Headache & Pain
Headache associated with intracranial neoplasms
Sep. 30, 2024
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US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
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The author outlines the clinical manifestations, etiology, differential diagnosis, diagnostic evaluation, and management of tension-type headache. Updated diagnostic criteria from the International Headache Society’s International Classification of Headache Disorders (ICHD-3) on tension-type headache are the focus, with some discussion on differentiation from other conditions like migraine and medication-overuse headache where relevant.
• Tension-type headache is bland and characterized as head pain devoid of migrainous characteristics. | |
• The fundamental difference between tension-type headache and migraine is that tension-type headache lacks features of sensory sensitivity (eg, photophobia and phonophobia) and severe throbbing pain. | |
• Virtually any and all structural and metabolic diseases may cause a phenotypic tension-type headache. | |
• First-line acute treatments for tension-type headache are aspirin or acetaminophen, whereas second-line are NSAIDs and caffeine combinations. | |
• Nonpharmacologic management should be first-line for tension-type headache preventive treatment before medications. These nonpharmacologic treatments include cognitive behavioral therapy, biofeedback, relaxation, physical therapy, occupational therapy, and optimization of sleep hygiene. | |
• Preventive medications should be considered when attacks occur more than 2 days a week, with a goal of 50% reduction. After 6 months response, consider stopping the preventive treatment to assess for maintained benefit. | |
• First, second, and third-line preventive medications are amitriptyline, mirtazapine, and venlafaxine, respectively. |
Tension-type headache is the most common primary headache, and perhaps because of this, it has been called by several different names over the years (124; 56). In the current International Classification of Headache Disorders (ICHD-3), based on the frequency of attacks, the International Headache Society (IHS) divides tension-type headache into episodic tension-type headache and chronic tension-type headache types. Tables 1 and 2 include diagnostic criteria of episodic tension-type headache, and Table 3 details criteria for chronic tension-type headache (57). Episodic tension-type headache is classified as either infrequent (less than 1 day per month or 12 days per year) or frequent (1 to 14 days per month or 12 to 179 days per year). Chronic tension-type headache occurs on greater than or equal to 15 days per month or greater than or equal to 180 days per year. The ICHD-3 further classifies each type of tension-type headache based on the presence or absence of associated pericranial tenderness on manual palpation. The pericardial tenderness is assessed using small rotating movements with index and middle fingers or with a palpometer in the following muscles: frontal, temporal, master, pterygoid, sternocleidomastoid, splenius, and trapezius. A score of 0 to 3 can be used for degree of tenderness.
The updated ICHD-3 allows chronic tension-type headache to be diagnosed in the presence of overuse of acute medication(s) (simple analgesics greater than or equal to 15 days a month; ergotamine, triptans, opioids, or combination analgesics on greater than or equal to 10 days a month). Previously, such patients could not be diagnosed with chronic tension-type headache until the overused medication had been discontinued, and it was demonstrated that the headache persisted. Now, with the updated guidelines, such patients are diagnosed with both chronic tension-type headache and medication-overuse headache, which is a separate ICHD-3 diagnosis. A retrospective pediatric study that included 250 cases of tension-type headache found that 11 had concurrent medication overuse headache (52).
According to the ICHD-3, chronic tension-type headache must be separated from new daily persistent headache. New daily persistent headache can phenotypically resemble chronic tension-type headache, but it is daily and unremitting from onset (ie, it starts 1 day and never goes away). In contrast, chronic tension-type headache evolves from episodic tension-type headache in most cases (79).
(A) At least 10 episodes occurring on less than 1 day per month on average (fewer than 12 days per year) and fulfilling criteria B to D. | |
(B) Headache lasting from 30 minutes to 7 days | |
(C) Headache has at least two of the following characteristics: | |
(1) Bilateral location | |
(D) Both of the following: | |
(1) No nausea or vomiting (anorexia may occur) | |
(E) Not attributed to another disorder | |
|
(A) At least 10 episodes occurring 1 to 14 days per month for at least 3 months (or 12 to 179 days per year) and fulfilling criteria B to D. | |
(B) Headache lasting from 30 minutes to 7 days | |
(C) Headache has at least two of the following characteristics: | |
(1) Bilateral location | |
(D) Both of the following: | |
(1) No nausea or vomiting (anorexia may occur) | |
(E) Not attributed to another disorder | |
|
(A) Headache occurring on 15 or more days per month on average for more than 3 months (180 or more days per year) and fulfilling criteria B through D* | |
(B) Headache lasts hours or may be continuous | |
(C) Headache has at least two of the following characteristics: | |
(1) Bilateral location | |
(D) Both of the following: | |
(1) No more than one of photophobia, phonophobia, or mild nausea | |
(E) Not attributed to another disorder** | |
*Chronic tension-type headache evolves over time from episodic tension-type headache. When criteria A through E are fulfilled by headache that, unambiguously, is daily and unremitting within 3 days of its first onset, physicians should code it as new daily persistent headache. If onset is gradual or not recalled, it should be coded as chronic tension-type headache. **When medication overuse is present, the patient should be diagnosed with both chronic tension-type headache and medication-overuse headache. |
Patients can have both migraine and tension-type headache (80). Authors have long suggested that the variety of headaches in those with migraine might be a manifestation of the same underlying pathophysiology (80). The Spectrum Study examined the effectiveness of sumatriptan in treating the range of headache attacks seen in migraine patients. In a double-blind, placebo-controlled, multiple-attack study, Lipton and colleagues investigated migraine with associated phenotypic tension-type headache and patients with pure tension-type headache. Oral sumatriptan was equally effective for phenotypic tension-type headache and clear migraine attacks in the group of patients who had migraine with tension-type headache but was ineffective for the patients with only tension-type headache (80). The authors of the Spectrum Study suggest that the attacks of phenotypic tension-type headache in the setting of migraine are pathophysiologically related to migraine, even though their symptom profiles vary (80).
