hpr-2024-0025.pdf

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這篇綜述文章全面探討了緊縮型頭痛 (TTH)，這是全球最普遍但常被科學界忽視的頭痛疾病。作者詳細說明了其臨床特徵，包含雙側、非搏動性的緊繃感，並對比了其與偏頭痛在生物標記物及 CGRP（降鈣素基因相關胜肽）機制上的差異。文中分析了引發疼痛的外周與中樞機制，指出肌肉緊繃與神經系統的敏感化是導致症狀慢性化的關鍵要素。最後，文章評估了從急性止痛藥物、預防性抗抑鬱藥到非藥物介入手段（如認知行為治療與物理治療）的整合管理策略，旨在喚起對此病症的臨床重視與研究投入。

© 2025 The Korean Headache Society This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons. org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

INTRODUCTION

Tension-type headache (TTH) is the most common head-

ache disorder. It is characterized by mild to moderate

intensity, bilateral, pressing, or tightening pain quality in

the forehead, occiput, and neck. The term “tension” em-

phasizes the role of muscle contraction and emotional ten-

sion, leading to various treatments that focus on muscle

relaxation and stress management.

Despite knowing the nature of how TTH and migraine

can co-occur and having similar medical treatments, such

as non-steroidal anti-inflammatory drugs (NSAIDs) or

Update on Tension-type Headache

Hye Jeong Lee1 , Soo-Jin Cho2 , Jong-Geun Seo3 , Henrik Winther Schytz4

1Department of Neurology, Chung-Ang University Gwangmyeong Hospital, Gwangmyeong, Republic of Korea 2Department of Neurology, Dongtan Sacred Heart Hospital, Hallym University College of Medicine, Hwaseong, Republic of Korea 3Department of Neurology, School of Medicine, Kyungpook National University, Daegu, Republic of Korea 4Headache Diagnostic Laboratory, Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health Sciences, University of Copenhagen, Glostrup, Denmark

Review Article Headache Pain Res 2025;26(1):38-47 pISSN: 3022-9057 · eISSN: 3022-4764 https://doi.org/10.62087/hpr.2024.0025

Received: September 7, 2024; Revised: October 1, 2024; Accepted: October 4, 2024 Correspondence: Hye Jeong Lee, M.D. Department of Neurology, Chung-Ang University Gwangmyeong Hospital, 110 Deokan-ro, Gwangmyeong 14353, Republic of Korea Tel: +82-2-1811-7800, Fax: +82-2-2610-6624, E-mail: hjlee@cauhs.or.kr

Abstract

Tension-type headache (TTH) is the most common type of headache, characterized by mild to moderate intensity, bilateral, with a pressing or tightening (non-pulsating) quality. Migraine and TTH can occur in the same person, and their risk factors and treatments can overlap. However, TTH receives less attention than migraine. Furthermore, despite the expanding market for migraine treatments targeting calcitonin gene-related peptide (CGRP) mechanisms, the lack of evidence regarding mecha-nisms related to CGRP-related mechanisms in TTH continues to be neglected. There remains a need to develop effective pre-ventive treatments for chronic TTH, which imposes a very high burden of disease. From this perspective, this review aims to provide the latest evidence on TTH.

Keywords: Headache, Tension-type headache, Headache disorders, Primary, Migraine

amitriptyline, TTH remains less researched, poorly diag-

nosed and treated than migraine.1 For example, a PubMed

search for the word “migraine” yields to almost 50,000 hits,

compared to less than 5,000 hits for the word “tension-type

headache.” It is also interesting to note that while migraine

and TTH can become interchangeable over time and share

similar risk factors, triggers, and comorbidities in indi-

viduals, they have distinctly different headache charac-

teristics.2 The distinctive features of migraine, as opposed

to TTH, appear to be influenced in part by the calcitonin

gene-related peptide (CGRP) mechanism, which has re-

cently received a great deal of attention. In contrast, TTH

Lee et al. Update on Tension-type Headache

39www.e-hpr.org

has been neglected as a research topic due to the lack of a

clear biomarker and the absence of randomized controlled

trial-based effective preventive medications for frequent

episodic or chronic TTH.

