Clinical manifestations

Presentation and course

Tension-type headache is bland and is characterized as head pain devoid of migrainous characteristics (106). Evidence suggests that there are two types of tension-type headache (76). 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 (132). 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 (58).

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 (53). 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 (110). It is helpful to remember that most disabling, episodic, primary headache is migraine, not episodic tension-type headache (76).

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 (45). Coexistent neck pain is associated with greater pericranial tenderness in individuals as well possibly related to worsening sensitization.

Prognosis and complications

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 (83). Poor outcome was associated with baseline chronic tension-type headache, coexisting migraine, not being married, and sleeping problems (83; 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 (70).

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 (96). 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 (19). 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 (74). Despite no prior history of mood disorders, chronic tension-type headache is closely associated with depression and anxiety (109). Network analysis supports that depression in particular is important to consider and manage to optimize treatment of tension-type headache (38). 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 (71).

Clinical vignette

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 two 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.

Biological basis

Etiology and pathogenesis

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 (63). However, pericranial muscles are harder and more tender in tension-type headache patients than in controls (69; 112). 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; 53). One study noted an associated between tension-type headache and hypertension with a possible connection through nitric oxide signaling (123). 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 (92).

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 (100; 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 (30). The presence of pressure pain hypersensitivity seems to be most related to chronic tension-type headache (39). There may also be gender differences, with one study showing lower pressure pain thresholds in women (23). 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 (136).

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 (118). 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 (118). 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 (65). These studies support a central mechanism for tension-type headache given white matter and gray matter changes.

Researchers from Brazil have conducted cross-sectional studies on individuals with tension-type headache, evaluating serum levels of various inflammatory mediators (32). 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 (33). 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 (93). 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 (35). 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 (111).

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.

Epidemiology

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 (48). The incidence in 2019 was 528.8 million (48). In a telephone-based population sample in the United States, the 1-year prevalence of episodic tension-type headache was 38% (121). Chronic tension-type headache is seen in about 2% of the population (116). The prevalence of tension-type headache peaks between the ages of 30 and 39 years and then declines with age (107). However, according to the Global Burden of Disease study, tension-type headache has increased in prevalence by 37% since 1990 in the pediatric population (73). In a pediatric prevalence study (n=5944) conducted in Istanbul, the prevalence of tension-type headache was 26.1% (64). Another pediatric study (n=2958) performed in Iran diagnosed tension-type headache in 32.1% of students aged 6 to 18 years (133). 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 (122). Tension-type headache is more prevalent in females than in males, with a female to male ratio of 5:4 (80). 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 (43).

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 (47). In the 2016 study, tension-type headache caused 7.2 million years of life lived with a disability (46). 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 (79).

Prevention

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 (115).

Differential diagnosis

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 (76). Stress is a trigger for both migraine and tension-type headache with equal frequency; therefore, it has no diagnostic utility when reported by patients (114).

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 (127).

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 (127). 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 (119). Hemicrania continua is a continuous unilateral headache punctuated by periodic exacerbations associated with ipsilateral cranial autonomic features (127). 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 (128). 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 (99; 88; 128; 126).

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 (128). 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 (59). In a systematic review, using treatments like oral splint, which is typically used for temporomandibular disorders, has not shown benefit for tension-type headache (85).

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 (55). The associated pain is typically unilateral (128). 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 (55).

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 (22). 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) (20). 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 (126; 51). 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 (126). Chronic tension-type headache and fibromyalgia are frequently comorbid (40). Furthermore, stress may increase pain perception in primary headache disorders (139).

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 (102). One study of 580 patients found that 54% of patients otherwise met criteria for tension-type headache (81). The headache presentation was often independent of fever and seem to occur on day 3 of symptoms (103). 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.

Diagnostic workup

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 (124). A good approach to identify red flags was described by Dodick as seen in Table 8 (31).

Table 4. “SNOOP4”: Red Flags for Secondary Headache

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 (134).

