Muscle Contraction Tension Headache

Etiology

The exact cause of TTH is not fully understood. However, various factors are linked to this condition, including nutritional, muscular, environmental, and genetic conditions. The literature reports that TTH causes greater disability and accounts for more missed work days than migraine with multiple etiologies, specifically genetic and environmental causes.[5]

Numerous correlational studies implicate vitamin deficiencies as factors in the development of TTH. A possible vitamin B12 correlation has been studied in Turkish children, with nearly a quarter of the 75 children ages 11 to 15 in the control group having headaches and serum vitamin B12 levels less than 200 pg/ml. Some participants had what researchers defined as "severe vitamin B12 deficiency," with a vitamin B12 level below 160. Upon vitamin supplementation, all 18 of these children stopped having headaches.[6]

Data also shows that vitamin D deficiency correlates with TTH. A case-control study that included 100 patients with chronic TTH and 100 healthy controls found that nearly 70% of the patients with chronic TTH had vitamin D deficiency. In contrast, only a quarter of the participants in the control group had vitamin D deficiency.[7] However, a recent study suggests that the association between TTH and vitamin D is more likely a secondary byproduct of the simultaneous relationship of other comorbid conditions with both TTH and low serum vitamin D. Evidenced-based indications for vitamin D supplementation in TTH are currently lacking.[8]

Environmental and muscular influences may also cause tension headaches, with stress and poor posture appearing to be the most significant.[9] The exact mechanism by which these conditions cause TTH is not entirely understood. However, poor posture, such as when the neck is excessively flexed while playing video games or watching the computer screen, leads to more stress placed on the atlantoaxial joint and upper cervical vertebrae. The shoulders attempt to compensate by stooping forward to reduce the stress that leads to muscular imbalances, with some areas tightening to create a tension headache. 

Recent studies noted that, besides stress, the factor that most commonly triggered TTH was disturbed sleep.[10] Chronic TTH is the most common headache type due to sleep apnea and other sleep-related breathing disorders. Psychiatric disorders are comorbid with both TTH and insomnia and may further complicate diagnosis and treatment. Empirical evidence supports a bidirectional relationship between TTH and sleep. Sleep dysregulation triggers episodic TTH, and sleep disorders can lead to complications and exacerbation of headaches. Most patients with chronic TTH were found to have insomnia. Longitudinal data and observational studies suggest that sleep disturbance and insomnia are risk factors for new-onset TTH, with the former leading to progression from episodic to chronic TTH (ie, headache "chronification").[11]

Epidemiology

TTH is the most common type of primary headache disorder and one of the most prevalent conditions and neurologic disorders in the general population, according to the Global Burden of Disease (GBD) study.[12] TTH affects about 1/5 of the world's population, with a worldwide lifetime prevalence of 46% to 78%. The condition also has a high economic and psychosocial impact.[13][14]

Although TTH had an increased prevalence in the Middle East and North Africa from 1990 to 2019, the incidence rate has remained the same. Furthermore, the burden of TTH in these regions was higher than at the global level for both sexes and all age groups.[15]

A Danish epidemiological study revealed that about 78% of the adult population had at least 1 episode of TTH in their lives. TTH is also more common in women than in men, with a female-to-male ratio of 3:1.[16][17] Recent studies found that TTH was more prevalent among adult Western women and Saudi female university students. The results of these investigations demonstrated a high prevalence of headaches and an association between headaches and depression.[18] Another study reported a strong relationship between trapezius muscle tenderness and headache intensity, as well as days with a headache, among female office workers. However, no correlation was observed between trapezius muscle tenderness and headache duration or analgesic use.[19]

Current reviews examine the impact of sex-based biological, psychological, emotional, and social differences on TTH. The results showed complex interactions between TTH, emotional stress, and sleep, with these interactions differing between men and women. The authors hypothesized that treatment for men with TTH should prioritize improving sleep quality and addressing depression, while treatment for women should focus on nociceptive mechanisms and emotional or stress-related factors.[20]

TTH is also the most common headache type in children. A study linked anxiety in children and adolescents with TTH and recommended screening and evaluation of their psychological symptoms.[21] The average age of patients with TTH is between 25 and 30 years. Although exact incidence rates are difficult to determine, a Danish study reported an incidence of 14.2 per 1,000 person-years for frequent episodic TTH.[22]

