Tension-type headache in adults: Pathophysiology, clinical features, and diagnosis

Author:
Frederick R Taylor, MD
Section Editor:
Jerry W Swanson, MD, MHPE
Deputy Editor:
John F Dashe, MD, PhD

Contributor Disclosures

INTRODUCTION — Tension-type headache (TTH) is the most prevalent headache in the

general population [1], and the second-most prevalent disorder in the world [2]. The typical
presentation of a TTH attack is that of a mild to moderate intensity, bilateral, nonthrobbing
headache without other associated features.

Understanding the pathophysiology and clinical aspects of TTH is important for accurate
diagnosis and optimum treatment. However, TTH is a relatively featureless headache,
making it the least distinct of all the primary headache phenotypes. In addition, it is the
least studied of all the primary headache disorders, despite having a very high
socioeconomic impact [1].

This topic will review the classification, pathophysiology, epidemiology, clinical features,
and diagnosis of TTH in adults. Treatment is discussed separately. (See "Tension-type
headache in adults: Acute treatment" and "Tension-type headache in adults: Preventive
treatment".)

Tension-type headache in children is also reviewed separately. (See "Tension-type

headache in children".)

CLASSIFICATION — There are three main subtypes of TTH:

●Infrequent episodic TTH, with headache episodes less than one day a month

●Frequent episodic TTH, with headache episodes 1 to 14 days a month

●Chronic TTH, with headaches 15 or more days a month

This division is relevant for several reasons. The underlying pathophysiology, impact on
quality of life, and therapy differ among the subtypes, with peripheral pain mechanisms
having more importance in episodic TTH, and central mechanisms having greater
importance in chronic TTH [3]. Acute symptomatic treatments are used for infrequent or
low frequency episodic TTH, while prophylactic treatments are used for high frequency
episodic TTH and chronic TTH. The category of infrequent episodic TTH identifies
individuals who typically do not require medical management, and separates them from
those with frequent or chronic TTH; this avoids categorizing most people as having a
significant headache disorder [1]. Therefore, a precise diagnosis should be established.
(See 'Diagnosis' below.)

Patients who meet all but one of the criteria for the episodic subtypes of TTH and do not
fulfill criteria for migraine without aura are considered to have probable episodic TTH.
Patients who meet the criteria for chronic TTH and also meet criteria for medication
overuse headache are considered to have probable chronic TTH. (See "Medication
overuse headache: Etiology, clinical features, and diagnosis", section on 'Diagnosis'.)

Each of the subtypes of TTH is additionally classified as occurring with or without

pericranial muscle tenderness [1]. However, there are no data showing that patients with
or without pericranial muscle tenderness differ in terms of TTH pathophysiology or
response to treatment.

The term tension-type headache replaces previous terms such as stress or tension
headache, muscle-contraction headache, psychomyogenic headache, and psychogenic
headache [1]. Tension headache was originally named for its suspected etiology (ie,
excessive stress or tension leading to muscle contraction). Sustained contracture of
pericranial muscles was long believed to be causative in TTH, although the concept is no
longer considered valid. (See 'Pathophysiology' below.)

PATHOPHYSIOLOGY — The pathogenesis of TTH is probably multifactorial, but the

precise mechanisms are uncertain [4]. Environment influences development of episodic
TTH more than chronic TTH, while genetic factors appear to play an important role in
development of chronic TTH [5-7]. Given the wide variation in frequency and intensity in
TTH, not only between individuals, but within individuals over time, it is likely that the
underlying pain mechanisms in TTH are dynamic and vary from one individual to another,
and potentially from one attack to another in the same individual.

The current pathophysiologic model of TTH posits that peripheral activation or

sensitization of myofascial nociceptors are most likely of major importance in episodic
TTH, while sensitization of pain pathways in the central nervous system due to prolonged
nociceptive stimuli from pericranial myofascial tissues seems to be responsible for the
conversion of episodic to chronic TTH [4,8-12]. Thus, stimuli that are normally innocuous
are misinterpreted as pain in chronic TTH. Continuous nociceptive input from peripheral
myofascial structures may induce central sensitization. The increased nociceptive
stimulation of supraspinal structures results in increased facilitation and decreased
inhibition of pain transmission at the level of the spinal dorsal horn/trigeminal nucleus, and
in increased pericranial muscle activity. Measurements of pain tolerance thresholds and
suprathreshold stimulation have shown presence of generalized hyperalgesia in patients
with chronic TTH, while diffuse noxious inhibitory control (DNIC) function is reduced in
chronic TTH. One voxel-based morphometric brain MRI imaging study showed loss of gray
matter structures involved in pain processing in patients with chronic TTH, which
correlated with increasing years of headache [11].

Pharmacologic studies have shown that tricyclic drugs such as amitriptyline and nitric
oxide synthase inhibitors can reverse central sensitization and the chronicity of headache.
Finally, low frequency electrical stimulation has been shown to rapidly reverse central
sensitization and may be a new modality in treatment of chronic TTH and other chronic
pain disorders. (See "Tension-type headache in adults: Preventive treatment".)