This review aims to provide an overview of recent find-

ings on the epidemiology, pathophysiology, diagnosis, and

treatment of TTH.

EPIDEMIOLOGY

The global prevalence of TTH is approximately 26% of

adults, with wide variation between studies and ethnic-

ities, but it is generally estimated that 30% to 80% of the

adult population will be affected at some point in their

lives.3-6

The incidence of TTH is higher in women than in men,

and this gender difference may be due to hormonal fac-

tors, stress, and psychosocial influences. TTH can occur

at any age, but the greatest burden in terms of years of life

lived with disability is in the between 15 and 49 age group.7

The incidence of TTH tends to decrease with age, although

it remains a significant health problem in the elderly pop-

ulation.7

Lower socioeconomic status is often associated with

higher levels of stress, poorer access to healthcare, and

lower levels of education, all of which may contribute to

the prevalence and severity of TTH.8 Cultural attitudes to-

ward pain and healthcare-seeking behaviors may influence

how individuals report and manage their headache symp-

toms. In some cultures, headache may be underreported

due to stigma or misconceptions about headache. In ad-

dition, infrequent episodic TTH may be under-reported in

epidemiological studies.9

CLINICAL PRESENTATION

TTH is characterized by a diffuse, mild to moderate, bi-

lateral headache that is often described as a tightening

sensation. Unlike migraine, the headache is not typically

pulsating and does not worsen with routine physical ac-

tivity. Also, TTH is also not usually associated with nausea

or vomiting, although mild photophobia or phonophobia

may be present in some cases. The clinical presentation

of TTH is highly variable between individuals, with some

experiencing infrequent episodic headaches and others

suffering from chronic daily headaches.10

The frequency of TTH episodes can vary widely, ranging

from infrequent episodic TTH (occurring less than 1 day

per month) to chronic TTH (occurring more than 15 days

per month).

Factors that contribute to the chronicity of TTH include

high levels of stress, co-existing migraine, fatigue, anxiety,

and depression, and an inability to relax after work.11

DIAGNOSIS

The diagnosis of TTH is primarily clinical and based on the

patient’s history and symptoms according to the criteria of

the International Classification of Headache Disorders, 3rd

edition (ICHD-3) (Table 1).12 However, due to the non-spe-

cific nature of TTH symptoms, diagnosis can be challeng-

ing because of overlap with other headache disorders and

medical conditions. This diagnostic ambiguity can lead to

misdiagnosis, inappropriate treatment, and unmet patient

needs. Therefore, it is important to rule out other diseases

on the basis of the headache history.

Headache diaries are the best assessment tool for diag-

nosis and classification. However, additional diagnostic

tests such as neuroimaging, blood sampling, and lumbar

puncture may be necessary if any red flags are present.13

Without strict criteria are applied, both migraine and

TTH may coexist and sometimes overlap, further com-

plicating the diagnostic process. Migraine and TTH may

have some overlap in their clinical features. Photophobia

and phonophobia are more common in migraine than

in TTH, also nausea and vomiting are more common

in migraine than in TTH, although mild nausea may be

present in chronic TTH according to the ICHD-3.14,15 This

can lead to clinicians misdiagnosing a patient as having

migraine when they are actually have TTH, and vice versa.

In children and adolescents, the transition from migraine

to TTH or from TTH to migraine occurs within a few years,

supporting the continuum theory of headache in this sub-

group of individuals. Not only are mixed presentations and

diagnostic shifts common at younger ages, but the chal-

lenges associated with distinguishing TTH from migraine

in clinical practice, clinical research, and epidemiologic

studies have been widely recognized.16,17 TTH with mi-

graine comorbidity is associated with genetic factors.18 Re-

cently, machine learning models have demonstrated high

Table 1. Diagnostic criteria of tension-type headache according to the International Classification of Headache Disorders, 3rd edition (ICHD-3)1

