Tension-Type Headache in Adults

Quick Reference

Critical Alerts

⚠️ Red Flag: Rule out secondary causes first: Red flags mandate imaging/lumbar puncture before attributing headache to TTH

⚠️ Red Flag: Medication overuse headache risk: Analgesic use > 10-15 days/month transforms episodic TTH to chronic daily headache

Clinical Pearl: Most common primary headache worldwide: Lifetime prevalence 38-78%, but often underdiagnosed and undertreated [1]

Clinical Pearl: Diagnosis of exclusion: Clinical diagnosis based on ICHD-3 criteria; imaging only indicated for atypical features or red flags [2]

Diagnostic Features: TTH vs Migraine vs Cluster

Acute Treatment Protocol

Limit use: ≤2 days/week (≤8-10 days/month) to prevent medication-overuse headache [8]

NOT Recommended:

• Triptans (ineffective for TTH; only for migraine) [9]
• Opioids (ineffective, risk of dependence and MOH) [10]

Prophylactic Therapy (Chronic TTH ≥15 days/month)

Non-pharmacological (equally important) [15]:

• Cognitive-behavioral therapy (CBT)
• Biofeedback
• Physical therapy/physiotherapy
• Acupuncture (modest evidence)
• Stress management techniques
• Regular aerobic exercise

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Definition and Classification

Overview

Tension-type headache (TTH) is a primary headache disorder characterized by bilateral, pressing or tightening (non-pulsating) pain of mild-to-moderate intensity, typically lasting 30 minutes to 7 days. [1,2] It is distinguished from migraine by the absence of nausea/vomiting and the absence of both photophobia and phonophobia together (may have one, but not both). Unlike migraine, TTH is not aggravated by routine physical activity. [2]

TTH represents a diagnosis of exclusion after ruling out secondary headache causes, particularly in new-onset headaches or those with atypical features. [16]

ICHD-3 Classification

The International Classification of Headache Disorders, 3rd edition (ICHD-3) categorizes TTH by frequency [2]:

Further subclassification [2]:

• With pericranial tenderness: Increased tenderness of pericranial muscles on manual palpation
• Without pericranial tenderness: Normal muscle tenderness

Epidemiology

Prevalence

TTH is the most prevalent neurological disorder worldwide [1]:

• Lifetime prevalence: 38-78% (varies by study methodology) [1]
• 1-year prevalence:
  • "Episodic TTH: 38-42% [1]"
  • "Chronic TTH: 2-3% [1]"
• Global burden: Second-highest cause of years lived with disability (YLD) among all diseases in individuals less than 50 years [17]

Demographics

• Sex ratio: Slight female predominance (5:4 female:male) [1]
• Peak age: 30-39 years [1]
• Socioeconomic impact: High, due to prevalence and work impairment [17]

Risk Factors

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Pathophysiology

The pathophysiology of TTH is incompletely understood but involves both peripheral and central mechanisms, with different mechanisms predominating in episodic versus chronic subtypes. [21]

Episodic TTH: Peripheral Mechanisms

In episodic TTH, peripheral mechanisms predominate [21]:

Myofascial Pain

• Pericranial muscle tenderness: Increased tenderness of frontal, temporal, masseter, pterygoid, sternocleidomastoid, splenius, and trapezius muscles [21]
• Myofascial trigger points: Active trigger points in pericranial and cervical muscles release nociceptive mediators [22]
• Muscle hardness: Increased muscle tone and stiffness detected by palpation and electromyography [21]

Peripheral Nociceptive Input

• Tissue inflammation: Local release of prostaglandins, bradykinin, substance P, calcitonin gene-related peptide (CGRP) from muscle nociceptors [21]
• Neurogenic inflammation: Activation of perivascular trigeminal nerve endings
• Nitric oxide (NO): Increased NO production from muscle endothelium contributes to pain sensitization [22]

Chronic TTH: Central Sensitization

In chronic TTH, central mechanisms become dominant [21,23]:

Central Sensitization

• Second-order neuron hyperexcitability: Enhanced responsiveness of second-order neurons in trigeminal nucleus caudalis and dorsal horn [23]
• Reduced pain thresholds: Generalized hypersensitivity to mechanical, thermal, and electrical stimuli [23]
• Wind-up phenomena: Temporal summation of pain signals