Heightened sensitivity — Heightened sensitivity of pain pathways in the central nervous

system, and perhaps in the peripheral nervous system, is thought to play a critical role in
the pathogenesis of TTH [3,13,14].

Central factors — General pain sensitivity in the central nervous system is increased in
chronic TTH, whereas central pain processing seems to be normal in episodic TTH [14-
16]. However, in TTH, as in migraine without aura, there may be a lack of habituation
when recording sympathetic skin responses compared with normal controls [17]. This
electrophysiologic similarity to migraine without aura supports the hypothesis that some
patients with TTH might be at the mild end of the migraine spectrum. Since lack of
habituation was not always observed in TTH, it seems to be relevant only for a subgroup
of patients. Decreased pain, thermal, and electrical thresholds reported in patients with
chronic TTH probably represent a central misinterpretation of incoming signals [18-20].
Increased excitability of the central nervous system generated by repetitive and sustained
pericranial myofascial input may be responsible for the transformation of episodic TTH into
the chronic form.

Altered brainstem nociceptive reflex findings, including significantly lower subjective pain
and reflex thresholds, have suggested that limbic-controlled descending pain systems may
be abnormal due to deficient descending inhibition in patients with chronic TTH [21-23].

Nitric oxide may play a key role in the pathophysiology of TTH, and novel treatments for
TTH that apply the antinociceptive effect of nitric oxide synthase inhibitors are under study
[9]. Compared with control subjects without headache, subjects with TTH (unlike those
with migraine) have no significant difference in levels of serum N-acetyl-aspartate (a
marker of neuronal dysfunction) or serum brain derived neurotropic factor (which interacts
with calcitonin gene related peptide) [24,25].

Peripheral factors — Firm evidence for peripheral abnormalities in TTH is still lacking, but
muscular factors may be important, especially in episodic TTH [12,14]. Compared with
matched control subjects without headache, subjects with episodic TTH demonstrate
increased numbers of active and latent trigger points, forward head posture, and lesser
neck mobility [26-28]. Increased muscle tenderness is the most pronounced and
consistent finding in TTH patients and probably represents the activation of peripheral
nociceptors [29]. The intensity and frequency of TTH positively correlates with pericranial
muscle tenderness [4]. Although the origin of muscle tenderness is unknown, nociceptors
around blood vessels in striated muscle, tendon insertions, and fascia have been
suggested as sources of the pain [3,14].

In a small case-control study, levels of the inflammatory mediator interluekin-1 beta were
significantly elevated in chronic TTH [30]. Although this finding requires confirmation in
additional studies, it lends support to the hypothesis that the pathology of chronic TTH
involves sterile neurovascular inflammation.

As previously noted, sustained contracture of pericranial muscles was long believed to be

causative in TTH, but this concept is no longer considered valid.

Genetic factors — In contrast to migraine, hereditary factors seem to play a minor role in
the pathogenesis of episodic TTH. However, genetic factors may be more important in the
development of chronic TTH than episodic TTH. These conclusions are supported by the
following observations:

●A Danish twin study found no significant difference in concordance rates for episodic
TTH between monozygotic and dizygotic twin pairs [5], suggesting little if any role for
genetic factors

●Another study found that first-degree relatives of probands with chronic TTH had
more than a threefold increased risk of chronic TTH compared with the general
population, suggesting that a genetic factor played a role [6]

●Evidence from a genetic study employing complex segregation analysis suggests

that chronic TTH has a multifactorial inheritance, whereas episodic TTH may be
caused by multiple genes in combination with environmental factors, or may have no
genetic component at all [7]

EPIDEMIOLOGY — Headache is one of the most common reasons for neurologic

consultation, and TTH is the most prevalent type of primary headache in the general
population [31]. In the population-based Danish twin registry, the one-year-period
prevalence of TTH among 12- to 41-year-old subjects was 86 percent [32]. Furthermore,
the prevalence of TTH may be increasing [33].

Although the overall prevalence of TTH is high, most patients with TTH have the infrequent
episodic subtype, with headaches less than one day a month. Using the International
Classification of Headache Disorders-2 (ICHD-2) criteria to classify TTH subtypes, the
Danish twin registry found that the one-year-period prevalences of infrequent episodic
TTH, frequent episodic TTH, and chronic TTH were 63.5, 21.6, and 0.9 percent,
respectively [32]. An earlier population study from the United States found that the one-
year prevalences of episodic and chronic TTH were 38.3 and 2.2 percent [34].
Women have a slightly higher prevalence of TTH than men, especially with regard to the
frequent episodic and chronic subtypes of TTH. In a Danish population study, the lifetime
prevalence of episodic TTH in men and women was 69 and 88 percent [35]. In another
Danish population-based study that evaluated 40-year-old subjects, men were more likely
than woman to have no TTH and infrequent episodic TTH, while women were more likely
than men to have frequent episodic TTH and chronic TTH [36]. These differences were all
statistically significant.

Data regarding age dependence of TTH are limited. In a population-based study from the
United States, the prevalence of episodic TTH peaked in the fourth decade [34]. A Danish
study found a decreasing prevalence of TTH with increasing age [35]. Other studies have
shown that TTH continues to be a problem in older patients, occurring in 20 to 30 percent
of those over 60 years of age [34,37,38].