The results of the Spectrum Study also raised the question of whether patients with chronic tension-type headache and episodic migraine really have a single unifying disorder: chronic migraine.
In the ICHD-3, chronic migraine is the diagnosis if there is headache on 15 days or more per month with at least 8 days meeting migraine criteria. The other headache days can be phenotypically tension-type headache, but the overall diagnosis is still coded as chronic tension-type headache (57).
The criteria do not require a truly featureless headache for tension-type headache as mild nausea, photophobia, or phonophobia may be allowed, but even this detail varies on whether tension-type headache is considered chronic or episodic. Given that phenotypic tension-type headache in migraine may have a migrainous biology and given that the ICHD-3 criteria do not require a strictly featureless headache, one wonders how many patients who have contributed to the tension-type headache literature in fact have migraine. The realization that some or perhaps many of the patients with previously reported chronic tension-type headache may be better classified as chronic migraine makes prior studies of chronic tension-type headache somewhat difficult to interpret.
To further clarify how to diagnosis headache based on these various headache types, consider these scenarios:
(1) A patient with at least 15 headache days per month, of which at least 8 meet criteria for migraine: this patient would be diagnosed with chronic migraine, even though the other headache days are consistent with tension-type headache. | |
(2) If this patient also had medication overuse, they would receive an additional diagnosis of medication overuse headache. | |
(3) If a patient has at least 15 headache days per month of headache in which none of the days meet migraine criteria, chronic tension-type headache is diagnosed. Technically, if 7 or fewer days meet migraine criteria, the ICHD-3 would not consider this presentation chronic migraine, although opinion among headache specialists may vary regarding whether the pathophysiology in this case would actually represent chronic migraine. | |
(4) If a patient presents with both chronic tension-type headache and medication overuse, they receive both diagnoses. | |
(5) If a patient meets criteria for chronic tension-type headache but had an onset of headache over 3 months ago with no previous headache history, then the diagnosis of new daily persistent headache is given if it became daily within 1 to 3 days. They are not given the diagnosis of chronic tension-type headache in this case. Medication overuse headache can only be added to new daily persistent headache if the headache predates the medication overuse, otherwise chronic tension-type headache or chronic migraine should be considered. |
To further complicate the distinction, there is also the diagnosis of probable migraine, which allows for a headache that is essentially in-between criteria for migraine and tension-type headache (57). This headache type is diagnosed, with assumed underlying migraine pathophysiology, if one of the migraine criteria are not met. For example, a patient with seven headaches a month meets all criteria for migraine except that it is bilateral, mild, not pulsatile, not aggravated by activity, and it is accompanied by nausea. This patient would be considered to have probable migraine, not tension-type headache.
Unfortunately, the diagnosis of primary headache disorders continues to be an issue for physicians and allied health. Incorrect diagnosis means incorrect enrollment for research studies, incorrect headache counselling, incorrect workup, and most importantly, incorrect treatment. Even when diagnosed correctly as migraine or tension-type headache, understanding of medication overuse headache is limited, with one study showing that one third of physicians would not prescribe prophylactic medications due to incorrect thinking that it would cause medication overuse headache (68). Another study showed poor knowledge that opioids and butalbital-containing products can cause medication overuse (90). A further example includes a study of physiotherapists where only 26.4% self-identified as being moderately or very familiar with the criteria for headache disorders (28). A major issue is that headache medicine is still under taught in neurology programs; in a study of 133 program directors in neurology, 96% of directors stated that their residents are not prepared for headache management (01). Eventually we may have biomarkers to help differentiate primary headache disorders. For example, a study comparing episodic tension-type headache (n=32) to healthy controls (n=32) using resting state functional MRI found altered functional connectivity of the insula and posterior cingulate (152). Unfortunately, the use of biomarkers is still at the level of research study and is not used clinically.
Tension-type headache is bland and is characterized as head pain devoid of migrainous characteristics (112). Evidence suggests that there are two types of tension-type headache (78). The phenotypic tension-type headache seen in migraine cases likely represents mild migraine. Pure tension-type headache is featureless and does not have concomitant migraine. Just how featureless tension-type headache should be is a matter of debate, as the ICHD-3 criteria for both episodic tension-type headache and chronic tension-type headache allow a minimal number of migrainous features. According to the ICHD-3, episodic tension-type headache and chronic tension-type headache allow photophobia or phonophobia, but not both. Mild nausea is allowed in chronic tension-type headache, but not episodic tension-type headache without clear rationale. The author's bias is to demand a completely featureless headache (bilateral, nonthrobbing pain, plus the absence of nausea, vomiting, photophobia, phonophobia, osmophobia, and movement exacerbation) before diagnosing tension-type headache in preference to the diagnosis of migraine. There is even a prospective study on 193 who found osmophobia to be predictive of migraine, with it being present in more than 25% of migraine attacks but in no tension-type headaches (141). The headache history also requires careful questioning as a patient may initially deny migraine characteristics like photophobia and phonophobia, but when asked differently (eg, if they prefer being in the dark or prefer being away from loud noises), the answer becomes yes. As an interesting example, a study of 400 patients with tension-type headache who were assessed for triggers, including sunlight and noise, suggested that photophobia and phonophobia were misinterpreted as triggers rather than symptoms (60).