A recent report described the rising incidence, prevalence, and disability associated with TTH among adolescents and young adults, particularly in male individuals, older youth, and populations with middle sociodemographic indices. This trend was most notable in East Asia, the Middle East, North Africa, and certain high-income countries, including Singapore, Norway, and Iran. However, a decline in prevalence was observed in countries like Qatar, Thailand, and Ethiopia.[23]

Pathophysiology

Multiple theories have been proposed for the presumed pathophysiology of TTH, but the exact mechanism is unknown. Both central and peripheral sensitization processes were observed to be clearly involved. Patients with episodic TTH demonstrate higher levels of peripheral excitability, while individuals with chronic TTH clearly show manifestations of central sensitization.[24][25][26]

Functional magnetic resonance imaging (fMRI) studies investigated the pathophysiology of TTH, focusing on central mechanisms. The findings consistently showed a significant increase in white matter hyperintensity in patients with TTH and identified the potential involvement of various brain areas related to pain perception. These areas included cortical regions (anterior and posterior cingulate cortex, prefrontal cortex, and anterior and posterior insular cortex), subcortical sites (thalamus, caudate, putamen, and parahippocampus), and the cerebellum. However, no significant association was found between TTH and intracranial abnormalities or total intracranial volume.[27]

Some reviews on the peripheral origins of TTH discussed initial events occurring outside the brain barrier, suggesting that vascular and musculoskeletal factors play a role at the onset of a tension headache attack. These factors may contribute to the sensitization of the peripheral nervous system due to sustained sensory input.

Another study found that TTH showed less activation at the start of sternocleidomastoid muscle contraction. No association was noted between the presence of a headache and alterations in longus colli muscle dimensions, median frequency, or sternocleidomastoid muscle activation toward the end of contraction.

Myofascial trigger points (MTrPs) have been implicated in the possible pathogenesis of TTH and are considered vital treatment components.[28] Trigger points are specific areas, usually located in skeletal muscles. Pressure on these sites may elicit pain in the area and related regions of the body. For TTH, the pericranial musculature is the presumed trigger point. Excessive pericranial muscle contractions may lead to ischemia and the release of noxious substances, such as substance P, which may cause further pain. Over time, these trigger points may become latent, radiating pain only with palpation, or active, causing constant pain.[29] Osteopathic studies suggest that tightening of the suboccipital and upper neck musculature can lead to a "pull" of the dural matter, forming the myodural bridges, which can be very painful.[30]

Another hypothesis is that autonomic dysfunction may play a role in the pathophysiology of TTH, particularly due to sleep disturbances. Sleep loss can increase fatigue, leading to greater sympathetic overdrive, which may subsequently worsen or trigger a headache. Growing evidence links TTH with sleep disturbances, including insomnia, poor sleep quality, excessive daytime sleepiness, insufficient sleep, and shift work. Clinical manifestations of TTH are more pronounced in patients with sleep disturbances than in those without.

A stronger correlation has also been reported between TTH and sleep disturbances in individuals with chronic TTH than in those with episodic TTH. Increasing evidence highlights the association of TTH with psychiatric comorbidity, which is also closely linked to sleep disturbances.[31] The present study also suggested that autonomic dysfunction is associated with TTH due to mental distress, as well as the influence of age and gender.[32]

TTH may also occur due to dysfunction within the brain's cortical matter, particularly the trigeminovascular system.[33] The trigeminal nucleus caudalis contains the nociceptive pathways of the face, which transmit pain signals to the ventral posteromedial thalamus. The nociceptive pathways within the trigeminal nucleus caudalis become inhibited when stimulated by the molecule orexin. Researchers postulate that the release of orexin decreases with inconsistent sleep. The resulting disinhibition of the trigeminal nucleus caudalis is thought to produce headaches.[34]

Mechanisms mediated by nitric oxide (NO) may also play a role in chronic TTH, as treatments have shown that inhibiting NO is effective in managing the condition. This subject is under further investigation.[35]

History and Physical

The 3 subtypes of TTH are infrequent episodic, frequent episodic, and chronic. Patients usually characterize the pain as pressing, dull, and with the sensation of a tight band around the head.

