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

INTRODUCTION — Tension-type headache (TTH) is a primary headache disorder characterized by a bilateral, nonthrobbing headache of a mild to moderate intensity, typically without other associated features. TTH is the most common headache and prevalent neurologic disorder in the population. Due to its high prevalence, TTH causes a high burden of disability.

TTH was previously known by several other terms that referred to its suspected etiology, including stress headache, tension headache, muscle-contraction headache, psychomyogenic headache, and psychogenic headache [1].

This topic will review the etiology, epidemiology, clinical features, and diagnosis of TTH in adults. Other aspects of TTH are discussed separately.

●(See "Tension-type headache in adults: Acute treatment".)

●(See "Tension-type headache in adults: Preventive treatment".)

●(See "Tension-type headache in children".)

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 [2-4].

●Prevalence – The worldwide prevalence of TTH was estimated in 2016 to be 26 percent in the Global Burden of Disease Study [5]. However, prevalence estimates of TTH vary by methodology, patient age, and specific population studied. In a telephone survey of individuals age 18 to 65, the one-year prevalence of episodic TTH in the United States was 38 percent [6]. In a population-based Danish twin registry, the one-year prevalence of TTH among 12- to 41-year-old subjects was 86 percent [7].

Reported TTH prevalence also varies when stratified by headache frequency. TTH may be classified as infrequent episodic headache, frequent episodic headache, and chronic headache, based on monthly average headache occurrence of <1, 1 to 14, or ≥15 attacks, respectively. Most patients with TTH have the infrequent episodic subtype [4]. Using the International Classification of Headache Disorders, 2nd edition (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 [7]. 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 [6].

The prevalence of TTH may be underreported because only a small percentage of persons with mild and/or infrequent TTH seek medical care for this diagnosis. In fact, some experts regard the infrequent episodic subtype of TTH not as a disease, but as an expected, normal phenomenon that does not require medical attention in many instances [8].

Limited data suggest that White Americans have a higher prevalence of TTH compared with Black Americans [6].

●Role of sex and age – Females appear to have a slightly higher prevalence of TTH than males. In a Danish population study, the lifetime prevalence of episodic TTH in females and males was 99 and 69 percent, respectively [9]. A female predominance is more apparent with increased frequency of headache attacks. In another Danish population-based study that evaluated 4000 40-year-old subjects, males were slightly more likely to have infrequent episodic TTH, while females were more likely to have both frequent episodic TTH (43 versus 25 percent) and chronic TTH (3 versus 1 percent) [10].

Data regarding age dependence of TTH are limited. In data from the Global Burden of Disease Study, the prevalence of TTH was found to sharply increase during adolescence, peak in the fourth decade of life, and gradually decrease thereafter [5]. Similar results were found in a population-based study from the United States [6]. A Danish study found a decreasing prevalence of TTH with increasing age [9]. However, other studies have shown that TTH continues to be a problem for many older patients, occurring in 20 to 30 percent of those over 60 years of age [6,11,12].

●Burden of disease – The societal burden of TTH is high. In one population study, individuals with episodic TTH reported a mean of nine work days lost and another five reduced-effectiveness days per year, while persons with chronic TTH reported a yearly mean of 27 lost work days and 20 reduced-effectiveness days [6]. A cross-sectional population study found TTH was associated with reductions in several measures of health-related quality of life [13]. The burden is particularly high for the subset of patients who have substantial and complicating comorbidities, such as hypertension, cardiovascular disease, and depression [14]. The impact of TTH appears to be greatest on those who continue to be symptomatic into their older years of life [6,11,12].

ETIOLOGY — The etiology of TTH is probably multifactorial, but the precise mechanisms are uncertain [15]. Environmental factors such as stress and muscle tenderness appear to be most impactful in the development of episodic TTH, while genetic factors appear to play a key role in development of chronic TTH [16-18]. However, the wide variation in frequency and intensity in TTH suggests that the underlying pain mechanisms and contributing factors have dynamic and variable roles in the pathogenesis of TTH, both from one individual to another and from one attack to another in the same individual.

Pathogenesis — Peripheral activation or sensitization of myofascial nociceptors is most likely a major contributor to the development of episodic TTH. In addition, continuous nociceptive input from peripheral myofascial structures may induce central sensitization and lead to the conversion of episodic to chronic TTH [15,19-23].