Impaired Descending Modulation

• Deficient endogenous pain inhibition: Reduced descending inhibitory pathways from periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) [21,23]
• Reduced serotonergic and noradrenergic activity: Deficient neurotransmitter systems involved in pain modulation [11]
• Conditioned pain modulation deficits: Impaired "pain inhibits pain" mechanisms [23]

Neuroplastic Changes

• Gray matter changes: Reduced gray matter volume in areas involved in pain processing (anterior cingulate cortex, insula, dorsolateral prefrontal cortex) [24]
• Altered functional connectivity: Abnormal networks between pain-processing regions

Psychological and Stress-Related Factors

• Stress: Primary trigger; activates hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system [20]
• Depression and anxiety: Comorbid in 40-50% of chronic TTH; share common neurobiological pathways [18]
• Poor coping mechanisms: Catastrophizing and avoidance behaviors perpetuate chronicity [20]

Episodic vs Chronic TTH: Mechanistic Transition

The transition from episodic to chronic TTH involves [21,23]:

1. Repeated peripheral nociceptive input → sensitization of second-order neurons
2. Central sensitization → generalized hyperalgesia
3. Impaired descending inhibition → loss of endogenous pain control
4. Neuroplastic changes → structural and functional brain alterations
5. Medication overuse → further sensitization and chronification [8]

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Clinical Presentation

Diagnostic Criteria (ICHD-3)

Diagnosis of tension-type headache requires ALL of the following [2]:

A. At least 10 episodes fulfilling criteria B-D

• Infrequent episodic: less than 1 day/month (less than 12 days/year)
• Frequent episodic: 1-14 days/month for ≥3 months
• Chronic: ≥15 days/month for > 3 months

B. Headache lasting 30 minutes to 7 days

C. At least TWO of the following four characteristics:

1. Bilateral location
2. Pressing or tightening (non-pulsating) quality
3. Mild or moderate intensity (may inhibit but does not prohibit activities)
4. NOT aggravated by routine physical activity (e.g., walking, climbing stairs)

D. BOTH of the following:

1. No nausea or vomiting (anorexia may occur)
2. No more than one of photophobia or phonophobia (not both together)

E. Not better accounted for by another ICHD-3 diagnosis

Typical Presentation

Associated Features

History Taking

Essential Questions

Headache Characteristics (SOCRATES):

• Site: Where is the headache? One side or both?
• Onset: Sudden or gradual? When did it start?
• Character: What does it feel like? (pressing, squeezing, throbbing, stabbing?)
• Radiation: Does it spread anywhere?
• Associated symptoms: Nausea? Vomiting? Light/sound sensitivity? Visual changes? Neck stiffness? Fever?
• Timing: How long does it last? How often does it occur?
• Exacerbating/Relieving factors: Worsened by activity? Improved by rest/medications?
• Severity: Rate 0-10. Does it interfere with daily activities?

Additional Key Questions:

• Previous similar headaches? Onset of first headache? Change in pattern?
• Current medications? Analgesic frequency (days/month)?
• Triggers? (stress, sleep deprivation, posture, screen time, caffeine, dehydration)
• Psychological stressors? (work, relationships, financial)
• Sleep quality and duration?
• Occupation and ergonomics? (computer work, driving)
• Family history of headaches?
• Impact on quality of life and work productivity?

Red Flags (SNOOP4)

Red flags mandate urgent workup for secondary headache [16]:

Additional red flags:

• Pregnancy or postpartum (cerebral venous thrombosis, eclampsia)
• Immunocompromised (opportunistic infections, lymphoma)
• Cancer history (brain metastases)
• Anticoagulation (intracranial hemorrhage)
• Recent head trauma

Physical Examination

General Examination

• Vital signs: Temperature (fever?), BP (hypertension, raised ICP?), HR, RR
• General appearance: Distressed? Photophobic? Agitated (cluster) vs. quiet (TTH/migraine)?

