INTRODUCTION — Tension-type headache (TTH) is 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 in the population, TTH causes a high degree of disability.
This topic will review the classification, pathophysiology, 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".)
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 [1]. 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 [2]. 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 [2]. 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 [2]. 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 [3]. Environment influences development of episodic TTH more than chronic TTH, while genetic factors appear to play an important role in development of chronic TTH [4-6]. 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.
Nociceptor sensitization — 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 [1,7,8]. 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 [3,9-13]. 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 [12].
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".)
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 [8,14,15]. However, in TTH, as in migraine without aura, there may be a lack of habituation when recording sympathetic skin responses compared with normal controls [16]. 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 [17-19]. 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 [20-22].
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 [10]. 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) [23,24].
Peripheral factors — Firm evidence for peripheral abnormalities in TTH is unavailable, but muscular factors may be important, especially in episodic TTH [8,13]. Compared with matched control subjects without headache, subjects with episodic TTH demonstrate increased numbers of active and latent trigger points, lower pain threshold at nerve trunks, forward head posture, and lesser neck mobility [25-28]. 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 [3]. 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 [1,8].
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 [30-33]. Additional studies are warranted to confirm these findings and to identify causal mechanisms in the development of TTH.
Sustained contracture of pericranial muscles was long believed to be causative in TTH, but this concept is no longer considered valid.
Genetic factors — 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 [4,34].
However, genetic factors may be more important in the development of chronic TTH than episodic TTH [35]. 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 [5]. Evidence from a genetic study employing complex segregation analysis suggests that chronic TTH has a multifactorial inheritance [6].
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 [36-38].
●Prevalence – In the population-based Danish twin registry, the one-year-period prevalence of TTH among 12- to 41-year-old subjects was 86 percent [39]. Furthermore, the prevalence of TTH may be increasing [40].
Although TTH is the most prevalent neurologic disorder, most patients with TTH have the infrequent episodic subtype, with headaches less than one day a month [38]. 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 [39]. 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 [41].
Limited data suggest that White Americans have a higher prevalence of TTH compared with Black Americans [41].
●Role of sex and age – Females have a slightly higher prevalence of TTH than males, especially with regard to the frequent episodic and chronic subtypes of TTH. In a Danish population study, the lifetime prevalence of episodic TTH in males and females was 69 and 88 percent [42]. In another Danish population-based study that evaluated 40-year-old subjects, males were more likely than females to have no TTH and infrequent episodic TTH, while females were more likely than males to have frequent episodic TTH and chronic TTH [43]. 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 [41]. A Danish study found a decreasing prevalence of TTH with increasing age [42]. 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 [41,44,45].
Societal impact — The prevalence of TTH is greater than migraine [46], and the overall cost of TTH is high. In one population study, persons with episodic TTH reported a mean of nine lost work days and five reduced-effectiveness days, while persons with chronic TTH reported a mean of 27 lost work days and 20 reduced-effectiveness days [41]. A cross-sectional population study found TTH was associated with reductions in several measures of health-related quality of life [47]. The burden is particularly high for the minority who have substantial and complicating comorbidities [48]. The impact is greatest on those with TTH who continue to suffer into their older years of life [41,44,45].
While TTH is the most common form of headache, only a small percentage of persons with TTH 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 [49].
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 severe, pulsating, or unilateral. In three Danish studies, for example, severe pain was found in 13 percent [40], pulsatile pain was found in 14 to 20 percent [42,50], and unilateral pain in 10 percent [51].
Increased pericranial muscle tenderness is the most important abnormal finding in patients with TTH [2]. Blood work, brain imaging with computed tomography or magnetic resonance imaging 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 [13]. 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. Muscle tenderness may be elevated in patients with TTH, independent of measures of muscle stiffness. The presence or absence of pericranial muscle tenderness should be elicited from the history and confirmed on examination by manual palpation [52,53].
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 [2].
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 [54]. 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 females [55].