Management

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 (130). Aspirin 500 to 1000 mg by mouth had low quality evidence for frequent tension-type headache in a Cochrane review (27). Ibuprofen 400 mg by mouth has also been shown in a Cochrane review to be beneficial for frequent episodic tension-type headache (28). Ketoprofen 25 mg by mouth has been shown in a Cochrane review to be beneficial for frequent episodic tension-type headache (138). Although NSAIDs are generally recommended, the combination of metoclopramide and diphenhydramine was superior to parenteral ketorolac in systematic review (140). In a systematic review, mepivacaine, meperidine given with promethazine, and subcutaneous sumatriptan were not superior to placebo (140). 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 (140). 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 (130; 138; 27).

Acute medications should be limited to two days per week to prevent medication overuse headache (128; 25; 126; 11).

Table 5. Acute Headache Treatment for Tension-Type Headache

First-line acute treatment	- Aspirin - Acetaminophen
Second-line acute treatment	- NSAIDs* - Caffeine combinations**
* NSAIDs with the highest level of evidence are ibuprofen and ketoprofen, but there is some evidence for naproxen and diclofenac. ** 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. (See below section for further discussion.)

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 (126). 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 (44). 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 (144), 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 (52; 135; 10). See Table 6 for preventive treatment recommendations.

Other medications that have been studied include tizanidine alone or in combination with amitriptyline (113; 13), gabapentin (Spira and Beran 2003), and topiramate (68). 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 (42). 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 (29). This treatment is not FDA-approved for tension-type headache due to lack of clear benefit (34; 98; 120; 125). 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 (21).

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 (126). 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.

Table 6. Prevention Headache Treatment for Tension-Type Headache

First-line	Amitriptyline
Second-line	Mirtazapine
Third-line	Venlafaxine

Nonpharmacologic treatments. Nonpharmacologic approaches to treatment include regular exercise, good sleep hygiene, and healthy eating (119). Symptoms of depression and poor sleep have been shown to contribute to the worsening of tension-type headache (100; 97). Systematic review supported psychological sleep interventions for improvement of headache frequency and for sleep, but evidence was conflicting for headache intensity (131).

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 (41). 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 (86). Pilates may be beneficial based on a small case series with nine subjects (72).

Psychological treatment can be beneficial for some patients (119). A 2008 meta-analysis concluded that biofeedback is an evidence-based treatment option for tension-type headache (94). One systematic review found limited evidence that cognitive behavioral therapy was more effective than no treatment for chronic tension-type headache (15). These techniques can be used alone or in combination with a preventive medication like amitriptyline (56). 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 (91).

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 (61). 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 (108).

One systematic review found that manual therapy was beneficial for headache disability in tension-type headache and migraine, but inconsistent for cervicogenic headache (36). 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 (60); 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 (101). Another randomized controlled trial of 45 patients found that manipulation outperformed myofascial release for headache frequency and severity (24). 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 (82). 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 (62). 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 (95).

A Cochrane review found 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 (75). A second systematic review of nine randomized controlled studies supported the use of dry needling (137). 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 (104). One pilot randomized controlled study found that adding acupuncture to standard medical care was significantly beneficial at 3 and 6 months (117). A randomized controlled trial with 218 patients comparing true acupuncture to a placebo group with superficial acupuncture found that headache frequency was decreased over 32 weeks in chronic tension-type headache (143). A systematic review and meta-analysis found that acupuncture is effective with mild side effects, but high-quality studies are needed (57).

At least one randomized controlled trial looking at massage focused on myofascial trigger points did show benefit for headache frequency in tension-type headache (90). Another randomized placebo-controlled trial suggested that massage with single or multiple myofascial trigger point release increased pressure point thresholds in tension-type headache (89). There is systematic review and meta-analysis on the use of a type of Chinese medicine in 1228 patients, showing benefits over medications with tolerable adverse effects; however, Fan and colleagues warned to interpret with caution due to low quality of studies (37). Another systematic review looked at miniscalpel-needle treatment, another type of Chinese medicine, with study quality being low (67). 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 (105). There was a significant reduction in pain severity, headache impact, and muscle activation.

Special considerations

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% (49). 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 (141).

Pregnancy

Retrospectively, tension-type headache is unchanged by pregnancy in 67% of patients and improved in 33% (84). Previously, the recommendations for acute medications used for tension-type headache in pregnancy be limited to acetaminophen or narcotics (84); 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.