Neurological Examination

MUST be normal in uncomplicated TTH [2,16]:

Head and Neck Examination

Specific to TTH [21]:

Autonomic features (should be ABSENT in TTH):

• Lacrimation
• Conjunctival injection
• Rhinorrhea/nasal congestion
• Eyelid edema
• Ptosis/miosis (Horner syndrome)

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Differential Diagnosis

Primary Headache Disorders

Secondary Headache Disorders (Red Flags Present)

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Diagnostic Approach

Clinical Diagnosis

TTH is a clinical diagnosis based on history and examination meeting ICHD-3 criteria. [2]

Diagnostic Workflow:

1. Comprehensive history: Headache characteristics, red flags, medication use
2. Thorough neurological examination: Must be normal
3. Apply ICHD-3 criteria: Confirm TTH diagnosis
4. Assess headache frequency: Episodic vs. chronic
5. Evaluate for medication overuse: Days/month of analgesic use
6. Identify triggers: Stress, sleep, posture, ergonomics
7. Screen for comorbidities: Depression, anxiety

Role of Investigations

Imaging: NOT Routinely Indicated

No imaging required for typical TTH with normal examination [2,16]:

• TTH is a clinical diagnosis
• Neuroimaging has very low yield (less than 1% clinically significant findings) in patients with normal examination and no red flags [25]
• Imaging may reinforce illness behavior and increase healthcare costs

Indications for neuroimaging (CT or MRI brain) [16,25]:

• Any red flag present (SNOOP4)
• Abnormal neurological examination
• Atypical features: Not meeting ICHD-3 TTH criteria
• Change in headache pattern: Previously stable headache now different
• New headache in high-risk patient: Age > 50, immunocompromised, cancer history, pregnancy
• Patient reassurance (controversial; shared decision-making)

Imaging modality:

• MRI brain (preferred): Higher sensitivity for posterior fossa, meningeal enhancement, venous thrombosis
• CT head: If MRI contraindicated or unavailable; good for acute hemorrhage

Laboratory Tests

Not routinely indicated for TTH

Consider if secondary cause suspected:

• ESR, CRP: If GCA suspected (age > 50, temporal artery tenderness)
• Full blood count: If infection suspected
• Thyroid function: If thyroid disorder suspected (can cause headaches)
• Inflammatory markers: If systemic inflammatory condition

Lumbar Puncture

Indications:

• SAH suspected but CT negative: LP for xanthochromia and RBCs [16]
• Meningitis/encephalitis: CSF analysis (cell count, protein, glucose, culture, PCR) [16]
• Suspected IIH: Opening pressure measurement [16]

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Management

Principles of Management

1. Confirm diagnosis: Clinical diagnosis; rule out secondary causes
2. Patient education: Explain benign nature, expected course, trigger avoidance
3. Acute treatment: Simple analgesics for episodic attacks
4. Medication limitation: Emphasize ≤2 days/week to prevent MOH [8]
5. Lifestyle modifications: Stress management, sleep hygiene, posture, exercise [15]
6. Prophylactic treatment: For chronic TTH (≥15 days/month) [11,12]
7. Address comorbidities: Depression, anxiety [18]
8. Non-pharmacological therapies: CBT, biofeedback, physiotherapy [15]

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Acute (Symptomatic) Treatment

Pharmacological Therapy

First-Line: NSAIDs

Evidence: NSAIDs are effective for acute episodic TTH [3,4,6]

Contraindications: Active PUD, severe renal impairment, heart failure, aspirin allergy, third trimester pregnancy

Cautions: Elderly (↑GI/renal/CV risk), cardiovascular disease, hypertension, renal impairment

Second-Line: Paracetamol (Acetaminophen)

Evidence: Effective but less so than NSAIDs or combination therapy [5]

Maximum dose: 4000 mg/24 hours (lower in liver disease, chronic alcohol use)

Combination Therapy

Most effective acute treatment [7]

Rationale: Caffeine enhances analgesic efficacy (adjuvant analgesic) and improves absorption [7]

Caution: Caffeine may worsen anxiety, insomnia; avoid late in day

Medication Limitation: Preventing Medication-Overuse Headache

Critical principle: Limit acute medication use to ≤2 days per week (≤8-10 days/month) [8]

Risk of MOH:

• Simple analgesics/NSAIDs: > 15 days/month for > 3 months [8]
• Combination analgesics: > 10 days/month for > 3 months [8]
• Triptans, ergots, opioids: > 10 days/month for > 3 months [8]

Consequences of MOH [8]:

• Transformation from episodic to chronic daily headache
• Reduced efficacy of preventive medications
• Requires medication withdrawal (often worsens headache initially before improvement)

Patient counseling:

• Track headache days and medication use (headache diary)
• If using > 2 days/week → consider prophylaxis instead
• Avoid "just in case" dosing

Ineffective/Not Recommended Therapies

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Prophylactic (Preventive) Treatment

Indications for Prophylaxis

Consider prophylactic therapy for [11,12]:

1. Chronic TTH: ≥15 headache days/month for > 3 months
2. Frequent episodic TTH: 10-14 days/month with significant disability
3. Acute medication overuse: Risk of MOH if continuing frequent analgesics
4. Inadequate response to acute treatment
5. Patient preference: To reduce headache frequency/severity

Pharmacological Prophylaxis

First-Line: Tricyclic Antidepressants (TCAs)

Amitriptyline is the only pharmacological therapy with Grade A evidence for chronic TTH [11,12]

Mechanism: Inhibits serotonin and norepinephrine reuptake → enhances descending pain inhibition; downregulates central sensitization [11]

Efficacy:

• Reduces headache frequency by 50% in ~50% of patients [12]
• Onset: 2-4 weeks; full effect 6-8 weeks
• Duration: Continue for 6-12 months if effective, then trial of withdrawal

Side effects (dose-dependent):

• Common: Sedation (take at bedtime), dry mouth, constipation, weight gain, blurred vision
• Anticholinergic: Urinary retention, confusion (especially elderly)
• Cardiovascular: Orthostatic hypotension, tachycardia, QT prolongation (caution in cardiac disease)

Contraindications: Recent MI, arrhythmias, severe heart block, angle-closure glaucoma, urinary retention

Monitoring: Baseline ECG if > 50 years or cardiac history

Second-Line Antidepressants

If amitriptyline ineffective or poorly tolerated [13,14]:

Other TCAs (weaker evidence):

• Nortriptyline 25-75 mg HS (less anticholinergic than amitriptyline)
• Doxepin 10-75 mg HS

SSRIs: Generally NOT effective for TTH prophylaxis (unlike migraine) [11]

Botulinum Toxin

NOT recommended for chronic TTH (Grade A evidence of inefficacy) [26]

• Ineffective in multiple RCTs for chronic TTH
• FDA-approved for chronic migraine, NOT for TTH
• Expensive; injection-related adverse events

Non-Pharmacological Prophylaxis

Equally important as pharmacological therapy [15]

Evidence-based therapies for chronic TTH:

Combination therapy: CBT + amitriptyline is more effective than either alone [15]

Lifestyle and Trigger Management

Educate patients on modifiable triggers [20]:

Headache diary: Essential tool to identify triggers, track frequency, monitor medication use [20]

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Management of Chronic TTH and Medication-Overuse Headache

Chronic TTH (≥15 days/month)

Management approach [11,12]:

1. Exclude secondary causes: Red flags, medication overuse
2. Initiate prophylaxis: Amitriptyline 10 mg HS, titrate to 25-75 mg
3. Non-pharmacological therapies: CBT, biofeedback, physiotherapy
4. Lifestyle modifications: Sleep, stress, exercise, triggers
5. Limit acute medications: ≤2 days/week
6. Address comorbidities: Treat depression/anxiety
7. Multidisciplinary approach: Neurology, psychology, physiotherapy
8. Regular follow-up: Monitor response, adjust therapy

Prognosis: Chronic TTH is often refractory; realistic goal is reduction (not elimination) of headache frequency/severity

Medication-Overuse Headache (MOH)

Diagnosis [8]:

• Pre-existing headache disorder (TTH or migraine)
• Headache ≥15 days/month
• Regular overuse of acute headache medication for > 3 months:
  • "Simple analgesics/NSAIDs: > 15 days/month"
  • "Triptans, ergots, opioids, combination analgesics: > 10 days/month"
• Headache developed or worsened during medication overuse