Furthermore, research suggests that a headache meeting tension-type headache criteria but that is throbbing has different pathophysiology than a nonthrobbing tension-type headache. Interictal calcitonin gene related peptide (CGRP), a protein elevated in migraine, is only elevated in chronic tension-type headache with throbbing pain (06). In Goadsby's view, the fundamental difference between tension-type headache and migraine is that tension-type headache lacks features of sensory sensitivity of any description (ie, no sensitivity to light, sound, smell, or movement) and lacks the usual triggers associated of migraine, such as aggravation by menses, skipping meals, or changing sleep patterns (55). However, a case series of 95 women with menstruation-related headache reported 13 pure menstrual tension-type headache cases and 14 menstruation-related tension-type headache cases (116). It is helpful to remember that most disabling, episodic, primary headache is migraine, not episodic tension-type headache (78).
In addition to headache, there is a high prevalence of neck pain. One study showed the prevalence of neck pain in tension-type headache was 88.4% (07). The presence of neck pain has been associated with increased pericranial tenderness, particularly in those with chronic headache likely associated with sensitization (04). Neck pain is also associated with higher headache frequency (47). Coexistent neck pain is associated with greater pericranial tenderness in individuals as well possibly related to worsening sensitization. Interestingly, a cross-sectional study assessing tension-type headache and migraine compared to healthy controls found that both primary headache disorders had postural alterations and musculoskeletal dysfunction, but it is unknown whether these alterations are a consequence or a driver of disease (29).
There may also be cranial autonomic symptoms in tension-type headache despite these symptoms being more associated with trigeminal autonomic cephalgias and migraine (138). These symptoms can include conjunctival injection, lacrimation, ptosis, and rhinorrhea, among others. A cross-sectional study performed a post-hoc analysis on a survey of 3225 respondents, of which 166 met criteria for episodic tension-type headache. Interestingly, 51.8% reported at least one cranial autonomic symptom during a headache. These patients tended to have higher burden and more depression. Tension-type headache may have more than just cranial autonomic symptoms. A 2023 cross-sectional study looked at heart rate variability in tension-type headache as a measure of autonomic function in general (145). The authors found that although there was no difference in heart rate variability between those with versus without tension-type headache, extrapolations from this analysis did show higher mental distress in those with tension-type headache.
In a 2005 study of 146 patients with frequent episodic tension-type headache and 15 with chronic tension-type headache at baseline, 45% experienced infrequent or no tension-type headache, 39% had frequent episodic tension-type headache, and 16% experienced chronic tension-type headache at follow-up (86). Poor outcome was associated with baseline chronic tension-type headache, coexisting migraine, not being married, and sleeping problems (86; 09). Predictive factors for remission included older age and absence of chronic tension-type headache at baseline. Patients with frequent episodic tension-type headache may be at increased risk of developing chronic tension-type headache over a period of years (72).
In terms of association between migraine and tension-type headache, one population-based study determined the course of tension-type headache and migraine between 2008 and 2013 (100). Although nausea, throbbing pain, severe pain, and osmophobia were predictors of persistent migraine, no predictors of persistent tension-type headache were found. The authors also noted that migraine and tension-type headache do not have a liner bidirectional relationship of worsening from tension-type headache to migraine or vice versa, suggesting different pathophysiology.
Although tension-type headache does not cause the same level of disability as migraine, it is ranked as the second most common cause of chronic disease worldwide (09). Despite not causing the same degree of burden, it can lead to absenteeism and presenteeism at work, with one study showing 2.3 lost days of work per month with chronic tension-type headache leading to 8.9 days per month of lost work time (20). A study has proposed a theoretical model where disability from tension-type headache has a complex interaction with sleep, psychological factors, and duration of pain (76). Despite no prior history of mood disorders, chronic tension-type headache is closely associated with depression and anxiety (115). Network analysis supports that depression in particular is important to consider and manage to optimize treatment of tension-type headache (40). However, a systematic review and meta-analysis found that anxiety scores, but not depression scores, were higher in tension-type headache when compared to healthy controls (73).
A 34-year-old woman presented with a 10-year history of continuous bilateral headache. The pain was aching and felt like "a pressure bandage around her head." The pain was typically rated 5 out of 10, although it could vary from 3 to 6 of 10 during the day. The pain was never throbbing in nature. She denied associated nausea, vomiting, photophobia, phonophobia, osmophobia, aura symptoms, or cranial autonomic features. The headache did not awaken her at night. Acetaminophen helped somewhat, and she only used this medication once or twice a week. She was on no other medication. The headache was not worsened by exercise, coughing, sneezing, or alcohol. It was not orthostatic. Menses, missing a meal, or sleeping in on the weekends did not make the continuous pain worse. She did not smoke, drink alcohol, or use caffeine. There was no family history of headache. General and neurologic examinations were normal. MRI of the brain was normal. The patient was diagnosed with chronic tension-type headache and was placed on amitriptyline for headache prevention. Naproxen was found to be more useful than acetaminophen for the acute treatment of her headaches, and she limited it to 2 days per week. After being on amitriptyline at a dose of 75 mg at night for 3 months, her headaches became episodic, occurring two to three times per week.
