better side-effect profiles)
Second-line treatment
Works in patients who do not respond to amitriptyline
Effective treatment, but not a blinded study
Effective treatment in patients with CM/CTTH
and depression
Not a blinded study
Limited effect in lowering headache intensity
in women with CTTH
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