Central factors — Heightened sensitivity of pain pathways in the central nervous system is thought to play a critical role in the pathogenesis of TTH [24-26].

General pain sensitivity in the central nervous system is increased in chronic TTH. There may be a lack of habituation as evidenced by recording sympathetic skin responses compared with normal controls [25,27-29]. Decreased pain, thermal, and electrical thresholds reported in patients with chronic TTH probably represent a central misinterpretation of incoming signals [30-32].

Sustained pericranial myofascial input may increase excitability of the central nervous system. This neuronal excitability may result in increased facilitation and decreased inhibition of pain transmission at the level of the spinal dorsal horn/trigeminal nucleus and may further promote increased pericranial muscle activity. Altered brainstem nociceptive reflex findings (eg, reduced subjective pain and reflex thresholds) suggest that limbic-controlled descending pain systems may be abnormal due to deficient descending inhibition in patients with chronic TTH [33-35].

Centrally acting molecular factors have also been implicated in the pathogenesis of TTH. Nitric oxide has been shown to induce TTH, and nitric oxide synthetase inhibition has been shown to reduce TTH intensity [36,37]. Modest reductions in serum N-acetyl-aspartate (a marker of neuronal dysfunction) and serum brain-derived neurotropic factor (which interacts with calcitonin gene-related peptide) have also been reported in patients with TTH [38,39].

Peripheral factors — Firm evidence for peripheral sources of TTH is unavailable, but muscular factors may be important, especially in episodic TTH [23,25].

●Myofascial trigger points – Compared with matched control subjects without headache, subjects with episodic TTH demonstrate more active and latent trigger points, lower pain threshold at nerve trunks, forward head posture, and reduced neck mobility [40-43]. Increased muscle tenderness is the most pronounced and consistent finding in TTH patients and probably represents the activation of peripheral nociceptors [44]. The intensity and frequency of TTH positively correlates with pericranial muscle tenderness [15]. 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 [25,26].

●Inflammation – Peripherally mediated neurovascular inflammation may contribute to the development of TTH. Elevated levels of several inflammatory mediators (interleukin [IL]-1 beta, IL-8, and IL-10) have been reported in several small case control studies of patients with frequent episodic or chronic TTH [45-48].

However, other studies suggest that tender muscles are likelier due to activated peripheral nociceptors and not sites of ongoing inflammation. As an example, one in vivo study showed normal levels of inflammatory mediators and metabolites related to tender trapezius muscle in patients with chronic TTH during both rest and static exercise [49]. Additional studies are warranted to confirm these findings and to identify causal mechanisms in the development of TTH.

Sustained contraction of pericranial muscles was long believed to be causative in TTH, but this concept is no longer considered valid [50].

Genetic contributors — However, genetic factors may be more important in the development of chronic TTH than episodic TTH [51]. One 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 [17]. Evidence from a genetic study employing complex segregation analysis suggests that chronic TTH has a multifactorial inheritance [18].

Hereditary factors seem to play a minor role in the pathogenesis of episodic TTH. Twin studies found no substantial difference in concordance rates for episodic TTH between monozygotic and dizygotic twin pairs, suggesting little if any role for genetic factors [16,52].

Risk factors — Several risk factors have been associated with TTH in cross sectional studies. These include [4,50,53,54]:

●Female sex

●Younger age

●Fatigue

●Sleep disorders

●Migraine history

●Depression history

Educational level has been positively correlated with episodic TTH but negatively correlated with chronic TTH in one population-based telephone survey [6].

CLINICAL FEATURES — The typical presentation of a TTH attack is that of a mild to moderate intensity, bilateral, nonthrobbing headache without other associated features.

●Character of head pain – The pain in TTH may is typically mild to moderate but may infrequently be severe [55]. 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."

●Pericranial muscle tenderness – Increased pericranial muscle tenderness is the most common abnormal finding on examination in patients with TTH [1]. Muscle tenderness may be identified in the head, neck, or shoulders (ie, pericranial tenderness) chronically and is typically exacerbated during the headache attack.

The presence or absence of pericranial muscle tenderness should be elicited from the history and confirmed on examination by manual palpation [56,57]. 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].