The exact cause of tension-type headache is unknown. However, both peripheral and central pain mechanisms appear to play a role. Contrary to prior hypotheses, muscle contraction does not seem to play a role in tension-type headache. Neither resting muscle tension nor muscle tension during a headache has been found to be greater in tension-type headache than in migraine (65). However, pericranial muscles are harder and more tender in tension-type headache patients than in controls (71; 118). These changes could represent local pathology, but given that a nitric oxide synthase inhibitor (L-NMMA) significantly reduces headache pain intensity and muscle hardness in chronic tension-type headache, a central mechanism is probable for some aspects because nitric oxide synthase inhibitors reduce central sensitization (08; 05; 55). One study noted an associated between tension-type headache and hypertension with a possible connection through nitric oxide signaling (130). Ashina and colleagues have suggested that increased muscle hardness in patients with chronic tension-type headache may reflect sensitization of second order neurons due to prolonged nociceptive input from myofascial tissues (05). A retrospective cross-sectional study compared patients with tension-type headache (n=20) to healthy controls (n=20) and demonstrated smaller deep neck muscle stabilizers with a lower pain threshold in those with tension-type headache (96).
Studies of pressure pain thresholds in tension-type headache have found trigeminal and widespread body hyperalgesia, including over muscle and nerve trunks in women with tension-type headache compared to controls. This finding suggests that both peripheral and central mechanisms are involved in tension-type headache (104; 18). Additional work by researchers in Denmark revealed that the number of active myofascial trigger points increases with age, suggesting that hyperalgesia is a consequence of tension-type headache rather than a cause, thereby supporting the central origin of the pain (33). The presence of pressure pain hypersensitivity seems to be most related to chronic tension-type headache (41). There may also be gender differences, with one study showing lower pressure pain thresholds in women (25). Myofascial nociception may be more important in episodic tension-type headache, and central sensitization generated by prolonged nociceptive input from the periphery is likely crucial in the pathophysiology of chronic tension-type headache (146).
Using MRI and voxel-based morphology, Schmidt-Wilcke and colleagues investigated 20 patients with chronic tension-type headache, 20 patients with medication-overuse headache, and 40 controls with no headache history (123). Only patients with chronic tension-type headache demonstrated a significant gray matter decrease in regions known to be involved in pain processing, suggesting that the alterations are specific to chronic tension-type headache rather than representing a response to chronic head pain. Patients with a longer history of headache had less gray matter in these regions. The cause of the reduced gray matter is unclear, but it may be a consequence of central sensitization (123). In the HUNT-MRI study, which included migraine and tension-type headache, associations between headache, type frequency, and white changes on MRI were assessed showing a widespread increase in white matter mean diffusivity, fractional anisotropy and radial diffusivity compared to controls. Effect sizes were small and more significant in middle-age onset headache (67). These studies support a central mechanism for tension-type headache given white matter and gray matter changes. A 2024 study looked at resting state fMRI in patients with tension-type headache compared to healthy controls using the voxel-wise degree centrality method for local functional connectivity hubs; abnormalities were then used as seeds for functional connectivity analysis (154). Areas with degree centrality abnormalities included the left middle temporal gyrus, left anterior cingulate, and paracingulate gyri, whereas functional connectivity abnormalities were seen between the left anterior cingulate gyrus and the right cerebellum lobule IX, as well as with the left middle temporal gyrus. There was also abnormal functional connectivity between the left middle temporal gyrus and the right caudate as well as the left precuneus. A systematic review of MRI studies in tension-type headache noted evidence of increased white matter hyperintensities and involvement of brain regions associated with pain perception, but inconsistencies were found for abnormalities and volume (105). It was felt that studies support a central mechanism for tension-type headache and that some brain regions are potentially implicated, but neuroimaging studies for tension-type headache are still early.
Researchers from Brazil have conducted cross-sectional studies on individuals with tension-type headache, evaluating serum levels of various inflammatory mediators (35). From a sample of 48 adult subjects with tension-type headache and 48 age and gender matched healthy controls, these investigators discovered that the proinflammatory chemokine interleukin-8 (IL-8) is increased in those with tension-type headache. Furthermore, monocyte chemoattractant protein (MCP-1) levels were increased in subjects who were actively experiencing a headache at the time of evaluation. Using the same cross-sectional population, these researchers also found that adiponectin, an anti-inflammatory protein, is reduced in individuals with tension-type headache, which is consistent with findings seen in other proinflammatory conditions such as metabolic syndrome and insulin resistance (36). A systematic review and meta-analysis found elevated transforming growth factor beta (TGF-beta) and tumor necrosis factor alpha (TNF-alpha) in patients with tension-type headache when compared to healthy controls (97). These findings support the idea that proinflammatory mechanisms may be involved in the pathophysiology of tension-type headache.