Finally, limited data suggest that whites have a higher prevalence of TTH than blacks of
either sex in the United States [34].

Societal impact — Because of the high prevalence of TTH, the global burden of disability
caused by TTH is greater than that caused by migraine [31,39]. This indicates that the
overall cost of TTH may also be greater than that of migraine. In one population study,
episodic TTH sufferers reported a mean of nine lost work days and five reduced-
effectiveness days, while chronic TTH sufferers reported a mean of 27 lost work days and
20 reduced-effectiveness days [34]. The burden is particularly high for the minority who
has substantial and complicating co-morbidities [39]. The impact is greatest on those with
TTH who continue to suffer into their geriatric years [34,37,38].

While TTH is the most common form of headache, only a small percentage of TTH
sufferers seek medical care because of this diagnosis, probably because most individuals
with TTH have infrequent, mild headaches. In fact, some experts regard the infrequent
episodic subtype of TTH not as a disease, but as a normal phenomenon that does not
require medical attention [40].

CLINICAL FEATURES — The typical presentation of a TTH attack is that of a mild to

moderate intensity, bilateral, nonthrobbing headache without other associated features.
Descriptions of TTH pain are characteristically nondescript: "dull," "pressure," "head
fullness", "head feels large," or, more descriptively, "like a tight cap", "band-like," or a
"heavy weight on my head or shoulders."

The pain in TTH may infrequently be unilateral or pulsating. In the Danish TTH population,
a pulsating quality of pain with TTH was seldom or never present in 80 to 86 percent of the
respondents [35,41]. In another Danish study of TTH, the head pain was unilateral in 10
percent [42].
Increased pericranial muscle tenderness is the most important abnormal finding in patients
with TTH [1]. Blood work, brain imaging with CT or MRI scans, and spinal fluid analyses
are usually normal in patients with TTH.

Pericranial muscle tenderness — The tenderness of pericranial myofascial tissues and

number of myofascial trigger points are considerably increased in patients with TTH [12].
Muscle tenderness in the head, neck, or shoulders (ie, pericranial tenderness) is
associated with both the intensity and the frequency of TTH attacks and is typically
exacerbated during the headache experience. The presence or absence of pericranial
muscle tenderness should be elicited from the history and confirmed on examination by
manual palpation [43,44].

Manual palpation is performed by applying firm pressure with the second and third finger
and making small rotating movements on the pericranial muscles, including the frontal,
temporal, masseter, pterygoid, sternocleidomastoid, splenius, and trapezius muscles [1].

An in-vivo study in tender trapezius muscle in patients with chronic TTH during rest and
static exercise provided evidence of normal interstitial levels of inflammatory mediators
and metabolites [45]. This finding suggests that tender muscles are not sites of ongoing
inflammation. One case-control study found that reduced neck-shoulder strength and
aerobic power, in addition to increased pericranial muscle tenderness, was associated with
TTH in girls [46].

Precipitating factors — Stress and mental tension are reported to be the most common
precipitants for TTH [47]. However, they are found at the same frequency in migraine
[48,49]. In a small study comparing primary headache types, head and neck movements
were important trigger factors in patients with episodic TTH, while foods, hunger, and odor
were significantly more common in patients with migraine [50].

Can change in pain sensitivity of muscle be a risk factor? In a population-based study of

subjects with TTH who were followed for 12 years, those who developed frequent episodic
TTH had normal muscle tenderness at baseline but increased tenderness at follow-up
[51,52]. In these subjects, the pain thresholds were normal both at baseline and at follow-
up. This finding suggests that increased pain sensitivity is a consequence of frequent TTH
rather than a precipitating risk factor, and lends support to central sensitization as an
important mechanism for the chronification of TTH.

Relationship with migraine — Migraine may precipitate or aggravate TTH in patients

who have both types of headache. In a population study that compared clinical
characteristics of TTH, the one-year prevalence and male to female ratios of TTH were
similar in patients with and without migraine. However, the frequency and duration of TTH
attacks were greater in the migraineurs compared with nonmigraineurs [49,53].
(See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults".)
DIAGNOSIS — The diagnosis of TTH is based upon clinical impression. There are no
diagnostic tests specific for TTH.

The diagnosis of TTH is made when the patient's description of the attacks is consistent
with the typical features of TTH, the diagnostic criteria below are fulfilled, and the general
and neurologic examinations are normal, with the possible exceptions that increased
tenderness of pericranial myofascial tissues and the presence of trigger points are
compatible with the diagnosis of TTH. However, it may be difficult to distinguish episodic
TTH from mild forms of migraine (see 'Diagnostic challenges' below). Due to extensive
symptom overlap, critical attention to the temporal pattern of headaches is necessary to
distinguish TTH from secondary headaches (see 'Secondary headaches' below).

As already noted, infrequent episodic TTH is very unlikely to be a presenting chief

complaint in clinical practice. Because of the association of TTH-like symptoms with
secondary headaches, such as those due to medication overuse or structural brain
lesions, we suggest that practitioners strongly consider the possibility of a secondary
headache disorder when patients present for clinical care with presumed TTH.
(See 'Secondary headaches' below.)