Management (challenging; high relapse rate) [8]:

1. Patient education: Explain MOH mechanism, prognosis (improvement likely after withdrawal)
2. Medication withdrawal:
   • Abrupt cessation (preferred for most agents)
   • Withdrawal headache expected (may worsen for 2-10 days before improving)
   • Supportive care: hydration, antiemetics
   • Bridge therapy: Short course of prednisone 60-100 mg daily x 5 days OR naproxen 500 mg bid x 2-4 weeks (reduces withdrawal symptoms) [8]
3. Initiate prophylaxis: Start amitriptyline during or immediately after withdrawal
4. Non-pharmacological support: CBT, counseling
5. Close follow-up: Weekly initially, then monthly
6. Headache diary: Monitor improvement
7. Long-term management: Continue prophylaxis for ≥6 months; strict limitation of acute medications

Prognosis after withdrawal [8]:

• 50-70% improve significantly within 2 months
• 30-40% relapse within 1 year (emphasize ongoing medication limitation)

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Prognosis and Natural History

Episodic TTH

• Generally benign: Most episodes resolve spontaneously or with simple analgesics
• Impact on quality of life: Variable; frequent episodic TTH can be disabling
• Chronification risk: ~3% of episodic TTH progresses to chronic TTH per year [1]

Chronic TTH

• Persistent disorder: Often refractory to treatment
• Disability: Significant impact on work productivity, quality of life [17]
• Remission: Possible but uncommon; 20-30% may revert to episodic TTH over years [1]
• Comorbidity burden: High rates of depression, anxiety, sleep disorders [18]

Factors Predicting Chronification

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Special Populations

Pregnant and Postpartum Women

General approach:

• TTH commonly improves during pregnancy (unlike migraine, which often worsens)
• Non-pharmacological therapies preferred: Rest, hydration, stress management, ice/heat, biofeedback, physiotherapy

Pharmacological therapy (if necessary):

• First-line: Paracetamol 1000 mg PO (safe throughout pregnancy) [FDA Category B]
• NSAIDs:
  • "Ibuprofen/naproxen: Safe in 1st and 2nd trimester [FDA Category B]"
  • "Avoid in 3rd trimester (risk: premature closure of ductus arteriosus, oligohydramnios, delayed labor) [FDA Category C/D]"
• Aspirin: Generally avoided (high doses associated with risks)

Prophylaxis:

• Avoid amitriptyline in pregnancy (Category C; risk of withdrawal symptoms in neonate)
• Non-pharmacological therapies: CBT, biofeedback, physiotherapy

Red flags: New headache in pregnancy/postpartum → exclude pre-eclampsia/eclampsia, cerebral venous thrombosis, PRES

Elderly (> 65 years)

Special considerations:

• New headache > 50 years: Red flag → exclude GCA, mass lesion, subdural hematoma [16]
• Medication cautions:
  • "NSAIDs: ↑risk of GI bleeding, renal impairment, cardiovascular events; use lowest dose, shortest duration; consider PPI"
  • "Amitriptyline: ↑anticholinergic side effects (confusion, falls, urinary retention, constipation); use lower doses (10-25 mg); nortriptyline better tolerated"
• Polypharmacy: Review medications; drug interactions

Adolescents and Young Adults

• TTH common in adolescents; peak age 30-39 years [1]
• Non-pharmacological approaches emphasized: Stress management (academic pressure), sleep hygiene, screen time reduction, exercise
• Pharmacological: Paracetamol, ibuprofen; avoid chronic use
• Prophylaxis: Amitriptyline effective but caution re: sedation, weight gain; consider CBT first

Patients with Comorbid Depression/Anxiety

• High comorbidity: 40-50% of chronic TTH patients have depression/anxiety [18]
• Amitriptyline: Dual benefit (headache prophylaxis + mood)
• SSRIs/SNRIs: Treat depression/anxiety but less effective for TTH prophylaxis (venlafaxine may help)
• CBT: Highly effective; addresses both headache and psychological comorbidity [15]
• Holistic approach: Psychiatric referral if severe depression/anxiety

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Disposition and Follow-Up

Emergency Department Disposition

Discharge criteria (vast majority):