Patients with tension-type headache have been compared to the general population in terms of pain response. One study looking at the pain modulation profile for patients found it to be heterogeneous, suggesting variability in the underlying pathophysiology with possible autonomic contributions (38). Compared with the general population, first-degree relatives of chronic tension-type headache sufferers had a 3.1-fold increased risk of chronic tension-type headache, suggesting a genetic predisposition to chronic tension-type headache (117).
Overall, the pathophysiology of tension-type headache has been more simply summarized into three major categories: genetics, myofascial, and central sensitization (09). The myofascial mechanisms may produce muscle changes like tenderness and hardness with development of peripheral sensitization. The central sensitization is associated with dysfunction of descending pain pathways.
The Global Burden of Disease (GBD) study identified that the prevalence of tension-type headache in the study (1990-2019) was 1.55 billion world-wide, making it one of the most prevalent disorders (50). The incidence in 2019 was 528.8 million (50). In a telephone-based population sample in the United States, the 1-year prevalence of episodic tension-type headache was 38% (126). Chronic tension-type headache is seen in about 2% of the population (122). The prevalence of tension-type headache peaks between the ages of 30 and 39 years and then declines with age (113). However, according to the Global Burden of Disease study, tension-type headache has increased in prevalence by 37% since 1990 in the pediatric population (75). In a pediatric prevalence study (n=5944) conducted in Istanbul, the prevalence of tension-type headache was 26.1% (66). Another pediatric study (n=2958) performed in Iran diagnosed tension-type headache in 32.1% of students aged 6 to 18 years (142). A study of adults in Japan looked at the prevalence of primary headache disorders in nurses (n=229) and found that 14.4% had tension-type headache (127). Tension-type headache is more prevalent in females than in males, with a female to male ratio of 5:4 (82). One study looking at gender differences hypothesized that men have a greater association with sleep quality and depression whereas women have a greater association with nociception and stress, but further studies are needed (45).
Although migraine is generally identified as the more disabling condition, tension-type headache is still ranked as number 12 by the GBD study in 2015 (1990-2015) for neurologic disorders in terms of years of life lived with a disability (YLDs), which is based primarily on disability-adjusted life years (49). In the 2016 study, tension-type headache caused 7.2 million years of life lived with a disability (48). For comparison, migraine caused 45.1 million years of life lived with a disability. The findings were more significant in those aged 15 to 49 years. Likely contributing to disability is that headache disorders are underdiagnosed and managed. A study conducted in China of patients with headache (n=2868) diagnosed 23.3% with tension-type headache, but only 8.1% had received a previous correct diagnosis and only 4.7% had received prior treatment (81).
Possible risk factors for episodic tension-type headache include education level, fatigue, younger age, females, inability to relax after work, poor sleep, and poor self-assessment of general health (09).
Limiting acute medication use to two days per week or less could help prevent episodic tension-type headache from becoming medication-overuse headache and chronic tension-type headache. Risk for progression to chronic tension-type headache has also been associated with higher headache frequency, females, migraine history, and depression (09).
As general recommendations, headache patients should exercise regularly, eat a healthy diet, and employ good sleep hygiene. Patients with frequent headaches should avoid alcohol, nicotine, and caffeine. However, at least one systematic review has found no association between alcohol use and tension-type headache (14). Habitual snoring has been identified as a risk factor for chronic daily headache, and if this association proves causal, sleep-disordered breathing may provide a target for therapeutic interventions for chronic daily headache (121).
The main differential diagnosis for episodic tension-type headache is episodic migraine. The author requires a headache with no migrainous features before diagnosing episodic tension-type headache. Most severe, disabling, episodic, primary headache is episodic migraine (78). Stress is a trigger for both migraine and tension-type headache with equal frequency; therefore, it has no diagnostic utility when reported by patients (120).
The phenotype of chronic tension-type headache can occur with or without medication overuse, and the combination should always be considered to optimize treatment. Simply decreasing the frequency of acute medication use to no more than two days per week can sometimes decrease the frequency of tension-type headache (134).
Chronic tension-type headache is one of the four categories of chronic daily headache. The main four types of chronic daily headache are:
(A) Chronic migraine
(B) Chronic tension-type headache
(C) New daily persistent headache
(D) Hemicrania continua
All four of these can coexist with medication overuse headache (134). As described above, chronic tension-type headache can be confused with chronic migraine. New daily persistent headache typically starts abruptly on one specific day and then continues in a daily fashion thereafter, whereas chronic tension-type headache typically evolves from episodic tension-type headache (124). Hemicrania continua is a continuous unilateral headache punctuated by periodic exacerbations associated with ipsilateral cranial autonomic features (134). It is completely responsive to indomethacin.
Due to the nonspecific clinical features of tension-type headache, virtually any structural or metabolic disease may cause a phenotypic tension-type headache (135). Examples of etiologies that can cause phenotypic tension-type headache include intracranial mass lesions, idiopathic intracranial hypertension, carbon monoxide poisoning, low CSF volume (intracranial hypotension), sleep apnea, and giant cell arteritis (103; 91; 135; 133).
The pain of temporomandibular joint disease can radiate to the temple and be misinterpreted as tension-type headache, but to diagnose temporomandibular joint disorder there should be features like clicking on examination. Temporomandibular joint disorder causing tension-type headache is probably over-diagnosed (135). The concurrence of tension-type headache and temporomandibular joint disorder could be due to chance because both are extremely prevalent. One study found that the prevalence of temporomandibular joint disorder did not differ between migraine, tension-type headache, and headache-free individuals (61). In a systematic review, using treatments like oral splint, which is typically used for temporomandibular disorders, has not shown benefit for tension-type headache (88).