2.1. Infrequent episodic tension-type

headache

2.2. Frequent episodic tension-type

headache

2.3. Chronic tension-type headache

2.4. Probable tension-type headache 2.4.1. Probable

infrequent episodic tension-type headache

2.4.2. Probable frequent episodic

tension-type headache

2.4.3. Probable chronic tension-type

headache

A At least 10 episodes of headache occur-ring on <1 day/mo on average (<12 days/yr) and fulfill-ing criteria B–D

At least 10 episodes of headache occurring on 1–14 day/mo on average for >3 months(≥12and<180 day/yr) and fulfilling criteria B–D

Headache occurring on≥15day/moon average for >3 months(≥180day/yr), fulfilling criteria B–D

One or more epi -sodes of headache fulfilling all but one of criteria A–D for 2.1. Infrequent ep-isodic tension-type headache

Episodes of headache fulf i l l ing al l but one of criteria A– D for 2.2. Frequent episodic tension- type headache

Headache fulfilling all but one of criteria A–D for 2.3. Chronic episodic tension- type headache

B Lasting from 30 minutes to 7 days Lasting hours to days, or unremitting

Not fulfilling ICHD-3 criteria for any other headache disorder

C At least two of the following four characteristics: 1. bilateral location 2. pressing or tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity such as walking or

climbing stairs

Not better accounted for by another ICHD-3 diagnosis

D Both of the following: 1. no nausea or vomiting 2. no more than one of photophobia or pho-

nophobia

Both of the following: 1. no more than one

of photophobia, phonophobia or mild nausea

2. neither moderate or severe nausea nor vomiting

E Not better accounted for by another ICHD-3 diagnosis1

diagnostic accuracy in migraine from electronic health

records or questionnaires.19-21 However, these are not yet

sufficient for application to TTH.21

Premonitory or prodromal symptoms are characteristic

of migraine and include yawning, mood changes, fatigue,

and neck pain. These symptoms typically occur within 2–48

hours of the onset of migraine headache.22 There are no

of premonitory symptoms in patients with TTH. Migraine

headaches may also be associated with menstrual periods,

with the drop in estrogen levels affecting the frequency of

migraine headaches. Migraine attacks are common during

the perimenstrual period and usually improve during

pregnancy.23

And the selective 5HT1B/1D agonist is thought to relieve

migraine by stimulating the 5HT1B receptor on cranial

vascular smooth muscle to reduce the pain-inducing vaso-

dilation that may be responsible for the headache.24 How-

ever, it is not effective for the treatment of TTH, except in

people who also have migraine.25 The healthcare provider

caring for patients with headache should be aware of these

overlaps and their implications for the management of pa-

tients with headache.

PATHOPHYSIOLOGY

The pathophysiology of TTH is complex, multifactorial,

and not fully understood, involving both peripheral and

central mechanisms. The peripheral mechanisms are pri-

marily related to myofascial tissues and nociception, while

the central mechanisms of chronification are related to

pain processing in the central nervous system.26,27 There

has been some research into the mechanisms of nitric

oxide-induced TTH and drug development is current-

ly underway, but to date there have been no significant

results.20,28,29 The role of CGRP in the progression and re-

mission of chronic TTH is becoming a subject of interest,

although treatment response to anti-CGRP monoclonal

antibodies is poor.14,30

40 www.e-hpr.org

Headache Pain Res 2025;26(1):38-47

1. Peripheral mechanisms

The peripheral mechanisms of TTH are mainly related to

pericranial muscle tenderness during acute headache at-

tacks and myofascial trigger points.31-33 The most common

method used to assess tenderness is manual palpation of

the pericranial muscles and calculation of the total tender-

ness score.34 And muscle hardness can be measured using

the hardness meter, a quantitative method.35 Pericranial

tenderness is exacerbated during the acute headache

phase and increases with the severity and frequency of

TTH attacks, supporting the presence of more severe ten-

derness in individuals with chronic TTH than in those with

episodic TTH.36

Myofascial tissues, which include muscles and con-

nective tissues, can develop localized areas of tenderness

called trigger points. These trigger points can cause pain in

other areas, such as the neck or shoulder, which may con-

tribute to the headache pain experienced in TTH.37 Active

myofascial trigger points are common in TTH consistent

with the hypothesis that peripheral mechanisms are in-

volved in the pathophysiology.27 However, the relationship

between myofascial trigger points and the severity of TTH

varies between studies.