The most important goal of taking a detailed headache history is to ascertain whether the headache is of primary or secondary type. Primary headaches are recurrent headaches. A thorough history and physical examination can differentiate the key features of a benign primary headache from concerning symptoms that are likely due to a secondary headache and need further evaluation. The most common primary headache disorder is TTH.[36]

New-onset headaches should undergo assessment for secondary causes. For recurrent headaches, an important question to ask is whether the current episode is similar to previous headaches. If the current headache is similar to previous episodes, a primary headache disorder is the most likely cause. Otherwise, evaluation for secondary causes is necessary. For instance, a patient with migraine or TTH may present with a headache more severe than usual due to subarachnoid hemorrhage (SAH) or meningitis.

TTH often presents with recurrent headaches. Patients should maintain a headache diary, noting the frequency, duration, severity, and aggravating and relieving factors. The IHS requires at least 10 headache episodes for a diagnosis of TTH. These headaches vary from 30 minutes to 7 days in duration. The average duration is about 4 to 6 hours. The headaches are often bilateral in location and described as having dull, pressing, or band-like tightening (nonpulsating) quality. The headaches are also of mild or moderate intensity and are not aggravated by routine physical activity such as walking or climbing stairs. Patients can thus continue performing their routine activities, unlike patients with migraines, who usually prefer to stay in quiet, dark rooms. Tension headaches are usually better in the morning and worse in the evening.

Patients may also complain of shoulder or neck muscle tightness, as well as sleep disturbances. Symptoms such as nausea, vomiting, photophobia, and phonophobia are typically absent or very mild. These features easily differentiate TTH from migraine when present. Symptoms sometimes overlap, and confirmation of the exact diagnosis may only occur over time. Medication history is also critical. The type, frequency, and response to analgesic drugs must be evaluated in all patients.

Physical examination is normal in primary headache disorders, including TTH. However, a recent case-control study compared muscle strength in the neck and shoulder muscles of patients with TTH with that of healthy individuals by examining maximal voluntary isometric contraction during shoulder abduction, neck flexion, and extension, as well as the extension-flexion strength ratio of the neck. Individuals with TTH showed a decrease in muscle strength in the neck extensor muscles, resulting in a reduced cervical extension/flexion ratio compared to healthy subjects.

Although transient trigeminal cranial features of ptosis, conjunctivitis, or orbital swelling may occur with trigeminal autonomic cephalgias, physical examination is vital in excluding secondary causes, such as nuchal rigidity seen in meningitis and SAH, focal neurological deficits observed in space-occupying lesions, or papilledema in idiopathic intracranial hypertension.

"Red flags" for secondary disorders should always be ruled out during the history and physical examination.[37] These manifestations include the following:

• Sudden onset of headache
• Age of onset at or older than 50 years
• Very severe headache
• New onset of headache in the presence of an underlying medical condition
• Headache with concomitant systemic illness
• Focal neurologic signs or symptoms
• Papilledema
• History of head trauma

Secondary headache disorders may also be evaluated using the acronym "SNOOP4," which stands for the following:

• "S" stands for systemic symptoms, including fevers, chills, myalgias, and weight loss.
• "N" means neurological symptoms, especially focal neurologic deficits.
• The first "O" is for "older onset," meaning the age of onset is 50 years or older.
• The second "O" is for "onset," particularly if sudden, as in cases of SAH.
• "P1" is for papilledema.
• "P2" is for positional.
• "P3" means the Valsalva maneuver or exertion can precipitate the headache.
• "P4" means the headache is progressive or has substantial pattern change.