Disease of the cervical spine can cause pain that radiates to the head, but neck movement is the main trigger. This diagnosis can be reviewed in the ICHD-3 under cervicogenic headache (57). The associated pain is typically unilateral (135). Neck pain is common in tension-type headache and migraine; however, the appendix of the ICHD-3 is testing a new diagnostic category of headache attributed to cervical myofascial pain, which may add an additional diagnosis to consider in primary headaches with associated neck pain (57).
Tension-type headache has also been associated with sleep disturbances including insomnia, excessive daytime sleepiness, and shift working, occurring at a higher frequency than controls, particularly for chronic tension-type headache (24). According to a population-based study from Taiwan, patients with obstructive sleep apnea also had a greater likelihood of developing tension-type headache (hazard ratio, 1.18, 95% CI 1.06-1.31, p = 0.003) (22). Screening for sleep apnea is recommended.
Depression and anxiety coexist with chronic tension-type headache but may be a result and not a cause of chronic pain (133; 53). A population-based study based on lifetime data gathered at baseline showed that severe nonmigrainous headache was a risk factor for depression (17). A 2-year prospective study of the same patients after initial enrollment determined that nonmigrainous headache could not be securely ruled out as a risk factor for depression (16). Depression, anxiety, and chronic headache may be comorbid conditions with a common pathogenesis and pathophysiology (133). Chronic tension-type headache and fibromyalgia are frequently comorbid (42). Furthermore, stress may increase pain perception in primary headache disorders (149).
During the COVID-19 pandemic, many patients have presented with headache as part of the infection including a change in headache pattern or new-onset headache. Different phenotypes were seen including a presentation similar to tension-type headache (107). One study of 580 patients found that 54% of patients otherwise met criteria for tension-type headache (83). The headache presentation was often independent of fever and seem to occur on day 3 of symptoms (108). Patients in this study were healthcare workers of which 17.9% had a history of migraine and 7.1% had a history of tension-type headache.
A thorough history and neurologic examination including fundoscopy is the main workup required to diagnose tension-type headache. Red flags in the history or abnormalities on examination should prompt further investigation (131). A good approach to identify red flags was described by Dodick as seen in Table 8 (34).
Systemic symptoms or Systemic illness (ie, new headache in patients with immunosuppression, malignancy, pregnancy) |
Neurologic signs on examination (ie, neurologic deficits including papilledema) |
Onset: thunderclap (peak 10/10 severity at onset or within 1 minute of onset from 0/10) |
Older age of first onset: headache begins after age 40 years (important to consider giant cell arteritis particularly over the age of 50 years) |
Previous headache: change in pattern (ie, increased intensity of pain, increased frequency of attacks, development of new features, or decreased response to treatment) |
Positional (worse supine in idiopathic intracranial hypertension and worse upright in intracranial hypotension) |
Progressive (headache is subacute and progressive in nature) |
Precipitated by Valsalva |
In the appropriate population, sedimentation rate and c-reactive protein can help to rule out giant cell arteritis. MRI should be done if any red flags are present, as any structural or metabolic cause of headache can present as phenotypic tension-type headache. Even in the presence of neck pain, MRI or CT of the cervical spine is generally not required unless the neurologic exam is abnormal, though this option should be considered on an individual basis if there are specific concerns. For instance, one pediatric study found that the rate of incidental unrelated findings on MRI brain in tension-type headache was 12.7%; only one significant finding (brain tumor) was reported, and that child had papilledema (143).
Acute treatment. First-line acute treatments for tension-type headache are aspirin or acetaminophen, with second-line treatments being NSAIDs and caffeine combinations (11; 09). Paracetamol 1000 mg by mouth has been shown to be beneficial for episodic tension-type headache in a Cochrane review (137). Aspirin 500 to 1000 mg by mouth had low quality evidence for frequent tension-type headache in a Cochrane review (30). Ibuprofen 400 mg by mouth has also been shown in a Cochrane review to be beneficial for frequent episodic tension-type headache (31). Ketoprofen 25 mg by mouth has been shown in a Cochrane review to be beneficial for frequent episodic tension-type headache (148). A 2024 network meta-analysis of simple analgesia found that simple analgesia is more effective than placebo, with ibuprofen and diclofenac-K being the best options (153). Although NSAIDs are generally recommended, the combination of metoclopramide and diphenhydramine was superior to parenteral ketorolac in a 2014 systematic review (150). In a systematic review, mepivacaine, meperidine given with promethazine, and subcutaneous sumatriptan were not superior to placebo (150). A systematic review of parenteral acute treatment options found that metamizole, chlorpromazine, and metoclopramide were each superior to placebo; however, caution should be taken due to adverse effects (150). In general opioids are not recommended and treatments have not been found to be efficacious (09). A randomized control trial through an emergency department compared intravenous lidocaine and intravenous dexketoprofen to significantly greater pain severity reduction from intravenous lidocaine (02). See Table 5 for an approach to acute treatment of tension-type headache based on level A recommendations from the European Federation of Neurological disorders (09).
The goal of acute headache treatment is pain freedom at two hours (137; 148; 30).
Acute medications should be limited to two days per week to prevent medication overuse headache (135; 27; 133; 11).