●Triggers – Stress and mental strain are reported to be the most common precipitants for TTH [58]. However, the role of these factors in the development of TTH is unclear as they are found at the same frequency in migraine [59,60]. Head and neck movements have also been reported as triggers in some patients with episodic TTH [61]. Other reported triggers for TTH include sleep disturbance, dehydration, alcohol, and sunlight exposure [62,63].

The causal role of triggering factors is questionable due to the diversity of potential factors and their uncertain relationship to the pathophysiology of TTH. However, identifying and avoiding specific triggers in an individual may help reduce TTH burden. Patients may self-report triggers for TTH or these may be identified with use of a headache diary. (See "Tension-type headache in adults: Preventive treatment", section on 'Behavioral therapies'.)

DIAGNOSIS — The diagnosis of TTH is made when symptoms are consistent with the typical features of TTH, the diagnostic criteria are fulfilled, and the general and neurologic examinations are normal (other than increased tenderness of pericranial myofascial tissues and the presence of trigger points).

There are no diagnostic tests specific for TTH; testing is performed for patients with atypical presentations to identify or exclude alternative entities. (See 'Secondary headaches' below.)

Because of the extensive overlap of TTH symptoms with secondary headaches (eg, medication overuse or structural brain lesions), we suggest clinicians consider the possibility of a secondary headache disorder when patients present for clinical care with presumed TTH. TTH features are often mild and infrequent, unlikely to be a common cause of symptoms among patients presenting for evaluation in clinical practice. (See 'Diagnostic testing' below.)

Diagnostic criteria — The International Classification of Headache Disorders, 3rd edition (ICHD-3) specifies diagnostic criteria for episodic TTH (table 1) and chronic TTH (table 2) [1].

●Episodic TTH – 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:

•At least two of the following:

-Bilateral location

-Pressing or tightening (nonpulsating) 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 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).

●Chronic TTH – The ICHD-3 criteria for chronic TTH (table 2) require headaches 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:

•At least two of the following:

-Bilateral location

-Pressing or tightening (nonpulsating) 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 subtypes of TTH is additionally classified as occurring with or without pericranial muscle tenderness [1]. (See 'Clinical features' above.)

Patients may be diagnosed with probable TTH when headache features meet all but one of the ICHD-3 criteria for TTH.

The ICHD-3 criteria provide a diagnostic hierarchy for patients whose symptoms fulfill multiple sets of criteria [1]. When a patient has headaches that meet criteria for both TTH and migraine, then migraine supersedes TTH as the diagnosis. Patients who meet criteria for both TTH and probable migraine are considered to have episodic TTH. Patients who meet the criteria for both chronic TTH and medication overuse headache (MOH) are considered to have both conditions; following successful treatment of MOH, the diagnosis should be reevaluated because many patients may be reclassified as having episodic TTH alone.

Distinguishing other primary headaches — The ICHD-3 criteria were designed to distinguish between TTH, migraine, and cluster headache. The diagnostic criteria for TTH can be viewed in contradistinction to criteria that characterize other primary headache disorders. These distinctions can be summarized according to what TTH is not: localized, throbbing, severe at presentation, aggravated by activity, accompanied by aura, or associated with cranial autonomic symptoms.

Some patients with TTH may report symptoms that partially overlap with other headache syndromes, but these features are typically minor when due to TTH. The presence of either photophobia or phonophobia alone (but not both) may occur with TTH. In addition, mild nausea may accompany chronic TTH as long as there is no photophobia or phonophobia. However, 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 characteristic features of episodic TTH. The proportion of TTH associated with cranial autonomic features is currently unknown, but these are uncommon accompaniments in the author's experience.

Headache diaries or calendars may help improve the accuracy of reporting the frequency of TTH to help determine the subtype. The distinction between episodic and chronic headache types is complicated by inaccuracies in patient recall of headache frequency. In one large survey study of nearly 16,000 patients with headache, subjects tended to report monthly headache frequency rounded to the nearest five days. Females were more likely to round than males; rounding decreased with increasing age and increased with symptoms of depression [64].