Recent reviews mentioned that, in the USA, headache is the 5th most common complaint in the emergency department, but only a minority have a secondary etiology. In line with this, revised and validated severity criteria were also published in 2018 under the name "SNNOOP10." The IHS compiled information on red flags that indicate a secondary etiology. Furthermore, the concept of green flags emerged, which allows the diagnosis of a primary headache without further investigations. A systematic diagnostic approach using red and green flags can help decrease unnecessary testing, thereby focusing attention on potentially life-threatening cases when caring for patients with headaches.[38][39][40]

Using the systematic SNNOOP10 mnemonic or list to screen acute headaches presumably increases the likelihood of detecting life-threatening secondary causes of headaches. A recent study found that the red flags from the SNNOOP10 list showed 100% sensitivity in detecting high-risk headache disorders.[41]

Medical literature indicates that the following red flags increase the likelihood of identifying a secondary etiology: 

• Systemic symptoms, including fever
• History of neoplasm
• Neurologic deficit, including decreased consciousness
• Sudden or abrupt onset
• Older age, with onset after 65 years
• Pattern change or recent onset of new headache
• Positional headache
• Precipitated by sneezing, coughing, or exercise
• Papilledema
• Progressive headache and atypical presentations
• Pregnancy or puerperium
• Painful eye with autonomic features
• Posttraumatic onset of headache
• Pathology of the immune system, such as HIV
• Painkiller overuse or new drug at the onset of headache 

Another study also identified additional red flags, such as acute thunderclap headache, meningeal irritation on physical examination, papilledema with focal neurologic signs, impaired consciousness, and concern for acute glaucoma requiring immediate assessment.

Evaluation

TTH is a clinical diagnosis based on the IHS diagnostic criteria. No laboratory testing or imaging studies are usually necessary for diagnosing this condition. Primary headache disorders without red flags or abnormal examination findings do not require neuroimaging.

However, if 1 or more red flags are present, appropriate investigations, including but not limited to brain imaging, should be performed to rule out secondary causes. For emergent evaluations, a noncontrast computed tomography of the head may be necessary to exclude acute intracranial hemorrhage or mass effect. A lumbar puncture is also needed to rule out SAH if the scan result is within normal limits.

For less urgent cases, brain magnetic resonance imaging (MRI) is preferred for evaluating headaches with concerning features. An MRI with gadolinium contrast is the recommended imaging study in these patients.

The International Headache Society's Diagnostic Criteria for Tension-Type Headache

The IHS has proposed the diagnostic criteria for TTH in the 3rd edition of the International Classification of Headache Disorders (ICHD-3). The criteria are as follows:

A. At least 10 episodes of headache fulfilling criteria B to D

B. Lasting from 30 minutes to as long as 7 days

C. At least 2 of the following 4 characteristics:

• Bilaterally located
• Pressing or tightening (nonpulsating) quality
• Mild or moderate in intensity
• Not exacerbated by routine physical activity, such as walking or climbing stairs

D. Both of the following:

• No nausea or vomiting
• No more than 1 of either photophobia or phonophobia

E. Not better explained by another ICHD-3 diagnosis

The above is a set of general ICHD-3 diagnostic criteria for TTH. If one of the above ICHD-3 features for TTH is missing, and the patient does not fulfill the criteria for another headache disorder, a diagnosis of "probable TTH" is possible. Patients with probable TTH eventually require further evaluation, with clinicians often making a diagnosis of TTH. TTH is further classified into 3 subtypes based on the frequency of headache episodes.

• Infrequent episodic TTH: At least 10 episodes of headache occurring less than 1 day a month on average or less than 12 days per year
• Frequent episodic TTH: At least 10 episodes of headache occurring 1 to 14 days a month on average for over 3 months, or 12 or more and less than 180 days per year
• Chronic TTH: Headache occurring 15 or more days per month on average for more than 3 months, or 180 or more days a year [42]

Treatment / Management

A literature review identified 2 main therapeutic avenues for TTH: acute and prophylactic treatments. Simple or combined nonprescription analgesics are used for managing episodic TTH. Prophylactic treatment is recommended for patients with chronic and very frequent episodic TTH. Prophylactic therapy is also recommended for individuals who are difficult to treat, have an increased risk of medication overuse headaches, or cannot tolerate effective doses of 1st-line drugs. 