First-line acute treatment |
- Aspirin |
Second-line acute treatment |
- NSAIDs* |
** Caffeine combined with any of aspirin, ibuprofen, or acetaminophen. |
Preventive treatment. The current recommendation is to try nonpharmacologic management for tension-type headache prior to initiating pharmacologic treatment. These nonpharmacologic treatments include cognitive behavioral therapy, biofeedback, relaxation, physical therapy, occupational therapy, and optimization of sleep hygiene (09). These nonpharmacologic treatment can also be combined with preventive medications and with one another.
Preventive medication should be used for chronic tension-type headache when attacks occur more than two days a week, and they can help prevent medication overuse (133). The first, second, and third-line treatments are amitriptyline, mirtazapine, and venlafaxine, respectively (11; 09).
Amitriptyline has the best evidence for prevention of tension-type headache and is considered first-line with a number needed to treat (NNT) of 12 and number needed to harm (NNH) of 2 to 3 (09). One amitriptyline regimen is to start 10 or 25 mg at night and then increase by 10 or 25 mg every week until the patient is on 1 mg/kg at night. The average dose of amitriptyline is 50 to 75 mg per day (46). There is also low to moderate level of evidence of the use of mirtazapine and venlafaxine for preventive treatment of tension-type headache (09). Mirtazapine at 15 to 30 mg daily was effective in a placebo-controlled trial for chronic tension-type headache (12). Venlafaxine XR 150 mg daily was beneficial in one randomized control trial for tension-type headache (155), but a Cochrane review of SSRIs and SNRIs in tension-type headache found that venlafaxine was no better than amitriptyline or placebo and was less effective than amitriptyline in reducing the use of acute analgesics. A Cochrane review did not support its use (10). SSRIs have not been shown to be beneficial for tension-type headache (54; 144; 10). See Table 6 for preventive treatment recommendations.
Other medications that have been studied include tizanidine alone or in combination with amitriptyline (119; 13), gabapentin (136), and topiramate (70). Botulinum toxin has not been shown to be helpful for chronic tension-type headache due to low quality evidence in systematic review, but the authors felt the evidence was not sufficient to refute its use (44). A systematic review and meta-analysis of 11 trials found that onabotulinumtoxinA was associated with improvements in headache severity, frequency, duration, and acute medication use, with an NNT of 8 for chronic tension-type headache, but more high-quality and adequately powered studies are needed (32). This treatment is not FDA-approved for tension-type headache due to lack of clear benefit (37; 102; 125; 132). There is also a retrospective observational study that found targeted trigger point injections using isotonic saline in chronic tension-type headache reduced headache intensity and increased quality of life (23).
The goal of a headache prophylaxis is to decrease the headache frequency by at least 50%. Preventive medication should be started at a low dose and increased slowly until therapeutic effects develop, side effects develop, or the ceiling dose is reached. They should be continued for approximately 2 to 3 months at maximal tolerated doses before determining utility (133). It is recommended that after six months of pharmacologic treatment with a response rate of at least 50% in headache frequency, treatment be suspended (09). If no worsening of tension-type headache, then continue off treatment. If return of tension-type headache, then the medication may need to be restarted.
First-line |
Amitriptyline |
Second-line |
Mirtazapine |
Third-line |
Venlafaxine |
Nonpharmacologic treatments. Nonpharmacologic approaches to treatment include regular exercise, good sleep hygiene, and healthy eating (124). Symptoms of depression and poor sleep have been shown to contribute to the worsening of tension-type headache (104; 101). Systematic review supported psychological sleep interventions for improvement of headache frequency and for sleep, but evidence was conflicting for headache intensity (139).
A randomized controlled trial in a low-income community in Brazil looking at exercise, relaxation, or both showed that relaxation and relaxation, exercise, but not exercise alone, was beneficial in primary headache disorders (43). A randomized controlled trial comparing a 12-week strength training program (n=20) to a control group (n=20) found a significant improvement in headache duration and intensity in addition to reduced deep neck muscle hypertrophy, decreased sensitization, and improved deep cervical flexor strength (89). Pilates may be beneficial based on a small case series with nine subjects (74).
Psychological treatment can be beneficial for some patients (124) and is cautiously recommended over other complementary and alternative medicines in a 2024 systematic review and network meta-analysis (110). A 2008 meta-analysis concluded that biofeedback is an evidence-based treatment option for tension-type headache (98). One systematic review found limited evidence that cognitive behavioral therapy was more effective than no treatment for chronic tension-type headache (15). A 2024 randomized controlled study looked at intensive short-term dynamic psychotherapy for tension-type headache, with both improved emotional regulation as well as a reduction in symptoms (128). These techniques can be used alone or in combination with a preventive medication like amitriptyline (58).
There is evidence of benefit for physical therapy. Systematic review and meta-analysis demonstrated that physiotherapy combined with exercise and transcutaneous electrical stimulation was effective for headache severity and frequency (63). However, a systematic review notes that there is no standardized protocol despite all protocols targeting the cranio-cervical-mandibular region with evidence of improved headache intensity and frequency (114). A systematic review and meta-analysis of “hands-off therapies,” including relaxation, aerobic training, and pain education, found a paucity of studies but did see a significant signal of benefit (95).