Diagnostic criteria — The International Classification of Headache Disorders, 3rd edition

(ICHD-3) specifies diagnostic criteria for episodic (table 1) and chronic (table 2) tension-
type headache [1].

The ICHD-3 criteria for episodic TTH (table 1) require at least 10 episodes of headache,
each lasting 30 minutes to seven days, which fulfill the following conditions [1]:

●At least two of the following:

•Bilateral location

•Pressing or tightening (non-pulsating) quality

•Mild or moderate intensity

•Not aggravated by routine physical activity such as walking or climbing stairs

●Both of the following:

•No nausea or vomiting

•No more than one of photophobia or phonophobia

These diagnostic criteria can be viewed as based more upon what TTH is not: localized,
throbbing, severe, or aggravated by activity.

The infrequent episodic TTH subform is diagnosed if the headache episodes occur on <1
day per month on average (<12 days per year). The frequent episodic TTH subform is
diagnosed if the headache episodes occur on 1 to 14 days per month on average (≥12 and
<180 days per year).

The ICHD-3 criteria for chronic TTH (table 2) require headache lasting hours to days, or
unremitting, occurring on ≥15 days per month on average for more than three months
(≥180 days per year) and fulfilling, that fulfill the following [1]:

●At least two of the following:

•Bilateral location

•Pressing or tightening (non-pulsating) quality

•Mild or moderate intensity

•Not aggravated by routine physical activity such as walking or climbing stairs

●Both of the following:

•No more than one of photophobia, phonophobia or mild nausea

•Neither moderate or severe nausea nor vomiting

Each of the subforms of TTH is additionally classified as occurring with or without

pericranial muscle tenderness [1]. (See 'Pericranial muscle tenderness' above.)

The ICHD-3 criteria were designed to distinguish between TTH, migraine, and cluster
headache. There are no auras with TTH, whether visual, language, sensory, motor, or
coordination. Similarly, other features typically associated with migraine headache, such
as nausea, vomiting, or sensitivity to light and noise, are not features of episodic TTH.
However, the presence of photophobia or phonophobia (but not both) does not exclude the
diagnosis [1]. There is an exception for chronic TTH that allows mild nausea as long as
there is no photophobia or phonophobia [1]. The proportion of TTH associated with cranial
autonomic features is currently unknown, but these are uncommon accompaniments in the
author's experience.

When a patient has headaches that meet all but one of the TTH criteria, the attacks fulfill
ICHD-3 criteria for probable TTH [1]. However, the practitioner must also consider whether
criteria are met for migraine or probable migraine. If so, all other available information
should be used to decide whether the attacks are more likely to be probable migraine or
probable TTH.

The distinction between episodic and chronic headache types is complicated by

inaccuracies in patient-reported headache frequency when depending upon retrospective
patient recall. As an example, a large survey study found that subjects tended to report
monthly headache frequency rounded to the nearest five days. Women were more likely to
round than men; rounding decreased with increasing age and increased with symptoms of
depression [54]. Thus, daily calendars may improve the accuracy of determining headache
frequency.

Diagnostic testing — The approach to neuroimaging in adult patients with headache is

briefly reviewed here and discussed in greater detail elsewhere. (See "Evaluation of
headache in adults", section on 'Danger signs' and "Evaluation of headache in adults",
section on 'Indications for imaging'.)

Neuroimaging is not necessary in most patients with primary headaches, including those
with TTH, who have a stable headache pattern for over six months and a normal
neurologic examination. However, brain imaging should be considered in patients with
nonacute headache who have any of the following conditions:

●An unexplained abnormal finding on neurologic examination

●Atypical headache features or headaches that do not fulfill the strict definition of a
primary headache disorder

Patients with sudden severe "thunderclap" headache also need neuroimaging to exclude
serious conditions such as subarachnoid hemorrhage, cervical artery dissection, cerebral
venous thrombosis, and others. (See "Clinical manifestations and diagnosis of aneurysmal
subarachnoid hemorrhage" and "Approach to the patient with thunderclap
headache" and "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".)

Brain MRI with and without contrast is the test of choice for most patients when
neuroimaging is warranted. However, head CT is more expeditious for evaluating those
suspected of having acute intracranial hemorrhage.

No other diagnostic tests are typically necessary in patients with "garden-variety" TTH.

DIAGNOSTIC CHALLENGES — Diagnostic challenges occur in the evaluation of

suspected TTH when there are atypical or missing features, when features overlap with
other types of headaches, and when patients fail to report all symptoms.