Electromyography studies have shown increased muscle

activity and tension in individuals with TTH, suggesting

that sustained muscle contraction and tension play a role

in the development of headache pain.38

2. Central mechanisms

Central sensitization of second-order neurons in the spinal

cord or the spinal trigeminal nucleus is a key mechanism

in the pathophysiology of transformation from episodic

to chronic TTH.39,40 Patients with chronic TTH had higher

pain sensitivity and lower tolerance to pressure stimula-

tion of cranial and extracranial structures than patients

with episodic TTH patients.26,41

Comorbidities, such as back pain, fibromyalgia, and

sleep disorders, may alter pain sensitivity in patients with

chronic TTH and increase central sensitization compared

to patients with transient TTH, suggesting shared central

mechanisms between the two groups. Anxiety and de-

pression are in patients with TTH and are associated with

worsening symptoms.42,43

Functional magnetic resonance imaging studies have

provided insight into the central mechanisms of TTH by

examining dynamic brain changes between pain and pain-

free periods in patients with episodic TTH.44,45 These stud-

ies have shown changes in activation in pain-processing

regions of the brain, including the anterior cingulate cor-

tex, insula, and prefrontal cortex. These findings suggest

that individuals with TTH have abnormal pain processing

and modulation, which may contribute to the perception

of headache pain.

In addition, neurotransmitters such as serotonin and nor-

epinephrine have been found to be associated with TTH,

although several studies have yielded conflicting results.

TREATMENT

There are significant gaps in the management of TTH,

and many patients are not receiving adequate treatment.

A multidisciplinary approach tailored to each individual

patient. For example, patients with infrequent episodes

of TTH can be managed with acute medications and

non-pharmacological treatments such as lifestyle mod-

ifications, while patients with frequent episodes of TTH

or chronic TTH may require preventive pharmacological

treatments with behavioral interventions (Figure 1).

1. Acute pharmacological treatments

Acute treatment aims to provide rapid relief of headache

attacks quickly and is typically used at the onset of a head-

ache episode. Simple analgesics have evidence-based effi-

cacy and are widely accepted as the first-line treatment for

the acute treatment of patients with TTH.46

NSAIDs and acetaminophen are commonly used for

acute symptom management. Opioids, triptans, and mus-

cle relaxants are not generally recommended for symp-

tomatic TTH.47,48

• NSAIDs NSAIDs inhibit the enzyme cyclooxygenase, which reduc-

es the production of prostaglandins that which mediate in-

flammation and pain. Initial treatments for acute TTH in-

clude ibuprofen, ketoprofen, naproxen, and diclofenac.49,50

Side effects include gastrointestinal discomfort, ulcers, and

cardiovascular risks with long-term use.

Lee et al. Update on Tension-type Headache

41www.e-hpr.org

42 www.e-hpr.org

Headache Pain Res 2025;26(1):38-47

Figure 1. Current treatments for tension-type headache.

Acute pharmacological treatments

Acetaminophen

Other antidepressants Lifestyle modificationsCombination analgesics

Preventive pharmacological treatments

Non-pharmacological treatments

Non-steroidal anti-inflammatory drugs Tricyclic antidepressants

Acupuncture

Biofeedback

Physical therapy

Cognitive-behavioral therapy

• Acetaminophen Acetaminophen is the preferred initial therapy for patients

with TTH who are intolerant of or contraindicated for

NSAIDs for pregnant patients. Acetaminophen is typically

used in a single oral dose of 500 to 1,000 mg. It is generally

well tolerated, but overdose may cause liver toxicity.51

• Combination Analgesics Combination of caffeine with acetaminophen, aspirin, or

ibuprofen improves the efficacy for the acute treatment of

TTH.52 Caffeine may enhance the analgesic effects by pro-

moting their gastric absorption.53 However, frequent use

may increase gastrointestinal discomfort and increase the

risk of medication overuse headache.