One systematic review found that manual therapy was beneficial for headache disability in tension-type headache and migraine, but inconsistent for cervicogenic headache (39). Systematic review of six randomized controlled trials for suboccipital soft-tissue inhibition technique (SIT) + occiput-atlas-axis global manipulation (OAA) versus SIT found the combination to be most effective (62); however, a comparison to sham treatment was not a focus of this study. A trial did not see benefit for pain, but there was benefit for disability (106). Another randomized controlled trial of 45 patients found that manipulation outperformed myofascial release for headache frequency and severity (26). A systematic review from 2000 to 2013 looked at 14 trials and felt that studies were too heterogeneous for sufficient study but did note that some benefit appeared likely though more studies using standardized measures are needed (84). In one systematic review and meta-analysis, Kamonseki and colleagues felt more studies were needed but did find superiority compared to no treatment for pain severity and frequency (64). It is also important to consider that neurologists often cite concern for dissection with cervical manipulation with many case reports and case series available in the literature though the actual risk is not known (99).
A 2024 systematic review with network meta-analysis looked at traditional Chinese medicines for tension-type headache (129). The authors found that the combination of Shugan Jieyu capsules with Western medicine improved clinician efficiency, whereas Tangxue Qingnao with Western medicine was effective for reducing headache duration. Another systematic review looked at miniscalpel-needle treatment, another type of Chinese medicine, with study quality being low (69). A 2024 systematic review with meta-analysis found that the combination of Chinese medicine with acupuncture might reduce headache frequency (110).
A Cochrane review found a small but statistically significant benefit of acupuncture over sham, and the authors concluded that acupuncture could be a valuable nonpharmacological tool in patients with tension-type headache (77). A second systematic review of nine randomized controlled studies supported the use of dry needling (147). A systematic review and meta-analysis of dry needling with 11 randomized controlled studies, including four high-quality studies, showed similar short-term benefit when compared to other modalities for pain relief but had better short-term improvement in headache related disability (109). A systematic review and meta-analysis found that acupuncture is effective with mild side effects, but high-quality studies are needed (59). Another systematic review and meta-analysis looked at seven studies with 3221 participants demonstrating durable post-treatment effects for up to 6 months but no superiority over physical training or relaxation training (21). In a meta-analysis comparing acupuncture and tricyclic antidepressants like amitriptyline, there was a similar reduction in tension-type headache frequency and intensity, but less adverse events with acupuncture (140). A randomized controlled trial for chronic tension-type headache found that predictors of acupuncture response included higher headache intensity, low general health scores, and high social functioning scores (19).
A randomized controlled trial looking at massage focused on myofascial trigger points did show benefit for headache frequency in tension-type headache (94). A different randomized controlled trial used dry needling for myofascial trigger points, leading to a reduction in active triggers points and in short-term headache intensity (92). Another randomized placebo-controlled trial suggested that massage with single or multiple myofascial trigger point release increased pressure point thresholds in tension-type headache (93). A 2024 systematic review and meta-analysis found that myofascial release can reduce pain and disability in tension-type headache and cervicogenic headache, though results were inconsistent for migraine (85). A systematic review and meta-analysis of five randomized controlled trials was supportive of yoga in patients with tension-type headache but not migraine (03).
Trigger avoidance is also used by some patients and clinicians. These are often patient reported, and studies are limited (09).
One randomized controlled study (n=20) found benefit from low-frequency repetitive transcranial magnetic stimulation versus sham after 2 weeks in patients with chronic tension-type headache (111). There was a significant reduction in pain severity, headache impact, and muscle activation.
Headache diagnosis may be less clear in the pediatric population. One retrospective chart review study of 989 children aged 6 to 18 found migraine and tension-type headache to be equally prevalent with no clear diagnosis in 41.5% (51). Although patients with migraine required more analgesia, more emotional difficulties were reported in the tension-type headache group. Pharmacologic treatment in the pediatric population does have some support for acetaminophen and amitriptyline; however, the evidence for nonpharmacologic treatment is stronger (09).
In the elderly population, it is recommended that nonpharmacologic management be used as first-line treatment (09). If pharmacologic agents are needed, then acetaminophen as needed and amitriptyline nighty would be first-line. It is worth noting that a 2006 retrospective, population-based cohort study did show that tension-type headache is a risk factor for dementia (151).
Retrospectively, tension-type headache is unchanged by pregnancy in 67% of patients and improved in 33% (87). Previously, the recommendations for acute medications used for tension-type headache in pregnancy be limited to acetaminophen or narcotics (87); however, it should be noted that opioids can increase the risk of chronification due to medication overuse headache. NSAIDs and caffeine are not recommended (09). No preventive medication is typically recommended during pregnancy as most options are category C or worse; however, if pharmacologic agent is needed then amitriptyline would be first-line (09). The focus in treating tension-type headache during pregnancy should be on nonpharmacologic treatment and on ensuring if headache is new or changed that secondary causes are considered.
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Jennifer Robblee MD MSc FRCPC
Dr. Robblee of Barrow Neurological Institute received research support from Eli Lilly, AbbVie, and Barrow Neurological Foundation as principal investigator, speaker fees from Impel Pharmaceuticals, and served on advisory boards for AbbVie and Tonix.
See ProfileStephen D Silberstein MD
Dr. Silberstein, Director of the Jefferson Headache Center at Thomas Jefferson University has no relevant financial relationships to disclose.
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