Episodic tension-type headache — In the clinic, patients with a stable pattern of

episodic, disabling headache and a normal physical examination should be considered to
have migraine in the absence of contradictory evidence [55]. This hypothesis was
validated by the Landmark study, which evaluated 1203 patients visiting a primary
practitioner with a complaint of episodic headache [56]. The subjects then recorded their
next six headaches in diaries, and each headache was strictly classified according to the
original 1988 International Classification of Headache Disorders (ICHD) criteria [57].
Overall, ICHD-defined migraine was present in 94 percent of the subjects (including 76
percent with migraine and 18 percent with probable migraine), while TTH, by definition
episodic, was present in 3 percent.
Diagnostic challenges occur when patients underreport symptoms by poorly describing
them (typically underreporting migraine symptomatology) or when TTH-like headaches are
more severe than typical TTH and associated with photophobia or phonophobia. In the
Spectrum study, 32 percent of patients with an initial diagnosis of episodic TTH were
diagnosed with migraine or probable migraine when headache diaries were reviewed [58].
Those TTH sufferers reclassified as migraineurs responded to triptans in the study, while
episodic TTH sufferers not meeting criteria for migraine responded at placebo rates
[58,59]. The results provide further support for the notion that patients with disabling
episodic headache are more likely to suffer migraine than TTH.

Distinguishing episodic TTH from migraine without aura may be difficult. As an example,
the diagnosis of probable TTH can be made according to the International Classification of
Headache Disorders, 3rd edition (ICHD-3) classification in a patient with a unilateral,
severe, nonthrobbing headache that is not aggravated by normal physical activity and has
no associated symptoms [1]. This same individual also meets ICHD-3 criteria for probable
migraine. In such cases, the ICHD-3 recommends that all other available information
should be used to decide which of the alternative diagnoses are more likely [1]. This
information may include patient age, gender, longitudinal headache history (especially
regarding how the headache started), family history, the effect of drugs, whether
headaches are related to menses, and a range of other features. Fulfillment of all
diagnostic criteria for any headache disorder (eg, TTH or any of its subtypes) always
trumps fulfillment of criteria for any "probable" diagnostic category (eg, probable migraine)
[1].

As noted above, throbbing or pulsating pain may infrequently occur with TTH, presumably
when the pain is most intense [41]. Thus, another possible presentation of headache that
meets criteria for both TTH and migraine is that of a unilateral throbbing headache of mild
to moderate intensity without aggravation by normal physical activity and without
associated features. Nevertheless, one should be wary of classifying such a headache as
TTH rather than probable migraine, since underreporting of migraine symptoms is a
common problem. Descriptive reports of a series of headaches that record all details of
each episode are warranted before being definitive about a primary TTH diagnosis in
clinical practice.

Other headaches that may cause diagnostic confusion with episodic TTH include
cervicogenic headache and sinus headache. (See 'Secondary headaches' below.)

Chronic tension-type headache — The challenges for a diagnosis of chronic TTH

diagnosis are rather limited and fairly straightforward compared with episodic TTH.
Typically, chronic TTH must be differentiated from other primary chronic daily headaches
of long duration and, infrequently, from secondary headache disorders. (See 'Secondary
headaches' below.)
The chronic daily headache disorders as a group are not addressed by the International
Classification of Headache Disorders, 3rd edition (ICHD-3); rather, the classification of
chronic daily headache as a form of headache is based upon criteria proposed by
Silberstein and Lipton (SL criteria) [60,61]. In this paradigm, chronic TTH is classified
under chronic daily headache, long duration subtype (at least four hours a day) (table 3).
(See "Overview of chronic daily headache".)

New daily persistent headache (see "New daily persistent headache") and hemicrania
continua (see "Hemicrania continua") are distinct headache syndromes, and if the patient
with chronic daily headache does not have a sudden onset of persistent headache or
strictly unilateral pain, then the main diagnostic classification involves transformed or
chronic migraine. One of three situations pertains:

●The diagnosis is transformed or chronic migraine if there are eight or more days a
month of migraine headache or migraine-specific acute medication use
(eg, ergotamine or triptans)

●The diagnosis is pure chronic TTH if all headache days fulfill criteria for chronic TTH

●The diagnosis is chronic TTH associated with episodic migraine if there are fewer
than eight days a month of migraine headache or migraine-specific acute medication
use

Secondary headaches — Secondary headaches may present diagnostic challenges for

both episodic and chronic TTH.

Brain tumor headache — Brain tumor headache frequently mimics TTH, and less often
may resemble migraine or a variety of other headache types. Though only a minority of
patients with headaches have a brain tumor, it is crucial to recognize those headache
characteristics that may be more commonly associated with tumors. The features of brain
tumor headache are generally nonspecific and vary widely with tumor location, size, and
rate of growth. The headache is usually bilateral, but can be on the side of the tumor.
(See "Brain tumor headache", section on 'Clinical features'.)

Because pure TTH is uncommon in the office, practitioners must be especially vigilant
about the possibility of brain tumor when patients present with a new, subacute, or
progressive headache suggestive of TTH. (See "Brain tumor headache", section on
'Diagnosis'.)

Medication overuse headache — Medication overuse headache (MOH) is a commonly

encountered type of secondary headache that should be suspected in patients who have
frequent or daily headaches despite, or because of, the regular use of headache
medications. The development of MOH is typically preceded by an episodic headache
disorder, usually migraine or TTH, that has been treated with frequent and excessive
amounts of acute symptomatic medications. (See "Medication overuse headache:
Etiology, clinical features, and diagnosis".)

The goal of therapy for MOH headaches is cessation of the offending medications through
drug withdrawal and detoxification. (See "Medication overuse headache: Treatment and
prognosis".)