Precipitating factors — Stress and mental tension are reported to be the most common precipitants for TTH [56]. However, they are found at the same frequency in migraine [57,58]. 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 [59].
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 [60,61]. 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 and TTH may be considered related conditions with shared environmental and lifestyle factors [34]. Additionally, migraine may precipitate or aggravate TTH in individuals 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 individuals with and without migraine. However, the frequency and duration of TTH attacks were greater in persons with migraine compared with persons without migraine [58,62]. (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 'Patients with atypical features suggestive of a secondary headache' 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 'Patients with atypical features suggestive of a secondary headache' 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 [2].
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 [2]:
●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 [2]:
●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 [2]. (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 [2]. There is an exception for chronic TTH that allows mild nausea as long as there is no photophobia or phonophobia. 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 [2]. However, if criteria are also met for migraine or probable migraine, then migraine supersedes TTH as the diagnosis.
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. Females were more likely to round than males; rounding decreased with increasing age and increased with symptoms of depression [63]. 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 "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Overview of 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 due to aging, when there are atypical or missing features, when features overlap with other types of headaches, and when patients fail to report all symptoms.
Older adults — Older adults pose unique diagnostic challenges due to physiologic changes associated with aging and medical comorbidities [64]. Treatment challenges include potential polypharmacy and intolerance to pain medication.
Distinguishing between migraine and TTH — 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 [65]. This hypothesis was validated by the Landmark study, which evaluated 1203 patients visiting a primary practitioner with a complaint of episodic headache [66]. 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 [67]. 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 [68]. Those persons with TTH reclassified as migraineurs responded to triptans in the study, while persons with episodic TTH not meeting criteria for migraine responded at placebo rates [68,69]. 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 [2]. 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.
As noted above, throbbing or pulsating pain may infrequently occur with TTH, presumably when the pain is most intense [50]. 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 'Patients with atypical features suggestive of a secondary headache' below.)
Patients with chronic daily 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 'Patients with atypical features suggestive of a secondary headache' below.)
The chronic daily headache disorders as a group are not addressed by the 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) [70,71]. In this paradigm, chronic TTH is classified under chronic daily headache, long duration subtype (at least four hours a day) (table 3). (See "Chronic daily headache: Associated syndromes, evaluation, and management".)
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
Patients with 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 [72,73]. 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 [72,73].
Patients with atypical features suggestive of a secondary headache — Patients with headaches due to a secondary headache syndrome may present diagnostic challenges for TTH. Secondary headaches may be associated with specific historical features or examination that are atypical for both episodic and chronic TTH (table 4). (See "Evaluation of headache in adults", section on 'Specific features suggesting a secondary headache source'.)
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 clinical characteristics that may be more commonly associated with tumors. These include age >50 years, history of cancer, progressive symptoms, and an 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'.)
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'.)
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 patients presenting with sinus headache turn out to have migraine or, less often, TTH. (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 neither trigger a diagnosis of sinus headache nor exclude the diagnosis of other primary headaches, including TTH [74,75].
Cervicogenic headache — Cervicogenic headache should be considered if headache is strictly unilateral [76]. 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 and may be discriminated by associated clinical features. (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
●Definition and epidemiology – Tension-type headache (TTH) is the most prevalent headache in the general population and the second-most prevalent disorder in the world. The typical presentation of a TTH attack is that of a mild to moderate intensity, bilateral, nonthrobbing headache without other associated features. (See 'Epidemiology' above and 'Clinical features' above.)
●Pathophysiology – 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.)
●Classification – 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
●Diagnosis – The diagnosis of TTH is based upon clinical impression. The diagnosis 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.)
Diagnostic challenges occur in the evaluation of suspected TTH when older adults are affected, 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.)
●Evaluation – 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 an unexplained abnormal finding on neurologic examination or atypical headache features or headaches that do not fulfill the strict definition of a primary headache disorder. (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'.)