2. Preventive pharmacological treatments

Preventive treatments have been shown to help reduce

headache frequency and severity in patients with fre-

quent episodic TTH (1 to 14 headache days per month) or

chronicTTH(≥15headachedayspermonth).Preventive

treatment is also indicated in patients with infrequent TTH

when simple analgesics are ineffective, poorly tolerated, or

contraindicated.

The goal of treatment is to reduce the frequency, severi-

ty, and duration of attacks and to improve the response to

treatment of acute attacks. It is important to understand

patient expectations and consider patient preferences

when deciding which of the various preventive therapies

to use. For patients who respond well (over 50% reduction

in headache days per month), an adjunctive approach is to

discontinue treatment after 3 or 6 months and monitor for

headache recurrence, unless there are other comorbidi-

ties, such as depression or anxiety disorders.

• Tricyclic Antidepressants (TCAs) TCAs have moderate to high potency for TTH, and ami-

triptyline controls pain through its inhibitory effects on

serotonin and norepinephrine reuptake.

Amitriptyline also reduces pericranial muscle tender-

ness, resulting in peripheral antinociception and inhibition

of central sensitization. It is common for clinicians to start

amitriptyline at 2.5–10 mg nightly and increase by 5–10 mg

per week to a maximum of 70–80 mg. Common side effects

include sedation, weight gain, dry mouth, and constipation.

• Other Antidepressants Mirtazapine (noradrenergic and specific serotonergic an-

tidepressant) is comparable to amitriptyline and has a bet-

ter tolerability profile than amitriptyline. Evidence for the

effectiveness of venlafaxine (serotonin-norepinephrine re-

uptake inhibitor) in preventing TTH is weak and supports

a level B rating by the EFNS-TF.46

3. Non-pharmacological treatments

Non-pharmacological treatments such as cognitive behav-

ioral therapy (CBT), biofeedback, and relaxation therapy

are often recommended as first-line interventions. In ad-

dition, integrative medicine (acupuncture and massage)

and lifestyle modifications (sleep management, healthy

diet, hydration, and exercise) may be considered to reduce

headache triggers. However, the evidence for non-phar-

macological approaches in TTH are very limited.54

• CBT CBT is a psychological intervention that helps patients

identify and modify negative thought patterns and behav-

iors that cause stress and muscle tension, both of which

Lee et al. Update on Tension-type Headache

43www.e-hpr.org

are important factors in TTH.55 CBT techniques for TTH

include cognitive restructuring, behavioral activation, and

relaxation techniques, among others. Stress management

therapy has demonstrated efficacy in randomized and pla-

cebo-controlled trials and has been shown to be equivalent

to amitriptyline in preventing chronic TTH.56 Long-term

group behavioral therapy has been shown to be effective

in reducing headache frequency and intensity, improving

coping strategies, and improving overall mental health.57,58

CBT has been shown to improve quality of life and reduce

comorbid symptoms of anxiety and depression.

• Biofeedback Biofeedback is a technique that teaches individuals how to

regulate physiological processes such as muscle tension,

heart rate, and skin temperature through real-time feed-

back. Biofeedback helps patients become aware of and

voluntarily control these processes, which can help reduce

the frequency, duration, and intensity of headaches in pa-

tients with TTH.