Diagnostic testing — Diagnostic testing is warranted to identify secondary cause of headache for patients with symptoms or signs that are atypical for TTH as well as for those with typical TTH symptoms plus an additional historical feature suggestive of a secondary cause of headache (table 3). These include:

●Headache features atypical for TTH:

•Abrupt onset

•Localized or unilateral

•Severe or progressive in nature

•Throbbing quality

•Aggravated by activity or change in body position (eg, positional)

•Associated with neurologic or systemic features (eg, impaired vision, severe nausea, weakness, fever)

●Historical features associated with a secondary headache:

•Age >50 years old

•Neoplasm history

•Anticoagulant use

•Trauma

•Pregnancy

•Immunosuppressant state

Headache and historical features suggestive of an underlying structural, metabolic, or systemic cause are discussed in greater detail separately. (See "Evaluation of headache in adults", section on 'Danger signs'.)

Diagnostic testing to exclude alternative causes of headache generally consists of brain imaging. Other testing such as cerebrospinal fluid (CSF) analysis or laboratory testing is reserved for patients with a suspected secondary headache and clinical features suggestive of an infectious or other systemic condition or when neuroimaging is nondiagnostic.

●Neuroimaging – We typically perform brain magnetic resonance imaging (MRI) with contrast to assess for secondary causes of headache. Computed tomography (CT) of the brain with contrast may be performed in emergency settings to exclude conditions such as intracranial hemorrhage or as a less sensitive alternative test in nonemergency settings when MRI is unavailable or contraindicated.

In addition, vascular imaging may be warranted for patients with suspected arterial or venous cause to headache symptoms, such as those with ischemic stroke from carotid dissection, reversible cerebral vasoconstriction syndrome, or cerebral venous thrombosis. Arterial imaging options include MR- or CT-angiography. MR- or CT-venography is used to assess venous structures.

The approach to neuroimaging in adult patients with headache is discussed in greater detail separately. (See "Evaluation of headache in adults", section on 'Indications for imaging'.)

●Other testing – Lumbar puncture for CSF analysis is typically performed for patients with suspected secondary causes to exclude conditions such as subarachnoid hemorrhage or meningitis. Laboratory testing, such as erythrocyte sedimentation rate and C-reactive protein, are warranted for patients ≥50 years old with suspected giant cell arteritis. Additional testing for specific suspected secondary causes of headache is discussed in detail separately. (See "Evaluation of headache in adults", section on 'Lumbar puncture' and "Evaluation of headache in adults", section on 'Common clinical scenarios'.)

Diagnostic testing may be unnecessary for other patients who have characteristic features of TTH, a stable headache pattern for over six months, a normal neurologic examination, and no associated high-risk conditions.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of TTH includes other primary headache conditions and secondary headaches that may present with bilateral, nonthrobbing headache attacks. These alternative conditions are typically distinguished from TTH by specific clinical features and/or by results of diagnostic testing. (See 'Diagnostic testing' above.)

Diagnostic challenges may occur when symptoms are atypical or variable, when some clinical features are missing or not reported by patients, when features overlap with other types of headaches, and when patients have multiple headache conditions. Older adults pose unique diagnostic challenges due to physiologic changes associated with aging and medical comorbidities that can increase the risk of secondary and some primary headaches [65].

Migraine — Migraine may be the most common headache condition in the differential diagnosis of TTH.

●Relationships between migraine and TTH – Migraine may be mistaken for TTH due to overlapping diagnostic criteria, especially for patients with migraine without aura. Migraine may precipitate or aggravate TTH in individuals who have both types of headache. In addition, migraine and TTH may also occur as independent conditions with shared environmental and lifestyle factors [52]. In a population study that compared clinical characteristics of TTH, the one-year prevalence of TTH was similar for individuals with migraine as for those without a migraine history [60,66].

Diagnostic challenges occur when patients underreport symptoms by poorly describing them (typically underreporting migraine symptomatology) or when TTH headache symptoms overlap with features suggestive of migraine (eg, severe pain, associated with photophobia or phonophobia).

●Features suggestive of migraine – The presence of aura is the most characteristic distinguishing feature suggestive of migraine. Other features suggestive of migraine include unilateral pain, pulsatile quality, associated nausea, photophobia and/or phonophobia, and the presence of cutaneous allodynia (eg, discomfort with brushing hair). (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Clinical features'.)

Patients with disabling episodic headache are more likely to have migraine than TTH. In one study, 32 percent of patients with an initial diagnosis of episodic TTH were subsequently diagnosed with migraine or probable migraine when headache diaries were reviewed [67]. Individuals with TTH reclassified as having migraine responded to triptans in the study, while persons with episodic TTH not meeting criteria for migraine responded at placebo rates [67,68].