Treatment of Episodic Tension-Type Headache

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the primary treatment options for aborting TTH episodes. Recent meta-analyses suggest that ibuprofen 400 mg and acetaminophen 1,000 mg are the most effective pharmacological agents for the acute treatment of TTH. A synergistic effect appears to exist when these 2 drugs are used together, as the number needed to treat with ibuprofen alone was higher than when combined with acetaminophen. Although acetylsalicylic acid is frequently used over the counter, a 500-mg dose has been shown to be no more effective than a placebo.[43] (B3)

Acetaminophen may be preferred over ibuprofen for patients with a higher risk of complications, such as renal insufficiency or gastrointestinal bleeding.[44] A dose of 1,000 mg can provide pain relief within 2 hours for individuals with frequent episodic TTH experiencing acute moderate-to-severe headaches.(A1)

Other NSAIDs, including naproxen sodium (375 to 550 mg), ketoprofen (25 to 50 mg), and diclofenac (50 to 100 mg), are also more effective than placebo for acute TTH. Patients should avoid overusing analgesics, which can lead to medication overuse headaches. Muscle relaxants have limited evidence supporting their efficacy in TTH and carry a risk of habituation.

The local application of peppermint oil (oleum menthae piperitae) has demonstrated significant efficacy in some studies, with pain relief comparable to acetaminophen or acetylsalicylic acid. Solutions containing 10% peppermint oil in ethanol are approved for treating TTH in adults and children over 6 years of age. This modality is included in treatment guidelines and is considered a standard option for acute TTH management.[45]

Treatment of Chronic Tension-Type Headache

Therapies for chronic TTH are divided into pharmacological and nonpharmacological categories. These modalities address factors that persistently trigger the symptoms, including emotional and physical stress. However, not all treatments demonstrate equal effectiveness in managing the condition, and their selection should be tailored to the patient’s specific symptoms, triggers, and overall health profile.

Pharmacological modalities

Chronic TTH develops from episodic TTH, presenting with daily or very frequent headache episodes that last for hours or may become continuous. Various interventions have been reviewed, addressing the effectiveness and safety of nondrug treatments such as acupuncture and cognitive behavioral therapy being used alongside drug therapies, including amitriptyline, anticonvulsants like sodium valproate, topiramate, and gabapentin, benzodiazepines, botulinum toxin, noradrenergic and specific serotonergic antidepressants like mirtazapine, NSAIDs such as ibuprofen, opioid analgesics like codeine, paracetamol, serotonin reuptake inhibitor antidepressants [selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors SNRIs)], and tricyclic antidepressants (TCAs) other amitriptyline.[46]

The primary goal of chronic TTH therapy is to reduce headache frequency through preventive medications. Among pharmacologic treatments, the TCA amitriptyline is the most effective and well-studied. Amitriptyline should be initiated at a low dose (10 to 25 mg daily) and gradually increased (10 to 25 mg weekly) until a therapeutic response is achieved or adverse effects appear, which commonly include dry mouth, drowsiness, urinary retention, cardiac arrhythmias, and glaucoma. The therapeutic response usually occurs in 3 to 4 weeks. In responsive patients, amitriptyline is typically continued for at least 6 months, with withdrawal attempted afterward. Long-term use may be necessary if the headaches recur upon discontinuation.

The efficacy of other antidepressants, such as mirtazapine and venlafaxine, has been documented. Weaker evidence backs the efficacy of gabapentine, topiramate, and tizanidin. Research also demonstrated that SSRIs and SNRIs were not as effective as TCAs. Recent studies did not provide high-quality evidence supporting the use of SSRIs or the SNRI venlafaxine as preventive drugs for TTH. SSRIs or venlafaxine were no more effective than placebo or amitriptyline in reducing headache frequency in patients with chronic TTH after 2 months of treatment. SSRIs were also found to be less effective than TCAs in terms of analgesic medication use. However, TCAs were associated with more adverse events.[47](A1)

Evidence for the efficacy of muscle relaxants in TTH is weak. These medications also risk habituation.