MOH represents a significant problem in patients with primary TTH, as such patients suffer
stronger withdrawal symptoms on clean-out and have significantly higher relapse rates
than patients with MOH who have other primary headache types at both one and four-year
prospective follow-up [62,63]. This is probably due, at least in part, to the withdrawal
patterns peculiar to different agents used for different types of headache, since overuse of
mixed analgesics was associated with a significantly higher relapse rate than overuse of
triptans (typically used for migraine) at one year after drug withdrawal [62,63].

Sinus headache — Sinus headache is commonly diagnosed by clinicians and self-

diagnosed by patients, but acute or chronic sinusitis appears to be an uncommon cause of
recurrent headaches, and many patients presenting with sinus headache turn out to have
migraine or, less often, TTH. (See "Evaluation of headache in adults".)

The occurrence of nasal symptoms associated with headache in the region of the sinuses,
without fever or purulent nasal discharge, should neither trigger a diagnosis of sinus
headache nor exclude the diagnosis of other primary headaches, including TTH [64,65].

Cervicogenic headache — Cervicogenic headache should be considered if headache is

strictly unilateral [66]. Cervicogenic headache is a controversial entity caused by referred
pain from the upper cervical joints. This type of headache is characterized by unilateral
nonthrobbing, nonlancinating head pain of moderate to severe intensity and variable
duration that is increased by movement of the head and radiates from occipital to frontal
regions. The proposed clinical features of cervicogenic headache may mimic those
commonly associated with primary headache disorders, including TTH. Muscle tenderness
in the posterior head and upper neck is a primary diagnostic criterion of cervicogenic
headache, and is common in TTH as well.

While there is no consensus, a practical approach for establishing the diagnosis of

cervicogenic headache relies on the use of controlled anesthetic blocks of cervical
structures or their nerve supply. These anesthetic blocks are believed (by many but not all
experts) to pinpoint sources of pain in the neck when they provide complete, momentary
relief of pain.

Cervicogenic headache is discussed in detail separately. (See "Cervicogenic headache".)

Other secondary headaches — Rarer entities such as spontaneous low volume

cerebrospinal fluid syndromes, chronic meningitis, and others may occasionally be
associated with headaches that resemble TTH. (See "Spontaneous intracranial
hypotension: Pathophysiology, clinical features, and diagnosis" and "Approach to the
patient with chronic meningitis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines

from selected countries and regions around the world are provided separately.
(See "Society guideline links: Migraine and other primary headache disorders".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education

materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are
written in plain language, at the 5th to 6th grade reading level, and they answer the four or
five key questions a patient might have about a given condition. These articles are best for
patients who want a general overview and who prefer short, easy-to-read materials.
Beyond the Basics patient education pieces are longer, more sophisticated, and more
detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Basics topics (see "Patient education: Headaches in adults (The Basics)")

●Beyond the Basics topics (See "Patient education: Headache causes and diagnosis
in adults (Beyond the Basics)".)

SUMMARY AND RECOMMENDATIONS

●The typical presentation of a tension-type headache (TTH) attack is that of a mild to

moderate intensity, bilateral, nonthrobbing headache without other associated
features. Pure TTH is a rather featureless headache. (See 'Clinical features' above.)

●Heightened sensitivity of pain pathways in the central nervous system, and perhaps
in the peripheral nervous system, is thought to play a critical role in the pathogenesis
of TTH. Nitric oxide may be a molecular trigger for pain. Genetic factors seem to play
a minor role in episodic TTH but may be more important in chronic TTH.
(See 'Pathophysiology' above.)

●There are three main subtypes of TTH (table 1). Each of the subtypes is additionally
classified as occurring with or without pericranial muscle tenderness.
(See 'Classification' above.):

•Infrequent episodic TTH, with headaches <1 day a month

•Frequent episodic TTH, with headaches 1 to 14 days a month

•Chronic TTH, with headaches ≥15 days a month

 ●TTH is the most prevalent type of primary headache in the general population, but
most patients with TTH have the infrequent episodic subtype, with headaches less
than one day a month. (See 'Epidemiology' above.)

●Pericranial muscle tenderness is associated with both the intensity and the
frequency of TTH attacks. (See 'Clinical features' above.)

●The diagnosis of TTH is made when the patient's description of the attacks is
consistent with the typical features of TTH, the diagnostic criteria are fulfilled (table 1),
and the general and neurologic examinations are normal, with the exception of the
presence or absence of pericranial muscle tenderness. Attention to the temporal
pattern of headaches is necessary to distinguish TTH from secondary headaches.
(See 'Diagnosis' above.)

●Neuroimaging is not necessary in most patients with primary headaches, including

those with TTH, who have a stable headache pattern for over six months and a
normal neurologic examination. (See 'Diagnostic testing' above and "Evaluation of
headache in adults", section on 'Danger signs' and "Evaluation of headache in
adults", section on 'Indications for imaging'.)

●Because of the association of TTH-like symptoms with secondary headaches,

including those due to medication overuse or structural brain lesions, practitioners
should consider the possibility of a secondary headache disorder when patients
present with presumed TTH. (See 'Diagnosis' above and 'Secondary
headaches' above.)