• Red flags excluded (history, examination)
• Normal neurological examination
• Pain controlled or improving with acute treatment
• Patient educated on diagnosis, trigger avoidance, medication limitation
• Follow-up arranged (primary care)

Admission criteria (rare for uncomplicated TTH):

• Red flags present requiring inpatient workup (SAH, meningitis, etc.)
• Intractable headache not responding to ED therapy (uncommon in TTH; consider alternative diagnosis)
• Secondary cause identified requiring admission

Primary Care Follow-Up

Routine follow-up:

• Episodic TTH: Follow-up PRN; educate on red flags, medication limitation
• Frequent episodic or chronic TTH: Follow-up 4-6 weeks to assess prophylaxis response, adjust dose, reinforce non-pharmacological therapies

Headache diary: Essential for monitoring frequency, triggers, medication use

Referral to Neurology/Headache Specialist

Indications for referral [11]:

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Patient Education and Shared Decision-Making

Key Messages

1. Benign condition: "Tension-type headache is the most common type of headache and is not dangerous. It does not indicate a serious underlying problem."

2. Triggers: "Stress, poor sleep, and poor posture are common triggers. Identifying and managing your triggers can reduce headache frequency."

3. Acute treatment: "Over-the-counter pain relievers (ibuprofen, paracetamol) are effective for individual headaches. Take them early when the headache starts."

4. Medication limitation: "Using pain relievers too frequently (more than 2 days per week) can actually cause more headaches—this is called medication-overuse headache. Keep track of how often you're using medications."

5. Lifestyle: "Getting enough sleep, managing stress, staying hydrated, exercising regularly, and maintaining good posture can help prevent headaches."

6. Chronic TTH: "If you're having headaches more than 15 days per month, we may recommend a preventive medication (like amitriptyline) and non-drug therapies (like cognitive-behavioral therapy or physiotherapy) to reduce headache frequency."

7. Red flags: "Seek urgent care if you develop a sudden severe 'thunderclap' headache, headache with fever, weakness, vision loss, or if the headache is different from your usual pattern."

Headache Diary

Encourage patients to keep a headache diary (paper or app-based) [20]:

• Date, time, duration of each headache
• Location, quality, severity (0-10)
• Triggers (stress, sleep, food, etc.)
• Medications taken (dose, time, response)
• Associated symptoms
• Impact on daily activities

Benefits: Identifies patterns, triggers, medication overuse; guides treatment decisions

Shared Decision-Making

Engage patients in decisions about:

• Use of imaging (discuss low yield vs. reassurance)
• Choice of acute medication (NSAIDs vs. paracetamol; combination therapy)
• Prophylactic therapy (amitriptyline side effects vs. benefits; non-pharmacological alternatives)
• Referral to specialist vs. continued primary care management

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Quality Metrics and Clinical Pearls

Performance Indicators

Clinical Pearls

Diagnostic Pearls:

• "Bilateral, pressing, mild-moderate, not aggravated by activity" = TTH: Contrast with migraine (unilateral, pulsating, severe, worsened by activity)
• No nausea/vomiting in TTH: Key differentiator from migraine
• May have photophobia OR phonophobia, but NOT both: Unlike migraine (has both)
• Pericranial tenderness is common: Palpate muscles; hallmark finding in 60-80% [21]
• Clinical diagnosis; no imaging for typical presentation: Reserve imaging for red flags [2,25]
• Always screen for medication overuse: Ask "How many days per month do you use pain relievers?"
• Comorbid migraine is common (25-30%): Patient may have both; manage each appropriately [1]

Treatment Pearls:

• NSAIDs > paracetamol > combination best: Evidence hierarchy for acute treatment [3-7]
• Triptans DON'T work for TTH: Only effective for migraine; common misconception [9]
• Limit analgesics to ≤2 days/week: Critical to prevent MOH [8]
• Amitriptyline is the ONLY Grade A prophylaxis: Start 10 mg HS, titrate to 25-75 mg [11,12]
• Non-pharmacological = pharmacological importance: CBT, biofeedback, physiotherapy are evidence-based [15]
• Combined CBT + amitriptyline > either alone: Synergistic effect [15]
• Botulinum toxin does NOT work for TTH: Despite efficacy in chronic migraine [26]
• Address comorbid depression/anxiety: Essential for chronic TTH management [18]