Unilateral, severe, or throbbing pain can occur in a minority of patients with TTH, presumably when the pain is most intense [69]. 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. Typically, migrainous features are mild or inconstant when present in TTH. (See 'Distinguishing other primary headaches' above.)

Cataloging features of serial headache attacks may help to discriminate between migraine and TTH.

●Patients who meet diagnostic criteria for both migraine without aura and 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 without aura. In such cases, the diagnosis of migraine and its subtypes supersedes that of TTH and its subtypes.

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 [70]. This hypothesis was validated by a study that evaluated 1203 patients visiting a primary practitioner with a complaint of episodic headache [71]. 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 [72]. 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 was diagnosed in 3 percent.

Medication overuse headache — Medication overuse headache (MOH) is a commonly encountered type of headache disorder with clinical features that can often be nondescript and mimic chronic TTH. The development of MOH is typically preceded by an episodic headache disorder, usually migraine or TTH. However, MOH may be distinguished by the presence of frequent or daily headaches that occur despite, or because of, the regular use of headache medications. Withdrawal and detoxification of the overused medication improves symptoms due to MOH. (See "Medication overuse headache: Treatment and prognosis".)

MOH may occur as a result of TTH, especially when management is suboptimal or preventive treatment ineffective. Observational studies have found patients with MOH associated with TTH may have stronger withdrawal symptoms and higher relapse rates than those with MOH associated with other primary headache conditions at both one- and four-year prospective follow-up [73,74]. This is probably due, at least in part, to the withdrawal patterns particular to the medications used for different types of headache, since overuse of mixed analgesics (typically used for TTH) is associated with a higher relapse rate than overuse of triptans (typically used for migraine) after drug withdrawal.

Other primary headache disorders — Several less common primary headache syndromes may mimic TTH. Specific clinical features may help to identify these alternative conditions.

●Hemicrania continua – Patients with chronic TTH may have frequent or continuous headaches similar to those with hemicrania continua. However, patients with hemicrania continua also have cranial autonomic symptoms (eg, conjunctival injection, rhinorrhea, facial sweating, ptosis) and typically report a sense of restlessness during severe headache symptoms. In addition, hemicrania continua responds to therapeutic doses of indomethacin. (See "Hemicrania continua".)

●Hypnic headache – The specific features of hypnic headache are often bilateral, dull in character, and moderate in intensity, similar to patients with TTH. Unlike TTH, hypnic headache is uniquely characterized by onset during sleep. (See "Hypnic headache".)

●New daily persistent headache – Patients with new daily persistent headache may report somewhat nondescript headaches consistent with clinical features of TTH. However, these headaches are characterized by a specific, recalled date of onset followed by unremitting persistence of the headache. (See "New daily persistent headache".)

●External pressure headache – Headache may also be due to external stimuli that exert pressure on the head or neck. Such headaches may be suspected when headaches occur in the setting of wearing tight-fitting helmets or goggles or traction on the hair from a ponytail or braiding [50].

Secondary headaches — Patients with headaches due to a secondary headache syndrome may present diagnostic challenges because symptoms may overlap with TTH. Secondary headaches may be associated with specific clinical features or examination findings that are atypical for both episodic and chronic TTH (table 3). (See "Evaluation of headache in adults", section on 'Specific features suggesting a secondary headache source'.)

Brain tumor headache — Brain tumor headache frequently mimics TTH. However, only a minority of patients presenting for evaluation with headaches have a brain tumor. Specific clinical characteristics more commonly associated with tumors can help identify these cases. These include:

●New headache at age >50 years

●History of cancer

●Progressive symptoms

●Abnormal neurologic examination

The features of headache associated with a brain tumor 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'.)

Sinus symptoms — "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 of these patients actually have migraine or, less often, TTH [75,76]. (See "Evaluation of headache in adults", section on 'Sinus symptoms'.)

The occurrence of nasal symptoms associated with headache in the region of the sinuses, without fever or purulent nasal discharge, should prompt an evaluation for both sinusitis and primary headaches, including TTH [75,77].

Cervicogenic headache — The pain with cervicogenic headache can mimic that of TTH, including nonthrobbing pain, moderate intensity, and associated pericranial muscle tenderness. However, symptoms with cervicogenic headache are unilateral, often associated with restricted range of motion of or pain exacerbation with neck movement [78]. (See "Cervicogenic headache".)