●Diagnostic challenges occur in the evaluation of suspected TTH when there are
atypical or absent features, when features overlap with other types of headaches, and
when patients fail to report all symptoms. (See 'Diagnostic challenges' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Headache Classification Committee of the International Headache Society (IHS). The

International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia
2013; 33:629.
2. Martelletti P, Birbeck GL, Katsarava Z, et al. The Global Burden of Disease survey 2010,
Lifting The Burden and thinking outside-the-box on headache disorders. J Headache Pain
2013; 14:13.
3. Bendtsen L. Central sensitization in tension-type headache--possible pathophysiological
mechanisms. Cephalalgia 2000; 20:486.
4. Jensen R. Peripheral and central mechanisms in tension-type headache: an update.
Cephalalgia 2003; 23 Suppl 1:49.
5. Ulrich V, Gervil M, Olesen J. The relative influence of environment and genes in episodic
tension-type headache. Neurology 2004; 62:2065.
6. Russell MB, Ostergaard S, Bendtsen L, Olesen J. Familial occurrence of chronic tension-
type headache. Cephalalgia 1999; 19:207.
7. Russell MB, Iselius L, Ostergaard S, Olesen J. Inheritance of chronic tension-type
headache investigated by complex segregation analysis. Hum Genet 1998; 102:138.
8. Bendtsen L. Central and peripheral sensitization in tension-type headache. Curr Pain
Headache Rep 2003; 7:460.
9. Bezov D, Ashina S, Jensen R, Bendtsen L. Pain perception studies in tension-type
headache. Headache 2011; 51:262.
10. Bendtsen L, Fumal A, Schoenen J. Tension-type headache: mechanisms. Handb Clin
Neurol 2010; 97:359.
11. Schmidt-Wilcke T, Leinisch E, Straube A, et al. Gray matter decrease in patients with
chronic tension type headache. Neurology 2005; 65:1483.
12. Bendtsen L, Fernández-de-la-Peñas C. The role of muscles in tension-type headache.
Curr Pain Headache Rep 2011; 15:451.
13. Zagami AS. Pathophysiology of migraine and tension-type headache. Curr Opin Neurol
1994; 7:272.
14. Ashina M. Neurobiology of chronic tension-type headache. Cephalalgia 2004; 24:161.
15. Cathcart S, Winefield AH, Lushington K, Rolan P. Noxious inhibition of temporal
summation is impaired in chronic tension-type headache. Headache 2010; 50:403.
16. Ashina S, Bendtsen L, Ashina M, et al. Generalized hyperalgesia in patients with chronic
tension-type headache. Cephalalgia 2006; 26:940.
17. Ozkul Y, Ay H. Habituation of sympathetic skin response in migraine and tension type
headache. Auton Neurosci 2007; 134:81.
18. Langemark M, Jensen K, Jensen TS, Olesen J. Pressure pain thresholds and thermal
nociceptive thresholds in chronic tension-type headache. Pain 1989; 38:203.
19. Schoenen J, Bottin D, Hardy F, Gerard P. Cephalic and extracephalic pressure pain
thresholds in chronic tension-type headache. Pain 1991; 47:145.
20. Bendtsen L, Jensen R, Olesen J. Decreased pain detection and tolerance thresholds in
chronic tension-type headache. Arch Neurol 1996; 53:373.
21. Schoenen J. Depression in tension-type headache sufferers: bystander or villain? Pain
2004; 111:225.
22. Sandrini G, Rossi P, Milanov I, et al. Abnormal modulatory influence of diffuse noxious
inhibitory controls in migraine and chronic tension-type headache patients. Cephalalgia
2006; 26:782.
23. Pielsticker A, Haag G, Zaudig M, Lautenbacher S. Impairment of pain inhibition in chronic
tension-type headache. Pain 2005; 118:215.
24. de Tommaso M, Ceci E, Pica C, et al. Serum levels of N-acetyl-aspartate in migraine and
tension-type headache. J Headache Pain 2012; 13:389.
25. Fischer M, Wille G, Klien S, et al. Brain-derived neurotrophic factor in primary headaches.
J Headache Pain 2012; 13:469.
26. Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA. Myofascial trigger points, neck
mobility, and forward head posture in episodic tension-type headache. Headache 2007;
47:662.
27. Fernández-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, et al. Myofascial trigger
points and their relationship to headache clinical parameters in chronic tension-type
headache. Headache 2006; 46:1264.
28. Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, et al. Trigger points in the
suboccipital muscles and forward head posture in tension-type headache. Headache
2006; 46:454.
29. Ashina S, Bendtsen L, Ashina M. Pathophysiology of tension-type headache. Curr Pain
Headache Rep 2005; 9:415.
30. Della Vedova C, Cathcart S, Dohnalek A, et al. Peripheral interleukin-1ß levels are
elevated in chronic tension-type headache patients. Pain Res Manag 2013; 18:301.
31. GBD 2015 Neurological Disorders Collaborator Group. Global, regional, and national
burden of neurological disorders during 1990-2015: a systematic analysis for the Global
Burden of Disease Study 2015. Lancet Neurol 2017; 16:877.