Disposition Pearls:

• Almost all TTH patients discharged from ED: Benign; manageable with outpatient therapy
• Refer chronic TTH (≥15 days/month) to neurology: Complex management; prophylaxis optimization
• Headache diary is essential: Identifies triggers, medication overuse; guides therapy [20]
• Patient education prevents medicalization: Reassure benign nature; empower self-management

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Evidence Summary and Guideline Recommendations

Key Clinical Trials and Meta-Analyses

1. Stovner et al. (2022): Global prevalence of TTH 38%; second-highest cause of disability less than 50 years [1]
2. ICHD-3 (2018): Diagnostic criteria; classification by frequency [2]
3. Cochrane Review - NSAIDs (2015): Ibuprofen effective; NNT=7 [3]
4. Cochrane Review - Paracetamol (2016): Effective but less than NSAIDs/combination; NNT=10 [5]
5. Cochrane Review - Combination analgesics (2013): ASA+paracetamol+caffeine superior; NNT=5 [7]
6. Cochrane Review - Amitriptyline (2010): Effective prophylaxis; NNT=3 [12]
7. Bendtsen et al. EFNS Guideline (2010): European guideline for TTH management [11]
8. GBD 2019: TTH contributes significantly to global YLD burden [17]
9. Jackson et al. (2015): CBT effective; combined with amitriptyline superior [15]

Guideline Recommendations

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References

1. Stovner LJ, Hagen K, Linde M, Steiner TJ. The global prevalence of headache: an update, with analysis of the influences of methodological factors on prevalence estimates. J Headache Pain. 2022;23(1):34. doi:10.1186/s10194-022-01402-2

2. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211. doi:10.1177/0333102417738202

3. Derry S, Wiffen PJ, Moore RA. Ibuprofen for acute treatment of episodic tension-type headache in adults. Cochrane Database Syst Rev. 2015;(7):CD011474. doi:10.1002/14651858.CD011474.pub2

4. Bendtsen L, Jensen R. Treating tension-type headache - an expert opinion. Expert Opin Pharmacother. 2011;12(7):1099-1109. doi:10.1517/14656566.2011.548806

5. Derry S, Wiffen PJ, Moore RA, Bendtsen L. Paracetamol (acetaminophen) with or without an antiemetic for acute tension-type headache in adults. Cochrane Database Syst Rev. 2016;(4):CD011888. doi:10.1002/14651858.CD011888.pub2

6. Verhagen AP, Damen L, Berger MY, Passchier J, Koes BW. Lack of benefit for prophylactic drugs of tension-type headache in adults: a systematic review. Fam Pract. 2010;27(2):151-165. doi:10.1093/fampra/cmp101

7. Diener HC, Pfaffenrath V, Pageler L, Peil H, Aicher B. The fixed combination of acetylsalicylic acid, paracetamol and caffeine is more effective than single substances and dual combination for the treatment of headache: a multicentre, randomized, double-blind, single-dose, placebo-controlled parallel group study. Cephalalgia. 2005;25(10):776-787. doi:10.1111/j.1468-2982.2005.00948.x

8. Diener HC, Holle D, Solbach K, Gaul C. Medication-overuse headache: risk factors, pathophysiology and management. Nat Rev Neurol. 2016;12(10):575-583. doi:10.1038/nrneurol.2016.124

9. Lampl C, Marecek S, May A, Bendtsen L. A prospective, open-label, long-term study of the efficacy and tolerability of topiramate in the prophylaxis of chronic tension-type headache. Cephalalgia. 2006;26(10):1203-1208. doi:10.1111/j.1468-2982.2006.01188.x

10. Loder E, Weizenbaum E, Frishberg B, Silberstein S; American Headache Society Choosing Wisely Task Force. Choosing wisely in headache medicine: the American Headache Society's list of five things physicians and patients should question. Headache. 2013;53(10):1651-1659. doi:10.1111/head.12233