Recent reviews demonstrated that botulinum toxin had a significant correlation with the reduction of TTH pain intensity and severity. However, no clear clinical evidence supports prophylactic treatment for chronic TTH and cervicogenic headaches.[48][49] This modality is also usually not recommended as a 1st-line treatment. However, a trial of botulinum toxin A may be considered in refractory chronic TTH cases.(A1)

Nonpharmacological modalities

Certain types of supervised physical activity, psychological treatment, acupuncture or trigger point injection, physical therapy, manual joint mobilization techniques, electromyography biofeedback, and cognitive-behavioral therapy have all proven effective based on identified benefits, certainty of evidence, and patient preferences. A review showed positive effects on headache frequency, quality of life, pain intensity, and stress symptoms after using these modalities.[50][51](A1)

Relaxation, exercise programs, and improvement of posture are critical components of physical therapy. Exercise may be considered clinically significant for primary headache management.[52] A study analyzed the efficacy of a strength-based exercise program in patients with chronic TTH. The results revealed changes in pain intensity, duration, and physically related factors among TTH patients after a 12-week strength training program targeting the neck and shoulder regions.[53] Another study suggested combining passive physiotherapy techniques with exercise or transcutaneous electrical stimulation, as these physiotherapy interventions were found to be the most effective in reducing pain intensity and frequency in the short term.[54] Biofeedback, either alone or combined with other behavioral therapies, is also an effective treatment for headaches.[55](A1)

Several other therapies, including massage, manipulation, acupuncture, and osteopathic manipulative medicine, have also demonstrated improvement in both acute and chronic presentations, using measures such as increasing the range of motion of the head. Trigger point dry needling among patients with chronic TTH is also effective and safe in reducing headache intensity, frequency, and duration and in increasing health-related quality of life.[56](A1)

The combination of acupuncture and medical training therapy produced positive effects on depression, anxiety, and quality of life and was observed to be safe and effective for treating frequent episodic or chronic TTH.[57][58][59] The 8-week true acupuncture treatment was effective for chronic TTH prophylaxis.[60] However, low- to moderate-quality evidence indicates that neuromodulation, acupuncture, and aerobic exercises are related to attenuated headache symptoms among patients with episodic migraine or TTH.(A1)

Manual physical therapy techniques are widely used in the clinical field to treat the symptoms associated with TTH. Systematic reviews have determined the effectiveness of manual and noninvasive therapies in the treatment of individuals with TTH. No standardized physical therapy protocol is available for treating tension headaches, even though the approach to the craniocervical-mandibular region reports significant effects in terms of lowering pain intensity and frequency of headache episodes in the short and medium term.[61][62](A1)

Manual therapy showed positive effects on pain intensity, pain frequency, disability, overall impact, quality of life, and craniocervical range of motion in adults with TTH. None of the techniques, including suboccipital inhibitory pressure and suboccipital spinal manipulation, was observed to be effective in changing different dimensions of quality of life. However, combining the different techniques was noted to be the most effective approach. The results supported the effectiveness of treatments applied to the suboccipital region for patients with TTH.[63](A1)

Research has also demonstrated the benefit of TTH treatment with massage, with or without a manipulative technique. However, the added manipulative technique was more beneficial for increasing the range of motion of the upper cervical spine and for reducing headaches.[64] A recent study assessed the outcome of single and multiple massage treatments on the pressure-pain threshold (PPT) at MTrPs among patients with myofascial pain syndrome described as tension headaches. Results showed that single and multiple massage applications increased PPT at MTrPs. The pain threshold of MTrPs has a great capacity to improve; additional gain in PPT was noted even after multiple massage treatments.[65](A1)

Another study revealed that warming acupuncture and moxibustion at the temples, along with Deanxit, greatly reduced the number and duration of headache attacks and decreased the severity of tension headaches.[66] Additionally, active, noninvasive therapies, such as relaxation technique programs (eg, the Schultz Autogenic Training), cervical spine kinesiotherapy, and posture correction exercises—especially the combination of these 3 modalities—effectively alleviate tension headaches by preventing and managing potential psychophysical causes of this disorder.[67](A1)

Differential Diagnosis

Other headache disorders, whether primary or secondary, are part of the differential diagnosis of TTH. These clinical entities and their differentiating features are discussed in this section.

Migraine

Migraine is the 2nd most common primary headache disorder and requires differentiation from TTH, as these conditions warrant different treatment approaches. Migraine headaches are moderate to severe in intensity and last for 4 to 72 hours. The headaches may be unilateral in location and typically have a pulsating or throbbing quality. Migraine headaches are also aggravated by routine physical activity. Nausea, vomiting, photophobia, and phonophobia are commonly associated with migraines. A preceding aura may also be present in some patients.