• Physical Therapy Physical therapy involves the use of massage, cervical

spine manipulation, and exercise to improve muscle func-

tion, reduce tension, and promote relaxation.59 It is partic-

ularly useful for TTH patients with severe musculoskeletal

problems, such as poor posture, muscle imbalances, and

trigger points.60 However, there is no standardized protocol

for treating TTH, and a combination of techniques appears

to be more effective.61

• Acupuncture The exact mechanism by which acupuncture relieves TTH

is not fully understood, but it is believed to involve the

modulation of pain pathways, release of endogenous opi-

oids, and reduction of muscle tension and inflammation.62

As the efficacy of greater occipital nerve block in various

headache disorders has been confirmed, attempts have

been made to use it as a treatment for TTH.63-65 One sys-

tematic meta-analysis found acupuncture to be effective

and safe for frequent episodic TTH and chronic TTH.66

• Lifestyle Modifications Adopting healthy lifestyle habits can play an important

role in the management and prevention of TTH. Important

lifestyle changes include regular physical activity, healthy

sleep patterns, a balanced diet, and effective stress man-

agement.67,68

Regular exercise, such as aerobic exercise, yoga, and

stretching, has been shown to help reduce stress, improve

sleep quality, and relieve muscle tension, all of which can

help prevent TTH.

Strategies such as maintaining a consistent sleep sched-

ule, avoiding caffeine and electronic devices before bed-

time, and creating a comfortable sleep environment can

help prevent headaches caused by sleep deprivation.

Eating a balanced diet that includes a variety of nutrients

can help prevent and manage TTH.

FUTURE RESEARCH DIRECTIONS

Future research should focus on addressing the diagnostic

challenges and improving our understanding and treat-

ment of TTH. The co-occurrence of migraine and TTH

may be coincidental, but more research is needed to de-

termine whether there is a causal mechanistic relationship

between the two disorders.69

One of the major challenges in diagnosing these head-

aches is the lack of reliable biomarkers, with diagnosis

largely based on clinical criteria and patient self-report.

More research is needed to improve diagnostic accuracy.

While both migraine and TTH are associated with genetic

factors, the specific genes responsible for the heritability of

TTH remain unknown, in contrast to the multiple risk loci

identified for migraine.

Pharmacological provocation studies have provided

valuable insights into the pathophysiology of migraine,

leading to the discovery of important therapeutic targets.

However, similar studies have not been thoroughly per-

formed for TTH. Unfortunately, in the absence of identified

therapeutic targets, this approach is not currently feasible

for TTH patients.

In addition, the evidence supporting the use of botuli-

num toxin and anti-CGRP monoclonal antibodies in the

treatment of TTH is limited. We believe additional studies

are needed to evaluate the utility of botulinum toxin and

other emerging therapies for this common and debilitating

condition.

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Headache Pain Res 2025;26(1):38-47

CONCLUSION

TTH remains a common and often debilitating headache

disorder. Despite its high prevalence, TTH remains un-

der-recognized and under-treated, with significant public

health implications. A comprehensive understanding of its

epidemiology, pathophysiology, and clinical management

is essential to improve patient outcomes. Continued re-

search into the underlying mechanisms and public health

efforts are needed to address the diagnostic and treatment

gaps and ultimately improve the quality of life for individu-

als affected by TTH.

AVAILABILITY OF DATA AND MATERIAL

Data sharing is not applicable to this article as no new data

were created or analyzed in this study.

AUTHOR CONTRIBUTIONS

Conceptualization: HJL, SJC, JGS; Data curation: JGS,

HWS; Formal analysis: JGS, HWS; Investigation: SJC;

Methodology: HJL, SJC; Project administration: SJC, HWS;

Resources: JGS; Software: JGS; Supervision: SJC, HWS; Val-

idation: HJL, SJC, JGS, HWS; Visualization: HJL; Writing–

original draft: HJL, SJC; Writing–review & editing: JGS, SJC,

HWS.

CONFLICT OF INTEREST

Soo-Jin Cho is the Editor-in-Chief of Headache and Pain

Research and was not involved in the review process of this

article.

Hye Jeong Lee is the Editor of Headache and Pain Research

and was not involved in the review process of this article.

Jong-Geun Seo is the Editor of Headache and Pain Re-

search and was not involved in the review process of this

article.

All authors have no other conflicts of interest to declare.

FUNDING STATEMENT

Not applicable.

ACKNOWLEDGMENTS

Not applicable.

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