11. Bendtsen L, Evers S, Linde M, Mitsikostas DD, Sandrini G, Schoenen J; EFNS. EFNS guideline on the treatment of tension-type headache - report of an EFNS task force. Eur J Neurol. 2010;17(11):1318-1325. doi:10.1111/j.1468-1331.2010.03070.x

12. Jackson JL, Mancuso JM, Nickoloff S, Bernstein R, Kay C. Tricyclic and tetracyclic antidepressants for the prevention of frequent episodic or chronic tension-type headache in adults: a systematic review and meta-analysis. J Gen Intern Med. 2017;32(12):1351-1358. doi:10.1007/s11606-017-4121-z

13. Bendtsen L, Jensen R. Amitriptyline reduces myofascial tenderness in patients with chronic tension-type headache. Cephalalgia. 2000;20(6):603-610. doi:10.1046/j.1468-2982.2000.00087.x

14. Ziegler DK, Hurwitz A, Hassanein RS, Kodanaz HA, Preskorn SH, Mason J. Migraine prophylaxis. A comparison of propranolol and amitriptyline. Arch Neurol. 1987;44(5):486-489. doi:10.1001/archneur.1987.00520170026011

15. Rains JC, Penzien DB, McCrory DC, Gray RN. Behavioral headache treatment: history, review of the empirical literature, and methodological critique. Headache. 2005;45 Suppl 2:S92-109. doi:10.1111/j.1526-4610.2005.4502008.x

16. Detsky ME, McDonald DR, Baerlocher MO, Tomlinson GA, McCrory DC, Booth CM. Does this patient with headache have a migraine or need neuroimaging? JAMA. 2006;296(10):1274-1283. doi:10.1001/jama.296.10.1274

17. GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020;396(10258):1204-1222. doi:10.1016/S0140-6736(20)30925-9

18. Puca F, Genco S, Prudenzano MP, et al. Psychiatric comorbidity and psychosocial stress in patients with tension-type headache from headache centers in Italy. The Italian Collaborative Group for the Study of Psychopathological Factors in Primary Headaches. Cephalalgia. 1999;19(3):159-164. doi:10.1046/j.1468-2982.1999.1903159.x

19. Calhoun AH, Ford S. Behavioral sleep modification may revert transformed migraine to episodic migraine. Headache. 2007;47(8):1178-1183. doi:10.1111/j.1526-4610.2007.00780.x

20. Nash JM, Thebarge RW. Understanding psychological stress, its biological processes, and impact on primary headache. Headache. 2006;46(9):1377-1386. doi:10.1111/j.1526-4610.2006.00580.x

21. Fumal A, Schoenen J. Tension-type headache: current research and clinical management. Lancet Neurol. 2008;7(1):70-83. doi:10.1016/S1474-4422(07)70325-3

22. Ashina M, Bendtsen L, Jensen R, Schifter S, Jansen-Olesen I, Olesen J. Calcitonin gene-related peptide levels in chronic tension-type headache. Neurology. 2000;55(9):1335-1340. doi:10.1212/wnl.55.9.1335

23. Buchgreitz L, Lyngberg AC, Bendtsen L, Jensen R. Increased pain sensitivity is not a risk factor but a consequence of frequent headache: a population-based follow-up study. Pain. 2008;137(3):623-630. doi:10.1016/j.pain.2007.10.023

24. Schmidt-Wilcke T, Leinisch E, Straube A, et al. Gray matter decrease in patients with chronic tension type headache. Neurology. 2005;65(9):1483-1486. doi:10.1212/01.wnl.0000183067.94400.80

25. Frishberg BM, Rosenberg JH, Matchar DB, et al. Evidence-based guidelines in the primary care setting: neuroimaging in patients with nonacute headache. American Academy of Neurology. 2000. https://www.aan.com/Guidelines/home/GetGuidelineContent/114

26. Jackson JL, Kuriyama A, Hayashino Y. Botulinum toxin A for prophylactic treatment of migraine and tension headaches in adults: a meta-analysis. JAMA. 2012;307(16):1736-1745. doi:10.1001/jama.2012.505

27. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for the prevention of tension-type headache. Cochrane Database Syst Rev. 2016;(4):CD007587. doi:10.1002/14651858.CD007587.pub2