A recent review discussing the differences and similarities between TTH and migraine indicated that migraine may be identified by specific features, such as being more prevalent in women, aggravated by physical activity, linked to certain genetic factors, and associated with photophobia, phonophobia, nausea, vomiting, or aura. Migraine also responds to specific drugs. However, TTH and migraine share some common manifestations, including onset in the 20s, psychological triggers such as stress, moderate pain severity, and mild nausea, especially in chronic TTH. Both conditions involve the trigeminovascular system in their pathophysiology.

Medication Overuse and Rebound Headaches

Medication overuse and rebound headaches are chronic daily headaches that occur when analgesics, triptans, and ergotamines are taken frequently (ie, more than 15 days/month for more than 3 months) to relieve headaches. These entities may be present concomitantly with TTH or other headache disorders. Rebound headaches may mimic chronic TTH, making diagnosis and treatment more difficult. The patient often takes analgesic medications for more than 10 to 15 days a month. Patients may complain of headaches upon awakening that transiently respond to analgesics and return as the drug effect wears off. These individuals may also appear anxious, irritable, and restless. Central sensitization and psychological factors play an important role in initiating and maintaining rebound headaches.[68]

The primary treatment is detoxification of the headache medication, preferably on an outpatient basis, with abrupt withdrawal of all acute headache medication and caffeine-containing products. Vital for successful detoxification is education about the reasons for detoxification, the expected course, and the subsequent treatment.[69] Discontinuing the overused analgesic medication is the primary treatment, which the patient needs to understand.

Hypnic Headache

Hypnic headaches are less frequent but should be considered in the differential diagnosis of chronic daily headaches, especially when they are nocturnal and occur during sleep. This headache typically has an onset after the age of 50. Hypnic headaches occur only during sleep and usually wake the patient. Since older adults have a higher risk of developing secondary headaches in general, distinguishing primary from secondary headaches in this subset of patients is crucial. This distinction should also be made in all age groups with risk factors.

A recent study presented an 86-year-old female patient with chronic daily headaches of 1-year duration, exclusively nocturnal, waking her up daily around midnight. Clinical examination and diagnostic workup, including MRI, were unremarkable, and she did not respond satisfactorily to paracetamol, diclofenac sodium, mefenamic acid, tramadol, flunarizine, or sodium valproate but was responsive to indomethacin.[70]

COVID-19-Related Headache

COVID-19 presents with headaches, occurring more frequently in individuals who are relatively young, have a history of primary headaches or migraine, or present with anosmia, ageusia, and myalgia. The headache typically starts early in the symptomatic phase and is characterized as bilateral, moderate to severe, with a pattern similar to TTH.[71]

Secondary Headaches with Potentially Life-Threatening Etiologies

Secondary headaches should always be considered and evaluated, looking for "red flags" during the clinical assessment. Some causes of secondary headaches include giant cell arteritis, sleep apnea headaches, cardiac cephalgia, and cervicogenic headaches. A discussion of each secondary headache disorder is beyond the scope of this article.

Prognosis

The prognosis of TTH is usually good. Most people respond to treatment. In a Danish study of 549 people, approximately half of the patients with episodic TTH experienced remission, and only about 15% progressed to newly developed chronic TTH.[72] Another study revealed improvements after withdrawal therapy for chronic headaches lasting at least 9 years. However, patients with sustained chronic headaches and medication overuse had poor initial responses to withdrawal therapy.[73]

Recent reviews show that headache relief has been the primary endpoint most commonly assessed, but headache disappearance is now being more seriously considered. Secondary endpoints have expanded over time to include other outcomes, such as disability, quality of life, and patients' preferences.[74]

Complications

TTH is a nonfatal condition, though it causes significant morbidity. Frequent episodic and chronic TTH lead to absent days and reduced work productivity. TTH may also increase stress and the risk of mood disorders. TTH is usually exacerbated by medication overuse, and repeated headaches can produce central sensitization and conversion to chronic headaches that are intractable, difficult to treat, and cause significant morbidity.[75]