32. 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.
33. Lyngberg AC, Rasmussen BK, Jørgensen 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; 20:243.
34. Schwartz BS, Stewart WF, Simon D, Lipton RB. Epidemiology of tension-type headache.
JAMA 1998; 279:381.
35. Rasmussen BK, Jensen R, Schroll M, Olesen J. Epidemiology of headache in a general
population--a prevalence study. J Clin Epidemiol 1991; 44:1147.
36. Russell MB. Tension-type headache in 40-year-olds: a Danish population-based sample of
4000. J Headache Pain 2005; 6:441.
37. Wang SJ, Liu HC, Fuh JL, et al. Prevalence of headaches in a Chinese elderly population
in Kinmen: age and gender effect and cross-cultural comparisons. Neurology 1997;
49:195.
38. Couch JR. The long-term prognosis of tension-type headache. Curr Pain Headache Rep
2005; 9:436.
39. Jensen R, Stovner LJ. Epidemiology and comorbidity of headache. Lancet Neurol 2008;
7:354.
40. Bendtsen L, Jensen R. Tension-type headache: the most common, but also the most
neglected, headache disorder. Curr Opin Neurol 2006; 19:305.
41. Rasmussen BK. Epidemiology of headache. Cephalalgia 1995; 15:45.
42. Jensen R, Rasmussen BK, Pedersen B, Olesen J. Muscle tenderness and pressure pain
thresholds in headache. A population study. Pain 1993; 52:193.
43. Sandrini G, Antonaci F, Pucci E, et al. Comparative study with EMG, pressure algometry
and manual palpation in tension-type headache and migraine. Cephalalgia 1994; 14:451.
44. Jensen R, Fuglsang-Frederiksen A. Quantitative surface EMG of pericranial muscles.
Relation to age and sex in a general population. Electroencephalogr Clin Neurophysiol
1994; 93:175.
45. 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; 23:109.
46. Tornoe B, Andersen LL, Skotte JH, et al. Reduced neck-shoulder muscle strength and
aerobic power together with increased pericranial tenderness are associated with tension-
type headache in girls: A case-control study. Cephalalgia 2014; 34:540.
47. Spierings EL, Ranke AH, Honkoop PC. Precipitating and aggravating factors of migraine
versus tension-type headache. Headache 2001; 41:554.
48. Rasmussen BK. Migraine and tension-type headache in a general population: precipitating
factors, female hormones, sleep pattern and relation to lifestyle. Pain 1993; 53:65.
49. Ulrich V, Russell MB, Jensen R, Olesen J. A comparison of tension-type headache in
migraineurs and in non-migraineurs: a population-based study. Pain 1996; 67:501.
50. Karli N, Zarifoglu M, Calisir N, Akgoz S. Comparison of pre-headache phases and trigger
factors of migraine and episodic tension-type headache: do they share similar clinical
pathophysiology? Cephalalgia 2005; 25:444.
51. Buchgreitz L, Lyngberg AC, Bendtsen L, Jensen R. Increased prevalence of tension-type
headache over a 12-year period is related to increased pain sensitivity. A population study.
Cephalalgia 2007; 27:145.
52. Buchgreitz L, Lyngberg AC, Bendtsen L, Jensen R. Frequency of headache is related to
sensitization: a population study. Pain 2006; 123:19.
53. Rasmussen BK, Jensen R, Schroll M, Olesen J. Interrelations between migraine and
tension-type headache in the general population. Arch Neurol 1992; 49:914.
54. Houle TT, Turner DP, Houle TA, et al. Rounding behavior in the reporting of headache
frequency complicates headache chronification research. Headache 2013; 53:908.
55. Dowson AJ. Assessing the impact of migraine. Curr Med Res Opin 2001; 17:298.
56. Tepper SJ, Dahlöf CG, Dowson A, et al. Prevalence and diagnosis of migraine in patients
consulting their physician with a complaint of headache: data from the Landmark Study.
Headache 2004; 44:856.
57. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial
pain. Headache Classification Committee of the International Headache Society.
Cephalalgia 1988; 8 Suppl 7:1.
58. Lipton RB, Cady RK, Stewart WF, et al. Diagnostic lessons from the spectrum study.
Neurology 2002; 58:S27.
59. 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.
60. Silberstein SD, Lipton RB, Sliwinski M. Classification of daily and near-daily headaches:
field trial of revised IHS criteria. Neurology 1996; 47:871.
61. Silberstein SD. Chronic daily headache. J Am Osteopath Assoc 2005; 105:23S.
62. Katsarava Z, Limmroth V, Finke M, et al. Rates and predictors for relapse in medication
overuse headache: a 1-year prospective study. Neurology 2003; 60:1682.
63. Katsarava Z, Muessig M, Dzagnidze A, et al. Medication overuse headache: rates and
predictors for relapse in a 4-year prospective study. Cephalalgia 2005; 25:12.
64. Bigal ME, Lipton RB. Tension-type headache: classification and diagnosis. Curr Pain
Headache Rep 2005; 9:423.
65. Cady RK, Schreiber CP. Sinus headache or migraine? Considerations in making a
differential diagnosis. Neurology 2002; 58:S10.
66. 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; 17:1318.