tension-type-headache-in-adult.pdf

Official reprint from UpToDate www.uptodate.com ©2014 UpToDate

Author Frederick R Taylor, MD

Section Editor Jerry W Swanson, MD

Deputy Editor John F Dashe, MD, PhD

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

All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Oct 2014. | This topic last updated: Jul 30, 2014.

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:

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.

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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●

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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.

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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:

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

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

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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]

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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]

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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]:

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).

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•



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]:

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 on history' and "Evaluation of headache in adults", section on 'Indications for imaging studies'.)

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:

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"

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•

An unexplained abnormal finding on neurologic examination●

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

●



and "Thunderclap headache" and "Etiology, clinical features, and diagnosis of cerebral venous thrombosis".)

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:

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].

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

●



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 "Headache syndromes other than migraine", section on 'Sinus headache'.)

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 "Headache attributed to spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis" and "Approach to the patient with chronic meningitis".)

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th th

th th

Basics topics (see "Patient information: Headache (The Basics)")●

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

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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.)

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REFERENCES

Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013; 33:629.

1.

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.

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Bendtsen L. Central sensitization in tension-type headache--possible pathophysiological mechanisms. Cephalalgia 2000; 20:486.

3.

Jensen R. Peripheral and central mechanisms in tension-type headache: an update. Cephalalgia 2003; 23 Suppl 1:49.

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Ulrich V, Gervil M, Olesen J. The relative influence of environment and genes in episodic tension-type headache. Neurology 2004; 62:2065.

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Russell MB, Ostergaard S, Bendtsen L, Olesen J. Familial occurrence of chronic tension-type headache. Cephalalgia 1999; 19:207.

6.

Russell MB, Iselius L, Ostergaard S, Olesen J. Inheritance of chronic tension-type headache investigated by complex segregation analysis. Hum Genet 1998; 102:138.

7.

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 on history' and "Evaluation of headache in adults", section on 'Indications for imaging studies'.)

●

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.)

●

of 17Tension-type headache in adults: Pathophysiology, clinical features, a...


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Topic 3357 Version 6.0



GRAPHICS

Episodic tension-type headache diagnostic criteria

Description: Episodes of headache, typically bilateral, pressing or tightening in quality and of mild to moderate intensity, lasting minutes to days. The pain does not worsen with routine physical activity and is not associated with nausea, but photophobia or phonophobia may be present. Increased pericranial tenderness may be present on manual palpation.

A. At least 10 episodes of headache fulfilling criteria B through D. Infrequent and frequent episodic subforms of TTH are distinguished as follows:

Infrequent episodic TTH: Headache occurring on <1 day per month on average (<12 days per year).

Frequent episodic TTH: Headache occurring on 1 to 14 days per month on average for >3 months (≥12 and <180 days per year).

B. Headache lasting from 30 minutes to seven days.

C. At least two of the following four characteristics:

Bilateral location.

Pressing or tightening (nonpulsating) quality.

Mild or moderate intensity.

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

D. Both of the following:

No nausea or vomiting.

No more than one of photophobia or phonophobia.

E. Not better accounted for by another ICHD-3 diagnosis.

ICHD-3: The International Classification of Headache Disorders, 3rd edition (beta version); TTH: tension-type headache.

Data from: Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013; 33:629.

Graphic 79672 Version 5.0



Chronic tension-type headache diagnostic criteria

Description: A disorder evolving from frequent episodic tension-type headache, with daily or very frequent episodes of headache, typically bilateral, pressing or tightening in quality and of mild to moderate intensity, lasting hours to days, or unremitting. The pain does not worsen with routine physical activity, but may be associated with mild nausea, photophobia or phonophobia.

Diagnostic criteria:

A. Headache occurring on ≥15 days per month on average for more than three months (≥180 days per year) and fulfilling criteria B through D

B. Lasting hours to days, or unremitting

C. At least two of the following characteristics:

1. Bilateral location

2. Pressing or tightening (non-pulsating) quality

3. Mild or moderate intensity

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

D. Both of the following:

1. No more than one of photophobia, phonophobia or mild nausea

2. Neither moderate or severe nausea nor vomiting

E. Not better accounted for by another ICHD-3 diagnosis

ICHD-3: International Classification of Headache Disorders, 3rd edition

Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 2013; 33:629.




Chronic daily headaches of long duration

Chronic daily headaches of long duration are characterized by headache duration ≥4 hours a day with headaches occurring ≥15 days per month for >3 months

Chronic tension-type headache:

Bilateral, gradual onset, muscle tenderness common

Chronic migraine:

Daily or near-daily headaches of low to moderate intensity and mild migrainous features with superimposed severe intensity headaches with more prominent migrainous features

Medication overuse headache:

Usually preceded by an episodic headache disorder, typically migraine or tension-type headache, that has been treated with frequent and excessive amounts of acute symptomatic medications; often manifests as a headache that is present or develops upon awakening

New daily persistent headache:

Sudden onset, usually bilateral, typically unresponsive to treatment

Hemicrania continua:

Strictly unilateral, unremitting without pain-free intervals but with variable intensity, autonomic features ipsilateral to the side of pain, responsive to indomethacin

Modified from: Silberstein SD, Lipton RB, Sliwinski M. Classification of daily and near-daily headaches: field trial of revised IHS criteria. Neurology 1996; 47:871.




Disclosures: Frederick R Taylor, MD Nothing to disclose. Jerry W Swanson, MD Nothing to disclose. John F Dashe, MD, PhD Employee of UpToDate, Inc. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy

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