In addition, 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 diagnostic anesthetic blocks are posited to pinpoint sources of pain in the neck when they provide relief of pain. (See "Cervicogenic headache", section on 'Diagnostic anesthetic blockade'.)

Idiopathic intracranial hypertension — Headache symptoms due to idiopathic intracranial hypertension (IIH, also called pseudotumor cerebri) are nonspecific. The presence of additional symptoms associated with IIH may suggest the diagnosis, including visual obscurations or diplopia, tinnitus, or back pain. Papilledema may be identified on examination. The diagnosis of IIH is made by documenting elevated intracranial pressure in the setting of normal cerebrospinal fluid composition. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis".)

Others — Less common alternative causes of headache in patients with suspected TTH include rare conditions as well as more common conditions that uncommonly present with isolated nonspecific headaches, mimicking TTH. These entities are typically identified by the presence of specific features that are atypical for TTH, including historical details, abnormal findings on clinical examination or diagnostic testing, or nonresponsiveness to TTH treatment.

These conditions include [50,79]:

●Spontaneous intracranial hypotension

●Chiari I malformation

●Subdural hematoma

●Cerebral venous thrombosis

●Ischemic stroke

●Giant cell arteritis

●Obstructive sleep apnea

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 5^th to 6^th 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 10^th to 12^th 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

●Epidemiology – Tension-type headache (TTH) is the most prevalent type of primary headache in the general population with a worldwide prevalence estimated to be 26 percent. The prevalence of TTH sharply increases during adolescence, peaks in the fourth decade, and gradually decreases thereafter. (See 'Epidemiology' above.)

●Clinical features – The typical presentation of a TTH attack is that of a mild to moderate intensity, bilateral, nonthrobbing headache without other associated features. Increased pericranial muscle tenderness is the most common abnormal finding on examination of patients with TTH. (See 'Clinical features' above.)

●Diagnosis – The diagnosis of TTH is made when symptoms are consistent with the typical features of TTH, the diagnostic criteria are fulfilled, and the general and neurologic examinations are normal, other than the presence of increased tenderness of pericranial muscle tenderness. (See 'Diagnosis' above.)

The International Classification of Headache Disorders, 3rd edition (ICHD-3) specifies diagnostic criteria for episodic TTH, both infrequent and frequent subforms, (table 1) and chronic TTH (table 2). (See 'Diagnostic criteria' above.)

•Infrequent episodic TTH – headaches occur <1 day a month on average

•Frequent episodic TTH – headaches occur 1 to 14 days a month on average (for >3 months)

•Chronic TTH – headaches occur ≥15 days a month on average (for >3 months)

Each of the subtypes is additionally subclassified as occurring with or without pericranial muscle tenderness.

●Diagnostic testing for atypical presentations – Diagnostic testing is warranted to identify secondary cause of headache for patients with symptoms or signs that are atypical for TTH as well as for those with typical TTH symptoms plus an additional historical feature suggestive of a secondary cause of headache (table 3). (See 'Diagnostic testing' above.)

Diagnostic testing to exclude alternative causes of headache generally consists of brain imaging, typically brain MRI with contrast. Other testing for selected patients with suspected alternative conditions may include cerebrovascular imaging, lumbar puncture, and laboratory testing.

●Differential diagnosis – The differential diagnosis of TTH includes other primary headache conditions and secondary headaches that may present with bilateral, nonthrobbing headache attacks. (See 'Differential diagnosis' above.)

•Primary headache disorders – The most common headache disorders that may mimic TTH include migraine and medication overuse headache. Other primary headache disorders in the differential diagnosis include hemicrania continua, hypnic headache, new daily persistent headache, and external pressure headache. (See 'Migraine' above and 'Medication overuse headache' above and 'Other primary headache disorders' above.)

•Secondary headaches – Several secondary headaches due to an underlying structural cause may present with nonspecific headaches that can mimic TTH. Common secondary headaches include (see 'Secondary headaches' above):

-Brain tumor headache

-Sinus symptoms

-Cervicogenic headache

-Idiopathic intracranial hypertension

These alternative conditions may be distinguished by specific clinical features and/or by results of diagnostic testing.